Sudden Cardiovascular Death

by Ben Best


It is common to hear people say that they would most prefer to die in their sleep, or at least prefer to die suddenly. For cryonicists concerned about the effects of brain ischemia (loss of blood circulation) and autolysis (dissolution of the brain in putrefaction), such a scenario is a disaster.

On July 10, 1991 Jerry Leaf, Leader of the Alcor Suspension Team, died suddenly at the age of 50 from a cardiac arrest. Despite the fact that his death was witnessed, despite his years of work at the forefront of cryonics and despite the nursing expertise and rapid application of CPR by his wife, Jerry experienced 6 hours of ischemia above 20C. Sudden death (even under the best of circumstances) makes a cryonicist a "coroner's case", subject to legal delays before cryonic procedures can begin. More recently, John Erfurt, a 58-year-old Director of the Cryonics Institute, experienced sudden death on September 9, 1992. Although the medical examiner signed the death certificate almost immediately, his body was not discovered until several hours after clinical death. That such compromises of cryonic rescue capability is possible even among the most committed of cryonicists is a matter of serious concern.

Considerable autolysis can be expected of a person who is discovered dead in bed many hours after the cessation of heartbeat. Moreover, the blood vessels of the brain are very sensitive to loss of oxygen. In less than an hour after deanimation it can become virtually impossible to restart brain circulation by artificial means for the purpose of perfusing the brain with cryoprotectants. Even in the early stages, when recirculation is possible, reperfusion injury occurs if too many minutes of ischemia have occurred.

The avoidance of sudden death should be a high priority for cryonicists. A good suspension will involve a rescue team on standby with knowledge that deanimation is immanent. Ideally, this will occur outside of a hospital, with a co-operative nurse on duty who can sign a death certificate without delay. There should be no danger of becoming a "coroner's case" under these circumstances. Death is our enemy, a sudden and unexpected death is our most deadly enemy. Know your enemy! A greater knowledge of sudden death means a greater likelihood that it can be avoided or dealt-with.


In Roy Walford's book MAXIMUM LIFESPAN (1), he named the three contemporary leading causes of death to be: (1) heart disease (38.3%), (2) cancer (17.2%), and (3) stroke (10.8%). Only 2.8% of deaths were said to be caused by motor vehicle accidents, and even these are not all sudden fatalities.

The most long-standing, large-scale and careful epidemiological study of cardiovascular disease is the Framingham Heart Study, begun in the city of Framingham, Massachusetts in 1948. Nearly half of the original participants have now died, and their deaths have been diagnosed with care (2). The Framingham definition of "sudden death" is a death that occurs within one hour of the onset of symptoms, and this definition is the most commonly used among medical researchers. Sudden cardiac deaths (SCDs) accounted for 11% of Framingham deaths, with another 7% classified as "possible" SCDs. ("Possible" cardiac deaths are those which have not been witnessed, or those for which the deceased was discovered dead in bed. These statistics are supported by analysis of 1983 death certificates for the entire state of Massachusetts (despite the fact of diagnosis being less scrupulous)(3). A study based on data compiled from both Framingham and civil servants in Albany, New York (4) demonstrated that for men in the 45-75 age range, 60% of SCDs occurred in men with no prior evidence of coronary artery disease. In another study, 32% of deaths among men in the 20-64 age range was attributed to SCD, with 25% showing no prior recognized symptoms of heart disease (5).

A detailed pathological study was made of 130 random subjects who died suddenly in the Glasgow, Scotland area (6). 92 of these (70%) sudden deaths were due to ischemic heart disease, 13 (10%) were due to overdose, 8 (6%) were due to unknown causes and 6 were (4.6%) were due to non-ischemic cardiovascular disease. Only two cases (1.5%) were due to cerebrovascular disease (stroke). All of the subjects deemed to have died from ischemic heart disease in the Glasgow Study showed a loss of more than 75% of cross sectional area in one or more coronary arteries (arteries supplying the heart).

Although stroke ranks third as a cause of death in industrialized countries, only 15% actually die in the acute phase -- and even those deaths are frequently not rapid enough to be classified "sudden". Stroke is, however, the major cause of disability, with over 50% of stroke survivors being permanently disabled (7).

