Thursday, 21 August 2008



The most common cause of cardiac failure in the Western world is ischaemic (coronary) heart disease. Hence it receives first mention after cardiac failure. In addition, it is the world’s biggest killer, and increasingly so in other parts of the world (although George W. Bush is slowly catching up there).

Overall, it kills a quarter of a million a year in the United Kingdom, with a higher prevalence in men than women. An estimated 2.7 million people in the UK have it, and its death rate in the UK remains one of the highest in Europe, exceeded only by Finland and Ireland. It kills a quarter of all men who die in the UK every year, and a fifth of all women. Fortunately its mortality rate is getting better, thanks perhaps to earlier and better intervention. But there remains a lot of work to be done to stop this disease’s destructive influence.

The following risk factors for the condition, acting separately, or more frequently together, lead to the disease. They may be recalled by SHIFT MAID:

• Smoking
• Hypertension
• IDDM or NIDDM (diabetes) / Ischaemic heart disease (previous angina or ACS)
• Family history
• Triglycerides / cholesterol
• Male
• Age
• Inactivity
• Drinking (alcohol)

The first three together are known collectively as the medical ‘unholy trinity’. They interact together (with other factors) to cause atherosclerosis, damaging the coronary arteries, which are responsible for the fueling of the heart. The relative risks are shown in the diagram below.

So what is atherosclerosis? Since it is the pathological process responsible for 50% of mortality in the Western world (leading to cardiovascular, cerebrovascular and other vascular disease such as abdominal aortic aneurysms, aortic dissections and others), it is worthwhile spending a little time on it.

Atherosclerosis is a remarkable disease process, which despite its harms to human health, must be regarded with a kind of quiet respect. We are at war against this incredible enemy, probably our chief enemy, since it kills a great proportion of humanity. It is one our more recent wars, since it has only been recognised after the 1920s. As explained by Howell (2005):

“Heart disease was once behind pneumonia, influenza, tuberculosis, diarrhea, enteritis, and intestinal ulceration. A sharp upward trend in coronary artery disease became apparent around 1920, and it was recognized with increasing frequency throughout the first half of the twentieth century”.

The increasing frequency closely parallels developments and the rise of postmodernism; to quote Neville Woolf, Professor of Histopathology at UCL, “It is fair to say that many of the most significant risk factors are linked to lifestyle”.

The modern lifestyle is full of leisure – and smoking, overeating – leading to obesity and diabetes, stress and anxiety – leading to hypertension and ‘type A personality’ which places one at a greater risk of the condition. Alcohol abuse is contibuted to by stress and personality problems, and is another ‘leisure’ of modern day living.

As a result of all these excessive and in some cases forbidden pleasures, humanity has succumbed to this quite notorious enemy. The words of God ring true yet again:

“If only the people of the cities had believed and guarded against evil, We would have opened up to them blessings from heaven and earth. But they denied the truth so We seized them for what they earned. Do the people of the cities feel secure against Our violent force coming down on them in the night while they are asleep? Or do the people of the cities feel secure against Our violent force coming down on them in the day while they are playing games?”(7:96-98)

We are playing games with our lives, primarily through the neglect of God’s message. One wonders what the incidence of ischaemic heart disease would be in a perfect Islamic environment, where smoking is prohibited (as it ought to be, according to many scholars – as we will see in a later section ), stress and anxiety are kept to a minimum with the remembrance of God (“Verily, in the remembrance of God do hearts find rest”(13:28)), eating and drinking is kept to sensible limits, and man eats to live and not the other way round (“Eat and drink but do not be excessive for God does not love those who are excessive (in what they do)” (7:31)) and alcohol is banned. It would be almost ideal.

In any case, our battle with this powerful enemy is not going too well, but, through knowing it better, we would be more likely to succeed in defeating it in the future. All great military leaders were great tacticians, and they spent a great deal of time in understanding the tactics and strategies of their opponents. It is in this sense that one should approach the study of atherosclerosis, or ‘Atherosclerosis’.

