Heart Attacks – An Ounce of Prevention
Half of all heart attack victims die after their first attack. The other half, more often than not, wander the earth in an imitation of life, popping pills and practising self denial. Heart attacks are scary, and the average victim doesn’t want a repeat. On this basis, many feel grateful for the bewildering array of pills vasodilators, antiarrhythmics, antihypertensives, diuretics and cholesterol drugs and surgical techniques which are on offer. Some patients as well as doctors invest these things with magic, life giving potential, though there is little evidence of this.
While early mortality from heart attacks death within the first 15 days to a year depending on which study you read appears to be on the decline, the incidence of heart failure is increasing (Lancet, 1993; 341: 733-36). In US about 1 per cent of the population is having a heart attack at any one time (Cardiol Clin, 1989; 7: 1-9). In the UK about 1 million patients per year currently receive treatment for heart attacks. The question is, is it doing any good?
Each week whole forests are laid to waste reporting what we now know about heart disease. Yet the function of many heart drugs, indeed what causes heart attacks in the first place, is still not well understood. The standard risk factors smoking, high blood pressure and cholesterol account for only 50 per cent of total risks (JAMA, February 24, 1993). Because of this a wide ranging approach to heart health is likely to yield the most promising results. When considering lifestyle modifications this is a sound principle. When considering drug therapy and/or surgery it could be fatal.
A single drug can act in several different ways, sometimes unpredictably. Trials have shown that combining drugs can be fatal. For example, in trials where enalapril (an ACE inhibitor) or hydralazine (a vasodilator/antihypertensive) and isosorbide dinitrate (also a vasodilator) when added to digoxin (a glycoside to increase the force of the heart beat) and used in combination with diuretics (to treat hypertension) survival rates did improve but not by much. Within four years more than 40 per cent of the patients enrolled in these trials were dead (N Eng J Med, 1987; 316: 1429-35; N Eng J Med, 1991; 325: 293-302; N Eng J Med, 1991; 325: 303-10; N Eng J Med, 1986; 314: 1547-52).
One long term trial in Finland showed that patients on the receiving end of multiple interventions were actually more likely to die from heart failure than those who received no interventions (JAMA, 1991; 266: 1225-9). Another trial in Gottenburg following 10,000 middle aged men for 10 years showed no reduction in mortality from a multiple intervention programme (Eur Heart J, 1986; 7: 279-88). Another trial of more than 12,000 men showed similar results (JAMA, 1982; 248: 1465-77; JAMA, 1990; 263: 1795-801), as did a World Health Organization study of 61,000 men (Lancet, 1986; i: 869-72). In fact, in the British arm of the WHO study the death rate from heart disease was 8 per cent higher in the intervention group (Lancet, 1983; i: 1062-6).
Indeed, the latest study from North America demonstrates that this get in there early aggressive intervention doesn’t do one bit of good. The study, which compared the use of cardiac procedures and mortality rates of more than a quarter of a million elderly patients in both Canada and the US, found that America had strikingly higher rates of aggressive cardiac treatment than Canada: 11 times the rate of angioplasty, and 10 times the rate of bypass surgery. Although short term mortality after a heart attack was slightly lower initially (21 per cent versus 22 per cent), this small gap was closed after a year. In the long term, survival rates were virtually identical between the two countries (New Eng J Med, 1997; 336: 1500-5).
Drug treatment doesn’t seem to provide long term gains. Other studies show between a 3 and 7 per cent short term (30-35 days) post heart attack survival rate with early drug treatment (Lancet, 1994; 343: 311-22; N Eng J Med, 1993; 329: 673-82). While these numbers may provide comfort for the few who survive, the overall question still remains about the real benefit of conventional treatments or the policy of concentrating merely on keeping patients alive, rather than encouraging them to take steps to improve the quality of their lives.
