Heart: An American Medical Odyssey (3 page)

Eventually it would become the closest race I ever ran in Wyoming, but things didn’t really heat up until June 1978. When the filing deadline came that month, three of us were in the race. Fortunately for me, a potential fourth candidate, Tom Stroock, decided at the last minute not to run. Tom was an oilman in Casper and would later become US ambassador to Guatemala. He would have been a strong opponent, and he and I would have split the vote in Casper. In the primary, I faced two men, both formidable opponents. Ed Witzenburger was a decorated World War II Air Force pilot and the incumbent state treasurer, who had been elected four years earlier. Jack Gage was the Republican son of a former Democratic governor with solid name recognition throughout the state.

All five statewide elected officials were also up for reelection in 1978, and from the start I had to assume that if I made it through the primary, I could well be in for a tough general election fight. Although Wyoming is traditionally a Republican state where Republicans outnumber Democrats by two to one, over the years the state’s voters had elected Democrats every once in a while. Gale McGee served for eighteen years in the US Senate, Teno Roncalio represented Wyoming for ten years in the US House of Representatives, and Ed Herschler served three terms as governor. By mid-June, the race was taking shape, and I was in Cheyenne campaigning. The day before Father’s Day, we went to two events: a square dance contest and the Cheyenne Kiwanis Club clambake, which was nonpolitical but an important event for those running for office.

We stayed that night with Joe and Mary Meyer. Joe and I had known each other since we’d started playing football together at Natrona
County High School when we were fourteen years old, and he had been in our wedding. Joe, who would go on to serve as Wyoming’s treasurer, attorney general, and secretary of state, was the deputy director of the state legislative services office in 1978. This was a nonpartisan appointed position, so he couldn’t participate in the campaign. But he and Mary were happy to help out, providing us with a place to sleep whenever we were in Cheyenne. Around 2:00 a.m. on Father’s Day, I awoke with a tingling sensation in the two small fingers of my left hand. I had no chest pain or any other symptoms, but I thought immediately of my cousin, Gene Dickey, who had recently had a serious heart attack. I knew instinctively that I should have this odd feeling in my arm checked out. I woke Lynne up and told her I needed to go to the hospital. Then I went downstairs and woke up Joe. As Joe drove Lynne and me to the hospital, I remember telling them that this was probably nothing to worry about. I just wanted to be cautious.

When we arrived at the emergency room, I walked in on my own, sat down on an examining table, and passed out. When I regained consciousness, there was a good deal of excitement in the emergency room, and I suddenly realized it was focused on me. I was having a heart attack.

Over an eighty-year life, a human heart beats, uninterrupted, 2.5 billion times, an astonishing example of physical durability seldom, and maybe never, replicated by even the most sophisticated human engineering. An automobile motor, for comparison, will make less than 500 million revolutions if you’re lucky enough to keep it running for 100,000 miles.

The heart is powered by nutrient- and oxygen-rich blood delivered through slender arteries, fuel lines for the human engine, that arise from the aorta, adhere to the surface of the heart, and then dive deep into the muscle. These vessels are not simple passive pipes; they are
complex, living conduits capable of dilating, or contracting, when provoked, and they are lined with a single layer of cells that, when healthy, discourage the formation of blood clots. When these arteries are diseased, however, blood flow to the heart is imperiled, a condition that can yield catastrophic consequences, a harsh lesson I learned early in my career.

•  •  •

In July 1986, on my third day of internship, only my third day on the job as a doctor, I am paged stat to the exercise lab. North Shore University Hospital on Long Island is a sprawling place, and I have to run through a maze of corridors and stop to ask directions before I find the suite where cardiac stress tests are performed. When I finally arrive, I see one of my patients—I’ll call him Bob—lying on the floor, his legs propped on the stopped but still-inclined treadmill ramp. The patient, in his fifties, had been admitted a week before with a myocardial infarction (MI), that is, a heart attack. The cardiology fellow who had been supervising the test is kneeling next to the man, frantically trying to insert a large-bore IV into the patient’s arm. The fellow said that everything was fine until the patient’s knees suddenly buckled. Bob is still conscious but he doesn’t look good, and his blood pressure is barely detectable.

