Über die Autorin bzw. den Autor

STEPHEN T. SINATRA, M.D., formerly chief of cardiology and director of medical education at Manchester Memorial Hospital in Connecticut, has specialized in preventive cardiology for the last twenty years. He has written or coauthored ten books, including the recent The Fast Food Diet, and writes the popular nationally distributed monthly newsletter, Heart, Health, and Nutrition (drsinatra.com).

JAMES C. ROBERTS, M.D., has practiced invasive and integrative cardiology for twenty years and is the Medical Director of the EECP Center and Advanced Magnetic Research Institute of Northwest Ohio (www.heartfixer.com).

MARTIN ZUCKER, a former Associated Press newsman, has written many books on health and medicine.

Von der hinteren Coverseite

While most books focus solely on the role of cholesterol in heart disease, Reverse Heart Disease Now draws on new research that points to the surprising other causes. Leading cardiologists Dr. Stephen Sinatra and Dr. James Roberts draw on their collective fifty years of clinical cardiology research to show you how to combine the benefits of modern medicine, over-the-counter vitamins and supplements, and simple lifestyle changes to have a healthy heart?? whether you have acute or chronic disease or just want to prevent cardiovascular disease from developing.

Focusing on crisis prevention, Reverse Heart Disease Now gives you the practical information and strategies you need to stop heart disease in its tracks. You'll discover how:

• You can combat heart disease before the first heart attack
• Your arteries can become enveloped in inflammation and plaque that lead to heart attack, stroke, and heart failure?? and what to do about it
• Medications, scientifically proven supplements, and lifestyle changes can extinguish the flames of disease and purge and stabilize arteries?? even for the most compromised cases
• Fish oil, nattokinase, L-arginine, CoQ10, magnesium, vitamin C, and other supplements can help prevent arterial clogging
• CoQ10, along with L-carnitine and D-ribose, can powerfully recharge weak and ailing hearts

Through the breakthrough integrative program found in Reverse Heart Disease Now, you can become more involved in your own healing process and even prevent heart disease before it strikes.

Aus dem Klappentext

While most books focus solely on the role of cholesterol in heart disease, Reverse Heart Disease Now draws on new research that points to the surprising other causes. Leading cardiologists Dr. Stephen Sinatra and Dr. James Roberts draw on their collective fifty years of clinical cardiology research to show you how to combine the benefits of modern medicine, over-the-counter vitamins and supplements, and simple lifestyle changes to have a healthy heart?? whether you have acute or chronic disease or just want to prevent cardiovascular disease from developing.

Focusing on crisis prevention, Reverse Heart Disease Now gives you the practical information and strategies you need to stop heart disease in its tracks. You'll discover how:

• You can combat heart disease before the first heart attack
• Your arteries can become enveloped in inflammation and plaque that lead to heart attack, stroke, and heart failure?? and what to do about it
• Medications, scientifically proven supplements, and lifestyle changes can extinguish the flames of disease and purge and stabilize arteries?? even for the most compromised cases
• Fish oil, nattokinase, L-arginine, CoQ10, magnesium, vitamin C, and other supplements can help prevent arterial clogging
• CoQ10, along with L-carnitine and D-ribose, can powerfully recharge weak and ailing hearts

Through the breakthrough integrative program found in Reverse Heart Disease Now, you can become more involved in your own healing process and even prevent heart disease before it strikes.

Auszug. © Genehmigter Nachdruck. Alle Rechte vorbehalten.

Reverse Heart Disease Now

John Wiley & Sons

Chapter One

Inflammation is our body's first line of defense against injury or infection. It's what causes a burn to turn red or a bruise to swell. It's nature's design to help us heal. But if inflammation becomes chronic and goes into constant overdrive, it can cause disease.

In 2000, doctors at Harvard University published the first of a series of landmark research studies revealing the central role of inflammation in cardiovascular disease (CVD). Evidence from the Women's Health Study, a project that monitored the status of twenty-eight thousand initially healthy postmenopausal women, put a new risk factor into the spotlight: C-reactive protein (CRP), a key biochemical substance indicating the presence of vascular inflammation. People with the highest level of CRP had five times the risk of developing CVD and four times the risk of a heart attack or a stroke compared to individuals with the lowest level. CRP predicted risk in women who had none of the standard risk factors and was the best predictor among twelve risk factors studied, including cholesterol. The cardiologist Paul Ridker, who led the study, said that "we have to think of heart disease as an inflammatory disease, just as we think of rheumatoid arthritis as an inflammatory disease."