Heart attack, or myocardial infarction (“death” of the heart muscle caused by an inadequate blood supply) is usually caused by obstruction of the coronary artery due to atherosclerosis. The condition may occur suddenly or after a history of angina pectoris (chest pains). Some people have little evidence of blockage, in which case it is assumed that spasm of the coronary artery is responsible. To treat these two possible causes, patients are offered a range of drugs to unclog and/or dilate arteries, to thin the blood or strengthen the force of the heart beat.
Beta blockers which have both an anti arrhythmic and antihypertensive action only reduce the possibility of a further heart attack by a very small margin and have other implications for a person’s health. They cause dizziness, impotence, nausea, coldness in the extremities, nightmares and insomnia. In one study atenol doubled the risk of kidney cancer in hypertensive patients (Hypertension, 1996; 28: 321-4). Beta blockers can also produce sudden, irregular heart beats which can cause death. One trial was stopped early because the side effects were so alarming (Lancet, 1996; 348: 7-12) and the editorial which accompanied this research concluded that we must assume that all anti arrhythmic drugs are potentially lethal.
Calcium channel blockers such as verapamil, diltiazem and nifedipine are also used to treat hypertension. But the FDA has now cautioned against using nifedipine since it has been shown to create first a sharp drop, followed five hours later by a sharp rise in blood pressure, thus increasing the risk of heart attack (JAMA, 1996; 275: 423; JAMA, 1996; 275: 515).
Calcium channel blockers can stop blood coagulating, but what is good for the heart is not necessarily good for the stomach. They have been shown to cause severe stomach bleeding in the elderly (Lancet, 1996; 347: 1056). They can also double your risk of getting cancer (Lancet, 1996; 348: 49).
Anti arrhythmics can cause the problem they are trying to treat. In one large trial there were significant deaths in those taking encainide and flecainide. Nearly 6 per cent of patients died from arrhythmias while taking these drugs, as opposed to 2.2 per cent of those who took placebo (N Eng J Med, 1991; 324: 781-88). Equally, nearly 3 per cent died of heart attack compared with 0.7 per cent of the placebo group.
In the three year SOLVD (Studies of Left Ventricular Dysfunction) trial (N Eng J Med, 1992; 327: 685-91) ACE inhibitors the newest class of heart drug prevented three episodes of non fatal heart failure for each 100 patients treated per year. Because of this it has been suggested that patients should be given ACE inhibitors to prevent further episodes (N Eng J Med, 1992; 327: 725-27). But a look at the long term picture is revealing: ACE inhibitors (in this case enalapril) saved only one life for every 300 patients treated.
Angioplasty when a “balloon” is inserted to clear the blockage is no better than drug therapy in preventing death (N Eng J Med, 1996; 335; 1253-60). This conclusion was borne out by research which showed that angioplasty fared badly against bypass surgery (N Eng J Med, 1997; 336: 92-9). In the study, angioplasty patients were able to return to work earlier but bypass patients could perform more daily activities such as housework and walking. Both procedures added an average of 4.4 years to the lives of patients. But angina levels in the angioplasty group were 26 per cent, compared to 11 per cent in the bypass patients. Nearly 60 per cent of the angioplasty group had to have further treatment because the arteries started to clog up again.
It’s not all good news for bypass surgery, which has been associated with a high rate of stroke following the procedure. About 6 per cent of patients may suffer a stroke directly afterwards. Of these 5 per cent die and nearly half suffer deterioration in mental functions (N Eng J Med, 1996; 335: 1857-63).
There is much that heart attack victims can do for themselves. Diet and lifestyle are factors within an individual’s control. There is plenty of research to show that eating raw foods can prevent heart attacks. Two or three servings a day of fruit, high in vitamin C and soluble fibre, can reduce the risk of heart disease by as much as 25 per cent (N Eng J Med, 1987; 316: 235-40; Am J Epidemiol 1987; 126: 1093-102; Am J Epidemiol, 1994; 139: S47). One 17 year study showed that people who eat fresh fruit every day are less likely to suffer from heart problems, with 24 per cent less fatal heart disease, a 32 per cent reduction in death from stroke and overall a 21 per cent lower mortality rate (BMJ, 1996; 313: 775-79). The same study revealed that if you have a raw salad every day your risk of fatal heart disease is lowered by 26 per cent.