The problem in defeating this formidable enemy lies mainly in the lack of knowledge regarding it; despite our pretence to the contrary, and “despite our familiarity with this disease, some of its fundamental characteristics remain poorly recognized and understood”, as Professor Peter Libby put it recently. Without this knowledge, we will never be able to defeat it. Because of this, so far the weapons we have been using to combat it have not been that effective.

Atherosclerosis can be likened to a devastating ruler, who has conned and trained the body’s good but unnecessary members into fighting against itself. Because they are unnecessary and unemployed, so to speak, having ‘graduated’ from the various universities of the human body, such as the liver (LDL), the kidneys (blood pressure) and others, they ‘revolt’ against it, against the body that has decided to render all of them redundant. And in most cases, they succeed. Once the disease process is established, it is very hard to reverse, and Atherosclerosis is king.

Atherosclerosis usually target specific locations, which are especially vulnerable to damage, regions of ‘disturbed blood flow’. As explained by Libby:

“Atherosclerosis tends to occur focally, typically in certain predisposed regions. In the coronary circulation, for example, the proximal left anterior descending coronary artery exhibits a particular predilection for developing atherosclerotic occlusive disease. Likewise, atherosclerosis preferentially affects the proximal portions of the renal arteries and, in the extracranial circulation to the brain, the carotid bifurcation. Indeed, atherosclerotic lesions often form at branching points of arteries, regions of disturbed blood flow”.

These natural variations in blood flow, leading to regional turbulence, predispose to damage. Within those naturally weak points (as evidenced by increased endothelial cell turnover and permeability), Atherosclerosis aims to establish itself. What follows is an incredible plan, and what it really highlights is that intelligent design in the human body is not only apparent in health, but also in disease. Disease is the handiwork of God; He inflicts it through causing defects in the body’s defence mechanisms, or by setting up powerful ‘military’ strategists such as Atherosclerosis.

It is unclear who the first soldiers are, but according to the most commonly accepted model of atherogenesis, the ‘response to injury’ hypothesis, it is possible that excessive blood pressure, causing damage within that region, predispose to damage to the endothelium, or excessive lipoproteins cause a similar damage. They “may collect in the intima of arteries because they bind to constituents of the extracellular matrix, increasing the residence time of the lipid-rich particles within the arterial wall. Lipoproteins that accumulate in the extracellular space of the intima of arteries often associate with proteoglycan molecules of the arterial extracellular matrix, an interaction that may promote the retention of lipoprotein particles by binding them and slowing their egress from the intima.” It is also felt that:

“Lipoprotein particles in the extracellular space of the intima, particularly those bound to matrix macromolecules, may undergo chemical modifications. Accumulating evidence supports a pathogenic role for such modifications of lipoproteins in atherogenesis. Two types of such alterations in lipoproteins bear particular interest in the context of understanding how risk factors actually promote atherogenesis: oxidation and nonenzymatic glycation”.

Following this, and other sorts of damage, the endothelial cells start to express ‘adhesion molecules’ and recruit monocytes and other inflammatory cells. These cells then form ‘foam cells’, which release fibroblast growth factors and induce smooth muscle migration into the intima. This results in formation of the atherosclerotic plaque; the fibrous cap is linked to clinical events due to its tendency to fracture and ulcerate, and the necrotic core has clinical consequence as a result of its size, consistency and thromboplastic components.

There is a complex interaction of cytokines (PDGF and FGF cause proliferation of smooth muscle and endothelial cells, IFN and TGF-beta inhibit cell proliferation and thus could account for endothelial cell discontinuities, and IL-1 and TNF stimulate activation of PAF, Tissue Factor, and PAI (plasminogen activator inhibitor)) in endothelial cells.

Thus the chief components of the atherosclerotic plaque are:

1. Damaged endothelium (which has its own functions)
2. Intimal smooth muscle cells (which proliferate as a result of endothelial damage)
3. Lipids which are deposited at the centre of the plaque and within the smooth muscle cells, some glycated, others oxidised (LDL).
4. Fibrous cap made up of connective tissue.

The pathogenesis of atherosclerosis is illustrated below. It causes clinical events only if it is large enough to obstruct coronary blood flow or until the plaque ulcerates or is disrupted, resulting in embolisation or thrombotic occlusion of the affected vessel.

