The Heart Healers (29 page)
Authors: James Forrester
I started an infusion of dopamine, a drug to increase blood pressure, which raised the systolic blood pressure back over 100. An anesthesiologist inserted a tube into his trachea to supplement his breathing, and we added a drug to diminish his pulmonary congestion. To supplement his cardiac output we inserted a temporary pumping device into his aorta. My measurements showed that Alexi’s cardiac function improved substantially. I knew I was headed in the right direction, and I could adjust the dose of each drug to maximize his heart’s function.
Over the next forty-eight hours, Alexi’s damaged heart and congested lungs struggled to bring his body back from the looming chasm of death. I tested his recovery by turning off his circulatory assist device, nervously watching to see if his heart function collapsed. It did not … his measurements stayed stable. So I left the machine turned off. By the early afternoon of his third hospital day, I could see clear signs that Alexi was on his way to recovery. I disconnected his respirator from his tracheal tube, and again watched his response. He remained stable. Next we discontinued his dopamine infusion and still his blood pressure remained stable. When he remained stable overnight, we removed the monitoring catheter from his heart. It was an inspiring day. In the years before our ability to manage severe heart failure during myocardial infarction, Alexi would have had virtually no chance of survival. We had pulled a young man back from the brink.
By the end of the week, we were able to send Alexi to a room on the hospital floor. He began walking. A few days later, I was stunned to learn that after a visit from a friend, he had dressed, and walked out of the hospital. Not even a good-bye note. Over the years, I have often wondered about Alexi after he left. He was as irreverently off-kilter as the lyrics of one of the songs he admired: “I don’t give a damn about your greenback dollar, spend it fast as I can.” I never saw him again. When the Internet emerged at the turn of the century, I knew if he were alive, he would be my age. I googled his unusual name. Not a trace. So we will always be two ships that passed briefly in the night during our journey through life.
* * *
IN THOSE EARLY
days of heart attack management, when my fellows and medical students took me to the bedside of a man in his thirties with a premature heart attack, I would always ask, “How many packs a day does he smoke?” Most young men with a heart attack were smokers. Nowadays I ask another question: “Have you done a ‘tox screen’?” That’s a urine screen for the common recreational drugs. My clinical impression is that the cardiac risk from cocaine, or the current drug du jour methamphetamine, is vastly greater than cigarette smoke. Alone or combined with heroin as a “speedball,” cocaine claimed the lives of Hollywood celebrities John Belushi, River Phoenix, Jim Morrison, Chris Farley, and sports figures like National League MVP Ken Caminiti and Boston Celtics forward Len Bias. Cocaine users quickly become aware that it increases heart rate, blood pressure, and respiratory rate, but their two big cardiac risks are virtually unknown to them. Cocaine causes coronary arteries to constrict, diminishing blood flow. At the same time it increases the stickiness of platelets, the disk-shaped cell fragments that initiate clotting of blood. These two factors can come together in the sudden catastrophic development of an occlusive clot in a coronary artery. I suspect this was the cause of Alexi Kroon’s heart attack. The final blow is that chronic cocaine and methamphetamine use predisposes to the early development of plaques in coronary arteries. So even if you don’t have a sudden heart attack the first time you use the drug, you greatly increase your long-term risk.
The irony of Alexi Kroon’s case is that he found one more way to increase his risk. With his young first-time partner, he exercised vigorously immediately after snorting cocaine, adding further the release of a hormone called norepinephrine that mediates the biologic response to exercise, and also potentiates the effect of cocaine on coronary constriction and clot formation.
What about sex causing heart attacks? It’s overrated. The heart attack part. It is true that there are occasional tabloid headlines about a celebrity having a heart attack during sexual encounters, the most famous of which is former potential presidential nominee Nelson Rockefeller, who allegedly collapsed during sex with his twenty-seven-year-old mistress. Panicked, instead of calling an ambulance, she called a girlfriend, who then called the ambulance about an hour after he first collapsed. Rockefeller allegedly died in the ambulance on the way to the hospital. The world’s most famous victim was Attila the Hun, who history tells us died of heart attack in his wedding bed.