A recent study of heart attack patients used a CAT scanner to measure the arteries of those who followed a vegetarian diet. The results showed that over five years arterial disease was actually reversing in 99 per cent of them (JAMA, 1995; 274: 894-901). This good news needs to be taken in context. Some very low fat diets can change levels of HDL cholesterol or result in low levels of essential fatty acids, both of which have been associated with an increased risk of heart attack (JAMA, 1996; 275: 1402-3).
There is no agreement on whether it is best to follow a strict vegetarian diet or a low or high carbohydrate diet. Certainly the stress of radically altering your diet may do more harm than good. Low levels of cholesterol can also cause violent mood swings and suicidal depression (see box page 2).
This is particularly true in the campaign to lower cholesterol levels. Universal screening for cholesterol has been condemned by the American College of Physicians, who recommend that those over 75 can safely ignore screening since cholesterol is not a risk factor in this age group. It is also not recommended for men under 35 or women under 45 unless they have a family history or more than two of the following risk factors: high blood pressure, cigarette smoking and diabetes.
The cholesterol lowering drug pravastatin has been shown to be little better than a sugar pill in protecting against a second heart attack. In one study of 4000 heart attack survivors with average cholesterol levels, 10 per cent on pravastatin had a second attack, compared to 13 per cent on a placebo within the first five years (N Eng J Med, 1996; 335: 1001-9).
Ironically, saturated fats found mainly in meat may not be linked to heart disease at all. One review of the literature on saturated fat failed to show any link between it and heart disease (BMJ, 1996; 313: 84-90). The review cited three studies in the last 20 years which show no link between meat eating and cholesterol and heart disease. In fact, the link between meat eating and heart disease is made in only one major paper (BMJ, 1996; 313: 1258). Lowering fat intake and cholesterol does not, in any case, appear to make that much difference to total plasma cholesterol concentrations (JAMA, 1982; 284: 1465-77).
A number of studies suggest vitamins may have a more protective effect. Of these, magnesium shows the greatest promise. Deficiency in magnesium has been long been thought to increase kidney damage and as a result can cause hypertension and thus heart trouble (J Exp Med, 1957; 106: 767-76; Am J Clin Nutri, 1959; 7: 13-22; Lancet, 1980; ii: 720-2). More recent studies have shown that the mean daily intake of magnesium in men who later experienced heart disease is around 12 per cent less than in those who did not (Br Heart J, 1988; 59: 201-6).
Intravenous infusion of magnesium salts, if given soon after a heart attack, has been shown in a randomized, double blind placebo controlled trial to be comparable to that of more aggressive thrombolysis or antiplatelet therapy (Lancet, 1992; 339: 1553-8) with no long lasting side effects.
Some practitioners continue to argue that magnesium is less effective than standard treatments, usually quoting the ISIS-4 trial. However, in this leg of the large clinical trial investigating stroke and heart attack treatments, 7.64 per cent of patients receiving magnesium died compared to 7.24 per cent in the standard treatment group (Lancet, 1995; 345: 669-85), showing that magnesium is at least as effective as orthodox treatments.
Why, then, are these less aggressive measures not put into practice? Diagnosing and treating heart problems can be complicated. GPs routinely refer patients with suspected heart trouble directly to a specialist, even when this is not clinically justified (JAMA, 1996; 276: 481-5). One survey found that GPs attitudes to the prevention of coronary heart disease by health promotion was that it was “tedious, dull and boring” (Soc Health Illness, 1994; 16: 372-93). Doctors were unhappy with the uncertainties entailed in identifying risk factors, ambivalent about the effectiveness of changes in behaviour and concerned that their actions were a moral intrusion into their patient’s lives.
