Heart: An American Medical Odyssey

by Cheney, Dick

  Though it coincided with my reelection campaign for my fourth term in the House of Representatives, the 1984 heart attack did not lead me to question my choice to serve in elective office or my commitment to a long-term career in politics. I spent the next several weeks recuperating at home in McLean, Virginia.

  On October 2, 1984, I went to the Capitol when the Wyoming Wilderness Act was up for a vote in the House of Representatives. Along with my Senate colleagues Al Simpson and Malcolm Wallop, I had worked very hard on this legislation, which set aside nearly a million acres in wilderness area in my home state. I wanted to be sure it passed, and I wanted to be there to cast my vote for it.

  I spent the last two weeks in October campaigning in Wyoming and was reelected to my fourth term with 74 percent of the vote that November. I felt no aftereffects from my second heart attack and had been able to resume a full and active schedule.

  In February 1985, I took on additional responsibilities in the House when I was named to the Permanent Select Committee on Intelligence, which has responsibility for congressional oversight of all matters relating to the nation’s intelligence agencies, including the CIA, the Defense Intelligence Agency, and the National Security Agency. It is the kind of assignment some members don’t relish. The work is mostly highly classified, and you can’t explain to your constituents how you are spending your time. Studying the materials and intelligence reports is a significant commitment of many hours and must be done only in the secure committee facilities in the Capitol. But it is an assignment of real significance in terms of the security of the nation, and I found the work fascinating.

  In 1986, I was reelected as the House Republican Policy chairman for the Ninety-Ninth Congress. That November, Al Simpson and I had been planning to go elk hunting. The day before we were scheduled to leave, House Republican leader Bob Michel called and asked me to attend a meeting the White House had just called. It seemed I was the only member of the House Republican leadership in town that day.

  As it turned out, the meeting, on November 12, 1986, was a briefing delivered by national security adviser John Poindexter in the White House situation room. I sat around a table with the Senate majority leader, Bob Dole, the Senate minority leader, Robert Byrd, House Speaker Jim Wright, and a number of members of President Reagan’s cabinet. Poindexter explained to us that in an attempt to secure the release of American hostages being held by Iran’s ally, Hezbollah, the United States had been selling arms to what they believed were moderate factions in Iran. Some of the hostages had been freed, but the policy was badly misguided. It violated an existing arms embargo and put the United States in the position essentially of negotiating with terrorists.

  A few weeks later, we learned the picture was even more complicated when it was revealed that proceeds from the arms sales were being sent to the Contras, a rebel group in Nicaragua. Congress had prohibited the president from providing any assistance to the Contras when it passed a series of amendments, collectively known as the Boland amendment, in the early and mid-eighties. In the aftermath of the revelation about the diversion of funds, a joint select committee was formed in Congress to investigate what had happened. I was the ranking House Republican on the committee and presided, along with chairman Lee Hamilton, over committee hearings on the arms sales and fund diversion throughout the first half of 1987.

  The issues raised by Iran-Contra were significant and concerning. Clearly the administration made mistakes in carrying out a policy of essentially negotiating with terrorists. But there were also legitimate questions to be asked about the proper role of Congress in the conduct of US foreign and national security policy. And the political atmosphere in Washington meant that, in my view, many of the Democrats on the select committee were more interested in scoring partisan points against President Reagan than they were in understanding what truly went wrong and finding ways to prevent it from happening again.

  Against the backdrop of my involvement in the significant, highly scrutinized, and time-consuming Iran-Contra committee, I was still dealing with matters of my heart. On January 27, 1987, President Reagan was scheduled to deliver his annual State of the Union address to a joint session of Congress. This would be the One Hundredth Congress and the beginning of the year marking the bicentennial of our Constitution. I was booked to appear on several news programs that night after the speech. I was at work in my office and began to feel some chest discomfort. I took two nitroglycerin pills and called Pete Williams, my press secretary, and Patty Howe, my legislative director, into my office. I asked them to cancel my interviews for the evening and then asked Pete to walk with me over to the Capitol physician’s office. We walked the length of the hallway to the elevator. I was feeling worse by the minute and didn’t think I could make it over to the Capitol. Pete and I turned around and headed back to my office to call an ambulance.

