by Cheney, Dick
At the same time that tPA and streptokinase were revolutionizing the treatment of heart attacks, intense research was under way to identify drugs that would help to prevent such events. In the 1950s and 1960s, driven by the increasing body of data linking serum cholesterol to heart disease, numerous pharmaceutical companies developed an interest in the complex biology governing how cholesterol is manufactured in the body. In 1956, researchers at one of these companies, Merck, isolated mevalonic acid, a key precursor of cholesterol, and three years later, scientists at the Max Planck Institute in Heidelberg, Germany, discovered the enzyme HMG-CoA reductase, which regulated the key step in mevalonic acid production. Theoretically, inhibition of this enzyme should inhibit the production of cholesterol, and over the next twenty years, researchers around the world hunted for a drug that would do that.
The first HMG-CoA reductase inhibitor was discovered in 1976 in the fermentation broth of the bacterium Penicillium citrinum by Japanese researcher Akira Endo. The drug, called compactin, was soon found to be effective at lowering cholesterol levels in rabbits, monkeys, and dogs. Meanwhile, in fall 1978, Merck scientists isolated a substance produced by the fungus Aspergillus terreus. The agent, a pure inhibitor of HMG-CoA reductase, was given the name lovastatin, and a US patent was filed in June 1979. In April 1980, Merck began clinical trials of the drug.
In September 1980, the Japanese pharmaceutical company Sankyo abruptly ended development of compactin amid concerns regarding cancers in dogs. Although there had been no such adverse safety signals with lovastatin, Merck quickly terminated development of lovastatin, citing the safety issues with the closely related compactin. Almost two years later, several clinicians petitioned Merck and the FDA for access to lovastatin for patients with severely elevated cholesterol that could not be controlled by treatment with any commercially available drug. Patients with superaggressive coronary disease and off-the-chart cholesterol levels saw their cholesterol drop by 30 percent or more after just a few weeks of lovastatin therapy. Merck promptly reinstituted animal testing in the drug, including long-term toxicology studies in dogs. Even after high doses, no tumors were found in the animals. Human clinical trials of lovastatin resumed in 1984. Merck found that lovastatin was well tolerated, and resulted in great reductions in LDL cholesterol levels. In November 1986, Merck filed a new drug application with the FDA comprised of 160 volumes of lab, animal, and human data. On August 31, 1987, only nine months after the application was filed, the FDA approved lovastatin for use in patients with high cholesterol not controllable by diet. Sold under the trade name Mevacor, the drug was an immediate commercial success, with annual sales eventually reaching $1 billion.
Hospital admissions for acute myocardial infarction began to drop sharply in 1987, the same year that lovastatin was introduced in the United States. Four years later, pravastatin (Pravachol), a derivative of compactin, and simvastatin (Zocor), a synthetic derivative of lovastatin, were approved by the FDA, and collectively the “statins” became some of the most widely prescribed medications in the world. Although the drugs unequivocally and profoundly decreased cholesterol levels, there remained uncertainty about whether improved lab results would translate to improved outcomes such as a reduction in myocardial infarction or death.
Questions concerning the clinical impact of these drugs were put to rest in 1994 when the Scandinavian Simvastatin Survival Study was published. The trial had assigned several thousand patients with high cholesterol to treatment with simvastatin or placebo and followed these patients for five years. The group of patients treated with simvastatin demonstrated a 30 percent or greater reduction in mortality, coronary events, or need for angioplasty or bypass surgery. This study became a landmark, effectively removing any lingering doubt concerning the benefit of cholesterol reduction. The studies that followed, using a variety of statins, including the newer atorvastatin (Lipitor) and rosuvastatin (Crestor), confirmed these results for patients both with and without a prior history of coronary disease, as well as those with a history of diabetes, peripheral vascular disease, and stroke.
