The Heart Healers (46 page)

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Authors: James Forrester

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Diabetes is the perfect storm for CAD, raising blood lipids and blood pressure, oxidizing LDL cholesterol, and creating chronic inflammation that affects every blood vessel in the body. The worst-looking coronary angiograms I have ever seen, with every millimeter of every vessel covered with atherosclerosis, belong to diabetics. And that is why, on the brink of victory over CAD, we must also admit the possibility of defeat, not at the hands of the enemy, but ourselves.

*   *   *

AFTER HIS LIFESTYLE
conversion, Donald’s LDL cholesterol was still in the 150 mg/dl range. We needed to bring it into the normal range. Yet here is the deepest irony of cardiology: we do not know the normal range of LDL cholesterol. Among people without signs or symptoms of CAD in the United States, the value for bad LDL cholesterol is now about 120 mg/dl, but we know from Framingham that half the people who had a heart attack or sudden death had no symptoms prior to their cardiac catastrophe. In other words, on the day before their catastrophe they would have been members of the “clinically normal” population.

But Mother Nature is giving us some advice about the normal level of blood cholesterol if we will only listen. Humans are the only species that spontaneously develop CAD. No wild animal in the entire animal kingdom develops atherosclerosis. So intrepid epidemiologists have measured blood cholesterol in wild animals like the elephant, bear, wild pig, and rhinoceros. The average LDL in wild animals is approximately 60 mg/dl (recall the average U.S. adult has twice this value). The entire wild animal kingdom is also pursuing a healthy lifestyle without atheroma or heart attacks. (The Angus steer that donated the steak you had last night, however, is not of this group because it was specially prepared for you by the cattle industry to have delicious “marbling.”) Let’s look at humans with the animal kingdom in mind. We are born with an LDL level in the same range as animals. It gradually increases as we get older. A few adult human populations, however, do not exhibit this progressive increase in LDL with age. The world’s remaining hunter-gatherer societies, diverse in geographic location and ethnicity, but arguably living the way humanity did 10,000 years ago, have LDL levels in the range of the rest of the animal kingdom. In modern societies, rural Chinese blood levels often fall within this range. And here is the most important trivia you’ve never heard. Among this diverse group of humans, CAD is rare. The consistency of these diverse human data sources, taken together with the mammalian species data, supports the idea that the normal range of LDL in adult humans is approximately 40 to 70 mg/dl.

Does lowering LDL into this range translate into measurable beneficial clinical outcomes? The most recent trial of this idea showed that reduction of LDL cholesterol from 108 mg/dl to 55 mg/dl in high-risk patients without known CAD resulted in a 44% reduction in actual cardiac events over a two-year period. The results were considered sufficiently powerful that an independent safety monitoring board called for the trial to be stopped, believing that it was unethical to withhold treatment from the placebo group. In patients whose LDL level reached values less than 50mg/dl, an even greater reduction in adverse events occurred. Sanjay and I chose to reduce Donald’s LDL to 70 mg/dl using statin therapy, and we were successful.

My message for you is that lower is better. In my view, if you have CAD or diabetes, you should be taking a statin and your LDL cholesterol should be in the 70s or lower. If you do not have CAD, still aim for the same level. It’s the same disease, whether or not we have symptoms.

Not everyone, of course, needs a statin. Can you assess your risk of having CAD if you have no symptoms? Yes, but it can cost you as much as $200. We cannot spend that amount of money on every adult because it would destroy our health-care budget. None of our tests are perfect, but two stand out as superior to all others. These are the two I would ask you to focus on. The first is the risk score used in our national guidelines, which includes age, smoking, diabetes, blood pressure, and blood lipids. The score provides your ten-year risk of a cardiac event. The blood lipid test runs about $75, and is covered by all insurance plans. You should have the test every five years after age 20. Our guidelines urge that you begin statin therapy if you have a greater than 7.5% risk of a heart event in the next ten years. Your doctor can calculate your risk.

Setting the guideline at 7.5% risk for ten years is a wise suggestion, but quite honestly, it is insufficient for you and me. We know that among those classified as low risk by the risk score, more than a third already have CAD. How do we detect these people, who also clearly need statin therapy?

