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InternalMed_Harrison. FIGURE 270e-25 Acute left anterior descending artery distribution myocardial infarction at end systole showing akinetic region (arrows). PART 10 Disorders of the Cardiovascular System Some patients demonstrate progressive left ventricular dilatation and dysfunction, known as cardiac remodeling, after myocardial infarction. Assessment of cardiac function and regional wall motion is useful in the follow-up period, generally between 1 and 6 months following infarction. The persistence of left ventricular systolic dysfunction following infarction is used to determine the type of therapy (e.g., angiotensin-converting enzyme inhibitors or angiotensin receptor blockers are typically used in patients with systolic dysfunction following myocardial infarction).


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InternalMed_Harrison. In patients with acute or subacute myocardial infarction, investigation of residual ischemia and/or viability is occasionally an important clinical question, especially among those with recurrent symptoms after myocardial infarction (Fig. 270e-26). All cardiac imaging techniques can provide information regarding myocardial viability and ischemia. In the absence of definitive trials offering head-to-head comparisons between techniques in large series of patients, uncertainty persists concerning the relative accuracies of each method for predicting functional and prognostic benefit after revascularization. Thus, one should exercise caution in the interpretation of the relative diagnostic accuracy of each imaging technology. Nevertheless, the available data suggest that radionuclide imaging, especially PET, is highly sensitive, with higher negative predictive value than dobutamine echocardiography. In contrast, dobutamine echocardiography tends to be associated with higher specificity


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InternalMed_Harrison. especially PET, is highly sensitive, with higher negative predictive value than dobutamine echocardiography. In contrast, dobutamine echocardiography tends to be associated with higher specificity and positive predictive accuracy than the radionuclide imaging methods. The experience with CMR suggests that it offers similar predictive accuracies as those seen with dobutamine echocardiography.


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InternalMed_Harrison. Role of Imaging in New-Onset Heart Failure Echocardiography is usually a first-line test in patients presenting with new-onset heart failure. As discussed above, this test provides a direct assessment of ventricular function and can help distinguish patients with reduced ejection fraction from those with preserved ejection fraction. In addition, it provides additional structural information including an assessment of valves, myocardium, and pericardium. Although coronary angiography is commonly performed in patients with reduced ejection fraction, the determination of heart failure etiology in an individual patient may be difficult even if angiographically obstructive CAD is present. Indeed, patients with heart failure and no angiographic CAD may have typical angina or regional wall motion abnormalities on noninvasive imaging, whereas patients with angiographically obstructive CAD may have no symptoms of angina


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InternalMed_Harrison. FIGURE 270e-26 Examples of myocardial viability patterns obtained with cardiac magnetic resonance imaging (MRI) and positron emission tomography (PET) in three different patients with coronary artery disease. The top panel demonstrates extensive late gadolinium enhancement (bright white areas) involving the anterior, anteroseptal, and apical left ventricular walls (arrows), consistent with myocardial scar and nonviable myocardium. The lower left panel demonstrates rubidium-82 myocardial perfusion and 18F-fluorodeoxyglucose (FDG) images showing a large and severe perfusion defect in the anterior, anterolateral, and apical walls, indicating preserved glucose metabolism (so-called perfusion-metabolic mismatch) consistent with viable myocardium. The right lower panel shows similar PET images demonstrating concordant reduction in perfusion and metabolism (so called perfusion-metabolic match) in the lateral wall, consistent with nonviable myocardium.


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InternalMed_Harrison. FIGURE 270e-27 A case of cardiac amyloidosis. Note on this late gadolinium enhancement image that there were multiple foci of gadolinium accumulation in the left ventricle (LV) myocardium (red arrows), as well as the left atrial (LA) walls (blue arrows). The LV walls were markedly increased in thickness, and both atria were dilated, consistent with a restrictive cardiac morphology. The blood pool signal was diminished after contrast injection, which was consistent with high burden of amyloid disease in other organs that causes gadolinium concentration in the blood to rapidly go down. RA, right atrium; RV, right ventricle.


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InternalMed_Harrison. or history of myocardial infarction. Thus, the appropriate classification for any given patient is not always clear, and it often requires the complementary information of coronary angiography and noninvasive imaging. Stress radionuclide imaging and echocardiography can be helpful in delineating the extent and severity of inducible myocardial ischemia and viability. Multiparametric CMR can be quite helpful in the differential diagnosis of heart failure etiologies. Apart from quantifying left and right ventricular volumes and function, CMR can provide information about myocardial ischemia and scar. The pattern of LGE helps differentiate infarction (typically starting in the subendocardium and involving a coronary territory) from other forms of infiltrative or inflammatory cardiomyopathies (typically involving the midor subepicardial layers without following a coronary distribution) (Fig. 270e-27). In addition, it can assess the presence of myocardial edema (e.g., myocarditis)


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InternalMed_Harrison. (typically involving the midor subepicardial layers without following a coronary distribution) (Fig. 270e-27). In addition, it can assess the presence of myocardial edema (e.g., myocarditis) cardiomyopathy has variable degree of increased ventricular thickness, 270e-21 and often is seen to have outflow obstruction and intense LGE in regions with marked hypertrophy (Fig. 270e-28). CMR also can quantify myocardial iron content in patients at risk of iron-overload cardiomyopathy (Video 270e-7).


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InternalMed_Harrison. PET metabolic imaging has a complementary role in the evaluation of inflammatory cardiomyopathies, especially sarcoidosis. In patients with suspected cardiac sarcoidosis, the presence of focal and/or diffuse glucose uptake can help identify areas of active sarcoidosis. In addition, for patients undergoing immunosuppressive therapy, PET is frequently used to monitor therapeutic response (Fig. 270e-29). In patients with ischemic cardiomyopathy, radionuclide imaging in general and PET in particular are frequently used to quantify the presence and extent of myocardial ischemia and viability to assist with clinical decision making related to myocardial revascularization (Fig. 270e-26).


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InternalMed_Harrison. Therapies used to treat cancer can adversely affect the cardiovascular system. As the efficacy of cancer treatment and survival improve, many patients are presenting with late adverse consequences from chemotherapy and/or radiation therapy on cardiovascular function. Thus, the morbidity and mortality from late cardiovascular complications threaten to offset the early gains in cancer survival, especially among children and young adults. Early recognition and treatment of cardiomyocyte injury are critical for successful application of preventative therapies, but difficult because the adverse effects on cardiac function are a relatively late manifestation after exposure to anticancer therapy.


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InternalMed_Harrison. The accepted standard for clinical diagnosis of cardiotoxicity is defined as a >5% reduction in LVEF to <55% with symptoms of heart failure, or a >10% drop in LVEF to <55% in patients who are asymptomatic. Thus, noninvasive imaging plays a major role in diagnosing and monitoring for cardiac toxicity in patients undergoing cancer treatment. Radionuclide angiography has been the technique of choice


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InternalMed_Harrison. CHAPTER 270e Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging and quantify myocardial iron deposi-FIGURE 270e-28 This figure demonstrates three pulse sequence techniques by cardiac magtion that can potentially lead to cardiac netic resonance that are often used to assess patients with hypertrophic cardiomyopathy, all toxicity. Infiltrative cardiomyopathy such displayed in the mid short-axis scan plane. The center panel demonstrates that the left ventricle as amyloidosis typically has a restrictive (LV) was markedly thickened in its wall thickness especially in the LV septum (red arrows). This findcardiomyopathy pattern (bilateral atrial ing was matched by marked regions of late gadolinium enhancement (LGE), which was consisenlargement and biventricular increased tent with fibrosis in these segments (right panel, white arrows). The left panel was cine myocardial wall thickness). CMR of patients with car-tagging in the


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InternalMed_Harrison. and biventricular increased tent with fibrosis in these segments (right panel, white arrows). The left panel was cine myocardial wall thickness). CMR of patients with car-tagging in the same slice plane. Myocardial tagging is used to assess the normal intramyocardial diac amyloidosis often also demonstrates strain by assessing distortion of the myocardial grids during systole. In this case, despite normal-a characteristic pattern of diffuse endo-appearing systolic radial wall thickening, the myocardial strain as assessed by the distortion of cardial infiltration of the left ventricle grids was markedly reduced (left panel, white arrows). This finding is consistent with substantial and the atria (Fig. 270e-27). Hypertrophic myofibril disarray in the anterior and anteroseptal segments in this patient. RV, right ventricle.


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InternalMed_Harrison. PART 10 Disorders of the Cardiovascular System FIGURE 270e-29 Representative cardiac magnetic resonance (CMR; top panel) and positron emission tomography (PET; lower panel) images from a 45-year-old male presenting with complete heart block. The CMR images demonstrate extensive late gadolinium enhance-ment in the subepicardial left ventricular (LV) anterior and anteroseptal walls and also in the right ventricular (RV) free wall (arrows). The PET images demonstrate extensive fluorodeoxyglucose uptake in the same areas, most consistent with active inflammation due to sarcoidosis. for quite some time. However, this is rapidly changing, and echocardiography now plays a major role in this application.


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InternalMed_Harrison. for quite some time. However, this is rapidly changing, and echocardiography now plays a major role in this application. Recently, more novel imaging approaches have been advocated, including deformation imaging with echocardiography and fibrosis imaging with CMR. These techniques have shown promising results in experimental animal models and in humans. In addition, there are also proof-of-concept studies in animal models using molecular imaging approaches targeting the mechanisms of cardiac toxicity (e.g., apoptosis and oxidant stress), which can presumably provide the earliest signs of the off-target effects of these therapies. However, all of these techniques are currently considered experimental.


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InternalMed_Harrison. The fibroelastic pericardial sac surrounding the heart consists of a visceral, or epicardial, layer and a parietal layer, with a generally small amount of pericardial fluid in between layers. The pericardium is generally quite pliable and moves easily with the heart during contraction and relaxation. Abnormalities of the pericardium can affect cardiac function primarily by impairing the heart’s ability to fill. Inflammation of the pericardium can lead to an accumulation of fluid between the two layers, or pericardial effusion, which can be visualized by echocardiography, CMR, or CT. Other reasons for accumulation of pericardial fluid include infection, malignancy, and bleeding into the pericardium. The latter can be the result of catastrophic processes such as trauma, cardiac rupture, perforation in the setting of a cardiac procedure, cardiac surgery, or dissection of the aorta with extension in the pericardium.