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Throughout most of the 1980s, Dick Cheney’s cholesterol proved resistant to a variety of drugs like cholestyramine and gemfibrozil. In late 1987, Allan Ross started him on newly approved Mevacor, carefully increasing the dose over the next several months and ultimately reaching 80 mg, the maximum daily dose. In October 1988, Cheney’s total cholesterol level, which a year earlier was over 300, was down to 133. The low-density lipoprotein (LDL) component (aka “bad cholesterol,” because elevated levels are associated with an increased risk of heart disease) had plunged from 163 to 65, a 60 percent reduction.
The clinical impact of this effect in this patient cannot be overstated. In the ten years prior to beginning statin therapy, Dick Cheney was hospitalized six times and experienced three myocardial infarctions, resulting in a loss of about 30 percent of his heart’s ability to contract. In the twelve years that followed, even during periods of high stress, including time as secretary of defense during the Gulf War and CEO of a large multinational corporation, Cheney had not a single cardiac event.
CHAPTER 6
Bypass
VICE PRESIDENT CHENEY
The year 1988 was shaping up to be an active and important one for the nation and for me personally. Ronald Reagan’s second term as president was coming to an end, and there was a major battle in the Republican Party for the nomination to succeed him. I did not get involved in the presidential contest because I was focused on my own campaign to win the second-ranking leadership post among House Republicans.
The incumbent GOP whip, my good friend Trent Lott of Mississippi, was stepping down to run for the Senate. If I could win the race to replace him by a unanimous vote of the GOP Conference, I would be well positioned to succeed Bob Michel as GOP leader or even become the first GOP Speaker in more than thirty years if we captured the majority. As chairman of the House Republican Conference, I was slated to serve as the chair of the Convention Rules Committee. I wanted to take advantage of that assignment to get a rule adopted that would grant floor access at national conventions to all GOP members of Congress. The existing rule allowed only members who had been elected as convention delegates from their home states to have floor access. In addition, I had to get reelected to Congress by the voters of Wyoming for my sixth term in the House.
On the morning of June 29, 1988, believing that I might be having another heart attack, I checked myself into George Washington University Hospital. As before, I didn’t experience any major chest pain or other significant symptoms that I can remember, just a general sensation that something was wrong. EKG and enzyme tests confirmed that I was indeed having my third heart attack. Dr. Ross recommended that we try to reopen the offending heart artery by administering a newly approved clot-busting drug designed to clear a blocked artery. It seemed to work initially, but two days later, the pain returned, and I was given a second dose. Of my five heart attacks, this one did the most damage. I have a distinct memory of a crisis, with many hospital personnel hurrying into my room trying to deal with my “crashing blood pressure.” During that period, I also recall lying in bed listening to reports that an American cruiser, the USS Vincennes, had accidentally shot down an Iranian airliner, with significant loss of life, in the Persian Gulf.
After checking out of the hospital, I issued a press release on July 9 indicating that I planned to attend the Republican National Convention in New Orleans in August. I made it clear that my recent stay in the hospital would not alter my political plans. The heart attack did not force me to make a single major change in my professional schedule, but it did require me to back out of a wilderness pack trip with Jim Baker. We had planned it for July while the Democrats were holding their national convention, but given my health situation, I couldn’t justify a weeklong horseback trip into the Yellowstone backcountry. (When I told Jim I couldn’t make it, he quickly found a replacement: George H. W. Bush.) I returned to w
ork in the House of Representatives on July 22.
After further tests showed there clearly had been some progression in my coronary artery disease, Dr. Ross raised with me the possibility of undergoing bypass surgery. He didn’t present it as necessary to save my life, but thought it was advisable because of my lifestyle. I noticed I was having some difficulty traveling through airports carrying luggage. I found it necessary to stop and rest occasionally. I clearly lacked the stamina I’d once had. Having open heart surgery wasn’t something I looked forward to, but if I wanted to continue my career in the Congress and continue my skiing and pack trips in Wyoming and all of the other activities I loved, it was necessary.
