When the Beat Goes Bad
All you baby boomers can be sure of one thing: You will not have your fathers' hearts. What emanated from the American Heart Association annual meeting in Dallas last week is that the heart faces problems that were not center stage even a generation ago, thanks to greater longevity and increased survival with underlying cardiac disease. Look at atrial fibrillation. Once its focus was as much about overactive healthy hearts as diseased ones. Now the emphasis has shifted from those fleeting bursts of fast, wild rhythms in the young to chronic AF in the older set. With age and survival, it's estimated that the 2.3 million Americans with this condition will double their numbers in the decades ahead.
Think of atrial fibrillation as an electrical storm. The thin-walled atria, the two chambers at the top of the heart, become quivering, overstretched bags of blood as they desperately try to contract at 300 to 400 times a minute and simply can't. This happens for two reasons: First, renegade clusters of atrial cells at the base of the pulmonary veins that feed into the left atrium start generating electrical discharges that override the normal sinus rhythm that keeps the heart rate mostly between 50 to 100 beats per minute. And second, the ventricular chambers that propel blood throughout the body are smart enough not to keep up with the atria, as they ordinarily would. Doing so would cause instant death from ventricular fibrillation. They ward off the death threat because of the atrioventricular node, a brake that keeps more than half of the atrial pulses from getting through. Nonetheless, the bombardment forces the ventricles to beat faster and irregularly. The racing rhythm makes patients feel rotten, fatigued, short of breath, and even lightheaded. Sometimes they're just spooked by the pounding or the sensation that their hearts will jump right out of their chests.
That rogue cells paralyze the atria and throw ventricles into disorder is bad enough. What's worse is that this behavior is a major cause of stroke among those with risk factors like hypertension, diabetes, or poor cardiac function. For them, we now jump in with stroke protection using the powerful blood-thinning drug Coumadin. But Coumadin carries its own baggage, like easy bleeding, and demands meticulous dose regulation. Safer alternatives would be nice, but that hope was dashed at last week's meeting when a new trial showed that Coumadin was superior to an aspirin strategy.
Robust arsenal. Another treachery of AF is the unexpected cost to a heart in overdrive: It remodels itself and becomes failure prone. That has led doctors to become aggressive about rate control, something we can do easily with our robust arsenal of drugs like digitalis, beta blockers, and calcium channel blockers. And the blood pressure-lowering ACE inhibitors have a special knack for preserving normal heart shape. We also have better drugs to stabilize heart rhythm and have grown comfortable with trying a few electrical jolts, under sedation, to restore normal sinus rhythm.