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InternalMed_Harrison. Echocardiography remains the initial test of choice for assessing pericardial disease, especially effusions (Fig. 270e-30). Moreover, echocardiography can be useful in evaluating for pericardial constrictive physiology, in which a thick noncompliant pericardium impairs cardiac filling. The location, size, and physiologic consequences of accumulated pericardial effusion can generally easily be determined by echocardiography. Pericardial tamponade occurs when enough pericardial fluid accumulates so that the intrapericardial pressure exceeds filling pressures of the heart, generally the right ventricle. The balance between intrapericardial pressure and ventricular pressure is more important than the extent of fluid accumulation. Conditions in which pericardial effusions accumulate over a long period of time, as can be the case in the setting of malignant effusions, can lead to large pericardial fluid accumulations without the classic hemodynamic findings associated with pericardial


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InternalMed_Harrison. a long period of time, as can be the case in the setting of malignant effusions, can lead to large pericardial fluid accumulations without the classic hemodynamic findings associated with pericardial tamponade. In contrast, rapid accumulations of pericardial fluid, such as those that occur due to cardiac rupture or perforation, can lead to tamponade physiology without very large effusions. In patients with suspected pericardial effusion or tamponade, echocardiography can usually be performed rapidly, at the bedside, and even by operators with limited skill. The distance from the parietal to the visceral pericardial layer can be measured, and when this exceeds approximately 1 cm, an effusion is considered significant. Echocardiographic features suggestive of tamponade include diastolic collapse of the right ventricular free wall, suggestive of pericardial pressures that exceed right ventricular filling pressures, and Doppler evidence of respiratory flow variation, which is the Doppler


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InternalMed_Harrison. of the right ventricular free wall, suggestive of pericardial pressures that exceed right ventricular filling pressures, and Doppler evidence of respiratory flow variation, which is the Doppler equivalent of pulsus paradoxus. Despite the benefits of echocardiography in suspected pericardial tamponade, the diagnosis of tamponade remains a clinical diagnosis, and other important features, such as patient’s blood pressure in the presence of pulsus paradoxus, needs to be taken into account when considering therapeutic options.


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InternalMed_Harrison. FIGURE 270e-30 Pericardial effusion with tamponade physiology. The right ventricle (arrow) is small and collapsing in end diastole due to increased pericardial pressure.


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InternalMed_Harrison. Chronic inflammation of the pericardium can lead to thickening and potentially calcification of the parietal pericardium, resulting in pericardial constriction in which diastolic filling can be severely impaired. In these cases, filling of the ventricles comes to an abrupt halt when the volume of ventricular filling is impaired by the constricting pericardium. Assessment of pericardial thickness in these patients is important, but it is just as important to note that approximately one in five patients with severe pericardial constriction have no significant pericardial thickening by imaging or at surgery. Thus, a lack of thickened pericardium does not rule out pericardial constriction, and patients’ signs and symptomatology and physiologic evidence of constriction should be assessed independently. Pericardial constriction typically demonstrates marked respiratory changes in diastolic flow on Doppler echocardiography, in contrast to restrictive cardiomyopathy, but substantial overlap


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InternalMed_Harrison. Pericardial constriction typically demonstrates marked respiratory changes in diastolic flow on Doppler echocardiography, in contrast to restrictive cardiomyopathy, but substantial overlap exists. CT and CMR offer tomographic, whole-heart assessment of pericardial thickening and other anatomy abnormalities in pericardial constriction (enlarged atria, vena cavas, pleural and pericardial effusions) (Fig. 270e-31 and Video 270e-8). CMR offers the additional information of pericardial fibrosis and inflammation by LGE imaging, as well as evidence of constrictive physiology (e.g., regional relaxation concordance due to myocardial adhesions, paradoxical septal motion at rest or during Valsalva maneuver).


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InternalMed_Harrison. Echocardiography is usually the modality that first detects the presence of a cardiac mass. Differential diagnoses of an intracardiac mass most often include thrombus, tumor, or vegetation. Given their unrestricted tomographic views and multiplanar three-dimensional imaging, CMR and CT can complement echocardiography by further characterizing the physical features of the cardiac mass. Compared to CT, CMR has the advantage of higher tissue contrast differentiation, more robust cine imaging, and the use of multifaceted techniques within the same imaging session to determine the physiologic characteristics of the mass. Gadolinium contrast enhancement patterns of increased capillary perfusion can help to determine the presence and extent of FIGURE 270e-31 A female patient developed pericardial constriction and right heart failure, secondary to radiation therapy for breast cancer. Note the multiple pericardial adhesions (red arrows).


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InternalMed_Harrison. FIGURE 270e-31 A female patient developed pericardial constriction and right heart failure, secondary to radiation therapy for breast cancer. Note the multiple pericardial adhesions (red arrows). FIGURE 270e-32 Cardiac thrombus (arrow) in an apical aneurysmal region following acute myocardial infarction.


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InternalMed_Harrison. vascularity within the mass, relevant for differentiating tumor from thrombus. Structures that are known to mimic a cardiac mass include (1) anatomic variants, such as the Eustachian valve, Chiari network, crista sagittalis or terminalis, and the right ventricular moderator band, and (2) “pseudotumors,” such as interatrial septal aneurysm, coronary or aortic aneurysm, lipomatous hypertrophy of interatrial septum, hiatal hernia, or a catheter/pacemaker lead. A number of coexisting conditions should raise the likelihood of a cardiac thrombus (Fig. 270e-32), including regional wall motion abnormality from infarction or ventricular aneurysm, atrial fibrillation leading to slow flow in the left atrial appendage, or presence of venous catheters or recent endovascular injury. CMR has the advantage of being able to assess regional wall motion and infarction or ventricular aneurysm in matching scan planes, adjacent to the cardiac thrombus, using cine and LGE imaging, respectively. For


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InternalMed_Harrison. advantage of being able to assess regional wall motion and infarction or ventricular aneurysm in matching scan planes, adjacent to the cardiac thrombus, using cine and LGE imaging, respectively. For ventricular thrombus, gadolinium-enhanced LGE imaging can detect thrombus at a higher sensitivity than echocardiography by depicting high-contrast difference between the dark thrombus and its adjacent structures and by imaging in three dimensions. In addition, mural thrombus does not enhance on first-pass perfusion and often has a characteristic “etched” appearance (black border surrounding a bright center) on LGE imaging, thus providing higher diagnostic specificity than anatomic information alone (Fig. 270e-33). Comparing the signal intensities of a mass before and after contrast injection may confirm the lack of tissue vascularity (i.e., thrombus)


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InternalMed_Harrison. CHAPTER 270e Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging FIGURE 270e-33 Late gadolinium enhancement image of a massive anterior infarction complicated by a dyskinetic left ventricular LV aneurysm and intracavitary thrombus (red asterisk). Disorders of the Cardiovascular System FIGURE 270e-34 A case of a cardiac fibroma. A patient presented with shortness of breath and was found to have a large myocardial mass on echocardiography. Cine cardiac magnetic resonance imaging confirmed the large myocardial mass involving the anterolateral wall. Shortly after gadolinium contrast was injected, the myocardial mass demonstrated intense accumulation of contrast on LGE imaging (right panel, asterisk). This is a case of cardiac fibroma. The patient also has gingival hyperplasia and bifid thoracic ribs, a part of the rare Gorlin’s syndrome.


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InternalMed_Harrison. by the lack of signal enhancement after contrast administration. Like intracardiac thrombus, regions of microvascular obstruction also appear dark, but microvascular obstruction is confined within the myocardium and surrounded by infarction and thus can be differentiated from intracardiac thrombus. CMR imaging for small thrombus in the left atrial appendage is difficult due to slow flow in the atrium and rhythm irregularity from atrial fibrillation, but it may be helpful in cases where transesophageal echocardiography is suboptimal or not feasible.


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InternalMed_Harrison. The majority of cardiac malignancy is metastatic, and metastatic cardiac malignancy is far more common than primary cardiac malignancies; these metastatic involvements of the heart are the result of direct invasion (e.g., lung and breast), lymphatic spread (e.g., lymphomas and melanomas), or hematogenous spread (e.g., renal cell carcinoma). Primary benign cardiac tumors are seen mostly in children and young adults and include atrial myxoma, rhabdomyoma, fibroma, and endocardial fibroelastoma (Fig. 270e-34). Atrial myxomas are often seen as a round or multilobar mass in the left atrium (75%), right atrium (20%), or ventricles or mixed chambers (5%). They typically have inhomogeneous brightness in the center on cine steady-state free precession imaging due to their gelatinous contents and may have a pedunculated attachment to the fossa ovalis. Primary malignant cardiac tumors are extremely rare and include angiosarcoma, fibrosarcoma, rhabdomyosarcoma, and liposarcoma.


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InternalMed_Harrison. Patients with suspected endocarditis often undergo echocardiography for the purpose of identifying vegetations or intramyocardial abscesses. Vegetations are generally highly mobile structures that most typically are attached to valves or present in areas of the heart with turbulent flow. The absence of a vegetation on echocardiography does not rule out endocarditis, because small vegetations below the resolution of the imaging techniques can be present. Echocardiography remains the best technique for assessment of vegetations because its high temporal resolution allows visualization of the typical oscillating motion, although large vegetations can be visualized with other techniques (Fig. 270e-35). The size and location of a vegetation do not necessarily provide any specific information about the type of infection. Abscesses, particularly around the aortic and mitral annuli, are particularly concerning in patients with endocarditis and should be suspected in patients with prolongation


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InternalMed_Harrison. the type of infection. Abscesses, particularly around the aortic and mitral annuli, are particularly concerning in patients with endocarditis and should be suspected in patients with prolongation of cardiac intervals in the setting of endocarditis. Visualization of both vegetations and possible abscesses is best done with transesophageal echocardiography, particularly in patients with prosthetic valves. Indeed, transesophageal echocardiography is the first test of choice in a patient with a mechanical mitral or aortic valve and suspected endocarditis (Fig. 270e-35). Vegetations should be measured because their size has prognostic importance and can be used to decide whether a patient should be taken to surgery.


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InternalMed_Harrison. PET metabolic imaging is emerging as a potentially useful imaging technique to identify the source of infection in patients with prosthetic valves, vascular grafts, and implantable pacemakers/defibrillators, especially in patients in whom echocardiography and/or blood cultures are negative. There is an emerging literature documenting the potential value of macrophage-targeted metabolic imaging with 18F-FDG and PET (Fig. 270e-36). Likewise, FDG PET is also useful to identify vascular inflammation and monitor the response to immunosuppressive therapy (Fig. 270e-37). While a discussion of complex congenital heart disease is beyond the scope of this chapter, a number of common congenital abnormalities are present in adults, and cardiac imaging is essential to diagnosing and managing these conditions. Abnormalities of the interatrial


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InternalMed_Harrison. FIGURE 270e-35 Vegetation on native mitral valve (left panel, arrow). Left atrium (LA) and left ventricle (LV) are indicated. Middle panel shows a vegetation on a mechanical prosthesis (St. Jude) indicated by an arrow; right panel shows vegetation on prosthesis after excision.