My confidence in the outcome grew when I learned that Dr. Ben Aaron, the surgeon who had saved President Reagan’s life in March 1981, would perform the operation. On August 9 I announced that I would undergo bypass on August 19, after the GOP convention. “While for me the bypass surgery is optional,” the statement said, “I have decided to do it now so that in the future, I can lead the same kind of active life I have in the past.”
My August 9 statement also noted that my dad had just undergone coronary bypass surgery in our hometown of Casper. Since my first heart attack ten years before, I had been asked frequently if there was any history of heart disease in my family. I always answered that Mom’s dad had died of a heart attack at age sixty-six, but that as far as we knew, there was no history of heart disease on Dad’s side of the family. Dad never talked about his health, and as far as I knew, he had rarely if ever seen a doctor since he had been discharged from the Navy at the end of World War II.
In early August 1988, Mom had finally persuaded him that he needed to have a doctor take a look at him, so he made an appointment. During that appointment, the doctor discovered that his condition was so serious that they took him directly into surgery and performed a six-way bypass on him. When they opened him up, they found he also had a large aneurysm in his aorta and evidence that he had experienced two previous heart attacks that he never told anyone about. The doctors didn’t believe he would survive the bypass and aneurysm repair if they did both at the same time, so they completed the bypass and sent him home to recover for eight weeks, then brought him back in to repair his aorta. He lived another ten years. Now I knew I had a history of heart disease on both sides of my family.
In Wyoming, I had primary opposition for the GOP nomination for Congress but won comfortably with 87 percent of the vote. That same day, I convened a meeting of the Convention Rules Committee and successfully passed the rules change that would allow all Republican members of Congress to have floor access at national conventions. Since George Bush had already sewn up the GOP nomination for president, the only excitement focused on his choice of Senator Dan Quayle for vice president.
For me, one of the most memorable moments of the convention was the private talk I had with Larry King, then a correspondent for CNN. Larry and I sat on the steps going up to the CNN broadcast booth during one of the regular convention sessions and talked about my scheduled coronary bypass surgery. Larry had recently undergone a similar procedure, and I had a lot of questions. He walked me through his experience and was very helpful.
On Wednesday night of the convention, George Bush was officially nominated for president. The following day, I flew back to Washington and checked into George Washington University Hospital. That evening, George Bush gave his acceptance speech and delivered the memorable line: “Read my lips, no new taxes.” What was memorable for me was that I watched his speech flat on my back in a hospital bed while a male nurse shaved the hair off my body to prep me for surgery the next morning.
Since this was my first open heart surgery, I was introduced to a number of technologies and procedures I had never before experienced. I was told at the outset that the anesthesia would have the effect over time of diminishing my memory of the operation. That was probably true, but I still have a recollection of certain aspects of the procedure twenty-five years later. I have a memory of being aware during part of the operation of what was going on around me. When I asked, the doctors explained they really had no idea what goes on inside an unconscious patient’s brain.
This was also my first experience with being on a respirator. When I came out from under the anesthetic, I discovered I was breathing with the aid of a machine that had been inserted into my throat, and I couldn’t speak. The discomfort I felt was more psychological than it was physical. I felt the same way about the catheter that had been placed in my bladder. The idea of being dependent on these devices bothered me.
On the second day of my recovery, my chest and back felt as if I’d been hit by a truck. Obviously the anesthetic had worn off by then, and I was feeling the effects of having my chest opened wide and my rib cage separated to get at my heart. For two or three days, it was very hard to find a comfortable position in the bed. In my subsequent open heart surgeries I didn’t experience that kind of discomfort, no doubt in part because there have been significant improvements in pain management. Other things have changed too. Lynne had purchased a CD player for me that allowed me to listen to music through a pair of earphones. In 1988 it played only one CD at a time.
After I checked out of the hospital on August 26, I spent several weeks getting my strength back. I had time to reflect on the fact that my dad and I both had bypass surgery within a few weeks of each other. He was seventy-three and I was forty-seven.
In October I returned to Wyoming in time to do some campaigning and easily won reelection with 67 percent of the vote. On December 5, my Republican colleagues unanimously elected me House GOP whip.