Atherosclerosis of the coronary arteries is the most common form of heart disease. Fatty cholesterol deposits (atheroma) line the walls of the arteries and are hardened (sclerosis) by deposits of calcium or lime salts. Arterial walls can be further narrowed by the clotting of blood (thrombosis). Clots that break loose and plug the artery downstream are called emboli. A region of the heart deprived of blood because a thrombus or embolus has stopped circulation is called a myocardial infarct (dead or dying heart muscle). Myocardial infarction is more commonly known as heart attack, whereas sudden cardiac death is more commonly known as cardiac arrest. Angina pectoris is a coronary atherosclerotic disease characterized by chest pain during exertion, particularly in cold weather. Although it can be relieved by nitroglycerin tablets (which dilate coronary arteries), it represents an increased risk of heart attack and cardiac arrest.

The most common sequence of events in an SCD is the slow progression of coronary artery atherosclerosis until the blood supplied to the heart ventricles is inadequate, stimulating further speedup of ventricular contraction and causing the contractions to become spasmodic and irregular (ventricular fibrillation). For this reason, cardiac arrest is sometimes referred to as "arrhythmic death". 75 to 90% of patients experiencing SCD are discovered to be in ventricular fibrillation by mobile cardiac resuscitation teams (8).

Sudden cardiac death involves arrhythmia (irregular beating) of the heart ventricles due to irregularity of electrical stimulation in those ventricles. SCD requires both that the ventricles be vulnerable to electrical instability and that some condition exists that can trigger that instability. In most cases, the condition that triggers SCD is coronary artery disease (CAD), but myocardial infarction is the trigger in less than 20% of cases (5,9). Analyzing the electrical patterns of the heart during exercise stress testing is the most effective means to determine the risk of electrical instability that can lead to SCD. In one study, patients demonstrating such electrical instability showed the greatest improvement (and the least side effects) when given the antiarrhythmic drug Ethmozin (5).

Psychological stress can also be a factor leading to SCD. In one cruel experiment, dogs placed in a sling and subjected to electrical shocks demonstrated significantly more arrhythmias than a control group. After conditioning, simply placing the dogs in a sling without such shocks was enough to induce arrhythmias (5).


According to one study (10) only 10% of all cases of cardiac arrest occur in a hospital, even among men with known coronary heart disease. Heart attack can be every bit as dangerous as cardiac arrest, because nearly half of heart attack victims die outside of a hospital -- despite a warning of two hours or more. Typically the victims try to convince themselves that the pressure, squeezing and pain in their chest isn't really a heart attack. Chest discomfort may spread to the shoulders, neck and arms. A feeling of weakness may accompany sweating, nausea and shortness of breath. But these feelings may come and go -- and since the typical heart attack victim has not had previous experience with having a heart attack, denial can be convenient and easy.

The most common time of death from all causes is 8 am, with a secondary peak at 6 pm. The pattern is similar for all people over 65, but for males under 65, the peak times are midnight, 2 pm and 8 am, in that order. For females under 65, peak times are 11 pm, noon and 8 am, in that order. Peak death times for ischemic heart disease and cancer are 8 am, but stroke death peaks at 6 am (11). It is possible that knowledge of such statistics could be helpful in both understanding the mechanisms of death and in planning strategies to prevent or deal-with death.

The Framingham Study (2) reveals that the risk of sudden cardiac death is at least 70% higher during the 7 to 9 am period than the average risk during other times of the day. This risk is similar for both sexes and for all ages. Nor does it seem to vary with day-of-week or month-of-year. And the rate of sudden cardiac death is lower during normal hours of sleep (11 pm to 6 am) than during waking hours.

A study was made of the blood pressure and heart rate of people with hypertension and normal blood pressure during continuous, 24-hour monitoring (12). For all subjects blood pressure was lowest at 3 am, and for all subjects the increase in blood pressure and heart rate was highest between 7 am and 9 am. Hypertensive patients reached a peak blood pressure at 10 am, which declined gradually during the day. People with normal blood pressure had a steady blood pressure from 9 am to 6 pm, after which a gradual decline was seen.


Genetic factors seem to be significant determinants in predisposing certain people to sudden cardiac death (SCD), yet these cannot yet be altered. Similarly, the likelihood of SCD is greatly influenced by age and sex.