Specialists have a greater faith in the drugs and technology at their disposal (N Eng J Med, 1994; 331: 1136-42). It can be difficult for doctors to believe that in some cases doing nothing may be the best course of action. Equally, it is sometimes difficult for patients who have suffered a heart attack to believe that what needs to be done needs to be done by them and not to them.
Sidebar: Heart drugs – the dangers
Vasodilators (nitrates, calcium channel blockers)
Headaches; dizziness; hypotension and potentially fata! altered heart rhythm (either too fast or too slow). Calcium channel blockers can cause constipation; vomiting; edema; sudden rapid heart beats; liver disorders; rashes; depression and gastrointestinal disorders.
Anti-hypertensives (Ace inhibitors, diuretics, potassium channel blockers)
Ace inhibitors can cause sudden drops in the blood pressure. A dangerous rise in potassium levels and when used with some diuretics, fluid on the lungs). Kidney malfunction; muscle cramps; diarrhea; nausea; fatigue; rashes; abdominal pain; heart palpatations; jaundice; sleep disturbances; mood swings and impotence.
Diuretics can cause gastrointestinal disturbances; dry mouth; skin rashes; photosensitivity; kidney damage and pancreatitis.
Beta-blockers
Potentially fatal slowing of the heart; asthma; fatigue; cold hands and feet; sleep disturbances; nightmares; stomach upsets and rashes.
Anti-arrhythmic
Heart failure; chest pain; choking sensations; light-headedness; impaired vision; skin discolouration; phototoxicity; diarrhea; fever; lupus-like symptoms; psychosis and liver damage.
Antiplatelets (aspirin, anticoagulants)
Gastrointestinal problems; respiratory disorders; stroke; diarrhea; vomiting; throbbing headaches and hypotension.
Cholesterol lowering drugs
Severe depression; suicidal violent tendencies; constipation; vitamin K deficiency and impotence. Also an established link with cancer of the lung, thyroid, testis and lymph nodes.
Sidebar: Depression and heart attack
Sadness, isolation and loneliness can cause heart attacks. In one study in San Francisco and another in Eastern Finland, of the 20,000 people observed for up to nine years, those who were lonely and socially isolated were two to three times more likely to die from heart disease and other causes than those who felt connected to others. These results were independent of other risk factors such as cholesterol levels and high blood pressure (Am J Epidemiol, 1979; 109: 186-204; Am J Epidemiol, 1988; 128: 370-80).
Depression after heart attack has also been recognized as having an influence on patients’ survival rate. Its impact is at least equivalent to that of left ventricular dysfunction and a history of previous heart attack (JAMA, 1993; 270: 1819-25). Again, this effect has been shown to be independent of the severity of the patient’s condition (JAMA, 1993; 270: 1819-25; Circulation, 1995; 91: 999-1005).Depressed patients experience physiological changes such as decreased heart rate variability (J Psychosom Res, 1988; 32: 159-64; Am J Cardiol, 1987; 59: 256-62). Studies also show that the hormone serotonin not only plays a major part in the development of depression but also influences the formation of blood clots (Pharmocol 1991; 17(suppl5): S6-S12).
The low cholesterol regimes which heart attack patients are often put on only exacerbate the problem. Men with low cholesterol levels are three times as likely to commit suicide (BMJ, 1996; 313: 664). Those with naturally low levels are most at risk, but those whose levels are lowered by drugs are still at double the risk.
Sidebar: Heart attacks and back strain
Is there a link between back strain and heart attacks? In his book The Heart Revolution (Arrow, lb6.99), Dr Paul Sherwood believes that the key to heart attacks brought on by spasm lies in the spinal column. In Dr Sherwood’s experience “many coronary attacks are the result of an old injury which has jolted or twisted the upper part of the back, giving rise to serious repercussions throughout the whole body.”
The muscles in the back have a vital role to play in helping to pump blood back into the heart. As the muscles contract they squeeze blood out of surrounding tissues. However, in a back which has been injured the muscles may stay in a continuous state of spasm, even when there appear to be no symptoms. In this state they are unable to pump efficiently. Over a period of years this damage can build up and affect surrounding organs including the heart.
