Posted on May 16, 2017, 10 a.m.
Research findings confirm that a respiratory infection can trigger a heart attack, increasing the risk by 17 times in the 7 days following the infection.
Researchers at the University of Sydney have determined the risk of suffering a heart attack is 17 times higher in the week after a respiratory infection. The study took place at Royal North Shore Hospital. The findings were recently published in the Internal Medicine Journal. It is the first study to show a link between respiratory infections like bronchitis, influenza and pneumonia and a heightened risk of heart attack in individuals confirmed through coronary angiography. Coronary angiography is an X-Ray that pinpoints artery blockages in the heart.
Why the Findings Matter
The findings are of significance as they confirm that respiratory infections can serve as a trigger for heart attacks. The study's data showed that a heightened risk for heart attack does not solely occur at the beginning of the respiratory symptoms. The risk peaks in the first week and slowly decreases. However, it is elevated for a full month.
About the Study
The study involved nearly 600 consecutive patients who suffered a heart attack as a result of a coronary artery blockage. They provided information on recent and common occurrences of respiratory infection symptoms. Just over 20 percent of the patients reported respiratory infection symptoms within the first month of their heart attack. Exactly 17 percent of the patients reported respiratory infection symptoms within a week of the heart attack.
Each subject was questioned about his activities prior to the onset of the heart attack. These interviews included questions about whether they endured recent flu-like sickness with a sore throat and/or fever. If a subject reported a cough, sore throat, sinus pain, fever or flu-like symptoms, he was considered to be affected. The same is true of those who reported a diagnosis of bronchitis or pneumonia.
Another analysis was performed amongst those with symptoms limited to the upper respiratory tract. These symptoms included sinusitis, rhinitis, pharyngitis and the common cold. Subjects who reported fairly mild infection symptoms of the upper respiratory tract endured less risk. However, this risk was still boosted 13-fold.
Though upper respiratory infections are not as severe, they are more common than the symptoms of lower respiratory tract infections. The research group desired to understand their relationship to the risk of heart attacks. This information is especially important during the winter. Heart attacks tend to occur at higher rates in the winter months in countries around the world. Part of the reason for this increase is due to an elevation of respiratory infections during the colder months. Medical professionals far and wide advise people to take precautions to minimize exposure to infection, whether it is a pneumonia vaccine, flu vaccine or other measures.
Why Respiratory Infections Trigger Heart Attacks
Though no one is completely certain why respiratory infections cause heart attacks, researchers point to the fact that blood clots occur at a higher frequency when one has a respiratory infection. There is also an increased tendency for other alterations in blood flow, inflammation, and toxins harming blood vessels. However, the odds of a single episode of a respiratory infection causing a heart attack are low. Yet it is still possible for such an infection to cause a coronary event.
Everyone should consider preventative strategies and take note of the symptoms that are an indication of a heart attack. As time progresses, medical professionals will eventually pinpoint effective treatment strategies to minimize the risk of heart attacks. This is especially important for those who face a higher susceptibility to heart attacks.
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Lorcan Ruane, Thomas Buckley, Soon Y. S. Hoo, Peter S. Hansen, Catherine McCormack, Elizabeth Shaw, Judith Fethney, Geoffrey H. Tofler. Triggering of acute myocardial infarction by respiratory infection. Internal Medicine Journal, 2017; 47 (5): 522 DOI: 10.1111/imj.13377