In search of reasons why people with HIV have about a 4.5-fold greater risk of sudden cardiac death, researchers have found evidence suggesting that the virus, especially if detectable, disrupts the resetting that occurs between heartbeats, according to a recent study.

Publishing their findings in the journal Circulation, researchers analyzed data from the Multicenter AIDS Cohort Study regarding 589 HIV-positive and 534 HIV-negative men.

Eighty-three percent of the men with HIV had a fully suppressed viral load. Sixty-one percent of the overall cohort was white, and 25% was African American.

The participants wore a portable electrocardiogram (ECG) to track QT interval variability. A QT interval is the time between the start of the heart’s Q wave and the end of its T wave according to the spikes on an ECG readout. It represents the time it takes for the heart’s ventricles to depolarize and repolarize, or “reset.” Higher QT interval variability is associated with a higher risk of cardiovascular disease.

Analyzing three to four days of QT data, the study authors found that the men with HIV, compared with those who did not have the virus, had a higher variability in their QT intervals, with a QT variability index of 0.077. Compared with the HIV-negative men, the men with HIV who had a fully suppressed viral load had a QT variability index of 0.064, while those with a detectable viral load had a QT variability index of 0.150.

The researchers estimated that the excess QT variation in the HIV-positive group was comparable to aging eight years, while for those with a detectable viral load, it was comparable to aging nearly 20 years.

Looking at inflammatory biomarkers, the researchers found that compared with the HIV-negative men, those with HIV had a 14% higher level of IL-6 and a 22% higher level of sCD163. Having a higher level of thesebiomarkers was associated with greater QT variability and risk of arrhythmia (irregular heart rhythm).

“HIV puts people in a state of chronic heightened inflammation, and that might be a major contributor to why the heart is prone to abnormal rhythms,” the study’s lead author Amir Heravi, a medical student at the Johns Hopkins University School of Medicine, said in the press release. “However, inflammation would only partly explain our findings, and our results showed even after adjusting for effects of inflammation, HIV infection was associated with higher QT variability. We think it may be a combination of the virus and the body’s reaction to the virus via inflammation that ultimately contributes to an increased risk of sudden cardiac death.”

To read the study abstract, click here.

To read a press release about the study, click here.