  I took a few steps, and there, in front of the Capitol policeman’s desk, fainted. Pete, pretty scared by this point, asked the policeman to call for a doctor. Instead, he called his superior and shouted, “Member down.” Pete ran down the hall to our office and had Patty call the House physician. The Cannon House Office Building nurse was on duty. She came out with a pillow and checked my blood pressure. Apparently, as I lay there sprawled out and unconscious on the marble floor with my shirt open, several of my colleagues walked by. As Pete tells it, they didn’t quite step over my body, but it was close.

  Eventually an ambulance came, and Pete rode with me to the George Washington University Hospital emergency room. Pete was understandably pretty worried and didn’t think I was getting medical attention quickly enough. At one point, he started yelling to no one in particular, “This is a United States congressman!” Either in light of that information or, more likely, because they wanted to get Pete to quit yelling, I was taken back for evaluation. After a few hours and tests, the doctors determined I had not had a heart attack but probably had an adverse reaction to the nitroglycerin. They released me to go home.

  I was somewhat surprised, given the dramatic nature of the event and the fact that several of my colleagues had strolled past me while I was unconscious on the floor, that the story never made the media. Pete Williams, a dear friend to this day, felt guilty that he’d been standing there when I passed out and hadn’t caught me. I couldn’t resist giving him a hard time about it when I got back to the office the next day. “Thanks, Williams,” I told him. “You dropped me!”

  A few months later, in May 1987, after I’d had an abnormal stress test, Dr. Ross performed another catheterization. In 1987, the standard procedure was to access the femoral artery through the groin. The area was shaved and prepped with antiseptic and a local anesthetic was administered. I was given mild sedation but was sufficiently awake to be aware of what was going on around me. On occasion, I remember being asked to cough during the procedure. I was sometimes able to see the screen the doctor used to steer the catheter into the arteries of my heart. When the dye was injected, I felt a warm flush. The only uncomfortable part of the procedure occurred after the catheter was withdrawn and the entry wound closed. The final step, to ensure there was no subsequent bleeding from the entry point, was to apply heavy pressure to the wound for approximately half an hour. This task was usually assigned to the largest member of the surgical team. The procedure has since been significantly improved.

  It wasn’t until I was reviewing my own medical records in preparation for writing this book that I realized this particular catheterization included some worrying moments. In the words of Dr. Ross:

  Unfortunately, during one injection he developed ventricular fibrillation requiring cardioversion x3 with 300 joules

  As happens sometimes, but not often, the dye had prompted my heart to fibrillate in a potentially deadly rhythm. It took three electric shocks to set things right.

  This catheterization showed that my right coronary artery had begun to narrow, but there had been no further progression of the plaque in other vessels in the heart
. At my follow-up appointment a few weeks later, Dr. Ross advised that I should restrict my most strenuous activities, particularly at high altitudes, in the hope that I would be able to continue to participate in less strenuous recreational pursuits without risking damage to muscle deprived of oxygen. We also agreed that given the results showing narrowing of an artery that had previously been plaque free, I would now have more regular stress tests.