Although suffering a heart attack during sex is extremely uncommon, about 75% of men experience sexual dysfunction after a heart attack, predominantly related to fear. Here are some facts. In controlled laboratory studies of sexual activity, volunteers have a significant increase in heart rate, breathing rate, and blood pressure pulse. The magnitude of increase approximates that of a moderate workout. But what about married couples in their own bedrooms? Twenty-four-hour heart rate monitors show that heart rates don’t increase, and remain lower than those recorded during normal daily activities. This is the reason that sexual activity rarely is identified as a precipitating factor in a myocardial infarction. An analysis of fourteen studies on the risk of cardiac death during sexual activity, from the Tufts University Center for Clinical Evidence Synthesis and the Harvard Department of Epidemiology in
The Journal of the American Medical Association,
concluded that the risk of death was 2.7 times more likely to occur during sexual activity, but only in the subgroup of people who rarely exercised or rarely had sexual relations. So if you have had a heart attack, a frequently quoted rule of thumb is that it is safe to have sex with your partner six to eight weeks after a heart attack, if you are able to walk up two flights of stairs without chest pain or feeling out of breath. For those who cannot pass that test, cardiac rehabilitation programs can assist in the return to normal daily activities.
* * *
IN THE YEARS
that followed, I could not have imagined the profound effect my role as director of the MIRU would have on my life as a doctor. Until that time I had always had a one-to-one relationship with my patients and families. Throughout my years in medicine, I had been fully immersed in the care of each of my patients. I took a detailed history from each patient, did a complete physical examination, read the chest X-ray and ECG myself, decided on appropriate treatment, and monitored each step in my patient’s return to good health. In my new role, three or four cardiology fellows who reported to me did all this before I saw the patient, and described their findings to me. My new role, while I was still in my early thirties, became that of a gray eminence. I still saw our patients, but now I would ask a few questions, listen to the heart and lungs, then step away from the bedside to discuss our patients’ care with my younger colleagues. As my relationship to patients became less tactile, my sense of fulfillment increasingly came from being a mentor. Our authority structure was transforming me from hands-on physician into a role model for other doctors.
When we won a huge new National Heart Institute grant called a Specialized Center of Research in Ischemic Heart Disease (known colloquially as a SCOR) with me as its director, my relationship with patients with heart disease was modified further by my responsibility for creating and supervising groundbreaking clinical cardiovascular research. I had to identify the most important problems in cardiologic patient care, then design and test potential solutions. The lessons I learned from living with several great mentors was fundamental: get a young colleague to discuss the critical unsolved problems in clinical care, get him/her enthused about solving it, get him/her the resources, and get out of the way. It was oddly similar to my direct patient care years: I was deeply committed to encouraging and supporting others, but now both doctors and patients. I’d get up every day looking forward to improving patient care. With $20 million to spend on cardiovascular research, a number of the young physicians in our previously unheralded Cedars of Lebanon Hospital advanced patient care and emerged as world leaders. I am deeply fulfilled today by their success in the dominant roles they played in bedside hemodynamic monitoring, nuclear stress testing, imaging inside the coronary arteries, heart disease in women, and interventional cardiology. I did not do the work, rather I created the environment where new ideas flourished and were translated into patient care. As I told my mentees, ideas are free: it’s the one who does the work that deserves the credit. Like so many others of our generation, we challenged established thinking. Yes, we, too, were misfits.