The rsult of all this could be any of TEA:

• Thrombosis
• Endothelial dysfunction
• Aneurysm

But, as we have mentioned time and time again, God has equipped the human body with a number of mechanisms to counter such insults. Within the coronary arteries, such narrowing is countered with attempts at coronary dilatation, mediated via the substance adenosine, “which is the ideal messenger because it has a very short half-life. Adenosine may be the cause of anginal pain when released from the ischaemic cell, acting as a self-protecting mechanism”.

Thus, we can immediately see that ischaemic heart disease is not simply a disease of ‘narrowing of the arteries’. It is a very dynamic interplay of multiple factors. In addition, it highlights a wonderful irreducibly complex system – the heart has considerable energy demands, is well vascularised, and even very short interruptions to the blood supply can produce catastrophic results. Although the heart can use virtually any fuel store it is given, it is dependent on a continuous supply.

So even if we were to state that the heart could have evolved in a step by step process, as the evolutionists claim, the period between every step of the evolutionary process has to be infinitesimal, to allow for proper function to take place. This is not what the evolutionists believe; they feel evolution takes thousands or even millions of years to proceed.

In addition, we see the importance of normal endothelial histological continuity and function, normal blood constitution – in particular lipids and glucose – as well as viscosity; one of the suspected mechanisms by which smoking causes ischaemic heart disease is by increasing blood viscosity. In addition, smoking can cause the following (Kalra, 2005):

• Increased platelet aggregation and adhesion
• Increased heart rate and catecholamine sensitivity and release
• Increased carboxyhaemoglobin levels and as a result, increased haematocrit
• Decreased HDL cholesterol and vascular compliance

Family history highlights the presence of possible genetic factors; many of these act at the lipid, glucose or blood pressure level. With age, all systems decline, and the coronary arteries are no exception. The damage that long term alcohol dependency can cause to the coronary arteries is another indicator of the wisdom of its prohibition.


While we said above that atheroscelosis is a modern disease, it is possible that some of our forefathers had developed it, particularly those who lived until an old age. A few examples would be John Hunter and Martin Luther, both of whom died in their 60s (way above the average life expectancy in their time), and Isaac Newton, who lived a grande 85 years.

I remember coming across a wonderful little book, which I cannot get hold of now, where the author tries to formulate the medical history of Martin Luther, linking it all together (such as his high salt diet, and other things with his speculated hypertension, and his eventual death from heart failure caused by a heart attack). It made for truly fascinating reading. It would have been interesting to discuss him in this context, but Martin Luther has other interesting aspects of his medical history, so we shall leave him to a later section.

As for John Hunter, he too led a led a fascinating life, and had a very educational death.

Rather unusually, let us start with Hunter’s death, and then take our way through his life. This came on October 16th 1793, following a meeting of the board of governors at St. George’s Hospital, “at which he was angered by some of the discussion, he said nothing, left the room and turned to one of the physicians of the hospital, groaned and dropped dead. Present at the meeting were the Reverend James Clarke, Drs George Pearson (1751-1828), Robertson and Matthew, and Mr. Walker.” Following this, his body was “taken to his house in Leicester Square in a sedan chair at about 4.45 p.m., and at a later date a postmortem was performed under the supervision of his brother-in-law and executor, Everard Home. The operators were his house pupils, Edward Bradley, Francis Kinlock, Percie Smith and Nicol, assisted by Robert Haynes, the dissecting-room attendant. William Clift, Matthew Baillie (an executor) and David Pitcairn were also present, and the examination confirmed the cause of death as atherosclerosis, involving the arteries of the heart and brain.” Famously, Hunter remarked before this event, “My life is in the hands of any rascal who chooses to annoy me!”