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InternalMed_Harrison. FIGURE 270e-36 Representative cross-sectional computed tomography (CT; left), fluorodeoxyglucose (FDG) positron emission tomography (PET; middle), and fused CT and PET (right) images before and after antibiotic treatment in a patient with fever and suspected infection of the stent placed in the descending portion of the aortic arch (arrow) for treatment of aortic coarctation. The FDG images before treatment demonstrate intense glucose uptake within the stent, consistent with inflammation/infection. The lower panel demonstrates significant attenuation of the FDG signal after treatment. (Images courtesy of Dr. Sharmila Dorbala, Brigham and Women’s Hospital.) septum probably represent the most common adult congenital cardiac abnormalities. Patent foramen ovale (PFO) can be identified in almost 25% of patients. In patients with PFO, a one-way flap in the region of the fossa ovalis is normally kept close by the left atrial pressure, which is generally higher than right atrial pressure for


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InternalMed_Harrison. 25% of patients. In patients with PFO, a one-way flap in the region of the fossa ovalis is normally kept close by the left atrial pressure, which is generally higher than right atrial pressure for the majority of the cardiac cycle. However, right-to-left flow through a PFO can occur any time the right atrial pressure exceeds the left atrial pressure, including with maneuvers or conditions in which intrathoracic pressure is increased. The presence of a PFO can increase the likelihood of the paradoxical embolus, and thus the presence of a PFO should be determined in patients with stroke or systemic embolus of unknown etiology. Because the one-way flap of the PFO will be closed during much of the cardiac cycle, color flow Doppler will usually not reveal a PFO. Instead, agitated saline (bubble study) is the best way to assess for PFO or atrial septal defect. Saline is agitated and injected peripherally and then enters the right atrium. If no shunt is present, only the right side of the


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InternalMed_Harrison. study) is the best way to assess for PFO or atrial septal defect. Saline is agitated and injected peripherally and then enters the right atrium. If no shunt is present, only the right side of the heart will be pacified because the air bubbles will be too small to traverse the lungs. Because PFO is a one-way flap, maneuvers should be used to temporarily increase right atrial pressure. Either a Valsalva maneuver or sniff maneuver can be effective.


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InternalMed_Harrison. Atrial septal defects occur most commonly in the region of the fossa extremely high to reflect the pressure gradient between the left and ovalis, referred to as secundum-type defects (Fig. 270e-38). Additional right ventricles. Defects can occur in both the muscular and membraatrial septal defects include defects of the sinus venosus and atrium nous portions of the ventricular septum. primum. Color flow Doppler echocardiography is usually sufficient for In patients with either atrial or ventricular septal defects, estimation of diagnosis of a secundum-type atrial septal defect, but agitated saline is the severity of the left-to-right shunt is essential and can be an important generally needed for the diagnosis of other types of atrial septal defects. determinant in management decisions. Shunts are generally assessed


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InternalMed_Harrison. Ventricular septal defects can generally be visualized by color by echocardiography by assessing the relationship between pulmonary flow Doppler as turbulent high-velocity jets from the left to the right flow and aortic flow, the Qp/Qs ratio. Shunts and cardiac anatomy of ventricle. In cases where the jet origin is unclear, continuous wave most congenital heart diseases can also be accurately evaluated by CMR Doppler can estimate the velocities. These would be expected to be (Fig. 270e-39). noted in the subcostal view with color flow Doppler showing flow through the defect (right). CHAPTER 270e Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging


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InternalMed_Harrison. CHAPTER 270e Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging FIGURE 270e-37 Representative coronal computed tomography (CT) angiographic (CTA; left panel), fluorodeoxyglucose (FDG) positron emission tomography (PET; middle panel), and fused CT and PET (right panel) images in a patient with suspected aortitis. The CTA images demonstrate thickening of the ascending aorta (Ao), which correlates with intense, focal FDG uptake consistent with active inflammation. LV, left ventricle.


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InternalMed_Harrison. FIGURE 270e-39 A and B are phase contrast images that display blood flow (phase images on A) and anatomy (structural images on B) of the aorta (red) and pulmonary artery (green). C demonstrates the flow curves of the aorta (red) and the pulmonary artery (green). Note that the total flow (area under the curve) was substantially higher in the pulmonary artery than the aorta, indicative of a marked elevated pulmonary-tosystemic shunt ratio, as a result of the partial anomalous pulmonary venous return that drained into the superior vena cava.


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InternalMed_Harrison. VIDEO 270e-1 Cine steady-state free precession (SSFP) imaging (left) in short axis in a patient who had a large anterior myocardial infarction. Only one cut of a stack of short axis is shown. This method allows quantification of left ventricular (LV) and right ventricular (RV) volumes in diastole and systole and calculation of the LV ejection fraction, stroke volumes, and cardiac output (a product of LV stroke volume and heart rate). Note that in this case there is anterior and anteroseptal akinesia (lack of systolic wall thickening, as shown by the left cine movie, red arrows) matching by a near-transmural myocardial infarction as seen by the matching late gadolinium enhancement (LGE) image (right picture, white arrows).


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InternalMed_Harrison. VIDEO 270e-2 This is cine cardiac magnetic resonance (CMR) imaging of a patient in the long-axis four-chamber view. Note that the basal aspect of the right ventricular (RV) free wall is thickened, aneurysmal, and akinetic (red arrows). The global RV systolic function is mildly reduced, and the RV is dilated. CMR can image the RV using tomographic views and can quantify the RV volumes and ejection fraction volumetrically. This is a patient who presented with syncopal spells and inducible ventricular tachycardia on subsequent workup. He was diagnosed to have arrhythmogenic right ventricular dysplasia. VIDEO 270e-3 Exercise echocardiogram showing rest images on left and poststress images on right, with parasternal long-axis, upper panel, and apical four-chamber, lower panel, end-systolic frames. Following exercise, the distal septal/apical region becomes akinetic. A = upper left (UL); B = upper right (UR); C = lower left (LL); D = lower right (LR).


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InternalMed_Harrison. VIDEO 270e-4 The video shows cardiac magnetic resonance (CMR) myocardial perfusion imaging during vasodilating stress, in three parallel-short-axis views. An bolus of gadolinium contrast was injected intravenously while rapid imaging acquisition occurred. The contrast enhances the right ventricle first, then travels through the pulmonary circulation, enters the left ventricle (LV), and then perfuses the LV myocardium. Myocardial perfusion defects with this technique show as black subendocardial rims, reflecting lack of contrast accumulation due to ischemia and/or scar. In this case, the anterior wall has a severe perfusion defect (red arrow). Figure 270-14 shows the late gadolinium enhancement (LGE) image of a mid short-axis view. There is no evidence of infarction in the anterior wall, which would be seen as bright white areas, indicating that the stress perfusion defect primarily represents myocardial ischemia. This patient had a significant stenosis of the left anterior descending


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InternalMed_Harrison. would be seen as bright white areas, indicating that the stress perfusion defect primarily represents myocardial ischemia. This patient had a significant stenosis of the left anterior descending coronary artery.


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InternalMed_Harrison. VIDEO 270e-5 A 60-year-old female presented with intermittent chest pain of 3 days in duration but was pain free at the time of assessment in the emergency room. Admission electrocardiogram (ECG) demonstrated T-wave inversion in the anterior precordial lead, but cardiac enzymes were normal. A resting cardiac magnetic resonance (CMR) study reviewed a large area of anteroseptal hypokinesia (left picture, region of hypokinesia shown by the red arrows), matching with a large resting perfusion defect (middle picture, perfusion defect shown by the blue arrows). Late gadolinium enhancement (LGE) imaging (right picture), however, did not show any enhancement to indicate any infarction in the anteroseptal wall, suggesting that the hypocontractile and hypoperfused anteroseptal wall was viable. Urgent coronary angiography demonstrated an acute thrombus in the mid left anterior descending coronary artery, which required coronary stenting. This case represents an example of acute coronary syndrome


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InternalMed_Harrison. coronary angiography demonstrated an acute thrombus in the mid left anterior descending coronary artery, which required coronary stenting. This case represents an example of acute coronary syndrome with hibernating but viable myocardium in the anteroseptal wall. The anteroseptal wall recovered contractile function when reassessed 6 months later.


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InternalMed_Harrison. VIDEO 270e-6 A patient with severe aortic regurgitation quantified by cardiac magnetic resonance (CMR). Notice the dark flow jet during diastolic across the aortic valve. For quantitation of the aortic regurgitation severity, a cross-sectional cut was made just below the aortic valve, perpendicular to the aortic regurgitation jet, using phase contrast flow imaging. Apart from aortic regurgitation fraction and 270e-27 volume, CMR also can volumetrically quantify ventricular sizes and dimensions of the aorta, which are useful in monitoring patients with aortic valve diseases. VIDEO 270e-7 These are T2* images of the heart (left panel) and the liver (right panel) of a patient who has hemochromatosis.


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InternalMed_Harrison. VIDEO 270e-7 These are T2* images of the heart (left panel) and the liver (right panel) of a patient who has hemochromatosis. Note that iron and the liver are markedly darkened in these movies, indicating high load of iron in the heart muscle and liver. The rate of signal reduction (decay) in the myocardium and liver can be calculated as T2∗ value expressed in milliseconds. In this case, the T2∗ was at 10 ms. T2∗ <20 ms in patients with cardiomyopathy has been shown to indicate iron toxicity as the etiology of the cardiomyopathy, and it carries prognostic valve for such patients at risk of cardiac iron toxicity. VIDEO 270e-8 This video shows the heart in long and short axis. Note the large atria, thickened pericardium, and extensive pericardial adhesions. Given the extensive pericardial adhesions, there is little shearing motion of the ventricles against the parietal pericardium.