This theory has gained some credence with the publication of Finnish research which showed a link between back pain and the risk of fatal heart disease (BMJ, 1994; 309: 1267-8). The risk was greatest in men aged between 30-49 years old.
Sidebar: Alternative treatment for heart patients
There is no magic bullet. Prevention of heart attack requires a wide ranging approach and often radical change in lifestyle.
Exercise. The usual suggestion is that you should take up vigorous exercise such as swimming, cycling or brisk walking. This does not suit everyone and has recently been challenged through the medical press. Regular programmes of walking can be even more beneficial. Yoga, which combines relaxation, stretching and flexibility, will lower your chances of having another attack (BMJ [Clin Res], 1985; 13: 1103-6; Lancet, 1975; ii: 93-5).Lose weight. Being overweight does not put you at increased risk of heart disease, but it does increase your risk of high blood pressure.
Weight loss usually involves diet changes. Rather than just restricting calories, a more sensible approach would, be to pay attention to what you eat. Certain foods are more effective heart protectors than others. In general Mediterranean or Indian diets high in fresh fruit and vegetables, onion and garlic, fish and chicken and polyunsaturated and monosaturated oils offer the best protection (J Cardiol, 1992; 69: 879-85).
In one study those on a Mediterranean diet decreased their risk of heart problems by a staggering 70 per cent (Am J Clin Nutri, 1995; 61(6 Suppl): 1360S-67S). The clinical effects of altering your diet in this way are thought to be the same as taking 180 mg of aspirin daily (Nutrition, 1991; 7: 119-23).
Increase folate. High levels of the amino acid homocysteine can cause cardiovascular disease, which affects the heart and blood vessels. Homocysteine levels can be lowered with even a small amount of folate (JAMA, June 26, 1996).
Supplement with antioxidant vitamins A, C and E for a general protective action (Lancet, 1991; 337: 1-5). Vitamin C has cardioprotective qualities (BMJ, 1995; 310: 1559-62). As little as one orange a day (equivalent to an extra 60mg daily) can decrease risk of heart attack by 10 per cent (Lancet, 1994; 343: 1454-9). Vitamin E is associated with a reduced risk of heart disease (N Eng J Med, 1993; 328: 1444-9; N Eng J Med, 1993; 328: 1450-55).
Coenzyme Q-10 is a vitamin like substance which is found in the heart muscle. Daily doses of around 150mg can also reduce angina attacks substantially. It can also help increase stamina (Am J Cardiol, 1985; 56: 247).
Increase fibre intake. Studies show that fibre (especially soluble fibre), has an role to play in the prevention of cardiovascular disease (JAMA, 1996; 275: 447-51) which is independent of other dietary measures. Fibre decreases LDL (“bad” cholesterol) and has little or no effect on HDL (“good”) cholesterol.
Avoid hydrogenated fats. Consumption of trans fatty acids produced by the partial hydrogenation of vegetable oils can lead to heart disease (Lancet, 1993; 341: 581-5). They interfere with essential fatty acids metabolism (Proc Natl Acad Sci, 1982; 79: 953-57), as well have having other deleterious effects on our health (N Eng J Med, 1990; 323: 439-45; Acta Paed Int J Paed, 1992; 81: 302-6). TFAs may be a greater health hazard than both dairy products and natural saturated fats (Lancet, 1993; 341: 1093).
Check toxic metal levels. High levels of cadmium are associated with potentially fatal cardiovascular disease (J Am Med Assoc, 1966; 198: 267; Ecologist, 1971; 1: 11).
Lead in your drinking water, especially in soft water areas, can contribute to hypertension (Medycyna Pracy, 1994; 45(2): 163-70). Consider chelation therapy a method which employs molecules called chelators to remove toxic metals in the body.
- This article first appeared in the July 1997 (Volume 8 Number 4) edition of What Doctors Don’t Tell You.
