What is Refractory Angina?

Patient Version

There was (and still is) a lot of confusion about when a stable angina patient becomes a refractory angina patient.

Most heart specialists agree that there is a subgroup of stable angina patients where the standard approaches don’t have a realistic chance of succeeding. Often this means the patient has tried a variety of drugs and has undergone one or more cardiac procedures. The European Society of Cardiology Joint Study group on the Treatment of Refractory Angina (European Heart Journal 2002; 23: 355–370) emphasises that refractory angina is a clinical diagnosis (i.e., based on a combinations of history, examination and investigations) and states:

“Refractory angina pectoris is a chronic condition characterized by the presence of angina caused by coronary insufficiency in the presence of coronary artery disease which cannot be controlled by a combination of medical therapy, angioplasty and coronary bypass surgery. The presence of reversible myocardial ischaemia should be clinically established to be the cause of the symptoms. Chronic is defined as a duration of more than 3 months.”

In table 1 the ESC Joint Study group states the diagnosis:

“Requires a cardiological and cardiothoracic surgical assessment that the patient has angina of ischaemic origin and that revascularization is unfeasible.”

The National Institute for Health and Clinical Excellence (NICE) considered the matter in 2010/11 and decided not to come up with an alternative definition for refractory angina. Instead NICE recommended all stable angina patients should be treated according to the same patient-centred principles that were previously only available to refractory angina sufferers. One big problem that arises from the NICE guidance is that cardiologists do not undergo training in patient-centred angina care, which is very different from the traditional approach.

An extremely important aspect of the NICE guidelines is that doctors must inform patients when proposed heart operations are life saving and when they are not. This is because many patients mistakenly assume procedures are life saving. It is yet to be seen whether patients will be offered the option of patient-centred angina care.


A diagnosis is a medical explanation of what is going wrong in the body. Most heart specialists focus on a very narrow diagnosis. What they want to know is whether the symptoms you describe is caused by blockage in the blood vessels that nourish the heart. They start with a working diagnosis based on the patient’s history (what the symptom feels like, when it happens, how it responds to GTN and other risk factors such as age, family history etc) but make the final diagnosis using tests which show up the blockages (angiogram or CT scan). Diagnosing blockages is a ‘disease-centred’ diagnosis.

Sufferers know that angina has wide ranging affects on the patient, their family and friends. Work and social planning often goes out of the window and these can have a major impact on the patient’s quality of life. In order to get to the bottom of how angina affects patients, the diagnosis must be widened to involve both the cause of angina and all the effects on the patient and their family. This patient centred approach is called a biopsychosocial diagnosis and it takes a lot more effort than simply sending a patient for tests or doing an angiogram. The big advantage of the patient centred approach is that it is greatly preferred by patients because it opens the way to a much wider range of low risk treatments. In practice, traditional cardiologists practice disease centred management and there are too few specialist patient-centred angina clinics.

Angina. Angina is a symptom and a symptom is a sensation of something happening in the body. One of the problems for angina sufferers is that internal organs (like the heart, lungs, bowels and kidneys) are very poor at letting the brain know what is happening. This is because the body did not evolve a system for dealing with problems with the innards. In other words, innards do not have built-in ‘warning’ pathways. Few people know this and it is not surprising that patients and their families commonly make major false assumptions that angina means something bad is happening. Most patients and carers are understandably anxious. Angina is bad enough on its own, but it is much worse if it accompanied by confusion and fear.

A lot of people are not even sure whether they have angina, let alone what they should do about it. The Virtual Angina Education portal might help.



This next bit is a bit complicated and it is worth taking your time over.

Symptoms arising from muscles, joints, skin and teeth are different. Everyone is familiar with pain and how accurately the source can be identified. The skin and joints are especially well supplied with special sensory nerves that have evolved to carry ‘warning’ signals. These peripheral sensory nerves are connected to specific parts of the nervous system in the spinal cord and these in turn relay the information to the brain. Brains assume that whichever spinal relay nerve transmitted the signal it must have started at the far end of the corresponding peripheral sensory nerve.