Bob’s recovery from the heart attack had been relatively uncomplicated, notable only for a bout of pericarditis, a painful inflammation of the fibrous sac that encases the heart. Pericarditis is not usually dangerous, but its appearance in this setting was a bit ominous because it suggested that Bob’s MI was not, as we’d previously suspected, small, involving only a limited inner rim of tissue, but instead involved the death of the full thickness of one of the walls of the heart, resulting in a significant loss of muscle. The stress test had been ordered as part of the standard procedure to determine if it would be safe to discharge him later in the day. Bob’s wife is already en route to the hospital intending to take him home.

Suddenly Bob stops breathing. We pull Bob off the treadmill, start
cardiopulmonary resuscitation (CPR), and call for the “code team.” Over the hospital-wide loudspeaker, the page operator intones “9-9-9 stress lab,” the euphemism at North Shore for the more widely known “code blue.” In less than a minute, a breathless parade of residents, nurses, cardiologists, fellows, and assorted other onlookers rushes through the doorway. A nurse opens the code cart, a rolling, fire-engine-red Sears Craftsman cabinet with a defibrillator on top and rows of drawers below, housing an array of drugs, drips, catheters, and emergency paraphernalia—an end-of-life toolbox. An anesthesiologist intubates the patient, placing a transparent plastic tube into the airway below Bob’s vocal cords, enabling us to breathe for the patient with the aid of an Ambu bag, a hand-squeezed, plastic, barrel-shaped bellows connected to 100 percent oxygen. I do chest compressions for a while, a laying on of hands equal parts resuscitative and ritual, until my effectiveness wanes and I am relieved by fresher arms.

It’s a choreographed chaos accompanied by a sound track of monitor beeps, pump alarms, and desperate voices all simultaneously struggling to be heard. Time is not our ally, and every minute that passes without restoration of a pulse makes it less and less likely that this is going to turn out well. Bob’s exercise clothes have been cut away to facilitate the placement of central lines and defibrillator paddles. Now remnants of shredded clothing lie scattered on the floor. Unadorned we come into this world and, in a hospital, unadorned we go out.

After multiple rounds of drugs and shocks and after what seems like a very long time, but probably not much more than about half an hour, chest compressions stop. The room gets very quiet and someone palpates the patient’s carotid. There is no pulse. The team is polled for suggestions. There are none. Very little is said as someone records the time of death, and people file out of the room leaving behind soiled gloves and gauze and IV bags still tethered to the now lifeless man and an electrocardiogram (EKG) monitor with a horizontal green line stretching into eternity.

Bob’s wife arrives at the hospital unaware of this terrible terminal event. She is informed only that her husband has had a complication,
and hospital staff take her to a room to wait. No one has told her that he is dead, a final responsibility left for me. The chief resident, David Cooper, who accompanies me on the short walk to the conference room, offers some quick advice on how to speak to the family and tells me to get permission for an autopsy. Postmortem examinations have been performed for millennia, and even today, when a patient dies unexpectedly, sometimes only an autopsy can determine the cause of death.

We introduce ourselves when we enter the room and sit down to talk. It is obvious that she is dreading what we are about to say, probably because of the way she was sequestered after she arrived at the hospital. Maybe she knows in the way that husbands and wives and mothers and fathers just seem to know when something bad has happened. I tell Bob’s wife that he collapsed while walking on the treadmill and, despite the efforts of many people, we were unable to resuscitate him. I don’t use euphemisms like
passed
or
gone
and instead say simply that I am so sorry to have to tell her that her husband has died. It’s an awful moment. I search without success for words of comfort. She asks us if he suffered at the end, and I tell her that I’m sure he did not.

Nurses clean Bob and dress him in a hospital gown before bringing him to a room where his wife spends some time with him before he is taken to the morgue. Cooper and I wait outside the door. When Bob’s wife finally comes out, I tell her that although we know he had a heart attack earlier in the week, we don’t know why he died today. I explain that an autopsy will answer some of these questions, and after some thought she gives her consent.