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InternalMed_Harrison. CHAPTER 270e Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging Atlas of Noninvasive Imaging Marcelo F. Di Carli, Raymond Y. Kwong, Scott D. Solomon This chapter provides “movie” image clips as they are viewed in clini-cal practice, as well as additional static images. Noninvasive cardiac imaging is essential to the diagnosis and management of patients with 271e known or suspected cardiovascular disease. This atlas supplements Chap. 270e, which describes the principles and clinical applications of these important techniques. 1.4 2.8 1.4 2.8


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InternalMed_Harrison. 1.4 2.8 1.4 2.8 Figure 271e-1 A 48-year-old man with new-onset substernal chest pain. Echocardiography shows evidence of acute anterior myocardial infarction involving the interventricular septum and apex secondary to an occlusion of the left anterior descending coronary artery seen from the parasternal long axis view (left) and the apical four-chamber view (right). LV, left ventricle; RV, right ventricle. (See Videos 271e-1 and 271e-2.) CHAPTER 271e Atlas of Noninvasive Imaging


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InternalMed_Harrison. CHAPTER 271e Atlas of Noninvasive Imaging Figure 271e-2 A 55-year-old man with exertional chest discomfort and dyspnea. He exercised for 12 min on a standard Bruce protocol, experiencing typical chest pain and ST-segment depression in V2–V5. End-systolic frame of a stress echocardiogram shows apical four-chamber view at rest (left) and after exercise (right). After exercise, there is a clear regional wall motion abnormality in the distal septum through the apex, consistent with a stenosis in the left anterior descending artery distribution (arrows). LV, left ventricle. (See Videos 271e-3 and 271e-4.)


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InternalMed_Harrison. Figure 271e-3 Exercise single-photon emission computed tomography (SPECT) myocardial perfusion technetium-99m (99mTc) sestamibi scan in a 54-year-old male with a history of coronary artery disease and a prior coronary stent. The stress images (left and middle) show a large defect involving the apex, all apical segments, mid-inferior, mid-inferoseptum, and mid-anteroseptum (arrowheads), which is completely reversible at rest (right), reflecting a large area of exercise-induced myocardial ischemia throughout the left anterior descending coronary territory. The bull's eye displays on the right panel depict the semiquantitative extent of ischemia (light yellow and blue areas represent the extent PART 10 Disorders of the Cardiovascular System and severity of ischemia).


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InternalMed_Harrison. PART 10 Disorders of the Cardiovascular System and severity of ischemia). Figure 271e-4 Coronary computed tomography angiography (CTA). Curved multiplanar reformations demonstrating coronary artery disease severity, defined as normal (no plaque or stenosis), mild (<40%), moderate (40–69%), and severe (>70%) luminal narrowing. By guidelines for CTA reporting, alternative classification provides for stenosis grading as normal, minimal (1–24%), mild (25–49%), moderate (50–69%), severe (70–99%), and occluded (100%). (From GL Raff et al: SCCT guidelines for the interpretation and reporting of coronary computed tomographic angiography. J Cardiovasc Comput Tomogr 3:122, 2009; with permission.) -CAC score 271e = 96th percentile for age, race and ethnicity1 10-year hard CHD risk is 6% (observed age) vs 30% (arterial age)2#


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InternalMed_Harrison. Figure 271e-5 Coronary artery calcium (CAC) scan on a 51-yearold white male without clinical cardiovascular disease or treated diabetes, referred for CAC for risk stratification to guide preventive therapies. A. Gated, noncontrast cardiac computed tomography (CT; 3-mm slice thickness), axial view, demonstrating calcified left anterior descending (LAD) artery atherosclerosis. B. Whole-heart three-dimensional image reconstruction, inverted maximum-intensity projection, demonstrating overall burden of CAC with predominant LAD distribution (arrow). Top right. CAC scores for each coronary artery with calcified plaque involvement, scored by Agatston method and total volume. #For white male with observed age 51 years, total cholesterol 220 mg/dL, high-density lipoprotein 45 mg/dL, nonsmoker, no hypertension, and systolic blood pressure 120 mmHg. Calculated arterial age is 81 years. CHD, coronary heart disease; CX, left circumflex artery; LM, left main artery. 1Data from RL McClelland et al:


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InternalMed_Harrison. hypertension, and systolic blood pressure 120 mmHg. Calculated arterial age is 81 years. CHD, coronary heart disease; CX, left circumflex artery; LM, left main artery. 1Data from RL McClelland et al: Circulation 113:30-37, 2006. 2Data from RL McClelland et al: Am J Cardiol 103: 59-63, 2009.


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InternalMed_Harrison. Figure 271e-6 Cardiac magnetic resonance (CMR) stress myocardial perfusion images in a 60-year-old patient with atypical chest pain. Cine movie short-axis image (left upper panel) shows normal left ventricle size and global and regional function at rest. During vasodilator stress, there is marked reduction of lateral wall perfusion (white arrow, right upper panel) as well as a mild defect in the septal wall. This region is confirmed to be viable by matching late gadolinium enhancement imaging (left lower panel), which demonstrated no evidence of infarction in the lateral wall. These findings are consistent with a severe coronary stenosis in the left circumflex artery. On angiography performed subsequently, there is a tight lesion in the left circumflex artery (red arrow, right lower panel). (See Videos 271e-5 and 271e-6.) LAD 79% 75% 1/8 1.05 1.40 LCX 65% 59% 2.22 0.89 2.49 RCA 76% 68% 1.99 0.96 2.08 TOT 74% 69% 1.75 0.98 1.79


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InternalMed_Harrison. Figure 271e-7 Adenosine positron emission tomography (PET) myocardial perfusion 13N-ammonia scan in a 60-year-old female with atypical chest pain. The stress images (left) show a large defect involving the apex, all apical segments, mid-inferior, mid-inferoseptum, and midanteroseptum (arrowheads), which is completely reversible at rest (right). This is consistent with a medium-sized area of stress-induced ischemia in the mid portion of the left anterior descending (LAD) coronary artery. The right panel illustrates the time-activity curves used for quantification of myocardial blood flow (in mL/min per g of tissue) at peak stress (upper panel) and at rest (lower panel). Coronary flow reserve is then calculated as the ratio of stress/rest myocardial blood flow. The coronary flow reserve is abnormal in the LAD territory, and normal in the left circumflex (LCX) and right coronary artery (RCA) territories (i.e., >2.0). TOT, total left ventricle.


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InternalMed_Harrison. Figure 271e-8 Coronary computed tomography angiography (CTA) obtained on a 35-year-old female presenting to an outpatient clinic with a history of unexplained syncope and a 6-month complaint of intermittent, atypical chest pain occurring primarily during rest. Physical examination is normal. An exercise treadmill test is performed demonstrating good exercise capacity with no exertional chest pain or ischemic ECG changes. For persistent, unexplained symptoms, coronary CTA is obtained. A. Three-dimensional cardiac CT image reconstruction demonstrating anomalous right coronary artery (RCA) origin from the left coronary cusp with an acute angle takeoff (arrow) and an intraarterial course between the aorta (Ao) and main pulmonary artery (PA). B, C. Contrast-enhanced CTA in two-dimensional axial (B) and coronal oblique views (C) demonstrating proximal RCA intraarterial course between the Ao and main PA. PART 10 Disorders of the Cardiovascular System


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InternalMed_Harrison. PART 10 Disorders of the Cardiovascular System Figure 271e-9 Coronary computed tomography angiography (CTA) obtained from a 13-year-old boy with a history of Kawasaki disease who presented with limited exercise capacity and occasional, atypical chest pain. A, B. Three-dimensional cardiac CT image reconstruction demonstrating large three-vessel coronary artery diffuse aneurysms with proximal, nondominant left circumflex (LCX) artery occlusion. C. Two-dimensional contrast-enhanced coronary CTA demonstrating mid-RCA and mid-LAD thrombi that are nonocclusive layered and near circumferential thrombi, respectively, and proximal LCX occlusion. Ao, aorta; CT, computed tomography; LAD, left anterior descending; RCA, right coronary artery.


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InternalMed_Harrison. Figure 271e-10 A case of viability assessment in a patient with inferior myocardial infarction. The cine movie in the upper panel shows an area of inferior akinesis (green arrows). Magnetic resonance image demonstrates transmural contrast enhancement of the inferior wall (red arrows) and the right ventricle (white arrows), which is consistent with infarction. Imaging the heart 10–15 min after injection of gadolinium allows for the accumulation of gadolinium in infarcted tissue (red arrows), which identifies nonviable infarcted myocardium as bright. Viability assessment, as in this case, can provide guidance for any benefits of invasive coronary intervention. In this case, the inferior wall is nonviable. Apart from the inferior wall infarction (red arrows), there is extensive right ventricular infarction (white arrows). (See Video 271e-7.)


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InternalMed_Harrison. Figure 271e-11 Rest myocardial perfusion and metabolism positron emission tomography (PET) scan obtained with 13N-ammonia (perfusion) and 18F-fluorodeoxyglucose (FDG; glucose metabolism) in a 48-year-old male with a prior myocardial infarction. The rest perfusion Atlas of Noninvasive Imaging images show a large defect involving the apex, apical segments, and mid-anteroseptal and anterior segments (arrowheads), which has associ-ated increase in glucose uptake (perfusion-metabolic mismatch), reflecting viable but hibernating myocardium throughout the left anterior descending coronary territory.


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InternalMed_Harrison. Figure 271e-12 A 70-year-old patient with known cardiac murmur and progressive shortness of breath and a recent episode of syncope. Echocardiography shows severe calcific aortic stenosis. A heavily calcified aortic valve (arrow) is shown in the parasternal long-axis views (top panels) and short-axis view (bottom left). Doppler interrogation shows a peak transaortic velocity of 5.2 m/s consistent with a peak instantaneous gradient of 109 mmHg and a mean gradient of 66 mmHg, and a corresponding aortic valve area of <0.6 cm2 (lower right). Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle. (See Videos 271e-8, 271e-9, and 271e-10.)


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InternalMed_Harrison. Figure 271e-13 A 66-year-old patient with multiple myeloma and progressive shortness of breath. Echocardiography shows features typical of cardiac amyloidosis, including thickened myocardium with a “sparkly” appearance and left atrial enlargement. Systolic function is mildly reduced, and diastolic function is severely reduced. LA, left atrium; LV, left ventricle; RV, right ventricle. (See Videos 271e-11 and 271e-12.)


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InternalMed_Harrison. Figure 271e-14 Magnetic resonance image with contrast enhancement in magnitude (A), and phase-sensitive reconstructed images (B) 5–10 min after injection of gadolinium in a patient with transthyretin (TTR)-mediated amyloidosis. The phase-sensitive reconstruction (B) enhances the region of abnormal collection of gadolinium, making gadolinium enhancement in the ventricle (red arrows) and the atrium (green arrows) more prominent. Amyloidosis causes accumulation of abnormal interstitial proteins, which results in late gadolinium enhancement in a diffuse subendocardial pattern (red arrows). Blood pool signal is characteristically dark (asterisk) owing to sequestration of gadolinium into other organs.


