Heart disease begins very young. Even children need to control their risk factors for heart disease. New heart studies of young men and women who died from accidental causes demonstrate that heart disease begins earlier than most people realized. In a recent study, researchers found 2 percent of the men aged 15 to 19 and 20 percent of those aged 30 to 34 had advanced artery disease. Although women aged 15 to 19 had no serious blockages, cholesterol deposits did begin at this age, and 8 percent of those aged 30 to 34 had significant disease. These coronary narrowings, the basis of future heart attacks, could be prevented with healthier lifestyles.

Marijuana may harm your heart. New findings suggest that the risk of heart attack in the middle-aged and elderly increases nearly five times in the first hour after smoking marijuana. In the second hour, the risk appears to be nearly twice the normal rate. In a study of 3,338 heart attack survivors, 124 were current marijuana smokers. Thirty-seven of them had smoked the drug within 24 hours of their attack, including nine who had used it within an hour of their symptoms’ onset. Marijuana smoking can increase the heart rate by about 40 beats a minute and can increase blood pressure. Some baby boomers began smoking the drug decades ago and continue to do so, despite accumulating increased risk for heart disease with age. The study raises concerns because some of these individuals have heart disease they are unaware of, and may be at risk without knowing it.

Recovering hearts need aspirin. Far too few heart attack survivors take aspirin, even though it is a powerful way to prevent a recurrence. Aspirin reduces the risk of blood clots forming in the arteries supplying the heart or brain (prime causes heart attack and stroke). For people who are not allergic to aspirin and who are having symptoms typical of a heart attack, the American Heart Association even recommends taking a single aspirin at the first symptoms of a heart attack. Yet a new study finds only 26 percent of those who have suffered a heart attack and could benefit from the drug use it regularly. More men (29 percent) than women (21 percent) take aspirin, as do those younger than age 80 (28 percent), compared to those 80 and older (17 percent). Because aspirin occasionally causes serious side effects, including gastrointestinal bleeding, the American Heart Association recommends that heart attack survivors and people with unstable angina, a form of chest pain, take aspirin daily only after consulting their physician.

Revolutionizing angioplasty. A biodegradable tube, or stent, could provide important benefits for the treatment of coronary disease. During angioplasty, a procedure commonly used to treat patients with chest pain due to coronary disease, a tiny balloon at the tip of a catheter is inflated in areas where fatty deposits narrow the walls of heart arteries. Flattening these deposits, called plaques, improves blood flow. Often a stent, a cylindrical meshwork made of metal, is put into the artery to help keep it open. Now a Japanese team has successfully tested a stent designed to degrade in two years. These degradable stents have the potential to reduce problems that can occur with metal stents.

Shining light on diseased arteries. Photoangioplasty may someday provide a new way to remove plaque in arteries. The new procedure uses a photosensitive drug and a red light. The drug concentrates in plaques and remains inactive until it is exposed to intense red light piped down a fiber-optic cable inserted into the artery through a catheter. When activated by light, the drug generates a chemical reaction that reduces or destroys the deposits. An early study in patients with narrowed leg arteries—which can cause severe pain when walking and lead to amputation—found that the procedure reduced blockage between 10 and 74 percent in 12 of 16 patients. Early testing has begun in heart patients.

Family and friends help survival. Friends and family can provide a lifeline for depressed heart attack survivors. Canadian researchers found that one-third of 887 survivors had mild to moderate depression soon after their heart attack. Within one year, 7.5 percent of the depressed patients died of cardiovascular disease, compared to 2.5 percent who were not depressed—a threefold difference. Among the depressed survivors, 50 percent were still depressed after one year. Patients who got strong support from close friends and relatives showed greater improvement in their depression, and this may make them more likely to successfully treat the conditions that increase their risk of a second attack. However, this support alone may not be enough. A patient’s physician needs to be told when depression persists to be sure it is treated effectively.

Exercise protects the heart in many ways. Whether you pump iron or prefer aerobics, exercise cuts your risk of heart attack in many different ways, according to a recent review of almost 100 studies. Physical activity may act to prevent high blood pressure and lower already high pressure. Serious exercise devotees can drop their total blood cholesterol levels as much as 24 percent, their “bad” LDL cholesterol as much as 10 percent, and raise their “good” HDL cholesterol 6 percent. Physical activity may reduce the risk of blood clots that trigger heart attacks or strokes. And it improves the ability of the cells in blood vessels to produce nitric oxide, which enables vessels to relax and contract more efficiently. Exercise also appears to reduce dangerous variability of the heart rate in heart attack survivors. Moderate exercise has important benefits, and vigorous exercise offers added gains. People at high risk for a heart attack should consult a physician before beginning an exercise program, to ensure that they get the most out of it.

“Fat hormone” hates exercise. Leptin, the so-called fat hormone, is a leading suspect in causing obesity, which increases the risk of heart disease. When researchers looked at the diets and lifestyles of 268 healthy men, they found the highest leptin levels in men who didn’t exercise and who ate diets rich in saturated fats and cholesterol. Men who worked out regularly and ate heart-healthy diets had the lowest leptin. Getting fatter appears to increase leptin production and set up a vicious circle of more weight gain. Exercise decreases leptin in the body and reduces weight, which lowers the risk of heart disease. The findings appear to apply to women as well as men.

Beta-blockers save lives. Surviving a heart attack may still leave patients with serious heart problems. If patients are not seen soon enough after a heart attack begins, enough heart muscle may be damaged to cause congestive heart failure, a life-threatening disorder in which the heart cannot pump blood efficiently to supply the body. Some 4.6 million Americans have congestive heart failure. For them, drugs called beta-blockers can be lifesavers because they reduce the heart’s workload. In an international study of 3,991 heart-failure patients, specialists in treating the disease compared the beta-blocker metoprolol to a placebo. The group taking the drug had fewer deaths from heart failure or any other cause than the placebo group, and it also had fewer hospitalizations. Finally, the drug group reported a higher quality of life. The findings support studies of other beta-blockers in heart failure. Although these medications must be given and monitored carefully, the message is clear: physicians need to ensure that patients who can benefit from beta-blockers get them.

A protein that cuts heart risk. Some people who eat a high-fat diet never develop heart disease. Why? Scientists studied two strains of mice, one that showed a strong tendency to develop heart disease when fed fat-rich foods and another whose arteries stayed healthy on the same diet. They exposed cells that lined the mice’s blood vessels to mildly oxidized human LDL, the so-called bad cholesterol, which can increase heart-attack risk. The oxidized LDL caused the cells to produce proteins that contribute to heart disease in the mice prone to the disease. But the strain that doesn’t get fatty deposits secreted a protein called HO-1, which appears to inhibit the disease. Further deciphering this phenomenon could lead to treatments in humans that block the production of “bad” proteins and stimulate the release of beneficial ones.

Genetic approaches to heart rate problems. In the era of genetic analysis, answers can often be found for problems that were previously insoluble. A number of young women, and some young men as well, experience unpleasant and sometimes incapacitating symptoms such as dizziness and high heart rates every time they stand up, a problem called orthostatic intolerance. These patients have high levels of norepinephrine, a stress hormone, driving these symptoms. In recent studies at Vanderbilt, my colleagues demonstrated that a single gene, responsible for making the protein that clears norepinephrine, does not function properly in some of these patients. By understanding this very specific cause, we may be able to develop a more effective treatment for these young patients.

Dr. Robertson is professor of medicine at Vanderbilt University School of Medicine and president of the American Heart Association.