Ridker estimates that approximately 25 percent of Americans have a normal to low cholesterol level, lulling them into complacency, but at the same time they have an elevated CRP without knowing it. Millions of Americans are unaware that they have an increased risk for future CVD, heart attack, or stroke.

Ridker's research confirmed what we as clinicians had suspected for years: that low-grade inflammation, like a silent, creeping fire, consumes arterial tissue and causes CVD. It leads to the weakening and eventual rupture of arterial plaques that directly trigger heart attacks and strokes. The CRP-inflammation link helps explain why more than half of heart attack and stroke victims have normal cholesterol levels.

Medical research has introduced us to other far-reaching and complex risk factors that go beyond the solitary threat of high cholesterol. Indeed, we have moved so far forward in recent years that the familiar model of diseased arteries as a network of inanimate pipes clogged by cholesterol-laden plaque seems almost as outmoded as the typewriter.

Life-threatening plaque is now regarded as an inflammatory injury-a lesion-that develops, almost like a boil, along the inner surface of the arterial walls where vital biological functions take place as blood rushes by. The walls become damaged by the inflammation-a process influenced by lifestyle, environment, and genetics. In some cases, the process unfolds slowly, stifling arterial wall chemistry and causing vessels to narrow. In other cases, deterioration occurs surprisingly fast, leading to vessel closure, stroke, or sudden death.

Plaque can be of two types. Stable plaque, covered with a fibrous cap, slowly expands inward and shrinks the diameter of blood vessels. Of greater danger is the vulnerable, unstable plaque, which can rupture and spill its noxious contents into the arteries and shut off blood flow. Identifying and combating the latter type of plaque has become the number one priority of today's cutting-edge cardiologists.

Indicative of a turnaround in thinking about the causes of CVD, the American Heart Association and the Centers for Disease Control and Prevention published new recommendations for CVD screening in 2003 that included a test for CRP. Today you may see posters on laboratory walls with information for patients about this new and potentially lifesaving blood test. There is more to inflammation than CRP and more to CVD than inflammation, but we see this kind of public awareness effort as a good first step in getting out the message about inflammation and CVD.

Cardiovascular System 101

The heart and its network of blood vessels deliver oxygen and metabolic fuel to the cells. Think of your heart as a fist-sized, cone-shaped muscular pump wrapped around four chambers. The chambers are connected by a series of one-way valves that let blood flow in one side and out the other. Oxygen-poor "used" blood returning to the heart collects in the right atrium chamber and is funneled into the right ventricle, which pumps it into the lungs to pick up oxygen. Oxygenated blood returns to the left atrium, passes through the mitral valve into the left ventricle, and is pumped out with great force (in a healthy heart) into the main artery of the body, the aorta. From the aorta, other arteries branch off to feed the body, including the two coronary arteries that supply the heart muscle.

Blood moves through your body's sixty thousand miles of blood vessels known as the circulatory system. Think of this system as the branches of a tree with many offshoots or a river with many tributaries. Large arteries branch off into smaller arterioles. These, in turn, branch off into the smallest vessels, called capillaries, which feed the cells of the body, then carry wastes and deoxygenated blood back out into venules (small veins), then into larger veins, and finally back to the right atrium.

This elaborate system needs to be clear to accommodate the forceful contractions of the heart and permit strong blood flow. The walls of the blood vessels have to be smooth and free of obstruction. We will concentrate on the arteries, since CVD primarily affects arteries rather than veins.

As Goes the Endothelium, So Go You

Artery walls are not hard and firm. Instead, they are composed of smooth muscle that contracts and expands in metronomic response to the rhythm of the heart, accommodating the pulsatile flow of blood. They are a living, breathing, dynamic organ, not a static system of tubes and pipes.