  As I was receiving news of a worsening heart condition, my responsibilities on the Hill continued to increase. On June 4, 1987, I moved up in the House leadership when I was elected chairman of the House Republican Conference, the number-three elected position in Republican leadership. Meanwhile I was still engaged in the high-stakes hearings about the Iran-Contra affair. At first glance, it might seem that my professional activities would have added to the stress of the somewhat negative health report. I think it was actually just the opposite. The job of ranking member on the Iran-Contra committee involved me in critically important matters—issues relating to the constitutional roles of the president and Congress, questions about how far the United States should go to secure the release of our hostages, and inquiries about how best we could prevent the Soviets from gaining a foothold in Latin America. I think it was the import of these issues and the sense that I was an important participant in a set of historic events that enabled me not to dwell on the negative developments with respect to my heart. I didn’t have time and was not inclined to sit around and feel sorry for myself. I believed Dr. Ross had laid out a reasonable course of action that involved some curtailing of my activity. He had also scheduled me to begin the new cholesterol-lowering drug, lovastatin, as soon as it received approval from the Food and Drug Administration (FDA). The combination of comfort with my physician and his judgments, a sense that we were doing all we could do to deal with the disease, and a knowledge that I had important work to do for the nation allowed me to continue to participate fully in all I was called on to do.

  DR. REINER

  You’re not sure what is happening, but somehow, in a visceral way you can’t articulate, you know that it is not good. At first, the symptoms were subtle. Maybe you awoke not feeling right; you might have had some of these symptoms yesterday, but you’re not really sure when it began. You thought it might be indigestion because you’re a bit nauseated, and you took some antacid a little while ago, but the discomfort hasn’t eased. Now you’re feeling something in your shoulder and chest, and your left arm is tingling. Someone tells you that you look pale, and you realize your shirt is drenched even though it is not warm in the room. You’re asked if you are having chest pain, and you say no, it’s not a pain, it’s more like a pressure or maybe a tightness. When you try to describe what you’re feeling, you subconsciously place a clenched fist over your chest. You have the sense that if you could manage to burp, you would feel better, but you can’t, and to make matters worse, you’re a little short of breath.

  You don’t know it yet, but a blood clot, smaller than a pencil’s eraser, is forming inside one of your coronary arteries, and if it is not dealt with quickly, it can kill you.

  • • •

  That’s what was happening when Dick Cheney awoke with chest pain in the early-morning hours of June 29, 1988, and was brought to George Washington University Hospital, in DC’s Foggy Bottom neighborhood, six blocks from the White House. When he arrived in the emergency room Congressman Cheney’s blood pressure was 115/70, and his pulse was 64, both normal. But his EKG showed signs of a new MI in the same region affected by heart attacks in 1978 and 1984. This was his third. Cardiologists Allan Ross and P. Jacob Varghese evaluated Cheney and recommended urgent cardiac catheterization to determine the site of the likely coronary occlusion.

  Dr. Ross had come to GW from Yale about a decade earlier and was an internationally known expert in the management of acute myocardial infarction, having helped to pioneer some of the revolutionary new drugs. Dr. Varghese, a legendary clinician, had come to GW from Johns Hopkins around the same time and was the director of the cardiac care unit.

  After puncturing the femoral artery at the top of Cheney’s right leg, Ross guided a catheter to the heart, maneuvering it into the aorta and the origin of the coronary arteries where an injection of contrast dye revealed an old occlusion of the circumflex branch (unchanged from 1984) and a new clot blocking the right coronary artery. Ross intended to open the artery with a balloon, but a mechanical malfunction in the cath lab forced him to change his plan. Instead Cheney was administered tissue plasminogen activator (tPA), the new intravenous “clot buster” approved by the FDA seven months earlier.

  • • •

  In the late 1970s, Dr. Marcus DeWood set out to prove once and for all that blood clots caused heart attacks. DeWood and his colleagues at the University of Washington performed coronary angiography in about three hundred heart attack patients admitted to hospitals in Spokane and Seattle. The demonstration that it was both feasible and safe to perform cardiac catheterization during an acute heart attack was itself a groundbreaking achievement. DeWood found that when angiography was performed within a few hours of symptom onset, it showed that almost 90 percent of the patients had a totally blocked coronary artery, and in many of these patients, a culprit blood clot could be extracted from the vessel. Importantly, when other patients in the study were imaged later, up to twenty-four hours after the onset of pain, fewer arteries were closed, suggesting that with time, some clots spontaneously dissolve, raising the possibility that this intrinsic “clot-busting” process might be induced therapeutically.