In the Framingham Study, the frequency of SCD increases slightly more than linearly for men over age 35, whereas for women there is an exponential increase over age 65. The incidence of SCD doubles every decade after age 45, but women in their 60s experience the same rate of SCDs as men in their 40s (13,14). In the 45 to 65 age range, the incidence of SCDs in men is four times as great as that in women. Only 2.5% of heart attacks by American women occur before the age of 65 (15). Estrogen is seen as protective against heart disease, although another theory holds that menstrual bleeding reduces the amount of iron in the circulation (which has led some to suggest that the protection against heart disease afforded by aspirin is due to gastric bleeding)(16). Iron is thought to damage heart muscle and oxidize LDL cholesterol, causing it to stick to artery walls (16).

Diabetics have a high rate of SCD, with the rate for diabetic women being slightly higher than that for diabetic men. Although there is often greater obesity and higher blood pressure among diabetics, it is likely that the disease also directly damages the small arteries of the heart (14).

Studies have been made which correlate heart attacks and cardiac arrests with psychological and social factors. External events can cause fatal stress in many instances, but there are personality types which can generate internal stress or high stress reactions to external events. The most famous of these personality types is the so-called "Type A behavior", characterized by a high level of ambition, a chronic sense of time-urgency, and a high susceptibility to anger. Most studies verify a correspondence of "Type A behavior" with CAD, but there is not sufficient evidence for believing that this personality type can be altered (17). One study demonstrated that "Type A" subjects were significantly more likely to live than other subjects ("Type B") if they survived the first 24 hours following a primary coronary event (18).


The most widely accepted and experimentally verified risk factors for both coronary artery disease (CAD) and sudden cardiac death (SCD) are the same: smoking, hypertension (high blood pressure) and hypercholesterolemia (high blood cholesterol). Since CAD is the most frequent trigger of SCD, this is not surprising. These three risk factors are less pronounced and less well documented in women than they are in men, so the discussion of controllable risk factors uses mainly data from men.

According to the Framingham Study (13,14), the risk of SCD for men is 3 times as great for a man who smokes over 20 cigarettes per day as for a man who smokes none. The risk of SCD for a man with high blood pressure (over 160/95) is nearly 3 times as great as for a man with "normal" blood pressure (under 140/85). And the risk of SCD is half as great for a man with a blood cholesterol level of 197 mg/dl (milligrams per tenth-of-a-litre, ie, per decilitre) as for a man with a level of 302 mg/dl (with the relationship for all values in between being very nearly linear). These data all apply to men in the 45-74 age group.

The effects of the three known controllable risk factors are additive. A person with any two of the three CAD risk factors has 4 times the mortality rate as someone with none. A person with all three risk factors has 8 times the mortality rate (19).

At least one study has denied that any CAD risk factors are controllable (20). This view is contrary to that of the great majority of researchers.


Cigarette smoking is deemed to be responsible for 25% of all CAD deaths in men under age 65, and 80% of all CAD deaths in men under age 45 (21). Nicotine has been implicated because it constricts blood vessels and increases heart rate. However, it has been established by the Framingham Study that filter cigarettes do not lower the rate of CAD deaths (22). Thus, the effect of cigarettes on CAD is probably more due to carbon monoxide, or to an unstudied tobacco compound, than to nicotine. Carboxyhemoglobin (blood hemoglobin bound to carbon monoxide) lowers the threshold for ventricular fibrillation in monkeys (22). Ten years after a man stops smoking, his risk of CAD mortality is nearly the same as that of a nonsmoker.

Part of the reason that the role of smoking in CAD and SCD has been so poorly documented in Framingham and other long-term studies is that very few women smoked when the study began, and those who did smoke, frequently did not inhale.

The added risk of myocardial infarction (MI) and stroke among women taking oral contraceptives is primarily among women over 35 and smokers. The yearly incidence of MI among 100,000 women in their 30s was 6 & 2 for users and non-users of contraceptives who smoke less than 14 cigarettes per day. For those who smoke more than 15 cigarettes per day, the incidence was 30 & 11, respectively, for women in their 30s, and 246 & 61, respectively, for women in their early 40s. The use of low-dose oral contraceptives has reduced the incidence of stroke and MI by as much as 80% (23).


Ninety percent of cases of high blood pressure are described as "essential hypertension". In this case, the word "essential" means "without known cause", rather than "necessary". Of the three controllable risk factors for SCD, only hypertension is also a proven risk factor for stroke (12,24).