We are most concerned with the innermost layer of the wall known as the endothelium. The blood meets the vessel walls at the endothelium. Though only one cell thick, this permeable lining carries out critical molecular exchanges between the blood-borne contents floating through the lumen and the smooth muscle and adventitial tissues behind it that form the bulk and structure of the arteries. A healthy endothelium produces chemical substances that allow for the normal expansion and relaxation of blood vessels. Endothelial health is critical to cardiovascular health. If you have a 40 to 50 percent narrowing of the arteries and impaired endothelial function, you are at greater risk for an adverse event than if you had an 80 percent narrowing of the arteries with intact endothelial function.

The endothelial lining is extremely delicate and sensitive to injury. It can be damaged by a variety of insults. Of course, you can injure the endothelium, along with the entire artery wall, if you cut yourself and slice an artery. Trauma aside, we are concerned with the steady damage from inflammation that develops over time from a less than healthy lifestyle. Unhealthy habits include overeating refined, packaged, and processed foods with lots of sugar, unnatural fats, and chemical preservatives; not eating enough fresh fruits and vegetables and not drinking enough water; smoking; and not being physically active. Living in an environment where you are regularly exposed to pollution and contaminants is an inflammation risk factor. Stress associated with work, relationships, and financial pressures can compound the problem.

Silent Inflammation Starts Early

A middle-aged person may go to the doctor, perhaps complaining of shortness of breath or maybe just for a checkup, and hear that his cholesterol is too high and he has the beginnings of atherosclerosis, commonly known as hardening of the arteries.

The news comes with a loud jolt. But the process itself has been going on silently for a long time, starting at a surprisingly young age. Studies going back to Korean War and Vietnam War casualties show that even some teenagers have early arterial disease. More recently, researchers specializing in the study of early-onset atherosclerosis reported in the medical journal Circulation that 20 to 25 percent of young people (aged fourteen to thirty-five) autopsied after death from homicide, auto accident, or suicide already had a major lesion in the coronary arteries. The study was performed on three thousand bodies.

Just over 3 percent of men aged fifteen to nineteen had 40 percent narrowing or greater in at least one coronary vessel. The prevalence increased to nearly 20 percent in thirty- to thirty-four-year-old men.

Narrowing of 40 percent or more was not found in women before the age of twenty-five. Occlusions of this magnitude were found in 8 percent of those aged thirty to thirty-four.

The presence of risk factors (such as smoking and diabetes) increased the likelihood of significant narrowing.

These numbers show that millions already have significant coronary disease at an early age. Most likely, they don't know it.

The message from these statistics is clear: you should not wait to begin a preventive program. Start as early as possible.

Arterial Hot Spots

The major cardiac hot spots are the left main coronary artery-the "left main" for short-and locations just beyond where it splits into the left anterior descending and left circumflex arteries on the outer surface of the heart. These blood vessels supply the front and side walls of the heart muscle.

The higher up in these vessels that blockages develop, the more damage that occurs "downstream." The left anterior descending artery is the potential site of the most dangerous lesion. We call it the "widow maker." It puts two-thirds of the heart muscle in jeopardy. The right coronary artery feeds the bottom and back portions of the heart muscle.

A blockage compromises the supply of oxygen and other blood-borne nutrients to the cells served by the artery and its branches. Denied their essential raw materials, these cells fail to generate adequate energy to sustain themselves and their multiple functions. If the blockage is incomplete, the cells starve. Pumping function ceases, but the cells remain alive. If the blockage closes the vessel, the cells die, and a myocardial infarct-a heart attack-is the result.

In the neck, the carotid arteries are the hot spots because they feed the front of the brain where you do your thinking. A stroke is like having a heart attack in the brain. There are four major arteries going into the brain: the left and right carotid arteries, which split into the external and internal branches; and the left and right vertebral arteries, which split into vessels serving the back of the brain. If a major blood vessel becomes blocked (especially before the split), a stroke is likely.

If you could take a miniature close-up camera and position it at a site of arterial inflammation, you would see a bulge along the artery wall, making the lumen (the flow area) narrower and less easily passable. The endothelium would look stretched out, like overstressed elastic. The spaces between the endothelial cells would be larger. Under the cap of this endothelial bulge, the plaque lesion forms-a virtual witch's brew of toxicity.