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InternalMed_Harrison. Figure 271e-15 A 34-year-old woman with known cardiac murmur and syncope with a family history of sudden cardiac death. Echocardiogram shows classic findings of hypertrophic cardiomyopathy, including marked left ventricular wall thickness, particularly in the interventricular septum, notable in the parasternal long-axis view (upper left) and apical view (upper right). Note reverse septal curvature in the apical view (upper left). There is substantial flow acceleration through the left ventricular outflow tract (lower left) with evidence of a late peaking systolic gradient (arrow, lower right) caused by outflow tract obstruction. Ao, aorta; IVS, interventricular septum; LA, left atrium; LV, left ventricle; PW, posterior wall; RV, right ventricle. (See Videos 271e-13, 271e-14, and 271e-15.)


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InternalMed_Harrison. Figure 271e-16 Magnetic resonance image with contrast enhancement in a patient with hypertrophic cardiomyopathy. Note the marked thickened anteroseptal wall (black arrows, left panel) consistent with asymmetric septal hypertrophy. After contrast is injected, this region demonstrated heterogeneous foci of contrast enhancement (right panel, red arrows) consistent with myocardial fibrosis due to myofibril disarray in this condition. This typical enhancement pattern of hypertrophic cardiomyopathy is found in the areas of maximum wall thickness, Atlas of Noninvasive Imaging typically at the anteroseptum as in this case. (See Video 271e-16.) Nonischemic cardiomyopathy sarcoid (with both MRI and PET) Apex Mid Base Perfusion FDG Short-axis MRI Late enhancement Perfusion FDG Horizontal Long-axis Vertical Long-axis LVRV LVRV


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InternalMed_Harrison. Figure 271e-17 Late gadolinium enhancement cardiac magnetic resonance imaging (MRI) (left panel) and rest myocardial perfusion and fluorodeoxyglucose (FDG) positron emission tomography (PET)/computed tomography (CT) studies (middle and right panels) in a 48-year-old male with a complete heart block. The MRI images demonstrate a linear area of mid-wall late gadolinium enhancement involving the inferior and inferolateral walls (arrows). The myocardial perfusion images were normal. However, the FDG images demonstrated a focal area of intense glucose uptake in the inferolateral wall, corresponding to the area of late enhancement on MRI. This is consistent with focal active sarcoidosis. LV, left ventricle; RV, right ventricle.


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InternalMed_Harrison. Figure 271e-18 A 46-year-old patient with malignant melanoma who presents with acute shortness of breath. Echocardiogram reveals a large pericardial effusion (arrow, upper left) with evidence of cardiac tamponade. M-mode echocardiography (upper right) shows evidence of collapse of the right ventricular free wall during diastole (arrow). Doppler echocardiography (lower panel) shows evidence of respiratory flow variation, consistent with a pulsus paradoxus. LA, left atrium; LV, left ventricle; RV, right ventricle. (See Video 271e-17.) PART 10 Disorders of the Cardiovascular System


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InternalMed_Harrison. PART 10 Disorders of the Cardiovascular System Figure 271e-19 Diffuse pericardial thickening (left; red arrows) and circumferential effusion (right; white arrows) associated with effusive-constrictive pericarditis. Effusive-constrictive pericarditis is a progressive condition that has varying degrees of hemodynamic consequences due initially to the collection of pericardial fluid and ultimately to pericardial constriction. It is typically suspected in cases where pericardiocentesis fails to normalize intracardiac pressures. In this example, pericardial fluid analysis resulted in a sterile exudate of leukocytes and erythrocytes. LV, left ventricle; RV, right ventricle.


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InternalMed_Harrison. Figure 271e-20 A 48-year-old woman with severe idiopathic pulmonary hypertension. Echocardiography reveals evidence of marked right ventricular volume and pressure overload as evidenced by enlarged right ventricle (upper left and right), small left ventricle (upper left and upper right), and flattening of the interventricular septum (D-shaped septum) in systole and diastole (upper right). Tricuspid regurgitation velocity, which reflects the pressure gradient between the right ventricle and the left ventricle, is markedly elevated at 5 m/s, consistent with a right ventricle to right atrial pressure gradient of 100 mmHg, which is consistent with systemic right-sided pressures. LA, left atrium; LV, left ventricle; RV, right ventricle. (See Videos 271e-18 and 271e-19.) CHAPTER 271e Atlas of Noninvasive Imaging


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InternalMed_Harrison. CHAPTER 271e Atlas of Noninvasive Imaging Figure 271e-21 Metastatic cardiac tumor diagnosed by cardiac magnetic resonance (MR) in a patient who presented with chest pain and inferior ST elevation. Left heart catheterization was normal. Cardiac MR demonstrates extensive myocardial edema (A, white arrows) with marked reduction in first perfusion (B) and accumulation of gadolinium within the cardiac mass 10–15 min after injection of gadolinium (C, red arrows). D. Positron emission tomography scan showed increased fluorodeoxyglucose uptake in a lung mass as well as in the cardiac mass, consistent with cardiac metastasis. Biopsy of the lung mass revealed adenosquamous carcinoma of the lung. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. (See Videos 271e-20 and 271e-21.) PART 10 Disorders of the Cardiovascular System


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InternalMed_Harrison. PART 10 Disorders of the Cardiovascular System Figure 271e-22 Fluorodeoxyglucose (FDG) positron emission tomography (PET)/computed tomography (CT) in a 52-year-old male with a prior aortic valve replacement who presented with fever and was found to have Haemophilus parainfluenzae bacteremia. The multiplanar reformatted fused PET/CT images demonstrate intense FDG uptake surrounding the aortic valve prosthesis (arrowheads), compatible with a paravalvular abscess. The patient was found to have purulent fluid around the valve during surgery, and he underwent an aortic valve replacement. Ao, aorta; AV, aortic valve; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.


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InternalMed_Harrison. Figure 271e-23 Cardiac computed tomography (CT) pulmonary vein mapping in a 62-year-old male with symptomatic, paroxysmal atrial fibrillation referred for cardiac CT for pulmonary vein mapping prior to planned pulmonary vein isolation. Three-dimensional image reconstruction, demonstrating (A) normal pulmonary vein anatomy and (B) common variant with presence of separate right middle pulmonary vein (RMPV) ostium. LLPV, left lower pulmonary vein; LUPV, left upper pulmonary vein; RLPV, right lower pulmonary vein; RUPV, right upper pulmonary vein.


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InternalMed_Harrison. Disorders of the Cardiovascular SystemDiagnostic Cardiac Catheterization and Coronary Angiography Jane A. Leopold, David P. Faxon Diagnostic cardiac catheterization and coronary angiography are 272 considered the gold standard in the assessment of the anatomy and physiology of the heart and its associated vasculature. In 1929, Forssmann demonstrated the feasibility of cardiac catheterization in humans when he passed a urological catheter from a vein in his arm to his right atrium and documented the catheter’s position in the heart by x-ray. In the 1940s, Cournand and Richards applied this technique to patients with cardiovascular disease to evaluate cardiac function. These three physicians were awarded the Nobel Prize in 1956. In 1958, Sones inadvertently performed the first selective coronary angiography when a catheter in the left ventricle slipped back across the aortic valve, engaged the right coronary artery, and power-injected 40 mL of contrast down the vessel. The resulting


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InternalMed_Harrison. coronary angiography when a catheter in the left ventricle slipped back across the aortic valve, engaged the right coronary artery, and power-injected 40 mL of contrast down the vessel. The resulting angiogram provided superb anatomic detail of the artery, and the patient suffered no adverse effects. Sones went on to develop selective coronary catheters, which were modified further by Judkins, who developed preformed catheters and allowed coronary artery angiography to gain widespread use as a diagnostic tool. In the United States, cardiac catheterization is the second most common operative procedure, with more than one million procedures performed annually.


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InternalMed_Harrison. INDICATIONS, RISKS, AND PREPROCEDURE MANAGEMENT Cardiac catheterization and coronary angiography are indicated to evaluate the extent and severity of cardiac disease in symptomatic patients and to determine if medical, surgical, or catheter-based interventions are warranted (Table 272-1). They are also used to exclude severe disease in symptomatic patients with equivocal findings on noninvasive studies and in patients with chest-pain syndromes of unclear etiology for whom a definitive diagnosis is necessary for management. Cardiac catheterization is not mandatory prior to cardiac surgery in some younger patients who have congenital or valvular heart disease that is well defined by noninvasive imaging and who do not have symptoms or risk factors that suggest concomitant coronary artery disease.


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InternalMed_Harrison. The risks associated with elective cardiac catheterization are relatively low, with a reported risk of 0.05% for myocardial infarction, 0.07% for stroke, and 0.08–0.14% for death. These risks increase substantially if the catheterization is performed emergently, during acute myocardial infarction or in hemodynamically unstable patients. Canadian Cardiology Society Class II, III, or IV stable angina on medical therapy Chest-pain syndrome of unclear etiology and equivocal findings on noninvasive tests Reperfusion with primary percutaneous coronary intervention Persistent or recurrent ischemia Pulmonary edema and/or reduced ejection fraction Cardiogenic shock or hemodynamic instability Risk stratification or positive stress test after acute myocardial infarction Mechanical complications—mitral regurgitation, ventricular septal defect Suspected severe valve disease in symptomatic patients—dyspnea, angina, heart failure, syncope Infective endocarditis with need for cardiac surgery


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InternalMed_Harrison. Suspected severe valve disease in symptomatic patients—dyspnea, angina, heart failure, syncope Infective endocarditis with need for cardiac surgery Asymptomatic patients with aortic regurgitation and cardiac enlargement or Prior to cardiac surgery in patients with suspected coronary artery disease New onset with angina or suspected undiagnosed coronary artery disease New-onset cardiomyopathy of uncertain cause or suspected to be due to coronary artery disease Prior to surgical correction, when symptoms or noninvasive testing suggests coronary disease Symptomatic patients with suspected cardiac tamponade or constrictive pericarditis Hypertrophic cardiomyopathy with angina Diseases of the aorta when knowledge of coronary artery involvement is necessary for management


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InternalMed_Harrison. Hypertrophic cardiomyopathy with angina Diseases of the aorta when knowledge of coronary artery involvement is necessary for management Additional risks of the procedure include tachyor bradyarrhythmias that require countershock or pharmacologic therapy, acute renal failure leading to transient or permanent dialysis, vascular complications that necessitate surgical repair, and significant access-site bleeding. Of these risks, vascular access-site bleeding is the most common complication, occurring in 1.5–2.0% of patients, with major bleeding events associated with a worse shortand long-term outcome.