Blood pressure is usually defined in terms of millimeters of mercury (mm Hg), and is actually a measure of two blood pressures: systolic and diastolic. Systolic pressure is the blood pressure when the heart is exerting its maximum force of contraction on the blood, whereas diastolic pressure is the pressure of the blood when the heart is relaxing between beats. Blood pressure is usually expressed as systolic/diastolic, with the upper limit of "normal" being around 140/85. Although elevated diastolic pressure is normally regarded as more diagnostic of atherosclerosis, the Framingham Study showed that elevated systolic and diastolic pressures are equally risk factors for SCD (14). A study indicates that 27_% of men and 37_% of women aged 40 to 59 have blood pressures in excess of 160/95, often regarded as the definitive boundary of "hypertension" (25).

Blood pressure rises with age for most North Americans, and this is considered normal. Systolic pressures average 113, 123, 126, 132, 139 and 147 for American whites in their teens, 20s, 30s, 40s, 50s and 60s, respectively. In one study (26), these figures are contrasted to the systolic pressures of tribesmen in the Solomon Islands, which never exceeds 120, even past the age of 60.

Overweight subjects in the upper third of the Metropolitan Life relative weight charts had more than double the incidence of SCD than subjects in the lower third (14). Nonetheless, obesity is not recognized as a separate risk factor because it is so often associated with hypertension. The Framingham Study showed that a 10% increase in weight results in a 6.5 mm Hg rise in systolic blood pressure (27). Another study found a 3 mm Hg and a 2 mm Hg increase in systolic and diastolic pressure (respectively) for a 10 kg increase in body weight (25).

Despite the wide publicity given to the use of salt to reduce blood pressure, there is considerable debate among researchers about the value of salt reduction (28). Most agree that only a minority (15% to 25%) of the population experiences a lowering of blood pressure with salt reduction, and claims have been made that salt restriction can actually increase blood pressure. The older (29) and obese (30) patients seem to be the most sensitive to the effects of salt, possibly due to decreased kidney function.

Approaches to the control of blood pressure and atherosclerosis are legion, and this is not the place to attempt an exhaustive study. Suffice it to say that beta-blocking drugs and diuretics are frequently the first choices by physicians for reducing blood pressure. The former reduces adrenalin-like stimulation of the cardiovascular system, whereas the latter simply reduces blood volume through increased urination. One study estimated the reduction in CAD death through the use of beta-blockers for a 10.5 year period to be 15% (31). Another study indicated that diuretics increase the risk of arrhythmias (32).

It is worth noting that two studies have demonstrated reduction of systolic blood pressure of 5 mm Hg by vegetarian diets lasting only a few weeks (33,34).


The literature on blood cholesterol, both scientific and in the popular press, is vast. It seems appropriate to begin the review here with a summary of a well-researched feature article in TIME magazine (35).

Although a total blood cholesterol level in excess of 240 mg/dl is regarded as high risk, the relative concentrations of HDL (high-density lipoprotein) to LDL (low-density lipoprotein) cholesterol are crucial. Unlike LDL cholesterol, which deposits cholesterol on artery walls, HDL actually seems to remove cholesterol from artery walls. William Castelli, medical director of the Framingham Heart Study, is quoted as saying, "If your ratio is 4.5 or higher, you are running a ratio typical of people who develop coronary heart disease in Framingham." For the average male heart patient, the ratio is 5.4 to 6.1. The average marathon runner has a ratio of 3.4, whereas the average vegetarian has a ratio of 2.5. A total blood cholesterol level of under 200 mg/dl is not considered safe if the HDL is below 35 mg/dl.

A large 5-year study in Finland (which has one of the world's highest heart-disease rates) showed that patients treated with the anticholesterol drug gemfibrozil had an 11% decrease in LDL, an 11% increase in HDL and 34% less heart disease. Niacin is reported to produce similar results. In another study, eight sedentary men who were put on a regimen of rigorous exercise for 48 weeks showed a 5 mg/dl HDL increase and a 16% drop in blood triglycerides (fats).

