Indeed, the balance has shifted so much that the effectiveness of treatment for cardiac disease is far more often on the good side of probable. That should not, however, be taken to mean that the once imperilled heart is now an immortal heart. Although the great majority of cardiac patients today survive their first episode, well over half a million Americans still die every year of some form of McCarty’s sickness. Another 4.5 million are newly diagnosed as being afflicted with it. Eighty percent of people whose heart disease eventually kills them are victims of this particular form of it: Ischemic heart disease (or coronary artery disease, or coronary heart disease, as it is variously called) is the leading cause of death in the industrialized nations of the world.
James McCarty’s heart died because it was not getting enough oxygen; it was not getting enough oxygen because it was not getting enough hemoglobin, the blood-borne protein whose function is to carry the oxygen; it was not getting enough hemoglobin because it was not getting enough blood; it was not getting enough blood because the heart’s nourishing vessels, the coronary arteries, were hardened and narrowed by a process called arteriosclerosis (literally, hardening of the arteries). The arteriosclerosis had occurred because of a combination of McCarty’s sybaritic diet, his cigarette smoking, his lack of exercise, an element of high blood pressure, and a certain degree of inherited predisposition. Very likely, the phone call from his pampered daughter had the same spasm-inducing effect on his severely narrowed coronary arteries as it did on his angrily clenched fists. That bit of acute tightening was probably just enough to rupture or crack one of the deposits of arteriosclerosis, called plaques, in the lining of a main coronary artery. Once this occurred, the disrupted plaque served as a focus on which fresh blood-clot formed, making the obstruction complete and choking off the already-compromised flow. This final stoppage caused so-called “ischemia” (pronounced
iskeemeeya
), or blood lack, thereby acutely starving a large-enough piece of McCarty’s heart muscle, or myocardium, to disrupt its normal rhythm into the chaotic squirming of ventricular fibrillation.
It is quite possible that none of McCarty’s heart muscle was actually killed by its acute blood lack. Ischemia alone may cause ventricular fibrillation, especially in a heart already injured by a previous attack And so may the adrenalinelike compounds produced by the body at times of stress. Whatever the cause, the electrical communication system upon which James McCarty’s heart depended for its regularity and coordination broke down, and so did McCarty’s life.
Like so many other medical terms,
ischemia
is a word with an interesting history and colorful associations. It will recur again and again in the telling of the stories in this long narrative of death, because it is so ubiquitous—and so insidious—a driving force toward the quenching of life’s energies. Though starvation of the heart may offer the most dramatic example of its lurking dangers, the process of choking off oxygen and nutrition is the common denominator in a wide variety of mortal illnesses.
The concept of ischemia and the word itself were introduced in the middle of the nineteenth century by a brashly brilliant little Pomeranian (the word, when applied to dogs, evokes a tiny and intensely spirited bundle of scrappy exuberance, which seems appropriate for the man being described) who began his multifaceted career as a kind of
enfant terrible
of research, and ended it sixty years later universally recognized by the sobriquet “the Pope of German Medicine.” No single individual has ever contributed more to the understanding of the ways in which disease wreaks its havoc on human organs and cells than did Rudolf Virchow (1821–1902).
Virchow, a professor of pathology at the University of Berlin for almost fifty years, produced more than two thousand books and articles, not only on medicine but on anthropology and German politics as well. So liberal a member of the Reichstag was he that the autocratic Otto von Bismarck once challenged him to a duel. Being given the choice of weapons, Virchow ridiculed the upcoming encounter out of existence before it took place—by insisting that it be fought with scalpels.
Among Rudolf Virchow’s many research interests was his fascination with the ways in which disease affects arteries, veins, and their contained blood constituents. He elucidated the principles of embolism, thrombosis, and leukemia and invented the words to describe them. Seeking a term to designate the mechanism by which cells and tissues are deprived of their blood supply, Virchow seized (this word is chosen advisedly) upon the Greek
ischano
—“I hold in check,” or “I quench”—derived from the Indo-European root
segh
, which refers to “seizing” or “holding” or “causing to pause.” By combining it with
aima
, or “blood,” the Greeks had created the word
ischaimos
, to signify a holding in check of the flow of blood.
