Researchers find a higher risk of coronary events during the 3 months after an infection. The body’s immune response, they suggest, may explain why infections “trigger” heart attack and stroke.
The term cardiovascular disease (CVD) covers a range of conditions: from heart attack and heart disease to stroke, hypertension, and heart failure.
As many as 84 million people in the United States are living with one of the conditions above, and 2,200 people die every day as a result.
Several factors may raise the risk of cardiovascular conditions. Some of these factors are modifiable, such as smoking, high cholesterol, and high blood pressure. Other factors, such as sex, race, age, and family history, cannot be modified.
However, there are also a number of “acute” risk factors, or triggers, that can lead to CVD. Some
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Dr. Kamakshi Lakshminarayan, a neurologist and associate professor of epidemiology at the University of Minnesota in Minneapolis, is the senior author of the study.
Dr. Lakshminarayan and colleagues examined 1,312 people who had had a coronary event such as a heart attack, or myocardial infarction, and compared them with 727 people who had had an ischemic stroke.
The study included both outpatients and people who were hospitalized to receive treatment for their infection.
The researchers looked for infections that these people developed up to 1–2 years before the cardiovascular event. The most commonly reported infections were urinary tract infections, pneumonia, and respiratory infections.
Overall, the study found that approximately 37 percent of the participants with heart disease had developed an infection in the 3 months leading up to the coronary event. Among people with stroke, this number was almost 30 percent.
In the first 2 weeks after having an infection, the risk of a stroke or a heart attack was the highest.
Though the analysis found this link among both inpatients and outpatients, people who received care in the hospital were more likely to have a coronary event.
Although the study was observational, the scientists speculate on the mechanism that may explain the results.
During an infection, explains Dr. Lakshminarayan, the body’s immune system produces more white blood cells to fight it off. However, this immune response also makes small blood cells, called platelets, stickier.
In a healthy body, the role of platelets is to bind to a damaged blood vessel and create a blood clot. This is very useful for accidental cuts, for example, but too many platelets, or platelets that are too sticky, can raise the risk of blood clots.
“The infection appears to be the trigger for changing the finely tuned balance in the blood and making us more prone to thrombosis, or clot formation,” says Dr. Lakshminarayan. “It’s a trigger for the blood vessels to get blocked up and puts us at higher risk of serious events like heart attack and stroke.”
“One of the biggest takeaways is that we have to prevent these infections whenever possible […] and that means flu shots and pneumonia vaccines, especially for older individuals.”
Dr. Kamakshi Lakshminarayan
In an accompanying
“And if the infection is that severe, we can assume a stronger inflammatory response will result in a higher cardiovascular risk,” he said in an interview.
Badimon is a professor of medicine and the director of the atherothrombosis research unit at Mount Sinai School of Medicine’s Cardiovascular Institute in New York City, NY.