Mistakes often happen and a common example is the tingling sensation in the little and ring fingers when you hit the ‘funny bone’ at the elbow. What actually happened is that you hit the nerve at the elbow joint which triggered the relay junction box in the spine belonging to the little finger. The brain suddenly receives lots of signals coming from the junction boxes are supposed to relay signals from the little finger, so you feel tingling in the little finger. Another common example is sciatica, where a piece of gristle bulges against a nerve to the leg at the point where the nerve enters the spinal cord in the lower back. Although the problem is at the lower part of the back, the pain is felt down the leg as far down as the foot.

Angina happens when the heart accidentally activates an innards nerve which then accidentally triggers one or more groups of relay nerves for pain in the spinal chord. As with the funny bone example, the brain will decide where the original signal came from according to which spinal nerve relayed the signal. The brain doesn’t know there is a short circuit, nor that the signal started in the heart. If the spinal nerves for the arm or jaw relay the signal, that is where the patient will feel their angina. If the relay nerves from the centre of the chest are involved, angina patients naturally assume it is coming from their heart. It is important to understand that the short circuit from the innards nerve to the relay nerve in the spine is unintentional and random. This explains why no two angina sufferers describe exactly the same symptoms.

The experts who developed the care pathway all agreed the best way to make a diagnosis is to take a very careful history often backed up by an examination. Unfortunately this time consuming phase is often bypassed in the rush to do tests. At clinics who follow the patient-centred approach, patients and carers spend around one and a half to two hours getting to the bottom of the diagnosis before tests are ordered. This nearly invariably identifies significant stress promoting misconceptions that are playing a major role in the overall impact of the condition.


Clinical jargon version

The old definition: “Chronic refractory angina is a clinical diagnosis. It is based on the presence of symptoms of stable angina that are thought to be caused by ischaemia due to advanced coronary disease and which are not controllable by a combination of maximal anti anginal medication, angioplasty or coronary artery bypass surgery. The presence of demonstrable myocardial ischaemia is desirable but is not an absolute requirement for offering patients the initial stages of care. However, as the patient moves through successive stages of the treatment algorithm it becomes increasingly important that ischaemia is confirmed especially when high risk, high cost procedures are considered. The choice of investigation must be at the discretion of the individual clinician considering local expertise and availability and the level of confidence in the clinical diagnosis.”

The original November 1998 definition of chronic refractory angina took insufficient account of paternalism, because it allowed clinicians to justify withholding information about simple evidence-based alternatives simply because revascularisation was technically feasible.

At the May 1999 UK national guideline group meeting it was decided to clarify the definition. This definition was fully implemented at the UK NHS National Refractory Angina Centre in June 1999 and was formally adopted by the UK Pain society angina special interest group in March 2000. It reflects current best consent practice and requires clinicians to involve patients fully in choosing from all the available therapies the one that is best suited to their needs.

The current UK national chronic refractory angina guideline group’s definition of chronic refractory angina differs from the ESC study group definition and is:“Chronic stable angina that persists despite optimal medication and when revascularisation is unfeasible or where the risks are unjustified.In practical terms, this definition has little or no impact on the outcome of consenting a patient with a tight left mainstem, proximal three-vessel disease or proximal left anterior descending disease, because bypass surgery remains the most effective evidence-based option. Also there is growing confidence that the newest generation of drug eluting stents also prolong life in certain situations. On the other hand the definition should have a significant effect on the process of obtaining valid consent for palliative (i.e. non-life prolonging) revascularisation for which low risk alternatives exist.

It appears that clinicians commonly ignore the risk justification caveat or have  failed to understand that whether or not risks are justified can only be judged with the full participation of the fully informed patient. Consequently, in breach of current professional guidance on consent, some doctors think it is reasonable to withhold information about low risk options if palliative revascularisation is a feasible option. This approach is risky for patients and clinicians. In our experience it leads to patients undergoing procedures that they might have avoided if they had had an opportunity to choose from lower risk options. Failure to inform patients about the range of options available for their condition invalidates consent and leaves open the possibility for negligence claims.

The 2011 NICE stable angina guideline does not explicitly define refractory angina. Instead it sets out general patient-centred principles that should be applied to all stable angina patients. Nevertheless, the term refractory angina is useful and will continue to be used to describe end-of-line patients who need the sort of time consuming overhaul only available in specialist patient-centred refractory angina clinics.


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