The Framingham Study found no influence of dietary cholesterol on the concentration of cholesterol in the blood (36). Most blood cholesterol is manufactured from the liver, and saturated fats seem to be the greatest stimulus for liver production of LDL. Animal fats are notoriously high in saturated fats, as are some "tropical oils" of plants (coconut and palm oil). Monosaturated fats like olive and canola (rapeseed) oil have a neutral effect on plasma lipid (fat) level (36).

Two polyunsaturated oils are regarded as "essential fatty acids" (necessary in human diet): linoleic and linolenic acids. Linolenic acid seems to be particularly effective in lowering VLDL (very low-density lipoprotein -- a form of LDL laden with triglycerides). Linolenic acid is a member of a family of polyunsaturates known as the omega-3 unsaturated fatty acids, all of which are effective in lowering serum triglyceride. (The "3" refers to the fact that the first double-bond occurs on the 3rd carbon from the methyl end of the fatty acid. Linoleic acid is an omega-6 unsaturated fatty acid.) 55% of the fatty acid in linseed (also known as flaxseed) oil is linolenic acid. Most fish oils are high in omega-3 fatty acid, in particular cod liver oil (25%) and mackerel oil (27%) (36).

Although many studies have verified that people with higher levels of physical activity have a lower incidence of CAD (37), all such studies have been criticized as providing only circumstantial evidence (38). Nonetheless, a fairly impressive experiment was done on 27 monkeys under observation for 36 months (39). The monkeys were divided into 3 groups of 9. One group served as a control, eating a normal diet of chow and living a sedentary life. The other two groups were given chow "enriched" with butter and cholesterol. One of those two groups was subjected to a one-hour session of treadmill exercise 3 times weekly, and the other group remained sedentary. All of the sedentary monkeys on the atherogenic diet (and none of the others) showed electrocardiogram abnormalities -- and one such monkey experienced an SCD after 23 months. The exercising monkeys showed elevated HDL. LDL and VLDL levels in the exercising monkeys, although still well above those seen in the controls, were significantly lower than those seen in the sedentary, atherogenic-diet group. This latter group showed marked atherosclerosis upon autopsy. The exercising monkeys had lower resting heart-rates, larger hearts and had coronary arteries that were "strikingly wider" than any of the sedentary monkeys. All monkeys showed a similar systolic and diastolic pressure, irrespective of exercise or diet.

In his book, RUNNING WITHOUT FEAR (40), Dr. Kenneth Cooper warns against exercise that does not involve a proper warm-up and cool-down period. Concerning the latter, it can be dangerous to suddenly stop vigorous exercise, because the blood-stream still contains high levels of adrenalin-like substances which can cause cardiac arrhythmias. Cooper mentions the ancient Greek Pheidippides, who ran 26 miles from Marathon to Athens to announce the defeat of the Persians, and promptly dropped dead after he had done so. Cooper suggests that Pheidippides experienced an SCD because he suddenly stopped running.


The Physicians Health Study (41) involved 22,071 physicians, half of whom received a 325 mg dose of aspirin on alternate days, and half of whom received an aspirin placebo. During the 5 years of the study there were 164 cardiovascular deaths, with no statistically significant difference between the two groups (81 in the aspirin group, 83 in the placebo group). There were 10 deaths due to myocardial infarction (MI) in the aspirin group, and 28 such deaths in the placebo group -- a statistically significant difference. However, the differences for stroke (10 aspirin, 7 placebo) and sudden cardiac death (22 aspirin, 12 placebo) were not regarded as statistically significant. I am not a statistician, but the evidence would lead me to believe that aspirin causes a statistically significant increase in non-MI cardiovascular deaths, which nullifies the effect of the significantly significant decrease in MI deaths.


Although controversy still surrounds the use of CPR, the widely quoted experiences in the Seattle area of Washington State (42,43) indicate that 43% of cardiac arrest patients survive if CPR is initiated within 4 minutes and definitive care is provided within 8 minutes. Survival is dramatically reduced if either time is exceeded.

A very significant reduction in cardiac arrests among high risk patients has been achieved by the use of small portable defibrillators. One such device can be worn, and will automatically deliver a shock if heart rate drops (44).


The use of exotic life-extension methods such as Deprenyl seems almost insignificant when contrasted to the real and high probability of fatality due to cardiac arrest or heart attack. This is all the more sobering when consideration is given to how greatly a cryonic suspension can be compromised by a cardiac fatality. A serious life-extension program requires a careful analysis of all the modes, dangers and probabilities of death.