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InternalMed_Harrison. In patients who understand and accept the risks associated with cardiac catheterization, there are no absolute contraindications when the procedure is performed in anticipation of a life-saving intervention. Relative contraindications do, however, exist; these include decompensated congestive heart failure; acute renal failure; severe chronic renal insufficiency, unless dialysis is planned; bacteremia; acute stroke; active gastrointestinal bleeding; severe, uncorrected electrolyte abnormalities; a history of an anaphylactic/anaphylactoid reaction to iodinated contrast agents; and a history of allergy/bronchospasm to aspirin in patients for whom progression to a percutaneous coronary intervention is likely and aspirin desensitization has not been performed.


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InternalMed_Harrison. Contrast allergy and contrast-induced acute kidney injury merit further consideration, because these adverse events may occur in otherwise healthy individuals and prophylactic measures exist to reduce risk. Allergic reactions to contrast agents occur in <5% of cases, with severe anaphylactoid (clinically indistinguishable from anaphylaxis, but not mediated by an IgE mechanism) reactions occurring in 0.1%–0.2% of patients. Mild reactions manifest as nausea, vomiting, and urticaria, while severe anaphylactoid reactions lead to hypotensive shock, pulmonary edema, and cardiorespiratory arrest. Patients with a history of significant contrast allergy should be premedicated with corticosteroids and antihistamines (H1and H2-blockers) and studies performed with nonionic, low-osmolar contrast agents that have a lower reported rate of allergic reactions.


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InternalMed_Harrison. Contrast-induced acute kidney injury, defined as an increase in creatinine >0.5 mg/dL or 25% above baseline that occurs 48–72 hours after contrast administration, occurs in ~2–7% of patients with rates of 20–30% reported in high-risk patients, including those with diabetes mellitus, congestive heart failure, chronic kidney disease, anemia, and older age. Dialysis is required in 0.3–0.7% of patients and is associated with a fivefold increase in in-hospital mortality. For all patients, adequate intravascular volume expansion with intravenous 0.9% saline (1.0–1.5 mL/kg per hour) for 3–12 hours before and continued 6–24 hours after the procedure limits the risk of contrast-induced acute kidney injury. Pretreatment with N-acetylcysteine (Mucomyst) has not reduced the risk of contrast-induced acute kidney injury consistently and, therefore, is no longer recommended routinely. Diabetic patients treated with metformin should stop the drug 48 hours prior to the procedure to limit the


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InternalMed_Harrison. acute kidney injury consistently and, therefore, is no longer recommended routinely. Diabetic patients treated with metformin should stop the drug 48 hours prior to the procedure to limit the associated risk of lactic acidosis. Other strategies to decrease risk include the administration of sodium bicarbonate (3 mL/kg per hour) 1 hour before and 6 hours after the procedure; use of lowor iso-osmolar contrast agents; and limiting the volume of contrast to <100 mL per procedure.


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InternalMed_Harrison. Cardiac catheterization is performed after the patient has fasted for 6 hours and has received intravenous conscious sedation to remain awake but sedated during the procedure. All patients with suspected coronary artery disease are pretreated with 325 mg aspirin. In patients in whom the procedure is likely to progress to a percutaneous coronary intervention, an additional antiplatelet agent should be started: clopidogrel (600-mg loading dose and 75 mg daily) or prasugrel (60-mg loading dose and 10 mg daily), or ticagrelor (180-mg loading and 90 mg twice daily). Prasugrel should not be selected for individuals with prior stroke or transient ischemic attack. Warfarin is held starting 2–3 days prior to the catheterization to allow the international normalized ratio (INR) to fall to <1.7 and limit access-site bleeding complications. Cardiac catheterization is a sterile procedure, so antibiotic prophylaxis is not required.


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InternalMed_Harrison. Cardiac catheterization and coronary angiography provide a detailed hemodynamic and anatomic assessment of the heart and coronary arteries. The selection of procedures is dependent on the patient’s symptoms and clinical condition, with some direction provided by noninvasive studies.


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InternalMed_Harrison. Vascular Access Cardiac catheterization procedures are performed using a percutaneous technique to enter the femoral artery and vein as the preferred access sites for left and right heart catheterization, respectively. A flexible sheath is inserted into the vessel over a guidewire, allowing diagnostic catheters to be introduced into the vessel and advanced toward the heart using fluoroscopic guidance. The radial artery (or brachial artery) may also be used as an arterial access site in patients, particularly those with peripheral arterial disease that involves the abdominal aorta, iliac, or femoral vessels; severe iliac artery tortuosity; morbid obesity; or preference for early postprocedure ambulation. Use of radial-artery access is gaining popularity due to a lower rate of access-site bleeding complications. A normal Allen’s test confirming dual blood supply to the hand from the radial and ulnar arteries is recommended prior to access at this site. The internal jugular or


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InternalMed_Harrison. bleeding complications. A normal Allen’s test confirming dual blood supply to the hand from the radial and ulnar arteries is recommended prior to access at this site. The internal jugular or antecubital veins serve as alternate access sites to the right heart when the patient has an inferior vena cava filter in place or 1461 requires prolonged hemodynamic monitoring.


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InternalMed_Harrison. Right Heart Catheterization This procedure measures pressures in the right heart. Right heart catheterization is no longer a routine part of diagnostic cardiac catheterization, but it is reasonable in patients with unexplained dyspnea, valvular heart disease, pericardial disease, right and/or left ventricular dysfunction, congenital heart disease, and suspected intracardiac shunts. Right heart catheterization uses a balloon-tipped flotation catheter that is advanced sequentially to the right atrium, right ventricle, pulmonary artery, and pulmonary wedge position (as a surrogate for left atrial pressure) using fluoroscopic guidance; in each cardiac chamber, pressure is measured and blood samples are obtained for oxygen saturation analysis to screen for intracardiac shunts.


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InternalMed_Harrison. Left Heart Catheterization This procedure measures pressures in the left heart as a determinant of left ventricular performance. With the aid of fluoroscopy, a catheter is guided to the ascending aorta and across the aortic valve into the left ventricle to provide a direct measure of left ventricular pressure. In patients with a tilting-disc prosthetic aortic valve, crossing the valve with a catheter is contraindicated, and the left heart may be accessed via a transseptal technique from the right atrium using a needle-tipped catheter to puncture the atrial septum at the fossa ovalis. Once the catheter crosses from the right to the left atrium, it can be advanced across the mitral valve to the left ventricle. This technique is also used for mitral valvuloplasty. Heparin is given for prolonged procedures to limit the risk of stroke from embolism of clots that may form on the catheter. For patients with heparin-induced thrombocytopenia, the direct thrombin inhibitors bivalirudin (0.75


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InternalMed_Harrison. procedures to limit the risk of stroke from embolism of clots that may form on the catheter. For patients with heparin-induced thrombocytopenia, the direct thrombin inhibitors bivalirudin (0.75 mg/kg bolus, 1.75 mg/kg per hour for the duration of the procedure) or argatroban (350 μg/kg bolus, 15 μg/kg per minute for the duration of the procedure) may be used.


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InternalMed_Harrison. A comprehensive hemodynamic assessment involves obtaining pressure measurements in the right and left heart and peripheral arterial system and determining the cardiac output (Table 272-2). The shape Arteriovenous oxygen difference (vol %) 3.5–4.8 Cardiac index ([L-min]/m2) 2.8–4.2


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InternalMed_Harrison. Hemodynamic measurements are also used to differentiate between cardiac tamponade, constrictive pericarditis, and restrictive cardiomyopathy (Table 272-3). In cardiac tamponade, right atrial pressure is increased with a decreased or absent “y” descent, indicative of impaired right atrial emptying in diastole, and there is diastolic equalization of pressures in all cardiac chambers. In constrictive pericarditis, right atrial pressure is elevated with a prominent “y” descent, indicating rapid filling of the right ventricle during early diastole. A diastolic dip and plateau or “square root sign,” in the ventricular waveforms due to an abrupt halt in ventricular filling during diastole; right ventricular and pulmonary artery pressures are elevated; and discordant pressure changes in the right and left ventricles with inspiration (right ventricular systolic pressure increases while left ventricular systolic pressure decreases) are observed. The latter hemodynamic phenomenon is the most


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InternalMed_Harrison. and left ventricles with inspiration (right ventricular systolic pressure increases while left ventricular systolic pressure decreases) are observed. The latter hemodynamic phenomenon is the most specific for constriction. Restrictive cardiomyopathy may be distinguished from constrictive pericarditis by a marked increase in right ventricular and pulmonary artery systolic pressures (usually >60 mmHg), a separation of the left and right ventricular diastolic pressures by and magnitude of the pressure waveforms provide important diag->5 mmHg (at baseline or with acute volume loading), and concordant nostic information; an example of normal pressure tracings is shown changes in left and right ventricular diastolic filling pressures with in Fig. 272-1. In the absence of valvular heart disease, the atria and inspiration (both increase). ventricles are “one chamber” during diastole when the tricuspid and mitral valves are open while in systole, when the pulmonary and aortic Cardiac Output


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InternalMed_Harrison. the atria and inspiration (both increase). ventricles are “one chamber” during diastole when the tricuspid and mitral valves are open while in systole, when the pulmonary and aortic Cardiac Output Cardiac output is measured by the Fick method or the valves are open, the ventricles and their respective outflow tracts are thermodilution technique. Typically, the Fick method and thermodiconsidered “one chamber.” These concepts form the basis by which lution technique are both performed during cardiac catheterization, hemodynamic measurements are used to assess valvular stenosis. although the Fick method is considered more reliable in the presence When aortic stenosis is present, there is a systolic pressure gradient of tricuspid regurgitation and in low-output states. The Fick method


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InternalMed_Harrison. FIGURE 272-1 Normal hemodynamic waveforms recorded during right heart catheteriza-tion. Atrial pressure tracings have a characteristic “a” wave that reflects atrial contraction and a “v” wave that reflects pressure changes in the atrium during ventricular systole. Ventricular pres-sure tracings have a low-pressure diastolic filling period and a sharp rise in pressure that occurs during ventricular systole. d, diastole; PA, pulmonary artery; PCWP, pulmonary capillary wedge pressure; RA, right atrium; RV, right ventricle; s, systole.


