The Heart Healers (43 page)

Should she go home to give her some breathing room? Should she return to the scene of her cardiac arrest for coronary angioplasty? Greta’s experience was so rare, so unheard of that there was no publication, no textbook to provide advice.

Jon reasoned that he did not know which of the obstructions he saw on her coronary angiogram just before her ventricular fibrillation was responsible for Greta’s angina or her ventricular fibrillation. She already had a stent in the left main coronary artery, but she still had an untreated severe stenosis in her right coronary artery. So she was still at risk for sudden death.

Jon concluded that the risk of going home exceeded any potential benefit. Greta would return to the site where her tumultuous journey began, but this time she would undergo right coronary balloon angioplasty. The stent he had placed during her cardiac arrest looked perfect. After a second stent was placed across the plaque in Greta’s right coronary artery, she returned home to her family.

With the use of a defibrillator, heart-lung machine, hypothermia, stents, and visits to the operating room and the CCU, Greta had nearly emptied cardiology’s metaphorical medicine cabinet. But not quite. With CAD at age thirty-five, the most important step in Greta’s care was now about to begin. Analysis of Greta’s blood revealed the likely cause of her early development of CAD. Greta had marked elevation of her LDL cholesterol. Greta needed a strategy designed to prevent the development of any new lesions in her coronary arteries and to prevent rupture of any existing plaques for the next fifty years. Before hospital discharge she started on a moderately high dose of a potent statin designed to lower her blood cholesterol into the low normal range. She was told that she would be expected to take the pill for the rest of her life.

About two months after Greta’s discharge, Jon called Greta at home to see how she was doing. There was no answer, so he left a message. When she did not return the call in a day or two, he called again, now concerned. Still no answer. So he got out her chart to find her emergency contact, which was Tyler’s cell phone. Again he called. No answer. His concern mounting, he left a message.

The next day Greta returned the call. She apologized for missing his call, she said. She and Tyler and Ben were camping, and doing a little hiking, in Yosemite.

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THREE YEARS AFTER
her hospitalization, Greta, Tyler, Jon, and I got together during a national cardiology conference. I described the book to Greta, Tyler, and Jon, and then asked Tyler to recount the details of Greta’s hospitalization as he experienced them. The three of us listened deeply moved in awed silence as deeply religious Tyler recalled every detail of the awful hours following Greta’s cardiac arrest. As he spoke Tyler seemed to be watching a long video replay. As image after image passed before him in his mind’s eye, he tearfully reexperienced his abject despair, his entreaties to God, his glimmers of hope, and finally his exaltation. It was so moving that at one point I noticed that all four of us had tears in our eyes. In that moment, I marveled how astonishing intellectual breakthroughs in cardiovascular medicine become truly profound when expressed in the life of a single patient. For me, the indelible image of Greta and Tyler, each smiling through their tears, personifies that profound insight.

25

CONQUERING CAD IN OUR LIFETIME

The past informs the present. Memory makes the map we carry, no matter how hard we try to erase it.

—CARA BLACK, AMERICAN MYSTERY NOVELIST

WHEN WE BEGAN
our journey at the end of World War II, we encountered disorders of the heart’s muscle, valves, electrical system, and arteries. Today, congenital heart disease is repaired early in life, mortality for valve surgery is a few percent, and rhythm disorders are managed with implantable defibrillator-pacemakers and ablation of abnormal electrical circuits in the cath lab. Since my days in Philadelphia, it is fair to say that we have delivered devastating blows to congenital heart disease, valvular heart disease, and disorders of the electrical system. In today’s world, that leaves the heart’s coronary arteries as our overriding concern. This year’s American Heart Association statistics suggest that the lifetime risk for developing atherosclerotic disease at age forty is 2 in 3 for men and 1 in 2 for women. CAD accounts for about a third of our annual mortality, and more than 2,200 Americans die of cardiovascular disease each day. So why do I claim that we are poised to subdue it?

