By Bernadine Healy, M.D.
The good news about coronary artery disease is that fewer people are having—or dying from—heart attacks in the prime of life. And those who have heart attacks are likely to survive and live on into ripe old age. The challenge, however, is that many of these heart attack survivors are left with weakened hearts that, over time, quietly give out, creating a virtual epidemic of chronic congestive heart failure in the elderly. Heart failure now accounts for a million hospitalizations a year and carries a high mortality—and has replaced heart attacks as the lethal face of cardiovascular disease in most of the Western world.
This evolution from heart attack to heart failure was made stark by a study from Canada reported last month in the Journal of the American College of Cardiology that, for five years. monitored nearly 8,000 men and women over age 65 who had survived their first heart attack. Not only did three quarters of the study patients develop heart failure, but close to 40 percent of them died from it. The tricky thing about heart failure in this older population is that its symptoms of fatigue, shortness of breath, and even swollen ankles all too often are attributed to age rather than a lethal cardiac condition. And up to half of those who succumb to heart failure do so suddenly and unexpectedly.
Heart failure happens when the muscle tires out and can't keep up with the demand of pumping up to six gallons of blood per minute through thousands of miles of blood vessels, large and small, to nourish and cleanse every tissue and cell in the body. A number of conditions put the heart at risk for failing at this daunting task, such as chronic high blood pressure, diseased heart valves, or intrinsically weak heart muscle cells (known as dilated cardiomyopathy). But coronary artery disease accounts for most cases of congestive heart failure—approximately 60 percent. And the elderly are most vulnerable. With age, hearts and blood vessels become stiffer and harder to fill with blood, and the heart's electrical conduction system shows sign of wear, as bouts of inappropriately fast and slow heart rhythms compromise normal heart function.
The heart's way of dealing with its weakness—whatever the cause—is to enlarge, in a process that occurs silently. And in this case, a big heart is not a good thing. The normal heart is about the size of a person's own clenched fist, but under stress the organ can remodel itself to twice or more that size. Since the Framingham study first began decades ago, it's been known that a thick heart wall—or left ventricular hypertrophy—is a worrisome risk factor for coronary artery disease and heart failure. What modern cardiology has learned is that the pathologically remodeled and hypertrophied heart is one that's also under constant hormonal stress.
Much of the stress relates to the heart's struggle to beat with limited oxygen or with muscle damaged by a prior heart attack. But the stress is aggravated when other organs in the body, unable to live without the heart's nourishment, secrete a raft of hormones—including norepinephrine and angiotensin—that constrict blood vessels to keep up blood pressure and stimulate the heart to work harder. This so-called neuroendocrine network is a lifesaver in an emergency—like sudden blood loss—but when activated on a chronic basis can flog the heart to exhaustion and cause it to thicken further. The heart fights back by making its own countering hormones called natriuretic factors, which calm the heart and signal blood vessels in the body to relax and give it a break. The battle of the hormones plays out largely unnoticed by the patient until at some point—the actual turning point is still a mystery—the overwhelmed heart can no longer keep up with the demands of propelling enough blood throughout the body. The patient begins to sense this as he or she fatigues more readily, blood backs up in the lungs (crackles in the chest), breathing gets short (dyspnea), and the legs swell (pedal edema).
When heart failure is very mild and limits only strenuous activity, it's labeled "class I," based on a widely used New York Heart Association tiered classification system that is commonly used to guide therapy. Class II means ordinary physical activity brings on fatigue, shortness of breath, and a faster heart rate. When fatigue is more severe and breathing markedly impaired even with minimal physical activity, the class is III. And in class IV, a patient is virtually incapacitated by shortness of breath and fatigue, even to the point of having to sleep sitting up.
Heart failure therapy reduces these symptoms by ridding the body of excess fluid using diuretics and by relaxing the heart and the stiff, constricted blood vessels by countering the hormones that drive the heart to exhaustion. Agents like ACE inhibitors counter angiotensin, for example, and beta blockers limit adrenaline's effects. In patients with serious heart rhythm problems, pacemakers including internal defibrillators have proven benefit. Such therapy relieves symptoms, improves quality of life, and reduces the many hormones whose levels track the progression of heart failure. Improvement is accompanied by fewer hospitalizations and longer life, providing an imperative for early detection of a failing heart.
Ultimately, of course, the way to dent the growing numbers afflicted with heart failure is to prevent coronary artery disease in the first place, by controlling the time-honored cardiovascular risk factors. Quit smoking; maintain normal blood pressure, blood lipids, and body weight; and engage in physical activity—at a time when the heart is able and ready to welcome such efforts.