An explanation of key terms and concepts by Robin Choudhury DM, FESC, FRCP Professor of Cardiovascular Medicine, University of Oxford Hon Consultant Cardiologist, Oxford Heart Centre
Heart attack (acute myocardial infarction) remains a huge clinical problem. Each year, over 80,000 heart attacks occur in the UK. The cost of heart attack and its sequelae are huge, estimated at over £2 billion annually to the NHS. Heart failure, which can be caused by myocardial infarction affects 900,000 patients in the UK.
Despite these astonishing figures, public understanding of some of the terminology around this medical area remains very patchy. This article will unpick and explain key terms including “angina”, “myocardial infarction”, “heart attack”, “cardiac arrest” and “heart failure”.
Normal heart function
In normal circumstances, the heart is a hollow muscular organ that works as a variable output pump. As a heavy duty mechanical pump, its energy requirements are relatively high. The heart has integrated electrical circuitry which allows its resident pacemaker to orchestrate organized, automatic beating activity at a baseline level and to respond to certain stimuli in response to increasing demand, notably on exercise. Because of this work as a perpetual pump it requires a reliable blood and nutrient supply, which is obtained from the coronary arteries. The three principal coronary arteries run along the surface of the heart, dividing
into branching structures that nourish the adjacent muscle.
Coronary Artery Disease
Most of the heart disease that will be discussed in this article relates to the consequences of interrupting blood supply to the heart. This is most usually due to the accumulation of“atherosclerosis” within the walls of the coronary arteries. Atherosclerosis reflects the buildup of fatty deposits, rich in cholesterol and attracting an inflammatory response mediated by the immune system. These deposits start in the second and third decades of life and build progressively over many years. They often come to light in the sixth and seventh decades (sometimes before) through the symptoms of “angina”. A patient with ‘stable angina’ experiences no symptoms at rest, but when the work of the heart increases due to physical exertion, fixed narrowings within the coronary arteries restrict the free flow of blood leading to inadequate nutrient supply and consequent discomfort. Symptoms are usually manifest as tightness / pressure / pain felt centrally in the chest, perhaps with radiation to the left arm, jaw, back. In this stable syndrome, the discomfort usually eases swiftly as the heart is returned to its resting state following exertion. This is a relatively benign condition.
In the context of angina described above, the narrowings in the arteries are stable and fixed. Their size changes slowly if at all. However, for reasons that are not always apparent, but sometimes related to surges in blood pressure or intense physical activity, these narrowly can change suddenly and dramatically. Rupture or fissuring of the lesion in the wall of the artery can lead to the rapid accumulation of a blood clot. Where this completely obstructs the passage of blood, a heart attack is imminent. This blood clot in the artery, otherwise known as a “coronary thrombosis” is a life-threatening and often intensely painful event. In this setting, a patient would typically experience extreme central crushing chest pain, often associated with nausea, vomiting, sweatiness and
profound pallor or greyness. This is a medical emergency.
Patients with this type of heart-attack usually present to the emergency medical services and the diagnosis is often made by paramedics in the community, based on the clinical history supported
by an ECG (Figure 1, below). The first principle of management is to transfer the patient to a place of safety so that the blocked artery can be opened as quickly as possible. Restoring blood flow and nutrient supply to the heart muscle is critical since the longer the muscle is deprived of blood, the more likely that in reversible injury, culminating in scarring and loss of function will occur.
Following large clinical trials in the 1980s, restoration of blood flow was generally achieved using powerful clot-busting enzymes (“thrombolysis”) that were injected intravenously and literally digested a blood clot, allowing the passage of blood to be restored. This is still a valid treatment used widely in much of the world, particularly where access to specialist cardiac centres in a timely fashion is restricted. More contemporary management, prevalent in the UK, is to restore blood through so-called “primary percutaneous coronary intervention”. In other words, the patient is transferred directly to a specialist cardiac centre where
the arterial blockage is relieved mechanically using techniques involving wires, balloons and stents all delivered through minimally invasive access in the radial or femoral artery.