The profound idea that CAD and its devastating complications are preventable is cardiology’s new mantra. Let me be explicit: if you have CAD, I now believe that you can arrest its progression, stop it in its tracks. If you don’t have CAD, you can prevent yourself from falling victim. But we know that in medicine, what sounds like an answer immediately raises new questions. Great scientific answers are not endpoints; they are new beginnings. So even as trials show us that CAD and its complications are preventable, to prevent CAD in yourself and your family, we need the answers to three new questions: at what age do atheromas begin to form, can we identify high-risk people before the atheroma begins to form, and can we reverse atheroma formation early in its course?

The answer to our first question, when do atheromas begin to form, has begun to emerge in just the past few years. At the Cleveland Clinic cardiologist Dr. Steven Nissen and his associates used a catheter with a miniaturized ultrasound probe to examine the wall of the coronary artery. In one study they have examined the coronary arteries of 262 donor hearts at the time of cardiac transplantation.

The investigators determined the percentage of donors who had coronary atheromas as a function of their age. It is 15% in fifteen-year-olds, and increases to 60% in thirty- to thirty-nine-year-olds. These shockingly high numbers parallel long-forgotten age-stratified autopsy studies of young soldiers killed in the Korean and in the Vietnam Wars. The conclusion is stunning and undeniable: although coronary atheromas cause symptoms in middle and older age, they actually begin to form in youth.

But can we identify the youth that are at high risk of developing atheroma? In Bogalusa, Louisiana, in the 1970s Dr. Gerald Berenson began a long-term follow-up of children in whom he recorded the risk factors for CAD. When the children were followed into middle age, he found that risk factors present in childhood tracked right into adulthood. So high-risk adults were identifiable as high-risk children. In a subgroup of Bogalusa middle-school children who died in their late teens and early twenties, autopsy showed that those who had more than two risk factors had eight times more atherosclerosis in their aorta than those with no risk factors. In a bizarre mimicry of ourselves, atheromas go through their own adolescence and early adulthood with us before blossoming to full adulthood in middle age. And thus the inescapable conclusion: we can identify people who are at high risk of a heart attack in middle age many years earlier, even as children and young adults.

The insight that CAD begins in youth and that risk can be identified at an early age raises the critical practical question for our times: can we halt and reverse atheroma formation years before symptoms? Our clinical trials show we can prevent the complications created by atheroma rupture, like heart attack and sudden death. But can we prevent atheromas from forming?

An experiment conducted by Mother Nature provides an insight into the potential impact of early prevention. The Atherosclerosis Risk in Communities study collects risk-factor information in four U.S. communities—Forsyth County, North Carolina; Jackson, Mississippi; suburbs of Minneapolis, Minnesota; and Washington County, Maryland. Approximately 3% of this population has a genetic mutation that confers a potentially beneficial 20% lower LDL cholesterol (bad cholesterol). Do these people, with modestly lower LDL cholesterol for a lifetime, do better? Yes, and how! Individuals with this mutation have had a 62% lower rate of cardiac events during the first fifteen years of the population study. An obvious inference is that a low LDL over a lifetime would have a similar impact in young high-risk individuals.

Our most recent statin drug trial confirms this idea. It was conducted in healthy people at high risk of CAD but with no known disease. Possibly someone like you, certainly like someone you know. Monitors stopped the planned five-year trial because they felt it was unethical to continue. After just two years the group randomized to rosuvastatin (Crestor) had a 44% reduction in cardiac events compared to the untreated group, and the gap between the groups appeared to widen each month.

What would you do if you knew the cause of a devastating disease, knew how to identify apparently healthy people at risk before it develops, and possessed the means to prevent the catastrophic illness before it developed? You would take action.

And that is why in November 2011 the Department of Health and Human Services, in partnership with many other organizations including the American Heart Association, announced the Million Hearts initiative. Our immediate stated goal is to prevent 1 million heart attacks and strokes over the next five years. I have not a single doubt that this goal is achievable, because in my personal odyssey I came to learn that CAD is a preventable disease. Last year heart disease ceased to be the leading cause of death in Canada. With Million Hearts, it will no longer be the U.S.’s number one killer. How does the initiative merge the past with the present and the future?