John Hunter was a fascinating figure, who should definitely be more widely known. Some regarded him as “the Richard Feynman of the medical establishment of the 18th century” (anyone who has read or seen the great physicist’s works will know what that means), one of the founders of modern surgery, the founder of experimental pathology and one of the greatest anatomists of all time. He was a great scientist, a first class anatomist, who is credited by many as one of the first to bring medicine out of the dark ages into the light. As explained by Krooglik (2005):

“We have John Hunter to thank for bringing medicine, quite literally, out of the dark ages and into the scientific age. Prior to Hunter's arrival, doctors believed that most ill derived from imbalances in "humors." By bloodletting, drinking your own urine, etc, etc, one could have a hope of regaining health. Frankly, as Hunter quickly learned, this was complete and utter hogwash and he systematically set out to prove that many of that age's theories were plainly wrong. Hunter succeeded in not only altering the understanding of medicine and anatomy in his time but also in inculcating a true scientific approach in his teaching role that reaches to today. He literally taught over a thousand doctors, including those who would go on to found the University of Pennsylvania's hospital in the capital of the American colony in Philadelphia. These doctors spread around the world in a wave and ultimately brought down the ridiculous knowledge base founded by Galen thousands of years before and replaced it with a rigorous, scientific one.”

He was also renowned for his generosity and great assistance to medical students of his time. He was also a philosopher of sorts, and made several interesting very philosophical statements in his time – two of which stand out for me. The first is, “All the causes of things cannot be seen, because they appear to depend on circumstances which are unknown, or appear to be accidental”, reminding me of the Quranic verse, “It is not ye who slew them; it was Allah: when thou threwest (a handful of dust), it was not thy act, but Allah's: in order that He might test the Believers by a gracious trial from Himself: for Allah is He Who heareth and knoweth (all things)” (8:17). (The second somewhat echoes the tabula rasa of John Locke, “Man is born or comes into the world ignorant; but he is furnished with the senses, so as to be impressed with the properties of things; by which means he gradually, of himself, acquires a degree of knowledge. But man goes farther, he has the power of receiving information of things that never impressed his senses; and, if he has that power, it is natural to suppose that one man has the power of communicating his knowledge of things to another, each giving and receiving reciprocally; which we find to be the case”.

Locke, the great 17th century philosopher-physician who we discussed in the first chapter of this work, wrote, in his ‘Essay Concerning Human Understanding’:

“Let us then suppose the mind to be, as we say, white paper [tabula rasa], void of all characters without any ideas; how comes it to be furnished? Whence comes it by that vast store, which the busy and boundless fancy of man has painted on it with an almost endless variety? Whence has it all the materials of reason and knowledge? To this I answer, in one word, From experience: in that all our knowledge is founded, and from that it ultimately derives itself. Our observation, employed either about external sensible objects, or about the internal operations of our minds, perceived and reflected on by ourselves is that which supplies our understandings with all the materials of thinking. These two are the fountains of knowledge, from whence all the ideas we have, or can naturally have, do spring”.

Twelve centuries before either was born however, we find the Quran say exactly the same to us, “It is God Who brought you forth from the wombs of your mothers, you not knowing anything, then made for you the ears, the eyes and the hearts, that you may give thanks”(16:78). But no one gives it any credit for revealing this astonishing psychological insight, because the world is unfair and unjust.

John Hunter was clearly a type A personality, as most surgeons are. It is often speculated that the great Isaac Newton was a victim of a heart attack too. Medical history books that detail his biographical details tend to stop short at mentioning his famous attacks of gout (which we shall discuss later), but never mention his likely cause of death. This is one convincing attempt by one biographer, Dale:

"Sir Isaac is said to have enjoyed fair health and never to have been seriously ill until the age of eighty three. Then he began to suffer acute attacks of pain, the location of which is not indicated. The paroxysms increased in severity until, in the last months of his life, he would sit pale and impassive, his face covered with cold sweat. The doctors diagnosed his trouble as "the stone". Since there is no mention of urinary disturbance, the physicians probably had kidney or ureteral stone in mind. It appears that the diagnosis was based entirely on the apparent severity of the pain. Fontonelle is quoted as saying in his Eloge de Newton, "Twas thought he certainly had the stone which could not be cured, when the pain was so violent that drops of sweat ran from his face." About three weeks before his death, the pain left him and he expired peacefully on March 20, 1727, at the age of 84.