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InternalMed_Harrison. between the left ventricle and the aorta; when mitral stenosis is present, there is a diastolic pressure gradient between the pulmonary capillary wedge (left atrial) pressure and the left ventricle (Fig. 272-2). Hemodynamic measurements also discriminate between aortic stenosis and hypertrophic obstructive cardiomyopathy where the asymmetrically hypertrophied septum creates a dynamic intraventricular pressure gradient during ven-200 tricular systole. The magnitude of this obstruction is measured using an end-hole catheter positioned at the left ventricular apex that is pulled back while recording pressure; once the catheter has passed the septal obstruction and is positioned in the apex of the left ventricle, a gradient can be measured between the left ventricular apex and the aorta. Hypertrophic obstructive cardiomy-100 opathy is confirmed by the Brockenbrough-Braunwald sign: following a premature ventricular contraction, there is an increase in the left ventricular–aorta pressure


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InternalMed_Harrison. obstructive cardiomy-100 opathy is confirmed by the Brockenbrough-Braunwald sign: following a premature ventricular contraction, there is an increase in the left ventricular–aorta pressure gradient with a simultaneous decrease in the aortic pulse pressure. These findings are absent in aortic stenosis.


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InternalMed_Harrison. Regurgitant valvular lesions increase volume (and pressure) in the “receiving” cardiac chamber. In severe 0 mmHg mmHg mitral and tricuspid regurgitation, the increase in blood flow to the atria takes place during ventricular systole, FIGURE 272-2 Severe aortic and mitral stenosis. Simultaneous recording of left leading to an increase in the v wave (two times greater ventricular (LV) and aortic (Ao) pressure tracings demonstrates a 62-mmHg mean than the mean pressure). Severe aortic regurgitation systolic gradient (shaded area) that corresponds to an aortic valve area of 0.6 cm2 leads to a decrease in aortic diastolic pressure with a (left). Simultaneous recording of LV and pulmonary capillary wedge (PCW) pressure concomitant rise in left ventricular end-diastolic pres-tracings reveals a 14-mmHg mean diastolic gradient (shaded area) that is consistent sure, resulting in equalization of pressures between the with critical mitral stenosis (mitral valve area = 0.5 cm2). d, diastole; e,


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InternalMed_Harrison. 14-mmHg mean diastolic gradient (shaded area) that is consistent sure, resulting in equalization of pressures between the with critical mitral stenosis (mitral valve area = 0.5 cm2). d, diastole; e, end diastole; s, two chambers at end-diastole. systole.


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InternalMed_Harrison. 1463TABlE 272-3 HEMoDYnAMiC FinDingS in TAMPonADE, ConSTRiCTivE PERiCARDiTiS, AnD RESTRiCTivE CARDioMYoPATHY Right atrium pressure ↑↑↑ (Fails to decrease by 50% or to <10 mmHg after pericardiocentesis) uses oxygen as the indicator substance and is based on the principle that the amount of a substance taken up or released by an organ (oxygen consumption) is equal to the product of its blood flow (cardiac output) and the difference in the concentration of the substance in the arterial and venous circulation (arterial-venous oxygen difference). Thus, the formula for calculating the Fick cardiac output is:


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InternalMed_Harrison. Oxygen consumption is estimated as 125 mL oxygen/minute × body surface area, and the arterial-venous oxygen difference is determined by first calculating the oxygen carrying capacity of blood (hemoglobin [g/100 mL] × 1.36 [mL oxygen/g hemoglobin] × 10) and multiplying this product by the fractional oxygen saturation. The thermodilution method measures a substance that is injected into and adequately mixes with blood. In contemporary practice, thermodilution cardiac outputs are measured using temperature as the indicator. Measurements are made with a thermistor-tipped catheter that detects temperature deviations in the pulmonary artery after the injection of 10 mL of room-temperature normal saline into the right atrium.


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InternalMed_Harrison. Vascular Resistance Resistance across the systemic and pulmonary circulations is calculated by extrapolating from Ohm’s law of electrical resistance and is equal to the mean pressure gradient divided by the mean flow (cardiac output). Therefore, systemic vascular resistance is ([mean aortic pressure − mean right atrial pressure]/cardiac output) multiplied by 80 to convert the resistance from Wood units to dyns-cm−5. Similarly, the pulmonary vascular resistance is ([mean pulmonary artery − mean pulmonary capillary wedge pressure]/cardiac output) × 80. Pulmonary vascular resistance is lowered by oxygen, nitroprusside, calcium channel blockers, prostacyclin infusions, and inhaled nitric oxide; these therapies may be administered during catheterization to determine if increased pulmonary vascular resistance is fixed or reversible.


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InternalMed_Harrison. Valve Area Hemodynamic data may also be used to calculate the valve area using the Gorlin formula that equates the area to the flow across the valve divided by the pressure gradient between the cardiac chambers surrounding the valve. The formula for the assessment of valve area is: Area = (cardiac output [cm3/min]/[systolic ejection period or diastolic filling period][heart rate])/44.3 C × square root of the pressure gradient, where C = 1 for aortic valve and 0.85 for the mitral valve. A valve area of <1.0 cm2 and a mean gradient of greater than 40 mmHg indicate severe aortic stenosis, while a valve area of <1.5 cm2 and a mean gradient >5–10 mmHg is consistent with moderate-to-severe mitral stenosis; in symptomatic patients with a mitral valve area >1.5 cm2, a mean gradient >15 mmHg, pulmonary artery pressure >60 mmHg, or a pulmonary artery wedge pressure >25 mmHg after exercise is also considered significant and may warrant intervention. The modified Hakki formula has also been used


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InternalMed_Harrison. artery pressure >60 mmHg, or a pulmonary artery wedge pressure >25 mmHg after exercise is also considered significant and may warrant intervention. The modified Hakki formula has also been used to estimate aortic valve area. This formula calculates the valve area as the cardiac output (L/min) divided by the square root of the pressure gradient. Aortic valve area calculations based on the Gorlin formula are flow-dependent and, therefore, for patients with low cardiac outputs, it is imperative to determine if a decreased valve area actually reflects a fixed stenosis or is overestimated by a low cardiac output and stroke volume that is insufficient to open the valve leaflets fully. In these instances, cautious hemodynamic manipulation using dobutamine to increase the cardiac output and recalculation of the aortic valve area may be necessary.


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InternalMed_Harrison. Intracardiac Shunts In patients with congenital heart disease, detection, localization, and quantification of the intracardiac shunt should be evaluated. A shunt should be suspected when there is unexplained arterial desaturation or increased oxygen saturation of venous blood. A “step up” or increase in oxygen content indicates the presence of a left-to-right shunt while a “step down” indicates a right-to-left shunt. The shunt is localized by detecting a difference in oxygen saturation levels of 5–7% between adjacent cardiac chambers. The severity of the shunt is determined by the ratio of pulmonary blood flow (Qp) to the systemic blood flow (Qs), or Qp/Qs = ([systemic arterial oxygen content − mixed venous oxygen content]/pulmonary vein oxygen content − pulmonary artery oxygen content). For an atrial septal defect, a shunt ratio of 1.5 is considered significant and factored with other clinical variables to determine the need for intervention. When a congenital ventricular septal


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InternalMed_Harrison. For an atrial septal defect, a shunt ratio of 1.5 is considered significant and factored with other clinical variables to determine the need for intervention. When a congenital ventricular septal defect is present, a shunt ratio of ≥2.0 with evidence of left ventricular volume overload is a strong indication for surgical correction.


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InternalMed_Harrison. Ventriculography to assess left ventricular function may be performed during cardiac catheterization. A pigtail catheter is advanced retrograde across the aortic valve into the left ventricle and 30–45 mL of contrast is power-injected to visualize the left ventricular chamber during the cardiac cycle. The ventriculogram is usually performed in the right anterior oblique projection to examine wall motion and mitral valve function. Normal wall motion is observed as symmetric contraction of all segments; hypokinetic segments have decreased contraction, akinetic segments do not contract, and dyskinetic segments appear to bulge paradoxically during systole (Fig. 272-3). Ventriculography may also reveal a left ventricular aneurysm, pseudoaneurysm, or diverticulum and can be used to assess mitral valve prolapse and the severity of mitral regurgitation. The degree of mitral regurgitation is estimated


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InternalMed_Harrison. FIGURE 272-3 Left ventriculogram at end diastole (left) and end systole (right). In patients with normal left ventricular function, the ventriculogram reveals symmetric contraction of all walls (top). Patients with coronary artery disease may have wall motion abnormalities on ventriculography as seen in this 60-year-old male following a large anterior myocardial infarction. In systole, the anterior, apical, and inferior walls are akinetic (white arrows) (bottom).


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InternalMed_Harrison. by comparing the density of contrast opacification of the left atrium with that of the left ventricle. Minimal contrast reflux into the left atrium is considered 1+ mitral regurgitation, while contrast density in the left atrium that is greater than that in the left ventricle with reflux of contrast into the pulmonary veins within three beats defines 4+ mitral regurgitation. Ventriculography performed in the left anterior oblique projection can be used to identify a ventricular septal defect. Calculation of the ventricular volumes in systole and diastole allows calculation of stroke volume and cardiac output.


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InternalMed_Harrison. Aortography in the cardiac catheterization laboratory visualizes abnormalities of the ascending aorta, including aneurysmal dilation and involvement of the great vessels, as well as dissection with compression of the true lumen by an intimal flap that separates the true and false arteries arising from the lumina. Aortography can also be used to identify patent saphenous vein grafts that elude selective cannulation, identify shunts that involve the aorta such as a patent ductus arteriosus, and provide a qualitative assessment of aortic regurgitation using a 1+−4+ scale similar to that used for mitral regurgitation.


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InternalMed_Harrison. Selective coronary angiography is catheterization and is used to define the coronary anatomy and determine the extent of epicardial coronary artery ease. Specially shaped coronary cath eters are used to engage the left and right coronary ostia. Hand injection of coronary “luminogram” that is recorded phy). Because the coronary arteries are three-dimensional objects that are in motion with the cardiac cycle, angio grams of the vessels using several differ ent orthogonal projections are taken to best visualize the vessels without overlap or foreshortening. The normal coronary anatomy is highly variable between individuals, but, in general, there are two coronary ostia and three major coronary vessels—the left anterior descending, the left circumflex, and the right coronary arteries with the left anterior descending and left circumflex left main coronary artery (Fig. 272-4).