The second test, calcium scanning, is more specific. If you have calcium in your coronary arteries, you have CAD. Period. The amount of calcium in your coronary arteries also is given a score, and it also predicts your ten-year risk. If there is no calcium (your calcium score is zero) your chances of a heart event in the next decade are vanishingly small. So if your LDL is low and you have no calcium in your coronary arteries, why take a statin?

If you want to prevent that cardiac catastrophe and you can afford to spend a couple hundred bucks, do these two tests. Your doctor can then design a risk modification program for you. What about me? Twenty-five years ago I had an LDL of 160 and just a wisp of calcium in my coronary arteries. I started on a statin. Today I have an LDL of 70 and no increase in the calcium in my coronary arteries. And that’s the way it will be when I hit age ninety.

How much does a statin cost? The prices for a generic statin vary widely. On the Internet I found pricing for $19 per month, but some chains like Walmart have plans for as little as $4 per month. If you were taught to pinch pennies (I was), be like me: get yourself a pill splitter for less than ten dollars, ask your doctor to double the dose of your statin pill, and then cut your pill, and bill, in half.

Given the cost of treating the complications of angina and heart attack, health-care economists have begun to wonder about applying a similar strategy in the entire population. The irony is that the cheapest strategy is to put everyone on a generic statin. Crazy? Maybe not. Two of my boys, both athletes, had an elevated LDL in their thirties, did not bother with the calcium scan, both take a statin, and their bad cholesterol is in the 70s. They experience no side effects from the drug. Many cardiologists might disagree, but my opinion is that, like me, they are better off than they were with an LDL in the 160s.

Among all the drugs I prescribe, generic statins are low risk and inexpensive. If you have an elevated LDL, talk to your doctor about a statin. For many of us it’s a very worthwhile inexpensive investment, provided you can take the pill with no side effects.

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WE STARTED WITH
statistics so let’s end with them. In December 2012 pathologist Bryant Webber compared autopsy results from 3,832 service members who died in Afghanistan and Iraq to similar studies performed in the Korean and Vietnam wars. In the Korean War, at the outset of our chronicle, 77% of the soldiers autopsied had evidence of coronary atherosclerosis. Twenty years later during the Vietnam War the prevalence of coronary atherosclerosis had fallen to 45%. Now, forty years after Vietnam, the prevalence of coronary atherosclerosis in soldiers dying in Afghanistan has fallen to a jaw-dropping 9%. We can reasonably attribute this change to lifestyle modification in our soldiers: more healthy diet, insistence on weight control, better exercise programs, and less smoking. We also know that over the last decade, the incidence of cardiac events in the general population has fallen by 36%. Over the last thirty-five years in the United States, mortality from heart disease has fallen five times as fast as the mortality rate for cancer.

That’s the past, but what about the future? In 2013, biostatistician Dr. Mark Huffman of Northwestern projected the number of CAD deaths in 2020, given recent trends in the six principal risk factors for CAD (total cholesterol, systolic blood pressure, physical inactivity, smoking, diabetes mellitus, and obesity). Even if we do not improve on our current trends, he projects a further 30% decrease in CAD mortality reflecting improvements in total cholesterol, systolic blood pressure, smoking, and physical activity (about 167,000 fewer deaths), offset by increases in diabetes mellitus and body mass index (about 24,000 more deaths). If these projections are correct, the annual mortality from CAD in the United States will fall from approximately 800,000 to 465,000. If we succeed in stemming the epidemic of obesity and diabetes, this mortality rate will be even less. The optimist sees the donut and the pessimist sees the hole … we are succeeding but even more is possible. We know what’s necessary to win the battle, but we cannot declare victory until the public takes responsibility for its own health. The opera won’t be over until the fat lady slims.

*   *   *

AND WHAT ABOUT
Donald, whose surgeon predicted his imminent demise? As he embarked on his new lifestyle and LDL cholesterol reduction, he had a few episodes of angina, but within a year, his chest pain on exertion disappeared. Two years ago Sanjay retired after taking care of Donald for twenty years. Donald’s surgeon retired. Donald and I still get together once or twice a year. Last month he had a stress test, which was normal. Donald likes to say that I saved his life. It’s not true. Donald’s foxhole conversion did. He made the decision to stop further progression of his CAD. From his normal stress test, I infer that some of his atheromas have regressed in size. From his two decades of absence of symptoms I infer that we have fended off the rupture of existing plaques. Every one of the steps Donald took was essential. I believe smoking cessation and exercise reduced chronic inflammation, proper diet and weight loss had multiple beneficial effects on his blood chemistry, and lowering his cholesterol stopped atheroma formation, induced regression, and cleared out inflammatory cells around the atheromas. I imagine that the atheromas are still there, smaller than they used to be, and in a deep sleep. And that’s the way they will stay. We have defeated a tiny monster as insatiable as the guillotine.