The probable cause of his pain was angina pectoris, symptomatic of the coronary artery disease that was to cause his death. Kidney colic causes the patient to writhe and cry out in agony; severe angina transfixes its victim with pain and a sense of imminent dissolution."

That seems much more likely, especially in view of the fact that Newton too died old, and had a type‘A’ personality throughout. His numerous quarrels, with many different eminent figures, most famously Leibniz, are testimony to this fact.


Chest pain is the most prominent feature of an ischaemic attack, be it stable angina, unstable angina or myocardial infarction (as illustrated on the following diagram). Angina is said to become unstable if it shows any of the following 4Rs:

• Recent origin
• Recurrent angina (in early post-infarction period).
• Resistant (progressive) angina.
• Rest angina.

The chest pain is usually retrosternal, severe, subacute in onset, gripping with radiation into the left arm, neck or jaw (reflecting common embryonic origins), or epigastrium (upper abdomen) and associated with breathlessness and autonomic symptoms (palpitations, dizziness, sweating, anxiety, impending feeling of doom). If associated with with syncope and breathlessness, aortic stenosis, causing increased demands on the heart (by increasing afterload), is a possibility. Claudication may be present; points towards diffuse atherosclerotic process If it lasts longer than 15 minutes, it is suggestive of unstable angine or MI (STEMI or NSTEMI) (ACS). A useful mnemonic characterising the pain is 6S:

 Sudden onset.
 Substrenal.
 Spread to right or left arm or both.
 Squeezing.
 Short duration.
 Sublingual nitroglycerin relieves.

It may be exacerbated by a number of things, usually exertion or eating. It is relieved by rest and nitrates in the case of stable angina; if it occurs at rest or is resistant to nitrates, it is more likely to be ACS. If it is unrelieved except with strong analgesia it is likely to be ACS.

To those who use the argument of evil, namely that, “If God is all powerful, all good, and all knowing, why does he allow pain and suffering in our lives?”, in order to negate the existence of God, we point them that there exists a condition called silent myocardial infarction, which contribute to the higher mortality of diabetic and elderly patients from cardiac events. It is felt that approximately one quarter of all myocardial infarctions are silent, without chest pain, and it is now established that, “Silent myocardial ischemia is proved to be a marker of unfavorable outcomes in coronary artery disease patients.” This is mainly because of a delay in seeking treatment. Thus pain here points in the direction of problems.

The patient almost invariably has some of the aforementioned SHIFT MAID risk factors. Therefore it is especially important to note the PMH and related risk factors (e.g. hypothyroidism and hyperlipidaemia). If a young patient is coming with what sounds like a cardiac event, then it is important to ask, within the drug history, if the patient is taking any cocaine or other sympathomimetic drugs. These cause vasospasm, rather than atherosclerosis.

The FH/SH cannot be neglected, for as we saw FH of IHD is relevant, as well as smoking and alcohol history. Certain occupations will be affected dramatically by the diagnosis; e.g. HGV driver will have license revoked if angina.

The physical examination is usually normal, and is an attempt to look for risk factors (e.g. tar stains, xanthelasma, xanthomata, hypertension), causes (e.g. AS – see above) or complications in case of MI (e.g. mitral regurgitation); MI patients should be regularly examined in the few days after admission to look for signs of complications.


The tools used in the investigation of coronary artery disease can be likened to the radars that nations use to detect threats or potential threats.

The only way to confirm that myocardial infarction has occurred is by viewing the heart; this can only be done directly in an operation or in an autopsy. The indirect way of confirming it is by echocardiography.

We are frequently taught that diagnosis of myocardial infarction is “based on the presence of at least 2 out of 3 of typical history, ECG changes, and cardiac enzyme rise” (OHCM). However, this is not strictly true, as many a pathologist who has done an autopsy on a patient who has sustained heart problem in his life, only to see a normal looking heart, or a cardiologist who has done an angiogram on a patient diagnosed via the fulfilment of those criteria (only to see normal coronary arteries) and an echocardiogram (only to have a very good result) would know. It is for this reason that a cardiologist of the stature of Richard Swanton writes regarding the diagnosis of MI, “This may pose a great problem, and there are no absolutely accepted criteria”.

