The Heart Disease Breakthrough: What Even Your Doctor Doesn't Know about Preventing a Heart Attack

Part One:

UNDERSTANDING

YOUR RISK

FOR HEART DISEASE

1

The Heart Disease Surprise: There Is No Immunity

If you opened this book, you or someone close to you has concerns about heart disease. And you’re right to be worried: Heart disease and its related problems will end the lives of more people than all the other diseases in the world combined. One of the reasons is that despite all the talk about this disease, despite all the advice handed out freely by doctors and laymen alike, most people still are unaware of how to avoid it. And avoid it you can. If you are properly armed with the latest information, heart disease is almost completely preventable.

Here’s a short quiz to determine how sophisticated your knowledge of heart disease really is. Which of the following statements are true, and which are false?

The process of atherosclerosis, which causes heart disease, begins at about the age of forty, so you only have to be careful from then on.

The first rule for preventing heart disease, which everyone should follow, is eating a low-fat diet.

Thirty minutes of moderate exercise accumulated over the length of the day, every day, will significantly reduce your risk for coronary artery disease.

If you keep your cholesterol level below 200, you will be fairly safe from getting a heart attack.

There are two different kinds of cholesterol, and you have to know both levels to determine your risk.

Although most people—even sophisticated people who are aware of medical facts—don’t know it, every one of these statements is false. In the last few years, research has made substantial progress in uncloaking heart disease’s secret code as it applies to each individual. In doing so, we have exposed some myths. Here is the real story:

The process of atherosclerosis begins in childhood, and in most Americans it is well advanced by the time they are in their twenties.

Low-fat diets can actually raise cholesterol and increase risk in certain groups of people. And a good low-fat diet for one person can actually be harmful for another.

Thirty minutes of moderate exercise in several short stretches during the day will do almost nothing at all to decrease your risk of coronary artery disease.

Many of the people with the most aggressive heart disease have total cholesterols under 200.

There are at least a dozen different kinds of cholesterol particles, and their balance in your blood can be the difference between longevity and an early death from heart disease.

You can prevent heart disease, but what you have to know and do to achieve such safety is dependent on your individual mix of risk factors. You have to know what your risk factors are and what you can do to reduce their power over your life. That’s what this book will tell you, and it can make the difference between healthy longevity or early death from heart disease. This book presents for the very first time the newest, cutting-edge information now being taught to doctors; it is information essential to anyone interested in preventing a heart attack or recovering from one. The following story shows how insidious heart disease can be.

There Is No Immunity from

Heart Disease

It was a routine evening on the maternity floor. When Dr. Pell, the intern on duty that night, was called to see Beth, it was hard for him to believe anything of great importance was happening. Probably another restless mom in need of a sleeping pill. But when Dr. Pell greeted her from the doorway, Beth didn’t answer. She just lay there, eyes open, then closed, restlessly tossing and turning under the sheets, speaking nonsense, apparently having a bad dream.

Dr. Pell and the nurse who had called him both tried to shake Beth awake, but nothing helped. She placed a blood pressure cuff on Beth’s arm and looked up at the intern. Seventy palp. Her blood pressure had dropped 30 points.

Fortunately, the chief resident was close by. We can’t wake her, and her BP’s real low, Pell informed his supervisor, Dr. Fisher. The resident peered at Beth. She took Beth’s hand in hers and felt her pulse, touched the fingers of Beth’s right hand with her palms, then the other hand. They were cold, the fingers a bluish gray, her eyes rolled back in her head. Beth’s breathing was fast but regular, and it sounded normal through a stethoscope. Then the resident’s eyebrows arched and she looked up. She’s bleeding. Call Dr. Reynolds. Get the OR ready. Get me a central line and 4 units of blood. She’s in shock!

Life-threatening bleeding is one of the more common of the uncommon complications of childbirth, but as Dr. Fisher scrubbed Beth’s chest and shoulder with disinfectant in preparation for placing a catheter in her subclavian vein, she realized she hadn’t checked the most obvious thing. With her gloved hand, she threw off the bedsheet covering Beth and parted her thighs. There was no blood! Hmm. This lady had a natural delivery, so if she were bleeding internally there would be blood. Even a ruptured uterus, and there would be the blood.