* * *
ONE OF MY
favorite mentees, Dr. Neal Eigler, has taken my research, in which I used a catheter to measure the pressure in the lung vessels during a heart attack, to a spectacular new level. Neal asked, “What about the patient after she leaves the hospital?” It’s a critical question because rehospitalization for symptoms of heart failure is today’s most expensive health-care problem. The symptoms of heart failure are due to backup of blood into the lungs. The resulting increase in pressure within lung vessels forces fluid across the exquisitely thin membrane that separates the blood from the air sacs in the lung. Fluid in the air sacs causes the patient to experience acute shortness of breath, precipitating an emergency room visit and hospitalization. Neal wondered if the rise in lung vessel pressure that precedes symptoms can be detected using modern technology and treated at a presymptomatic stage. He invented an implantable device that measures the pressure in the lungs. His device instructs the patient to take a dose of medication previously programmed into it by his/her doctor. The dose of drug varies with the pressure. Other devices send the pressure information to a central location that is accessed by the patient’s doctor.
Does controlling the pressure that causes the symptoms of heart failure work? The answer is yes. The FDA has just approved the first device that directly measures the pressures in the lung. It reduced heart failure hospitalizations by 30% at six-month follow-ups in 550 previously hospitalized patients. I got a lump in the throat reading the comment of noted Ohio State heart failure specialist Dr. William Abramson: “pulmonary artery pressure monitoring … represents our first meaningful improvement for the management of heart failure in nearly a decade … patients with chronic heart failure can reduce the need for costly and dangerous hospitalization while improving quality of life.”
* * *
THE EVOLUTION OF
the CCU now seemed complete. We had the capacity to monitor both disordered rhythm and the function of the heart following myocardial infarction, we had potent therapies, and we had the ability to assess the effectiveness of our treatment in each patient. Today, a destitute skid-row heart attack victim now receives far better care than the most powerful man in the world had received only a quarter century earlier. Three arrows: pacemakers, defibrillators, and methods of assessing cardiac function, aimed at different targets, had hit a bull’s-eye in myocardial infarction. When I saw Willie the Phillie, the in-hospital mortality rate was 30%. With these three advances in the CCU, in the passage of less than a decade, we had reduced heart attack mortality rate by half.
And yet, if you stood at the bedside of a patient experiencing a heart attack, as I did so often in those years, you had to admit an awful truth. We were standing helpless watching the progressive death of heart muscle, waiting to treat its consequences. We had no strategy for preventing the death of heart muscle as the heart attack occurred. Today, we have that strategy. I am proud to say it began with one of our former cardiology fellows.
I don’t want to play 10 years and then die of a heart attack when I’m 40.
—PETE MARAVICH, ALL-AMERICAN BASKETBALL PLAYER WHO DIED SUDDENLY AT AGE FORTY IN A PICKUP GAME
THROUGHOUT THE 1970S
I (and many others) focused on that era’s central topic: managing the devastation caused by myocardial infarction (heart attack). At that time we all believed that myocardial infarction was a final exclamation point, the culmination of a relentless progressive stenosis (narrowing) of a coronary artery plaque. A moderate narrowing caused angina, which was Mother Nature’s way of saying it’s time for bypass surgery. Left unattended, the narrowing ultimately became so severe that the need for oxygen in a segment of the heart muscle exceeded the supply. That segment could no longer survive. Without a way to open the narrowing during a heart attack, we focused on reducing its need for oxygen, using drugs that slowed the heart rate and diminished its vigor of contraction.
We imagined that a solution might lie with emergency bypass surgery, but creating such a program posed a logistic nightmare. If a heart attack occurred during the day, the surgeons, operating rooms, and heart-lung machines were typically busy with other elective procedures, so waits of three to four hours were often unavoidable. If the heart attack occurred at night, rapid mobilization of the entire team of surgeons, nurses, and technicians was at least as frustrating, and then wreaked havoc with the next day’s operating schedule.
In 1979 one of my former cardiology trainees, Dr. Marcus DeWood, came back to visit me. Marcus had recently settled into practice in Spokane, Washington, and sought me out for advice about the results of a small research project he had organized. He and his local cardiac surgery group had been able to establish a new program offering around-the-clock emergency bypass surgery for patients with acute myocardial infarction. At that time, no other hospital in the United States had yet succeeded in establishing a program like it. I was eager to see Marc’s results, believing that emergency coronary bypass might well reverse the imbalance between oxygen supply and demand precipitated by a heart attack.