The problem lies also in the fact that each of these three things – typical history, ECG changes and cardiac enzyme elevation can be caused by other things. A patient with an attack of oesophagitis may well present with exactly the same history as the patient with an MI, the ECG changes can also be caused by other things (see ECG section) and cardiac enzymes (including troponin – which is not strictly speaking an enzyme) can go up in other things).

Thus, myocardial infarctions cannot be ‘diagnosed’ (in the sense of knowing what problem the patient is suffering from), until a post-mortem or visualisation of the heart is undertaken. It can be the most likely suspicion, the closest approximation to the truth, and indeed this suspicion is increased with the fulfilment of more criteria. But it remains a suspicion, to be confirmed by the pathologist or cardiothoracic surgeon.

This is a very important point, because it highlights the point that medicine can never be a guide to truth. Much of what we believe and do is based on ‘faith’. The atheist physician ought to reflect on this, and note that his or her belief in medicine is based on exactly the same type of faith as that of any other person of faith. He or she cannot ridicule the man of faith and claim that ‘they believe in science only’, for even science, as David Hume showed, is based on faith, and medicine much more so.

In any case, in the majority of UK hospitals, “no longer do we find ourselves meticulously mapping out the rise and fall of traditional ‘cardiac’ enzymes over time. No longer do we necessarily relax in the absence of ST-elevation. With the advent of the routine measurement of the cardiac troponins, a whole new range of ischaemic entities, previously defying classification has been born”. There are many types of troponin-assays. Troponin T is better than troponin I as it is more specific and not raised in renal failure. In patients with renal failure presenting with chest pain, it is helpful to assess the troponin level at the baseline as well as at 12 hours after the onset of symptoms, and sometimes at later time points. In these circumstances only a rising troponin would be suggestive of ischaemic myocardial damage.

The other causes of high troponins are TROPS:

 Tachycardia
 Renal failure / Running (intense exercise e.g. marathon runners)
 Operations (cardiac surgery, heart transplant)
 Pulmonary embolism
 Sepsis (see above table)

 Cardiac amyloidosis
 Cardiac contusion
 Cardiac surgery and heart transplant
 Defibrillation
 Closure of atrial septal defects
 Coronary vasospasm
 Dilated cardiomyopathy
 Heart failure
 Hypertrophic cardiomyopathy
 Myocarditis
 Percutaneous coronary intervention
 Radiofrequency ablation
 Supraventricular tachycardia  Critical illness, e.g. sepsis
 High-dose chemotherapy
 Primary pulmonary hypertension
 Pulmonary embolism
 Renal failure
 Subarachnoid hemorrhage
 Scorpion venom
 Stroke
 Very heavy exercise (marathon)

As for other enzymes, their measurement is not advised now, but they can be done sometimes. With them, the sequence of elevated enzymes can be remembered as CASTLE:

 CK-MB and myoglobin first. Myoglobin is a storage molecule of oxygen in muscle. It is the earliest marker of MI and the first marker to clear. It rises within 2-4 hours of infarction, peak 6-12 hours, returns to normal in 24-36 hours
 AST second
 LDH third

As for ECG, these may show ST depression, flat or inverted T-waves and possible signs of previous MI in angina; in ACS, hyperacute T-waves, ST elevation or new LBBB occur within hours. T-wave inversion and the development of pathological Q waves follow over hours to days. Note that 20% of MIs, the ECG may be normal initially. Remember that ACS changes STart with ST changes, then T and eventually Q.

Note the crucial point that ECG is not sufficiently specific or sensitive to be used in isolation of the patient’s clinical history (BMA guidelines). Hence there is no point in extrapolating cardiac information from an ECG if there are no cardiac symptoms.