While waiting for help to move Beth to the ICU, the residents emptied a bottle of saline through the new catheter, placed a 100 percent oxygen mask on her face, and sent for every blood test they could think of to help make a diagnosis. There was very little time. Beth was dying. There were no clues, no suspicions other than what the three doctors saw right before them: a normal new mother mysteriously rendered senseless and in shock fourteen hours after a normal delivery.

In the ICU, Dr. Fisher, the senior medical ICU resident, the chief medical resident, and Beth’s attending obstetrician debated what might be happening. They examined and reexamined her. They were joined by both the pulmonary and the cardiology fellows on call, all of them trying to figure it out. But there was little time for discussion. They put the now unconscious woman on a mechanical ventilator. Another catheter was inserted into the large artery feeding her leg to monitor her blood pressure and oxygen level. And another catheter was inserted through Beth’s jugular vein deep into the heart to monitor exactly how effectively the heart was pumping. In an attempt to keep her blood pressure up, they pumped thick, protein-rich fluid into her bloodstream and infused adrenalinelike chemicals to force her arteries to constrict and her heart to pump more strongly.

Senior residents in prestigious teaching hospitals rarely bother to consult with attending physicians in the middle of the night. But I was called. The senior resident wanted someone with more experience, and he sensed the need for a pair of cold eyes, as he put it, to take control of what had become a confusing and emotionally charged case. I was barraged with information the moment I entered the ICU. I craned my neck to read the X ray one resident held up to the ceiling light; someone rustled EKG paper in my ear. The EKG was okay, but the X ray showed that her lungs, which should have appeared black on the film, were opaque white. Then the ICU resident began his systematic account: No, she wasn’t bleeding; no, the EKG was correct—she wasn’t having a heart attack; no, she had not become infected during delivery, since she had no fever and her white blood count was normal. And yes, the lungs were providing almost no oxygen to the blood.

Of even greater interest to me was the information we could garner from the catheter in Beth’s heart. Here we could measure the circulation pressures in the heart-lung system, gauge the amount of blood expelled by each heartbeat, and sample the blood as it was being ejected from the right ventricle into the lung—before it received any new oxygen from the lung. The right ventricle propels this returning blood into the lungs where it is recharged with oxygen. Then it flows through the left ventricle and into the arteries to bathe the cells of every organ. When the flow is thick and fast, the cells are saturated, and they tap only a small portion of the oxygen flowing by. But when the flow is meager, the cells suck up as much oxygen from the blood as they can, leaving it depleted of oxygen as it returns into the right side of the heart. Even though there was no reason to believe she was in heart failure, her heart wasn’t providing enough blood flow to her body. To compound the problem, her lungs were becoming increasingly incapable of recharging the blood with oxygen. Neither her heart nor her lungs were working right. She was in shock.

Fortunately, the role of the lungs could, up to a point, be duplicated by a ventilator. But circumventing the inadequately pumping heart and getting that oxygen to her kidneys, liver, and brain was more problematic. I watched the nurse enter with two bottles of fluid and saw her set the infusion pump to maximum. The OB/GYN resident’s first thought was that she had thrown a big blood clot into her lungs. The others had drawn more or less the same conclusion. It was either a large blood clot—that is, a pulmonary embolus—or, even more damaging, a lump of amniotic fluid that, on rare occasions, finds its way into the bloodstream rather than being completely delivered with the baby. Either event is catastrophic because they both physically block the flow of blood and set off a violent inflammatory reaction. The lungs become engulfed, choked with fluid, blocking the diffusion of air into the blood. It’s as if the patient were drowning.

We’d induced air pressures into the lungs, which can get transmitted everywhere in unpredictable ways. These pressures can distort the heart catheter readings and can also compress the veins that supply the heart, further blocking blood flow. That’s why the doctors believed that the heart was nearly empty, despite the readings we were getting.