Narrowed arteries place a strain on the cardiovascular system and create all sorts of other health problems, as the heart is overstressed to pump harder and compensate for the partially obstructed blood flow. In turn, this raises blood pressure, leading to further cardiac strain.

The Role of the Immune System

The immune system protects the body from foreign invaders such as bacteria. It fields a variety of cells armed with different weapons to fight the enemy. Some of these cells are released by the immune system and others by the injured tissue itself. Some are designed to engulf invading organisms, others to gobble them up, others to cart off the debris, and still others to seal off the injury and allow healing to begin.

This internal defense force is constantly challenged as it is involved in battle and repair operations. Without such a robust system, you would be overwhelmed by every germ you encounter and every injury you sustain.

Inflammation takes place when immune cells are summoned to the site of an injury such as an insect bite, a laceration, gum disease, or a broken ankle. The composition of cells depends on the nature and the location of the challenge, but all cause some characteristics of inflammation, namely redness, heat, and sometimes swelling. In the case of a viral or bacterial assault, the system may respond with fever, diarrhea, or nausea in addition to any localized distress.

In any case, the inflammatory response stirs up a complex array of chemicals throughout the body. In this alert mode, a normal defensive reaction in one place can contribute to unwanted inflammation elsewhere. An infection in the gums can leak bacteria into the bloodstream. The bacteria may find fertile ground in a weakened arterial wall or a defective heart valve and fan the flames of inflammation there. In rheumatoid arthritis, a highly inflammatory condition, researchers have discovered that a woman's risk for heart attack is doubled.

Inflammation may or may not be obvious. It can take place on a subtle or silent level. From head to toe, your body is always in a process of repairing itself, with countless mini-inflammation dramas going on that you are not aware of as you go about your daily business or sleep. Inflammation in the arteries is an example of this below-the-radar-screen activity.

From Inflammation to Plaque

The delicate endothelium can become damaged from a variety of elements, including cigarette smoke, toxic chemicals and metals, bad fats, poor diet, elevated insulin, bacteria, high blood pressure, and excess stress.

Singly, or in combination, these elements kindle inflammation that can evolve into plaque. Following is a stage-by-stage description of the process.

Stage 1

Under siege, the normally smooth endothelium becomes permeable or porous, attracting fatty particles such as circulating cholesterol. These particles wriggle into the lining and disturb biological activities. Usually, though not always, this occurs at locations where the endothelium tends to be under extra pressure. A typical hot spot is where the left main coronary artery splits into the anterior descending and circumflex arteries.

Once cholesterol becomes wedged in the arterial wall, a chemical process may take place in which the fatty molecules are damaged by free radicals to form oxidized LDL (low-density lipoprotein) cholesterol. Soon the ever-vigilant immune system takes notice that something is amiss and needs attention. The system goes into action.

Stage 2

Local cells surrounding a distressed site release immune chemicals that initiate an inflammatory process. The intima, the layer of tissue just behind the endothelium, secretes adhesion molecules to create a sticky endothelial surface like fly paper. Blood cells adhere, including monocytes, circulating immune cells instrumental in the inflammatory response. Meanwhile, the besieged endothelium secretes endothelin and other distress-signaling agents.

Stage 3

The endothelium and intima now release other chemicals. They cause more circulating monocytes to swarm across the endothelial barrier and mature into full-fledged scavengers called macrophages that are designed to seek and destroy foreign objects. Under ordinary circumstances, macrophages engulf invading cells, consume them, and are eliminated from the body by other specialized immune cells. But the developing situation here is no longer ordinary.

Stage 4

Oxidized LDL is not benign. It is toxic to the macrophage. Oxidized LDL immobilizes the macrophage, preventing it from returning to the bloodstream. The stressed macrophage sends out an SOS-a proinflammatory distress signal that draws other white cells into the area, where they, too, are destroyed by the oxidized LDL. Under the microscope, we see a fatty streak made up of dying macrophages loaded with oxidized LDL layering out from the inner area of the artery wall.

(Continues...)

Excerpted from Reverse Heart Disease Nowby Stephen Sinatra James C. Roberts Martin Zucker Copyright © 2006 by Stephen Sinatra. Excerpted by permission.
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