Table 5-3. ECG Localization of Myocardial Infarction
Infarct Location Leads Depicting Primary ECG Changes Likely Vessel* Involved
Inferior II, III, Avf RCA
Septal V1 and V2 LAD
Anterior V3 and V4 LAD
Anteroseptal V1-V4 LAD
Extensive anterior I, aVL, V1-V6 LAD
Lateral I, aVL, V5 – V6 CIRC
High lateral I, aVL CIRC
Posteriort† Prominent R in V1 RCA or CIRC
Right ventricular‡ ST elevation, V1 and, more specifically, V4R in setting of inferior infarction RCA

As for angina, the best test is the angiogram, directly visualising the coronary arteries and looking at the extent of narrowing. However, stress tests such as the ETT (or dobutamine stress test or thalium scan if debilitating joint, lung or peripheral vascular disease) are cheap, indirect ways of checking coronary blood flow, although up to 20% of patients with ischemic episodes do not show electrocardiographic changes with pain.

Once the diagnosis is confirmed by any of the above means, it is necessary to know the culprits of that damage. Is it raised glucose or lipids, building up the atheroma, or is it aortic stenosis, increasing the workload of the heart and increasing its oxygen demands. Thus blood tests checking for these things as well as an echocardiogram, are required in many such patients.

As for the consequences, these too may be the first pointer towards a coronary problem. They can be recalled as ACTRAPID:

 Arrhythmias (sometimes due to electrolyte disturbance)
 Cardiac failure
 Tamponade / Thromboembolism
 Rupture
 Aneurysm (left ventricular; occurs 4-6 weeks post-MI)
 Pulmonary oedema
 Infarction (re-infarction)
 Dressler’s syndrome

Thus echocardiograms (CHF, thrombus, papillary muscle rupture, septal rupture, ventricular aneurysm), ECGs (arrhythmias, pericarditis), CXR (pulmonary oedema, heart failure) and measurement of U &E s (especially K+), D-dimers, and cardiac enzymes (re-infarction) may be useful.

Dressler’s syndrome occurs 1-3 weeks after an MI, and consists of raised ESR (in word DrESsleR) plus 3P:

 Pyrexia
 Pericarditis
 Pleural effusion

To summarise the main features of the three main types of angina, the following table is of great use.

Table 9-2. Angina Pectoris
Type Pattern ECG Usual Coronary Abnormality
Stable Chronic unchanged pattern of precipitation and relief
Induced by physical activity or emotional stress; lasts 5-10 min, relieved by rest or sublingual nitroglycerin Baseline often normal or nonspecific ST-T changes, or signs of prior myocardial infarction
ST segment depression or T wave inversion during angina ≥ 70% stenosis resulting from atherosclerotic plaque in one or more coronary arteries
Unstable Recent increase in angina frequency or severity, especially with rest pain; new-onset angina if at low activity level; angina after a myocardial infarction
May last longer and be less responsive to sublingual nitroglycerin As with stable angina, although changes during discomfort may be more pronounced
Occasionally, ST segment elevation during discomfort Fissured plaque with platelet and fibrin thrombus contribute to stenosis
Prinzmetal's or variant angina Typically unpredictable rest pain, often in early morning hours Transient ST segment elevation during pain (ST segment depression and/or T wave inversion can also occur) Coronary artery spasm at a region of fixed but often nonstenotic lesion; can also occur in angiographically normal vessel


All acute coronary syndromes are medical emergencies, and because it may be difficult to differentiate between ACS and angina in the beginning, it is best to treat stable angina too as an emergency.

The principles of emergency, with ABCDEFG & MOVE are used; cardiac monitoring is vital (monitoring for prompt treatment of ventricular fibrillation remains the most cost-effective intervention to prolong life), and put on oxygen (100%). If the patient’s BM > 10 put on a sliding scale even if not known diabetic.

The most important task of the emergency doctor is to stabilise the patient and prevent immediate problems that can arise.

Giving oxygen and controlling symptoms with analgesia (with antiemetics) helps reduce the patient’s anxiety. Morphine is the analgesic of choice, although if the patient still complains of pain, start IV GTN 50 mg in 50 mls normal saline infused at 2-10 mg/hr, titrated to pain and blood pressure, aiming to keep the systolic BP > 100 mmHg.