I admired the sophisticated reasoning, but I didn’t agree. I scrutinized the numbers and matched them against what the residents were doing to reverse the shock. It appeared to me that the lungs weren’t the real problem at all; it was the heart. No matter how much blood flowed into it, the left ventricle was unable to expel enough blood. This occurs rarely in pregnant women. For some unknown reason, pregnancy produces a cardiomyopathy where the entire heart muscle becomes profoundly weakened and can’t pump blood effectively. To confirm this, I borrowed the ICU resident’s calculator and more carefully analyzed the resident’s readings. Yes, the heart muscle itself seemed weak.

But we couldn’t determine whether we should give more fluid for a blockage in the lung, or more medicine for strengthening the heart’s beat. To answer that question we would have to look at the heart itself. An echocardiogram could provide a moving picture of the heart, which would show us one of two things: If the heart was swollen and hardly moving, the diagnosis of a primary heart problem was correct. We would then treat it with the appropriate medication. If it showed a small, hyperactive heart desperately trying to supply a flow of blood to the body, that meant the damaged lungs were obstructing the blood return from the body back into the heart. Then fluids would be the correct treatment. Within an hour, we had our echocardiogram.

Gallerstein, the cardiologist, was annoyed. No, there’s something wrong here. I’ve got to get a better picture. He repositioned the transducer on Beth’s chest.

The left ventricle’s not moving well at all, I concluded, looking at the screen.

Look again, Gallerstein challenged, with his usual caustic tone and rapid-fire delivery. Does this lady have coronary artery disease?

I doubt it. She’s only thirty-five years old! I reassured him. Isn’t it just the anterior wall that’s not moving? Why? I asked.

Well, he answered, if I didn’t know better, I’d think I was looking at one of my big Mi’s upstairs, Gallerstein said, referring to his heart attack patients.

How often do you see a myopathic ventricle look like this? I asked.

‘You don’t. She looks like an MI, Gallerstein shot back. The heart’s not even big." A heart damaged from pregnancy is uniformly weak; all of the walls of its ventricles contract poorly. A heart damaged by a blocked coronary blood vessel will show weak contractions only in the wall of the ventricle supplied by that artery. The latter seemed the case with Beth’s heart.

We looked at each other in amazement. Let’s get another EKG now! I shouted to no one in particular.

No one had thought of repeating Beth’s EKG. There was no reason to. But when we did, the second EKG told a radically different story from the first. There in the sections of the EKG that corresponded to the section of the heart that was not moving on the echo screen were the unmistakable traces of an acute infarct. It showed us that at some time between the first EKG and now, Beth had had a massive heart attack that practically paralyzed the left ventricle.

My residents were expecting to see a normal heart. I was expecting a bloated sack, almost uniformly still. But what we were seeing was a large, discrete section of the left ventricular wall not moving as it should. This is the typical picture of an infarcted heart muscle because only the muscle supplied by the clogged artery dies. No wonder Beth remained in shock. To stay alive, Beth needed powerful medications to keep her blood pressure up and make her heart more forcefully squeeze out the blood it contained. But she was in complete heart failure, and now we worried that we’d soon see blockages of her other coronary arteries if this level of stress continued.

Beth did not get better. Her shock state was stabilized, but at a low level of heart performance, and as each day passed, the other organ systems began to show the effects of inadequate blood flow. Even so, she might have made it if pneumonia hadn’t invaded her lungs. It was a big infection, raising the demands on her heart and circulation to impossible levels. This time, we could not reverse the shock.

Two weeks after the birth of her son, Beth’s husband looked at me, pain on his face. I want to bring her our son. Can you wake her? I agreed to stop the infusion of sedatives that had kept Beth mercifully senseless. When they wore off, Beth opened her eyes and gazed randomly around the room. I couldn’t tell if she really saw her son, or felt his touch when her husband laid the baby on her chest. Beth died the next day.

This was 1984, when we were just beginning to drag the still cumbersome echocardiogram machines into ICUs to help us discover all sorts of surprises about our patients. Had we never done the echo, Beth’s death certificate would have read cause of death: peripartum cardiomyopathy, the intractable heart failure that rarely and mysteriously accompanies a pregnancy.