  At about the same time that DeWood’s study was under way, several groups were working to prove that not all of the at-risk heart muscle (the myocardium) died immediately after a coronary artery closed. Using a laboratory model involving the temporary occlusion of a dog’s coronary, Keith Reimer from Duke University and Robert Jennings from Northwestern demonstrated that myocardium died over hours, limited initially to the innermost layer of the heart (subendocardium) and over time extending through the full thickness of the muscle to the outermost layer (subepicardium). They showed that if blood flow was restored within fifteen minutes, no permanent heart damage occurred. Progressively longer occlusions resulted in progressively larger amounts of muscle death, and restoration of blood flow after about six hours would not salvage any muscle at all. The implication of this work was profound: a heart attack could be interrupted, but time was of the essence.

  With the cardiology community finally convinced that a typical heart attack resulted from a blood clot and with a potential therapeutic window of several hours, the approach to the management of heart attacks changed from the old largely defensive, watch-and-wait strategy, to a new offensive attempt to open the occluded vessel and salvage heart muscle. But how to open the artery?

  • • •

  Each of us has more than sixty thousand miles of blood vessels, mostly comprising a microscopic maze of billions of capillaries. The five liters of blood coursing through this complex vascular network must be kept in careful biochemical balance, also known as homeostasis. If blood is too “thin,” spontaneous hemorrhage may occur, and if it is too “thick,” clots may develop.

  In 1933, William Tillett and R. L. Garner, working at the Johns Hopkins Medical School in Baltimore, discovered the novel ability of cultures of streptococcal bacteria to completely liquefy a previously solid blood clot. This bacterial protein, which was later called streptokinase, was found to exert its “fibrinolytic” effects by activating a naturally occurring protein in human blood called plasminogen and converting it to the active enzyme plasmin, which dissolves the fibrin meshwork of a thrombus.

  Tillett and his colleagues initially used streptokinase to treat patients with pneumonia or tuberculosis who had developed large gelatinous collections in the pleural space that surrounds the lung. A direct injection of streptokinase into the pleural space between the lung and the chest wall dissolved much of the thick material, enabling drainage from t
he space and reexpansion of the lung. In 1951, Tillett showed that an experimentally induced clot in an ear vein of a rabbit could be opened when streptokinase was administered systemically, and in the late 1950s, intravenous streptokinase was evaluated in patients with acute myocardial infarction. Despite some data suggesting a potential mortality benefit when the drug was administered relatively early, streptokinase was largely abandoned in the United States because we did not yet know enough about the mechanics of a heart attack.

  Twenty years later, with the pathophysiology of heart attacks much clearer, interest in clot-busting drugs returned. In the late 1970s, Evgenii Chazov in the Soviet Union and Peter Rentrop in West Germany separately demonstrated that a direct injection of streptokinase by catheter into an occluded coronary could restore the flow of blood, and in 1984 the FDA approved streptokinase for intracoronary use during myocardial infarction. The downside of this approach was that it was fairly complex, took a significant amount of time to perform, and required the use of a cardiac cath lab, at the time available in only a limited number of hospitals in the United States.

  In the years that followed, several very large international clinical research trials, enrolling tens of thousands of patients, proved that streptokinase and tPA, a new drug at that time, produced using recombinant DNA techniques (a process whereby different strands of DNA are combined to produce a “designer” molecule), could open many of the arteries with a relatively simple intravenous administration, and compared with placebo, both drugs significantly improved a patient’s likelihood of surviving a heart attack. In November 1987, the FDA granted approval for the intravenous use of streptokinase and tPA in the United States. Manufactured by Genentech (and at $2,200 a dose, ten times the cost of streptokinase), tPA was enthusiastically embraced by the medical community in the United States. Accelerated by a study in the early 1990s that found myocardial infarction death rates lower after treatment with tPA than after treatment with streptokinase, annual tPA sales soared to more than $300 million.