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InternalMed_Harrison. When the right coronary artery is the origin of the atrioventricular nodal branch, the posterior descending artery, and the posterior lateral vessels, the circulation is defined as right dominant; this is found in ~85% of individuals. When these branches arise from the left circumflex artery as occurs in ~5% of individuals, the circulation is defined as left dominant. The remaining ~10% of patients have a codominant circulation with vessels arising from both the right and left coronary circulation. In some patients, a ramus intermedius branch arises directly from the left main coronary artery; this finding is a normal variant. Coronary artery anomalies occur in 1–2% of patients, with separate ostia for the left anterior descending and left circumflex arteries being the most common (0.41%).


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InternalMed_Harrison. FIGURE 272-4 Normal coronary artery anatomy. A. Coronary angiogram showing the left circumflex (LCx) artery and its obtuse marginal (OM) branches. The left anterior descending artery (LAD) is also seen but may be foreshortened in this view. B. The LAD and its diagonal (D) branches are best seen in cranial views. In this angiogram, the left main (LM) coronary artery is also seen. C. The right coronary artery (RCA) gives off the posterior descending artery (PDA), so this is a right dominant circulation. FIGURE 272-5 Coronary stenoses on cine angiogram and intra-vascular ultrasound. Significant stenoses in the coronary artery are seen as narrowings (black arrows) of the vessel. Intravascular ultrasound shows a normal segment of artery (A), areas with eccentric plaque (B, C), and near total obliteration of the lumen at the site of the significant stenosis (D). Note that the intravascular ultrasound catheter is present in the images as a black circle.


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InternalMed_Harrison. Coronary angiography visualizes coronary artery stenoses as luminal narrowings on the cine angiogram. The degree of narrowing is referred to as the percent stenosis and is determined visually by comparing the most severely diseased segment with a proximal or distal “normal segment”; a stenosis >50% is considered significant (Fig. 272-5). Online quantitative coronary angiography can provide a more accurate assessment of the percent stenosis and lessen the tendency to overestimate lesion severity visually. The presence of a myocardial bridge, which most commonly involves the left anterior descending artery, may be mistaken for a significant stenosis; this occurs when a portion of the vessel dips below the epicardial surface into the myocardium and is subject to compressive forces during ventricular systole. The key to differentiating a myocardial bridge from a fixed stenosis is that the “stenosed” part of the vessel returns to normal during diastole. Coronary calcification is also seen


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InternalMed_Harrison. systole. The key to differentiating a myocardial bridge from a fixed stenosis is that the “stenosed” part of the vessel returns to normal during diastole. Coronary calcification is also seen during angiography prior to the injection of contrast agents. Collateral blood vessels may be seen traversing from one ves(Fig. 272-5). Intravascular ultrasound (IVUS) is performed using 1465 a small flexible catheter with a 40-mHz transducer at its tip that is advanced into the coronary artery over a guidewire. Data from intra-vascular ultrasound studies may be used to image atherosclerotic plaque precisely, determine luminal cross-sectional area, and measure vessel size; it is also used during or following percutaneous coronary intervention to assess the stenosis and determine the adequacy of stent placement. Optical coherence tomography (OCT) is a catheter-based imaging technique that uses near-infrared light to generate images with better spatial resolution than IVUS; however, the depth of


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InternalMed_Harrison. placement. Optical coherence tomography (OCT) is a catheter-based imaging technique that uses near-infrared light to generate images with better spatial resolution than IVUS; however, the depth of field is smaller. The advantage of OCT imaging over IVUS lies in its ability to image characteristics of the atherosclerotic plaque (lipid, fibrous cap) with high definition and to assess coronary stent placement, apposition, and patency (Fig. 272-6).


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InternalMed_Harrison. Measurement of the fractional flow reserve provides a functional assessment of the stenosis and is more accurate in predicting longterm clinical outcome than imaging techniques. The fractional flow reserve is the ratio of the pressure in the coronary artery distal to the stenosis divided by the pressure in the artery proximal to the stenosis at maximal vasodilation. Fractional flow reserve is measured using a coronary pressure–sensor guidewire at rest and at maximal hyperemia following the injection of adenosine. A fractional flow reserve of <0.80 indicates a hemodynamically significant stenosis that would benefit from intervention.


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InternalMed_Harrison. Once the procedure is completed, vascular access sheaths are removed. If the femoral approach is used, direct manual compression or vascular closure devices that immediately close the arteriotomy site with a staple/clip, collagen plug, or sutures are used to achieve hemostasis. These devices decrease the length of supine bed rest (from 6 hours to 2–4 hours) and improve patient satisfaction but have not been shown definitively to be superior to manual compression with respect to access-site complications. With radial-artery access, bed rest is needed for only 2 hours. When cardiac catheterization is performed as an elective outpatient procedure, the patient completes postprocedure bed rest in a monitored setting and is discharged home with instructions to liberalize fluids because contrast agents promote an osmotic diuresis, to avoid strenuous activity, and to observe the vascular access site for signs of complications. Overnight hospitalization may be required for high-risk patients


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InternalMed_Harrison. agents promote an osmotic diuresis, to avoid strenuous activity, and to observe the vascular access site for signs of complications. Overnight hospitalization may be required for high-risk patients with significant comorbidities, patients with complications occurring during the catheterization, or patients who have undergone a percutaneous coronary intervention. Hypotension early after the procedure may be due to inadequate fluid replacement or retroperitoneal bleeding from the access site. Patients who received >2 Gy of radiation during the procedure should be examined for signs of erythema. For patients who received higher doses (>5 Gy), clinical follow-up within 1 month to assess for skin injury is recommended.


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InternalMed_Harrison. sel to the distal vasculature of a severely stenosed or totally occluded vessel. Thrombolysis in myocardial infarction (TIMI) flow grade, a measure of the relative duration of time that it takes for contrast to opacify the coronary artery fully, may provide an additional clue to the degree of lesion severity, and the presence of TIMI grade 1 (minimal filling) or 2 ABCDE (delayed filling) suggests that a significant coronary FIGURE 272-6 Optical coherence tomography imaging. A. The optical coherence artery stenosis is present.


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InternalMed_Harrison. tomography (OCT) catheter (*) in the lumen of a coronary artery with limited neointima INTRAVASCULAR ULTRASOUND, OPTICAL COHERENCE formation. The intima is seen with high definition, but unlike intravascular ultrasound TOMOGRAPHY, AND FRACTIONAL FLOW RESERVE imaging, the vessel media and adventitia are not well visualized. B. A fibrous plaque During coronary angiography, intermediate steno-(arrow) is characterized by a bright signal. C. A large, eccentric, lipid-rich plaque obscures ses (40–70%), indeterminate findings, or anatomic part of the vessel lumen. Because lipid in the plaque absorbs light, the lipid-rich plaque findings that are incongruous with the patient’s appears as a dark area with irregular borders (arrow). The plaque is covered by a thin symptoms may require further interrogation. In fibrous cap (arrowhead) typical of a vulnerable plaque. D. A thrombus (arrow) adherthese cases, intravascular ultrasound provides a ent to a ruptured plaque that is protruding into the


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InternalMed_Harrison. In fibrous cap (arrowhead) typical of a vulnerable plaque. D. A thrombus (arrow) adherthese cases, intravascular ultrasound provides a ent to a ruptured plaque that is protruding into the vessel lumen. E. A coronary stent is more accurate anatomic assessment of the coronary that is well opposed to the vessel wall. The stent struts appear as short bright lines with artery and the degree of coronary atherosclerosis dropout behind the struts (arrow).


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InternalMed_Harrison. Principles of Electrophysiology David D. Spragg, Gordon F. Tomaselli HISTORY AND INTRODUCTION The field of cardiac electrophysiology was ushered in with the devel-opment of the electrocardiogram (ECG) by Einthoven at the turn of 273e SECTion 3 DiSoRDERS of RHy THm


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InternalMed_Harrison. FIGURE 273e-1 A. Cellular atrial and ventricular action potentials. Phases 0–4 are the rapid upstroke, early repolarization, plateau, late repolarization, and diastole, respectively. The ionic currents and their respective genes are shown above and below the action potentials. The currents that underlie the action potentials vary in atrial and ventricular myocytes. B. A ventricular action potential with a schematic of the ionic currents flowing during the phases of the action potential. Potassium current (IK1) is the principal current during phase 4 and determines the resting membrane potential of the myocyte. Sodium current generates the upstroke of the action potential (phase 0); activation of Ito with inactivation of the Na current inscribes early repolarization (phase 1). The plateau (phase 2) is generated by a balance of repolarizing potassium currents and depolarizing calcium current. Inactivation of the calcium current with persistent activation of potassium currents


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InternalMed_Harrison. plateau (phase 2) is generated by a balance of repolarizing potassium currents and depolarizing calcium current. Inactivation of the calcium current with persistent activation of potassium currents (predominantly IKr and IKs) causes phase 3 repolarization.


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InternalMed_Harrison. the twentieth century. Subsequent recording of cellular membrane currents demonstrated that the body surface ECG is the timed sum of the cellular action potentials in the atria and ventricles. In the late 1960s, the development of intracavitary recording, in particular, His bundle electrograms, marked the beginning of contemporary clinical electrophysiology. Adoption of radiofrequency technology to ablate cardiac tissue in the early 1990s heralded the birth of interventional cardiac electrophysiology.


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InternalMed_Harrison. The clinical problem of sudden death caused by ventricular arrhythmias, most commonly in the setting of coronary artery obstruction, was recognized as early as the late nineteenth century. The problem was vexing and led to the development of pharmacologic and nonpharmacologic therapies, including transthoracic defibrillators, cardiac massage, and, most recently, implantable defibrillators. Over time the limitations of antiarrhythmic drug therapy have been highlighted repeatedly in clinical trials, and now ablation and devices are first-line therapy for a number of cardiac arrhythmias. In the last two decades, the genetic basis of a number of heritable arrhythmias has been elucidated, revealing important insights into the mechanisms not only of these rare arrhythmias but also of similar rhythm disturbances observed in more common forms of heart disease. SCN5A (Nav1.5) CACNA1C (Cav1.2) ICa-L SLC8A1 (NCX1.1) KCNJ2 (Kir2.1) IK1 KCND3/KCNIP2 (Kv4.3/KChIP2) to


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InternalMed_Harrison. SCN5A (Nav1.5) CACNA1C (Cav1.2) ICa-L SLC8A1 (NCX1.1) KCNJ2 (Kir2.1) IK1 KCND3/KCNIP2 (Kv4.3/KChIP2) to KCNH2/KCNE2 (HERG/MiRP-1) IKr KCNQ1/KCNE1 (KVLQT1/minK) IKs KCNA5 (Kv1.5)