Four months after my surgery, I was skiing at Vail and Beaver Creek in Colorado, something I could never have done without the bypass.
DR. REINER
An assignment to Dr. Robert Wallace’s service was a lucky break for me as a third-year medical student: I had the opportunity to learn from a famous heart surgeon and decide once and for all if surgery was for me.
Dr. Wallace had come to Georgetown from the Mayo Clinic where he had trained under the legendary John Kirklin, one of the pioneers of cardiac surgery. In 1968, Wallace became the first surgeon in the United States to perform the Rastelli procedure to correct transposition of the great arteries, a devastating congenital heart defect, where the aorta and pulmonary arteries arise from the wrong chambers of the heart. Dr. Wallace was old school, and rounds began in the ICU way before sunrise and moved forward at a rapid pace before concluding in time for the first OR case of the day. There was talk that he didn’t approve of students or residents with facial hair, a perhaps apocryphal story recounting a patient’s fatal infection and the beard Wallace had allowed the patient to keep at the time of his operation. On rounds the day before, I thought I saw Wallace take note of my well-groomed whiskers, the last vestige of my college years.
“Don’t worry about it,” one of the residents said.
Not reassured and not taking any chances, I wore a surgical hood for my first case, a kind of OR trapper’s hat replete with ear flaps. Now with my mask in place and revealing less of my face than a typical mummy, I tried to make myself invisible as Wallace entered the operating room. After donning his gown and gloves and moving quickly to the table, ignoring a series of “Good morning, Dr. Wallace” salutations, the chief leaned toward me, his head lamp and loupes (magnifying OR lenses) inches from my head, and fumed, “Step away from the table and cover your face! There’s no place for a beard if you want to be a surgeon.”
An inauspicious beginning.
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The British often refer to an operating room as an operating theater. It is part anachronistic description of the old tiered galleries from which young physicians once observed surgical procedures and part apt depiction of a highly choreographed space in which only dramas are staged.
You enter the cardiac OR through a door adjacent to a deep, stainless-steel sink and notice the discarded antiseptic scrub brushes littering the ba
se. When you push through the door, you immediately notice that the room is very bright, and very cold, and filled with a lot of people. At the head of the table, separated from the surgical field by a sterile drape suspended between two poles, is the anesthesiologist who has inserted an endotracheal tube, which protrudes from the patient’s mouth like a fat transparent cigar. The tube is mated via lengthy corrugated hose to a large machine that provides a mixture of vaporized anesthesia, nitrous oxide, and oxygen, keeping the patient asleep and ventilated. You gingerly slide next to the anesthesiologist, moving into the small space amid an organized jumble of IV tubing, pressure lines, and a rolling forest of infusion pumps. From this vantage point, the patient’s only visible body part is his head, and you watch as the anesthesiologist slips a transesophageal echo probe into the patient’s mouth. Unlike the endotracheal tube positioned in the airway, this much longer ultrasound transducer is destined for the esophagus, which lies behind the heart; it provides inside-out surveillance of cardiac function during the operation.
At the table you count four gowned participants. A surgeon’s assistant beside one leg has inserted an endoscope under the skin and is working to remove an eighteen-inch-long segment of vein through a one-inch incision below the knee, a bit of magic that eliminates the long scars and swollen legs common to bypass surgery patients a decade ago. A scrub nurse positioned near the waist presides over a broad back table filled with a gleaming menagerie of elegant stainless-steel instruments. Across the room, the perfusionist sits behind the heart-lung machine, its pump temporarily idle. You step onto a small platform and peer over the screen to watch the surgeon and first assistant open the chest with a sternal saw, a pneumatic-powered tool with a jagged reciprocating blade that slices effortlessly through the hard breastbone with a loud and angry growl, reminding you more of wood shop than science lab. An adjustable metal retractor is then wiggled into the breach and the chest is winched open revealing the beating heart still shrouded in its translucent pericardial sac.