In general, the quicker this therapy is delivered, the better. The benefit is greatest in the first 2 to 3 hours, falling quite steeply even within that time period and maintained at a lower level for up to 12 hours (Figure 2 below). Care providers actively monitor the times to effective treatment after (1) onset of symptoms; (2) first medical contact; (3) arrival at hospital. Integrated medical care systems, such as the National Health Service, where mechanisms of care delivery can be developed in a collaborative way that co-ordinates the ambulance system and the accepting hospitals have proven very effective in this emergency context.
Successful treatment of acute myocardial infarction typically involves the relief of obstruction by removal of the blood clot and inflation of a balloon within the affected artery (which is typically 2 to 4 mm in diameter); followed by placement of a metallic stent (Figure 3, see over). Where the procedure is uncomplicated, the patient is often discharged within 72 hours, with a package of medications and a structured rehabilitation program planned
The first presentation of this type of problem is often abrupt without any prior warning. However, not unusually, the definitive heart attack event is anticipated by episodic, milder though similar, symptoms in the preceding days. Unfortunately, is not unusual for patients and their carers to attribute these less dramatic symptoms to unrelated putative problems such as indigestion or acid reflux. Indeed without specific diagnostic testing, the actual diagnosis can be very difficult to pin down. Indeed the initial diagnosis often depends on clinical judgments. There are a number of diagnostic aids, including the measurement of troponin (a protein released from damaged heart muscle) and the electrocardiogram (ECG). However both of these tests are commonly normal even in the presence of significant coronary artery disease and should be considered ‘rule-in’ (when abnormal) rather than ‘rule-out’ (when normal).
In confirmed myocardial infarction, the objective of prompt effective treatment is to restore the blood supply to heart muscle in jeopardy and to prevent
permanent damage due to lack of oxygen and other nutrients. Where this is successful, damage to the heart can be very minimal, and sometimes discernible at all. It is frequently possible for a patient to return to a completely normal life. Unfortunately, this is not always the case. Irreversible damage may occur due to late presentation or delayed / ineffective treatment. Sometimes even where the treatment is apparently successful and the main coronary artery is opened,
the blood supply to the small blood vessel within the heart muscle remains compromised, perhaps due to obstruction with microscopic blood clot debris. In these cases, complications of myocardial infarction can ensue.
Complications of Acute Myocardial Infarction
It can be helpful to regard these as the immediate and early complications of acute MI and those occurring late.
Immediate and Early complications
As soon as the coronary artery is blocked (see above), the heart is in potential grave danger. The most significant potential hazard is that the lack of oxygen will render the heart susceptible to serious arrhythmias. In practice, this can mean very rapid, possibly disorganized contraction of the heart muscle. Where this is sufficiently severe, it can make the heart ineffective as a pump and may result in a catastrophic fall in blood pressure. Where there is insufficient blood pressure to perfuse the brain, loss of consciousness occurs. This constellation of events is a cause of “cardiac arrest”. Without immediate resuscitation, this would be fatal. Increasingly, with expanding awareness of cardiac arrest and cardio pulmonary resuscitation, patients are arriving at hospital following “bystander resuscitation”. This intervention can be a life-saving bridge to definitive treatment. Restoration of normal blood flow is often effective in removing the hearts susceptibility to these arrhythmias.
A similar presentation occurs when the heartbeats extremely slowly, a recognized complication of myocardial infarction. This usually resolves with effective treatment, but can occasionally require implantation of pacemaker.
Even where the heart rhythm is not disturbed, disruption to the blood supply to the heart can result in impaired pumping function. Not surprisingly, the larger the volume of blooddeprived heart muscle, the more significant is the likely negative impact on pump function. At the severe end of the spectrum, this can result in
extreme pump failure, with low blood pressure, accumulation of fluid in the lungs (“pulmonary oedema”) and sometimes failure of the kidneys and other organs. Happily, with the benefit of contemporary treatments this is now a relatively unusual scenario.
Even in patients who have sustained significant damage to the heart muscle, the future with appropriate medical management can be satisfactory from a symptom point of view. However, where there has been significant damage to the heart, “heart failure” can ensue in the succeeding months and years. This is often manifest as exertional breathlessness, ankle swelling and sometimes severe breathlessness requiring admission to hospital. The risk of heart failure can
be minimized by appropriate medical therapy, so-called ‘secondary prevention’.
