by Cheney, Dick
Like most other people in their thirties, I didn’t give a lot of thought to my mortality, and I operated as though I’d live forever. Bad habits and their long-term consequences frankly didn’t concern me much.
• • •
Although we came very close, we didn’t win the 1976 election. One of the hardest things I’ve ever had to do in politics was read President Ford’s concession to Jimmy Carter the morning after the election. While the campaign hadn’t seemed to take much of a toll on my health, by Election Day the president was suffering a bout of laryngitis. The next morning, just after 11:00, sun streaming through the windows of the Oval Office, his family gathered around him, he told me to have the White House operator get Governor Carter on the line. After some brief words of congratulations, President Ford turned things over to me, and I read the concession telegram that was on its way to Plains, Georgia:
Dear Jimmy:
It is apparent now that you have won out in our long, intense struggle for the presidency, and I want to congratulate you on your victory. As one who has been honored to serve the people of this great land—both in Congress and in the presidency—I believe that we must now put the divisions of the campaign behind us and unite the country once again in a common pursuit of peace and prosperity.
Certainly there will continue to be disagreements over the best means of reaching our goals, but I assure you that you will have my complete and wholehearted support as you take the oath of office this January. I also pledge to you that I and all the members of my administration will do all we can to ensure that you begin your term as smoothly and effectively as possible.
May God bless you as you undertake your new responsibilities.
Sincerely,
Jerry Ford
The call lasted three minutes.
• • •
Shortly after Election Day, job offers began coming my way. Lynne and I decided we would take a much-needed vacation and spend some time carefully considering what we’d do next. I decided this would also be a good time to see a doctor for a routine physical exam. I wasn’t having any problems and thought of myself as very healthy. The doctor told me that given my smoking, cholesterol levels, bad diet, and family history on my mom’s side, I was a prime candidate for a heart attack.
I didn’t believe him.
• • •
Losing a presidential campaign is painful, as anyone who has ever been through it will tell you. I had huge admiration for Jerry Ford and still believe he should have won that race. But the loss convinced me that I didn’t want to be in that position again with my future dependent on someone else. I loved politics, and I loved public policy even more. If I am going to continue to do this, I thought, I want it to be my name on the ballot. I knew if I were going to run, I had to get out of Washington and go home to Wyoming. When school ended that June, Lynne and I packed up the girls and our basset hound and headed out in a U-Haul for our hometown of Casper.
On June 11, 1977, at the annual convention of the Wyoming Stock Growers Association, Wyoming’s senior senator, Cliff Hansen, announced he would be retiring the following year. “When my wife, Martha, and I go home at the end of the 1978 session,” Hansen said, “we are coming back for good.” A rancher and member of one of the first families to settle in Jackson Hole, Cliff had also served as Wyoming’s governor and was loved throughout the state. His decision to retire meant that a lot of folks would be thinking about a run for the Senate. I was one of them. Later that summer, after we’d gotten settled in back in Casper, I drove down to Cheyenne to visit one of my mentors, former Wyoming governor Stan Hathaway. Hathaway had given me my first political job as an intern in the state legislature when I was a student at the University of Wyoming. He knew Wyoming politics and issues better than just about anyone else.
I sat across from Stan in his law office and told him I was considering running for Cliff Hansen’s seat. “Well,” Hathaway said, “you could do that, but Al Simpson is going to kick your butt.” At that point, Al had served for twelve years in the Wyoming State House of Representatives. He was a natural: he loved people and they loved him. He remains one of my closest friends to this day. And I remain glad I took Hathaway’s advice and didn’t run against Al in that first campaign. In 1977 I didn’t yet know Al well, but Stan’s warning meant a lot. I headed home to Casper resigned to the possibility that I wouldn’t be running for office after all in 1978. All that changed on September 17, 1977, at a football game in Laramie between the University of Wyoming and the University of Texas at El Paso. During half time, Congressman Teno Roncalio, a Democrat who held Wyoming’s only House seat, went up to the press box in the stands and announced he would not be seeking another term. Three months later, on December 14, 1977, I announced I would be a candidate for Congress. I was thirty-six, and there was no doubt in my mind that I was perfectly capable of running for and serving as Wyoming’s congressman. As far as I was concerned, I had no health problems whatsoever aside from a bum knee.
The idea of a statewide campaign in Wyoming was daunting, but I didn’t think of it as jeopardizing my health. Any obstacles to success in my mind were purely political, and I was confident I could overcome them.
At the beginning of the campaign, I traveled the state alone, talking to as many Wyoming citizens as I could, looking folks in the eye, asking for their support, and building an organization. Wyoming covers nearly a hundred thousand square miles and has only one congressman, making it one of the largest congressional districts in the country geographically. In a primary, I could expect there would be less than one voter per square mile. Running for office for the first time meant long hours and many miles of travel.
In November 1977 I attended my first political event—a spaghetti dinner at the high school gym in Lusk, Wyoming, hosted by the state auditor Jim Griffith—and spoke for the first time as a candidate for Congress. Lots of candidates were in attendance, and each of us was given ninety seconds to make our case. I had worked hard to prepare my remarks. I had rehearsed in front of Lynne and had my notes in large print on a stack of note cards for the event. Unfortunately, when I got to the gym, I discovered there was no podium, so no place to put my cards. There was just a bare microphone. I had to do the best I could from memory, and I was very nervous. The master of ceremonies for the event had a huge gong—The Gong Show was a big hit on TV in those days—and the challenge for all candidates was to say what we had to say before our time ran out and we were gonged off stage. I slid in under the wire. The whole thing was a bit disconcerting, but it taught me a valuable lesson: never to assume I could predict the conditions under which I’d have to speak.
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.
DR. REINER
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 mum
mies, 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.