(See also my essay Prevention of Cardiovascular Disease)



  1. MAXIMUM LIFESPAN by Roy Walford (1983) page 8
  2. AMERICAN JOURNAL OF CARDIOLOGY Vol 60,p.801-806 (1987)
  3. THE PREVENTION OF SUDDEN CARDIAC DEATH J.Kostis&M.Sanders, Editors (1990) pages 21-41
  4. CIRCULATION Vol 51,p.606-613 (1975)
  5. AMERICAN JOURNAL OF CARDIOLOGY Vol 43,p.313-328 (1979)
  6. BRITISH HEART JOURNAL Vol 57,p.329-335 (1987)
  7. CORONARY AND CEREBRAL VASCULAR DISEASE L.Rolak&R.Rokey, Editors (1990) pages 87-113
  8. SUDDEN CARDIAC DEATH Patricia Owen, Ed. (1991) pages 21-37
  9. CIRCULATION Vol 65,p.457-464 (1982)
  10. CIRCULATION Vol 51,p.606-613 (1975)
  11. THE AMERICAN JOURNAL OF MEDICINE Vol 82,p.266-274 (1987)
  12. THE LANCET Vol 1,p.795-797 (1978)
  13. THE PREVENTION OF SUDDEN CARDIAC DEATH J.Kostis&M.Sanders, Editors (1990) pages 1-12
  14. SUDDEN CARDIAC DEATH Patricia Owen, Ed. (1991) pages 3-20
  15. TIME November 9, 1992 page 58
  16. SCIENCE NEWS Vol 142,p.180 (1992)
  17. NEW ENGLAND JOURNAL OF MEDICINE Vol 294 p.987-994 (Part 1) and p.1033-1038 (Part 2) (1976)
  18. NEW ENGLAND JOURNAL OF MEDICINE Vol 318,p.65-69 (1988)
  19. JOURNAL OF CHRONIC DISEASE Vol 31,p.201-306 (1978)
  20. THE LANCET Vol 1,p.839-841 (1988)
  22. THE LANCET Vol 1,p.109-113 (1981)
  23. NEW ENGLAND JOURNAL OF MEDICINE Vol 305 p.612-618 (Part 1) and p.672-677 (Part 2) (1981)
  24. CORONARY AND CEREBRAL VASCULAR DISEASE L.Rolak&R.Rokey, Editors (1990) pages 330-334
  25. CIRCULATION Vol 39,p.403-421 (1969)
  26. JOURNAL OF HYPERTENSION Vol 9 (Suppl 6),p.S37-S41 (1991)
  27. FOOD, NUTRITION & DIET THERAPY M.Krause&L.Mahan (1984) page 560
  28. AMERICAN JOURNAL OF HYPERTENSION Vol 3,p.499-504 and 518-519 (1990)
  29. HYPERTENSION Vol 17 (Supp I),p.I102-I108 (1991)
  30. HYPERTENSION Vol 4 (Supp III),p.III43-III49 (1982)
  31. CIRCULATION Vol 82,p.1616-1628 (1990)
  32. JOURNAL OF CARDIOVASCULAR PHARMACOLOGY Vol 10 (Suppl 2) p.S61-S63 (1987)
  33. BRITISH MEDICAL JOURNAL Vol 293,p.1468-1471 (1986)
  34. THE LANCET Vol 1,p.5-9 (1983)
  35. TIME December 12, 1988, pages 60-67
  36. FOOD, NUTRITION & DIET THERAPY M.Krause&L.Mahan (1984) page 40-46 and page 565
  37. AMERICAN JOURNAL OF EPIDEMIOLOGY Vol 108,p.161-175 (1978)
  38. AMERICAN JOURNAL OF HYPERTENSION Vol 5,p.574-576 (1992)
  39. NEW ENGLAND JOURNAL OF MEDICINE Vol 305,p.1483-9 (1981)
  40. RUNNING WITHOUT FEAR by Dr. Kenneth Cooper (1985)
  41. NEW ENGLAND JOURNAL OF MEDICINE Vol 321,p.129-135 (1989)
  43. ANNALS OF INTERNAL MEDICINE Vol 90,p.737-740 (1979)
  44. SUDDEN CARDIAC DEATH Patricia Owen, Ed.(1991) pages 236-42