The logic of the Million Hearts initiative is compelling: in the Framingham study, half of the people who experienced a catastrophic heart attack or sudden death had no cardiac symptoms prior to their catastrophe. To overcome the scourge of CAD, therefore, we will have to prevent heart attack and sudden death in patients with no known disease. Our two-pronged approach is disarmingly simple: lifestyle modification and pharmacologic intervention when necessary. Lifestyle modification focuses on diet, exercise, stopping smoking, and controlling high blood pressure. The primary pharmacologic intervention will be medications that reduce the level of bad cholesterol in the blood.

How well have we done over the past twenty-five years, and how well might we do in the future? A 2013 analysis of the National Health and Nutrition Examination Surveys (NHANES) puts numbers on speculation. High blood pressure doubles the risk of CAD. Treatment reduces the risk of heart attack risk by about 25%. The national control of blood pressure has increased sixfold in the past twenty-five years. The control of LDL-cholesterol has improved by a similar magnitude. That’s why the mortality rate from CAD has fallen so precipitously. As effective as we have been, however, 70% of individuals who have both high blood pressure and high cholesterol still don’t have both risk factors controlled, and the majority is entirely untreated. So there is a huge opportunity for further improvement in this high-risk group. With the Affordable Care Act many of this untreated group will enter the healthcare system, and with the Million Hearts initiative, many more patients will be controlled through either lifestyle modification or drugs. Let’s use another of my patient-friends to illustrate what you need to do for yourself and your family.

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THE THREE OF
us had hilarious times as college fraternity brothers, and the friendships lasted a lifetime. Mort was the college politician and the head cheerleader. He became a university professor and served in the president’s cabinet as an adviser on Russia. Donald was the literary and artistic intellectual who later gained national notoriety as the lead prosecutor in one of the great criminal trials of our era. I was the varsity athlete and sportswriter. After graduation, through marriage, children, and changing jobs, we Three Musketeers held a reunion once or twice a year where we endlessly retold glorious tales of yesteryear. When we were in our early fifties, the reunion was a Texas-UCLA football weekend in Los Angeles. Both friends flew in from Houston.

Donald is a big man, about six foot two inches. In the thirty years since college, he had put on about forty pounds. He was a partner in one of Houston’s high-stress corporate law firms that bore his name. He lived life with joie de vivre; a cultured connoisseur of wine and art, he always had a big toothy smile, and another witty story to tell. In our college years, one of our friends toured the dorms a couple times a week handing out free packs of Winston cigarettes, four to a pack. That’s how we started smoking. I stopped, Donald didn’t. He now had a three pack-a-day habit.

Late Sunday night, as we waited outside a restaurant for a taxi to take my friends and their wives back to the airport, Donald pulled me aside, and casually, as if he were describing one of the abstract paintings that hang on his living room wall, said, “Jim, I felt some discomfort in my chest when I walked up the Rose Bowl steps yesterday at halftime. I’ve been fine since. I figure it was the chopped onions I put on those two hot dogs.” He postscripted an apology, “Nothing to worry about, I know, but you being a doctor, I thought I might as well mention it to you.”

Donald might as well have dangled from the nearby overpass and casually said, “Hey, look.” Really? Nobody, least of all a lifelong friend, gets a free pass after casually informing a cardiologist that he’s just started having chest pain with exercise. I yanked Donald out of earshot of the others and launched an inquisition. His discomfort had first come on a couple of weeks earlier walking up a hill after lunch to a rental car in San Francisco. He had experienced several episodes since that time. Each episode had its onset with either physical or emotional stress. Sometimes the discomfort went from behind his breastbone into his left arm. It was relieved in about a minute by rest. He had not mentioned the symptoms to anyone before me. An overweight fiftysomething smoking man in a high-stress occupation had just described typical angina, defined by its location, precipitation, and relief. I was momentarily dumbfounded. How could an intelligent person have such alarming symptoms, act as if he felt fine, and withhold such information until the last critical moment?