Archive for the ‘infective endocarditis’ Category

Getting really angry might be more dangerous than you think.

A new study found people who experienced severe anger outbursts were more at risk for cardiovascular events in the two hours following the outbursts compared to those who remained calm.

“The relative risk was similar for people who had known pre-existing heart disease and those who didn’t,” says Dr. Murray A. Mittleman, senior study author and an associate professor of medicine at Harvard Medical School.

The study was designed so that each patient was compared to his or her own baseline risk. “A person with pre-existing heart disease or cardiovascular disease, the absolute risk they are incurring is much greater than (that of) a person without cardiovascular disease or risk factors,” Mittleman says.
“If we look at somebody at higher risk for having cardiovascular events, and they get angry multiple times a day, this can lead to 650 extra heart attacks per year out of 10, 000 a year,” he says. “When we look at a person who is relatively low risk, but if they do have these episodes of anger fairly frequently, we estimate there would be about 150 extra heart attacks out of 10,000 a year.”

Smoking, high cholesterol, high blood pressure, being overweight and having diabetes are all risk factors for cardiovascular disease. An estimated 17 million people worldwide die of cardiovascular diseases, particularly heart attacks and strokes, each year, according to the Centers for Disease Control and Prevention.

The study published Monday in the European Heart Journal was a data analysis looking at nine studies where anger and cardiovascular events were self-reported over nearly two decades. The study found a 4.74 times higher risk of MI (myocardial infarction, or heart attack) or ACS (acute coronary syndrome, where the heart muscle doesn’t get enough oxygen-rich blood) following outbursts of anger.

“Anger causes our heart rate to increase through the sympathetic nervous system and causes our stress hormones to become elevated (the fight or flight mechanism),” says Dr. Mariell Jessup, president of the American Heart Association and medical director of the Penn Heart and Vascular Center at the University of Pennsylvania. “We breathe faster, all of which may trigger undesirable reactions in our blood pressure or in our arteries.”

This disruption may mean the heart or the brain doesn’t get the blood and oxygen they need resulting in a heart attack or a stroke, she says.

Researchers suggest more needs to be done to come up with effective interventions to prevent cardiovascular events triggered by anger outbursts. The American Heart Association suggests regular physical activity, finding a way to relax or talking with friends to help reduce stress and anger.

Mittleman suggests the best way to lower your risk for a heart attack or stroke during an angry outburst is to lower your overall baseline level of risk – exercise, eat healthy and don’t smoke – and then find ways to cope with stress and anger.

http://thechart.blogs.cnn.com/2014/03/03/angry-outbursts-may-raise-heart-attack-stroke-risk/?hpt=hp_t2

heart infection

University of Iowa researchers have discovered what causes the lethal effects of staphylococcal infective endocarditis – a serious bacterial infection of heart valves that kills approximately 20,000 Americans each year. According to the UI study, the culprits are superantigens — toxins produced in large quantities by Staphylococcus aureus bacteria — which disrupt the immune system, turning it from friend to foe.

“The function of a superantigen is to ‘mess’ with the immune system,” says Patrick Schlievert, PhD, UI professor and chair of microbiology at the UI Carver College of Medicine. “Our study shows that in endocarditis, a superantigen is over-activating the immune system, and the excessive immune response is actually contributing very significantly to the destructive aspects of the disease, including capillary leakage, low blood pressure, shock, fever, destruction of the heart valves, and strokes that may occur in half of patients.”

Other superantigens include toxic shock syndrome toxin-1, which Schlievert identified in 1981 as the cause of toxic shock syndrome.

Staph bacteria is the most significant cause of serious infectious diseases in the United States, according to the Centers for Disease Control and Prevention (CDC), and infective endocarditis is the most serious complication of staph bloodstream infection. This dangerous condition affects approximately 40,000 people annually and has a death rate of about 50 percent. Among patients who survive the infection, approximately half will have a stroke due to the damage from the aggressive infection of the heart valves.

Despite the serious nature of this disease, little progress has been made over the past several decades in treating the deadly condition.

The new study, led Schlievert, and published Aug. 20 in the online open-access journal mBio, suggests that blocking the action of superantigens might provide a new approach for treating infective endocarditis.

“We have high affinity molecules that neutralize superantigens and we have previously shown in experimental animals that we can actually prevent strokes associated with endocarditis in animal models. Likewise, we have shown that we can vaccinate against the superantigens and prevent serious disease in animals,” Schlievert says.

“The idea is that either therapeutics or vaccination might be a strategy to block the harmful effects of the superantigens, which gives us the chance to do something about the most serious complications of staph infections.”

The UI scientists used a strain of methicillin resistant staph aureus (MRSA), which is a common cause of endocarditis in humans, in the study. They also tested versions of the bacteria that are unable to produce superantigens. By comparing the outcomes in the animal model of infection with these various bacteria, the team proved that the lethal effects of endocarditis and sepsis are caused by the large quantities of the superantigen staphylococcal enterotoxin C (SEC) produced by the staph bacteria.

The study found that SEC contributes to disease both through disruption of the immune system, causing excessive immune response to the infection and low blood pressure, and direct toxicity to the cells lining the heart.

Low blood flow at the infection site appears to be one of the consequences of the superantigen’s action. Increasing blood pressure by replacing fluids reduced the formation of so-called vegetations – plaque-like meshwork made up of cellular factors from the body and bacterial cells — on the heart valves and significantly protected the infected animals from endocarditis. The researchers speculate that increased blood flow may act to wash away the superantigen molecules or to prevent the bacteria from settling and accumulating on the heart valves.

In addition to Schlievert, the research team included Wilmara Salgado-Pabon, PhD, the first author on the study, Laura Breshears, Adam Spaulding, Joseph Merriman, Christopher Stach, Alexander Horswill, and Marnie Peterson.

The research was funded in part by grants from the National Institutes of Health (AI74283, AI57153, AI83211, and AI73366).

http://www.infectioncontroltoday.com/news/2013/08/bacterial-toxins-cause-deadly-heart-disease.aspx