Ischemia
was chosen by Virchow to designate the consequences of diminishing or totally stopping blood flow to some structure of the body, whether as small as a cell or as large as a leg or a section of heart muscle.
Diminishing
is a relative term, however. When an organ’s activity increases, its oxygen requirements go up, and so does its need for blood. If narrowed arteries cannot widen to accommodate this need, or if for some reason they go into tight spasm that further restricts flow, the organ’s demands are not met, and it rapidly becomes ischemic. In pain and anger, the heart screams out a warning, and continues to do so until its shrieking exhortations for more blood are met, usually by the natural stratagem of the victim, who—alarmed by the distress within his chest—slows or stops the activity that is tormenting his cardiac muscle.
A ready example of this process is the suddenly overworked calf muscle of a weekend athlete who returns to jogging each year when the weather warms up in April. The discrepancy between the amount of blood required by his out-of-condition muscle and the amount that is able to force its way through his out-of-condition arteries may result in ischemia. The calf does not get enough oxygen and it cries out in an agonizing seizure, to warn the athlete manqué to stop his exertions before a clump of muscle cells are starved to death, the process known as infarction. The shriek of pain in the overtaxed calf is called a cramp or a charley horse. When it originates in the heart muscle, we use the much more elegant term
angina pectoris
. Angina pectoris is nothing else than a charley horse of the heart. If it lasts long enough, its victim sustains a myocardial infarction.
Angina pectoris
is a Latin phrase which translates literally as “a choking” or “throttling” (
angina
) “of the chest” (
pectoris
, the genitive case of
pectus
, “chest”). It is to another medical philologist, the remarkable eighteenth-century English physician William Heberden (1710–1801), that we owe not only the term but also one of the finest descriptions of the symptoms associated with it. In a 1768 discussion of the various forms of chest pain, he wrote:
But there is a disorder of the breast marked with strong and peculiar symptoms, considerable for the kind of danger belonging to it, and not extremely rare, which deserves to be mentioned more at length. The seat of it, and sense of strangling and anxiety with which it is attended, may make it not improperly be called angina pectoris.
They who are afflicted with it, are seized while they are walking, (more especially if it be up hill, and soon after eating) with a painful and most disagreeable sensation in the breast, which seems as if it would extinguish life, if it were to increase or to continue; but the moment they stand still, all this uneasiness vanishes.
Heberden had seen enough patients—“nearly a hundred under this disorder”—to be able to study its incidence and progress:
Males are most liable to this disease, especially such as have past their fiftieth year.
After it has continued a year or more, it will not cease so instantaneously upon standing still; and it will come on not only when the persons are walking, but when they are lying down, especially if they lie on the left side, and oblige them to rise up out of their beds. In some inveterate cases it has been brought on by the motion of a horse, or a carriage, and even by swallowing, coughing, going to stool, or speaking, or by any disturbance of mind.
Heberden was struck by the unremitting progression of the disease: “For if no accident intervene, but the disease go on to its height, the patients all suddenly fall down, and perish almost immediately.”
James McCarty never had the luxury of a succession of bouts of angina pectoris; he succumbed to his very first experience of cardiac ischemia. His brain died because the fibrillating and finally stilled heart could no longer pump blood to it. The ischemic brain was followed gradually into lifelessness by every other tissue in his body.
A few years ago, I met a man who was miraculously resuscitated from such an apparent sudden cardiac death. Irv Lipsiner is a tall, broad-shouldered stockbroker who has been an avid athlete all his life. Although he requires insulin for long-standing diabetes, the disease has had no physical effects on his vigorous good health, or so it would appear at first glance. But he did have a small heart attack when he was forty-seven years old, which is exactly the age at which his father died from the same cause. That episode left his heart muscle with only minimal damage, and he continued his active life without restriction.