The findings at Beth’s autopsy were shocking. The major branch of her left coronary artery had a large atherosclerotic plaque with a fresh thrombosis, a blood clot that completely sealed off any blood flow. One expected to find this in a sixty-five-year-old, not a new mother. Her other coronary arteries had smaller but similar lesions. So did her aorta, the big artery that receives all the blood directly from the left ventricle.

I don’t know if what he saw on my face was wonderment or horror, but as he was removing his gloves and cleaning up after performing the autopsy, Dr. Bala turned to me. Oh, yes, he assured me, we see a lot of this in young people. She’s an extreme case because of the infarction, but we see this kind of atherosclerosis all the time at this age. I shook my head, and Bala patted me on the shoulder. There’s no immunity from heart disease.

The inspiration for this book was born with that statement—that and the horrible image of the cooing baby lying on his dying mother’s breast. I scanned my memory of cases: The bicyclist with massive head trauma who mysteriously died in heart failure. The auto mechanic crushed by a car when a jack slipped who died of irreversible cardiac shock. Another postdelivery mother who threw a blood clot to her lung and whose autopsy showed a weekold heart attack.

Heart disease does not begin with chest pain. Even as a teenager growing up in the 1960s, I was aware of what is one of the most famous medical studies of all time, Major William Enos’s autopsy examinations of three hundred young soldiers killed in the Korean War. The average age of his soldiers was only twenty-two, yet three-quarters of them had significant atherosclerosis in the arteries of their hearts. A study of Vietnam casualties showed much the same thing, but the atherosclerosis was not as severe or widespread. Was this an indication that the population was adopting healthier lifestyles? One might have hoped so, but a study conducted in the 1990s gave little reason for optimism. This time, young people killed by homicide or accident, men as well as women, were studied in Louisville, Kentucky. The findings were depressing: 80 percent of these young people (their average age was twenty-six) had significant atherosclerotic lesions in their coronary arteries, and one in five had lesions so advanced they blocked more than half of the blood flow through the channel. One in ten had an almost completely blocked artery. These were virtually the same as the findings in Major Enos’s study forty years earlier.

We have come to understand that heart disease is more akin to arthritis than it is to pneumonia or peptic ulcer disease. It isn’t something that strikes us out of the blue or that is produced exclusively by behavior, in the way lung cancer is caused by smoking. Rather, it is a condition bestowed on us by our genes and is the result of a physiology that actually evolved to sustain life in humans. But early man lived under conditions that were quite different from those of men and women entering the twenty-first century. The human being for whom our physiology evolved lived a life of constant motion: chasing animals and being chased by them, dressing and cooking the catch, building and rebuilding shelter, foraging, migrating, fighting. The amount and type of food available was always in precarious balance with need. The things that bring misery and death to modern humans—LDL cholesterol particles, cholesterol receptors, triglycerides, blood-clotting factors, immune scavenger cells—not only helped our ancestors heal their wounds but also allowed them to store food in times of plenty against the inevitable times of scarcity that followed. Times of scarcity—at least for the fortunate—no longer exist. But the physiological mechanisms designed to deal with them live on. This book shows you what you can do about it.

2

Heart Disease Begins in Childhood

It has long been common knowledge that babies develop accumulations of cholesterol on the walls of their major arteries. These accumulations are contained within the bodies of predatory immune cells that are somehow stimulated to grab particles of cholesterol called low-density lipoproteins (LDLs) and intermediate density lipoproteins (IDLs) circulating in the bloodstream as they light upon the arterial wall. Once captured, the LDL and IDL cholesterol particles remain harmlessly contained within the bodies of these predatory cells.

In their first days of medical school future doctors used to learn about these so called foam cells, named for the foamy accretion of globules of cholesterol particles filling their interiors. Medical students were told they were harmless, for after a few years the cells would just melt away.

All true. But because foam cells in babies are harmless, doctors were thereby enticed to downplay the connection between the subsequent nascent cholesterol collections of older children and clinical heart disease.

But now, large-scale systematic studies document a slow but relentless reappearance of these foam cells as children approach puberty. Two-thirds of fourteen-year-olds have not only these isolated cells. They also have a coalescence of masses of these cells that are mixed with pools of free cholesterol oozing from the ruptured carcasses of foam cells that have died from overeating