For both Donald and me, the time had come to step down, to let go of the titles, and, well for me at least, to write a book. Combining mentoring with being on the cutting edge of the advances in clinical cardiology has been exhilarating. Although I loved my years on this larger world stage, even today I remain ambivalent, recalling my dreams as a little boy under my dad’s living room table. What would life have been if, like my father’s friends, instead of mentoring and consulting, I had spent my years seeing twenty patients a day? Daily hands-on patient care is deeply rewarding. Paradise Lost or Paradise Gained? Looking back, it seems to me I had both—the best of both worlds. So today I find myself more often asking young doctors questions rather then giving answers, suggesting they carry forward the legacy of a generation that never lost touch with compassion as they challenged conventional wisdom.

 

26

THE PRESENT CREATES THE FUTURE

The positive thinker sees the invisible and achieves the impossible.
—NISHAN PANWAR, CONTEMPORARY INDIAN WRITER

IF WE GAZE
only on the past and the present, we will surely miss the future. So let’s imagine the future management of diseases of the heart’s four components: its muscle, its electrical system, its valves, and its arteries. I envision a new landscape with awe-inspiring achievements by a next generation that matches those of my own.

H
EART FAILURE: CREATING NEW HEART MUSCLE

LET’S START WITH
damaged heart muscle. We estimate that 5.7 million people in the United States have heart failure, the natural outcome of heart muscle damage, most commonly during a heart attack. Currently, half of our patients with heart failure die within five years of diagnosis. The economic burden of heart failure is the largest in all of health care, costing $35 billion per year in the United States. So heart failure is one of medicine’s greatest problems. We currently rely on drugs, lifestyle measures, and cardiac transplantation for management of heart failure.

Here’s the great irony of heart failure: even though normal heart muscle cells are naturally replaced each year by its own stem cells, damaged cells are not. In other words, although we humans clearly possess the intrinsic capacity to regenerate heart muscle cells after a heart attack, it does not happen. But there’s more. Some animals like the zebrafish, newts, and mutant mice regenerate heart muscle as easily as a starfish regrows a limb. Somewhere along evolution’s wandering trail, we lost the capacity for regenerating heart muscle. The good news is we can get it back.

*   *   *

FOR SIXTY-SIX-YEAR-OLD
commodity broker Edward Sukyas his solitary one-hour walk along Third Street in Beverly Hills is his source of vitality, a metaphor for so much that is good about being alive: each unique smell emanating from competing restaurants and coffeehouses, the gabble of different languages, the hubbub of bustling humanity. After all, it mirrors his own ebullient life, one fully lived. His daily walk had begun more than a decade earlier soon after his father had died of a heart attack, and now it is an essential part of his day. With two children of his own, he looks forward to a grandchild already on its way.

Edward was educated at the Lycée Stendhal in Milan, Italy. He is fluent in seven languages. He has traveled the world. A Canadian citizen, he has lived in nine countries. Edward has been intimate with the back streets of Tangiers where he owned a carpet factory and he has lived the hectic nightlife of Cabo San Lucas as the owner of a French-Italian haute cuisine restaurant. And on this day his walk embodied the duality of his healthy-unhealthy lifestyle: adherence to both morning goat cheese omelets (“loosely rolled instead of folded, the French way, of course”) contrasted with a very good exercise regimen. The south side of Third Street, wafting aromas of garlic and oregano through the doors of Locanda Veneta, was a metaphor for the gourmet side of life. At the moment the chest pain began he could hardly imagine that on the north side of the street stood a new metaphor, Cedars-Sinai Medical Center. A plaque was poised to rupture in one of Edward Sukyas’s coronary arteries. He was about to have a heart attack. It was August 17, 2009.

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