Where normal heart muscle is replaced by scar tissue as a consequence of heart attack, a proportion of patients will be susceptible to lateoccurring arrhythmias. These may manifest as palpitation, but can also result in abrupt loss of consciousness (“syncope”). Clearly this abrupt, unheralded loss of consciousness can prove hazardous to the patient and potentially to those in the immediate surroundings. This would be particularly important in the context of driving or in the operation of machinery/working at heights etc. In some cases, for instance in patients with severely diminished pump function, it is possible to anticipate this arrhythmic complication and to implant a device known as an “implantable cardioverter defibrillator”, with the intention of rapidly detecting malignant arrhythmias and correcting them either with intensive pacemaker activity or with the delivery of an internal electric shock.
Risk factor and provocation
Risk factors for the development of atherosclerosis in the coronary arteries include genetic predisposition, high blood pressure, high plasma cholesterol, diabetes, tobacco smoking. Usually, it is not possible to determine the relative contributions of these factors. On occasion, there can be further contributory factors to the timing of acute myocardial infarction in susceptible individuals. For instance, cocaine use has been associated with surges in blood pressure, rapid heart rate,
increased coagulation of blood and spasm of the coronary arteries - all of which may contribute to heart attack. Similarly, intense physical exertion has been associated with a rise in heart-attack risk of over 100 fold. Significant emotional and can also place physiological strain on the heart predisposing to heart attack and / or arrhythmia in susceptible individuals.
Finally, it is worth noting that not all chest pain comes from the heart. Relatively common causes include oesophageal reflux and spasm, hiatus hernia, musculo-skeletal pain, pulmonary pathology including pulmonary embolus and, importantly, diseases of the aorta – most notably “aortic dissection”, which is a surgical emergency.
Pain or discomfort experienced in the chest, jaw or arm that is often provoked by exercise. Angina reflects inadequate nutrient supply to the heart muscle, usually due to atherosclerosis narrowing the coronary arteries.
Usually-spontaneous tear in the wall of the aorta. Can have very serious consequences including death and paralysis. Often present with severe chest and or back pain
Atherosclerosis Fibrous and fatty tissue that builds up in the walls of large arteries (such as the carotid arteries to the brain and the coronary arteries to the heart). Atherosclerotic diseases are very common and reflect a process that has often already begun by the second decade of life.
Catastrophic fall in blood pressure that is usually due to a heart dysrhythmia – either too fast or too slow. Commonly occurs in the context of heart attack.
Blood clot in the coronary artery. Most usual cause of a heart attack.
Damage to the heart muscle usually caused by blood clot in a coronary artery
Inability of the heart to work as a pump that can deliver nutrients to the other organs.
Implantable cardioverter defibrillator
Implanted device that monitors the heart electrical activity for abnormal rhythms and intervenes with an electric shock to correct the most malignant of them
Accumulation of fluid in the lungs, usually due to failure of the heart as a pump. Pulmonary oedema causes distressing breathlessness and requires prompt treatment.
About the author
Professor Robin Choudhury studied medicine at the University of Oxford with postgraduate training in London (Royal Brompton & Hammersmith), Boston (Massachusetts General Hospital), Oxford and New York (Mount Sinai). He is Professor of Cardiovascular Medicine at the University of Oxford, UK and Honorary Consultant Cardiologist at the Oxford Heart Centre.
His clinical practice is in interventional and general cardiology, including the management of patients presenting acutely. He is active in both clinical practice and research and has published approximately 150 papers and book chapters on aspects of cardiovascular disease. He is co-editor of the textbook “Cardiology Emergencies” (Oxford University Press). He has a particular interest and expertise in the assessment and management of chest pain and heart attack [myocardial infarction].
Professor Choudhury has been elected to Fellowships of the Royal College of Physicians, the American College of Cardiology, the European Society of Cardiology and of Balliol College. He is past President of the Royal Society of Medicine Section on Lipid and Vascular Risk. He serves on the Editorial Board of the Journal of the American College of Cardiology (Section Editor, Clinical Cardiology).
His professional bases are in Oxford and London.