Giving the patient antiplatelets and anticoagulants such as aspirin (300 mg stat), clopidogrel (300 mg stat) and clexane (1 g/kg bid) will stop platelet adhesion and clot formation around the ruptured plaque site, and prevents immediate problems. It is only in patients with evidence of ST-elevation or new LBBB, in whom there is potentially complete block by a plaque, rather than a mere ruptured aspect of it, that we consider thrombolysis. This should never be considered in patients who have any of the following, recalled by HEPAR:

• Haemorrhage / Hypertension (malignant)
• Esophageal varices
• Peptic ulcer disease / Pregnancy / Previous use in last year
• Allergy / Aortic dissection
• Recent surgery or trauma / Recent CVA or streptococcal infection

And one should always watch out for potential side effects such as:

• Allergic reaction – give IV hydrocortisone 100 mg and chlorpheniramine 10 mg
• Hypotension – stop infusion and if blood pressure improves, restart at half the rate.
• Haemorrhage – consult haematologist, stop infusion, give blood and FFP, or antagonise with tranexamic acid. Reduced GCS strongly suggests intracranial haemorrhage; an urgent CT head is needed.

With the patient stablilised, anticoagulated, ‘antiplateleted’, and possibly thrombolysed, medical referral becomes mandatory, and they ought to look after the patient until the time for measurement of the 12 hour troponin come. When it returns you can carry on treating as:

1. Stable angina – stop clexane and clopidogrel, and continue aspirin and GTN spray, as illustrated below:

2. Unstable angina / NSTEMI – carry on aspirin 75 mg od and clopidogrel 75 mg od and GTN spray, with consideration of angiography based on the TIMI score

3. STEMI - carry on aspirin 75 mg od and clopidogrel 75 mg od with thrombolysis considered or urgent angioplasty

All patients with unstable angina, NSTEMI and STEMI should be monitored in CCU. The main reason for this is that they are at risk of developing sudden arrhythmias.

Angiography and possible further intervention should be considered in all high-risk patients; these are identified by a high TIMI score, troponin positivity and haemodynamic instability. The TIMI score consists of 7 variables, highlighted in bold below, are STARCH:

 Stenosis (50% on recent angiography) / ST segment dynamic changes
 Troponin positive
 Age > 65 / Aspirin use in last 7 days
 Risk factors > 2 / Recurrent angina
 Cardiac enzymes elevated
 Hemodynamic instability

The complications of coronary angiography include DASH:

• Death
• Arrhythmias
• Stroke
• Haematoma (at site of puncture)/Heart attack (MI)

If the patient is not bradycardic, they should be put on a beta blocker; if very tachycardic, consider IV beta blockers, e.g. metoprolol 12.5 mg IV and 25 mg tds thereafter – which should be avoided if heart failure or asthmatic or COPD. If symptomatic bradycardia, give IV atropine 0.5 mg every 5 minutes to a maximum of 3 mg total; if persistent, consider temporary pacing.

Monitor the patient carefully subsequently for signs of ACTRAPID, and treat as appropriate.

To summarise the treatments used:

• Beta blocker (or calcium channel blocker)
• Aspirin
• Nicorandil

• Oxygen
• Beta blockers / Bed rest
• Aspirin & Clopidogrel
• Thrombolytics
• Morphine & Metoclopramide
• Antithrombotics
• Nitrates

In unstable angina you don’t thrombolyse. Always ensure long term management is instituted, with ABCDE:

• Antiplatelet agents (aspirin, clopidogrel)
• Beta-blockers/Blood pressure control
• Cholesterol lowering / Converting enzyme inhibition / Cessation of smoking
• Diet (heart-healthy)/Diabetes control
• Exercise

It is crucial to bear in mind the POSSETs of cardiovascular disease (like cardiac failure above), especially the need for cardiac rehabilitation. Remember that the patient should be off work and avoid air travel for 2 months, not drive and avoid intercourse for the same (one month).

Thus, we can see there is lot more to atherosceloris than is normally supposed. It is one of the most fascinating assassins around; silent, internal, and capable of killing by many modes, including damaging, by thrombosis, aneurysm rupture or complete atherosclerotic blockage, of the fuel supply to the most incredible machine known to man, the human heart.


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