Late on a Saturday afternoon in 1985, when he was fifty-eight years old, Lipsiner was beginning his third hour of tennis at the Yale indoor courts when two of his partners left, necessitating a switch from doubles to singles. The practice rally was just beginning when, without warning or premonitory pain, he slumped to the floor unconscious. Two physicians, by luck playing on an adjacent court, rushed to his aid and found him glassy-eyed, unresponsive, and not breathing. There was no heartbeat. Assuming correctly that he was in ventricular fibrillation, they immediately began cardiopulmonary resuscitation, continuing it for what seemed to them an interminable time, until the ambulance arrived. By then, Lipsiner had begun to respond, even resuming a spontaneous regular heartbeat as his airway was intubated and he was placed in the ambulance. Soon, he was wide awake in the Yale–New Haven Hospital emergency room and wondering, as he put it, “what the fuss was all about.”
In two weeks, Lipsiner was out of the hospital, fully recovered from his episode of ventricular fibrillation. I met him some years later, on the horse farm where he lives. Every day, he takes time out from work to go riding or play tennis, usually singles. Here is Irv Lipsiner describing what it felt like to drop dead on a tennis court:
The only thing I can recall is just—not hurting, but just collapsing. And then the lights went out, as if you’re in a little room and you flip the switch. The only thing different from that was that it was in slow motion. In other words, it didn’t go out like
that
[here he snapped his fingers]. It went out like this [he made a lazy downward circle with his hand, like an airplane turning gently in descent toward a landing], gradually and almost in a spiral, like—[he hesitated briefly in thought, then pursed his lips and blew his breath out in a slow diminuendo]—this. The change from light to dark was very evident, but the speed with which it happened was—well, gradual.
I was aware that I’d collapsed. I felt like somebody took the life out of me. It felt like—I’m thinking of a scene—I had a dog that was hit by a car, and when I looked at that dog on the ground—he was dead already—he just looked like the same dog, only shrunk. You know, shrunk—uniformly. That’s how I felt. I felt like—[he made a sound like air going out of a balloon] “Pffft.”
Lipsiner’s light went out precisely the way it did because the circulation to his brain had been suddenly shut off. As the oxygen in the organ’s now-stagnant blood was steadily used up, the brain began to fail—sight and consciousness were turned down as though by the gradual twist of a dial rather than the suddenness of a switch. That was Irv Lipsiner’s slow-motion spiral into oblivion, and almost death. The mouth-to-mouth breathing and chest massage of the cardiopulmonary resuscitation forced air into his lungs and drove blood to his vital organs until his heart decided, for reasons of its own, to resume its responsibilities. Like most sudden cardiac deaths in nonhospitalized people, Irv Lipsiner’s episode was caused by ventricular fibrillation.
Lipsiner felt no ischemic pain. The probable cause of his fibrillation was some transient chemical stimulation of a supersensitive area left on his heart muscle by the attack of 1974. As to why the fibrillation occurred when it did, there is no way to be certain; but a quite plausible guess is that it was related to the stress of too much tennis on that Saturday afternoon, which could have caused the release into his circulation of extra adrenaline, and this in turn may have made a coronary artery go into spasm and set off the irregular rhythm. Such are the occasional vagaries of ischemic heart disease that Lipsiner was left with no new damage to his heart, although he never again played more than two consecutive hours of tennis.
The fact that Lipsiner experienced no cardiac charley horse before he began fibrillating makes this particular case of heart seizure somewhat unusual—the majority of people who drop dead probably do feel ischemic pain of the characteristic sort. Like its equivalent in the calf, the onset of ischemic cardiac pain is sudden and severe. It has been most commonly described by its sufferers as constricting, or viselike. Sometimes it manifests itself as a crushing pressure, like an intolerable blunt weight forcing itself against the front of the chest and radiating down the left arm or up into the neck and jaw. The sensation is frightening even to those who have experienced it often, because each time it recurs it is accompanied by awareness of the possibility (and quite a realistic awareness it is) of impending death. The sufferer is likely to break out into a cold sweat, feel nauseated, or even vomit. There is often shortness of breath. If the ischemia does not let up within approximately ten minutes, the oxygen deficiency may become irreversible, and some of the deprived cardiac muscle will go on to die, the process called myocardial infarction. If that happens, or if the oxygen lack is sufficient to scramble the heart’s conduction system, some 20 percent of the afflicted will perish in the throes of such an episode before reaching an emergency room. That figure drops by at least half if transportation to a hospital is possible within the period cardiologists call “the golden hour.”