Bob’s autopsy removes all doubt as to why he died: a week out from his heart attack, his weakened myocardium ruptured, filling the pericardial space with blood, essentially strangling his heart. Although heart disease has been with humans for millennia and traces can be found in the remains of four-thousand-year-old Egyptian mummies, detailed knowledge of this affliction is relatively new.

•  •  •

In 1500,
Leonardo da Vinci returned to Florence where he served as an engineer for Cesare Borgia, painted the
Mona Lisa
, and rekindled his prodigious interest in anatomy. In the winter of 1507, Leonardo visited a one-hundred-year-old man in Florence’s Hospital of Santa Maria Nuova a few hours before the man’s death. After performing an autopsy on the centenarian da Vinci wrote:

And I made an anatomy in order to see the cause of a death so sweet, which I found to proceed from debility through lack of blood and deficiency of the artery which nourishes the heart and the other lower members. I found this artery very dessicated, shrunken and withered. . . . The tunics of the vessels behave in man as in oranges, in which the peel thickens and the pulp diminishes the older they become.

Da Vinci is undoubtedly describing atherosclerosis.

The term
atherosclerosis
is derived from the Greek words
athere
(gruel) and
skleros
(hard). Examine an artery afflicted with this disease, and you appreciate the aptness of its name. While a normal artery has an elastic quality, an atherosclerotic vessel is often stiff (“hardening of the arteries’), a consequence of cholesterol, calcium, and various cellular elements that have been deposited in the blood vessel wall. Over many years, the accumulating material can impede blood flow and become prone to blockage by blood clots. Until fairly recently, the disorder was thought to result mainly from the accumulation of lipids (fats). It is now known that the disease, which develops over decades, is caused by a complex interaction among lipids, inflammatory cells, and components of the immune and clotting systems.

Although noted for hundreds of years, atherosclerotic heart disease is largely a malady of the twentieth and twenty-first centuries, killing more people than any other disease in the United States every year since 1900 with the sole exception of 1918, when
the Spanish influenza pandemic infected 28 percent of Americans and killed a staggering 675,000 people.
Atherosclerotic
disease developed in the United States during an era of increasing life expectancy brought about by a precipitous decline in death due to infectious causes and a concomitant improvement in nutrition and wealth.

In 1971, Abdel Omran, an epidemiologist, published an influential paper, “The Epidemiologic Transition: A Theory of the Epidemiology of Population Change,” in which he described how a population’s death rate changes as a country industrializes. This landmark work described three progressive stages in the evolution of population longevity. In the United States, the first stage, what Omran called the “Age of Pestilence and Famine,” a period of high mortality and low life expectancy, when the top ten causes of death were all infectious diseases, persisted until about the year 1900. Prior to that time, the average life expectancy in the United States was only forty-eight years.

The second stage, the “Age of Receding Pandemics,” a time when mortality began to decline, occurred in the first half of the twentieth century. During this period,
there were steep reductions in deaths in this country from diseases such as dysentery, typhoid fever, and tuberculosis. Food-borne diseases declined following key improvements in food quality fostered by safeguards like the Pure Food and Drug Act of 1906. The discovery of penicillin by Alexander Fleming in 1928 led to the antibiotic era. Polio mortality dropped sharply after the introduction of the Salk vaccine in 1955. These steep declines in deaths from infectious diseases contributed to a significant increase in the nation’s average life expectancy, which reached sixty-eight years by midcentury, ushering in the third stage (the modern era), in which chronic diseases and cancer predominate, and no other disease kills more Americans than heart disease.

The rise of coronary heart disease occurred in part because Americans were living long enough to develop this illness, which most commonly presents in the fifth through seventh decades of life and also because life itself was changing in this country. As we became more affluent and more urbanized, the nation shifted away from a traditional low-fat,
agrarian diet and toward a diet high in saturated fats, found mostly in beef, pork, and lamb, as well as associated by-products such as lard, cheese, and cream.