Small study links prior SARS-CoV-2 infection with coronary vasomotor dysfunction
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Prior SARS-CoV-2 infection was associated with coronary vasomotor dysfunction, regardless of whether the patient required hospitalization, according to a brief communication published in the Journal of the American Heart Association.
“When compared with a matched control group without prior COVID-19 within a similar time frame, patients with prior COVID-19 had greater frequency and severity of coronary vasomotor dysfunction with lower maximal myocardial blood flow and myocardial blood flow reserve, a concordance that reflects the highest clinical risk,” Brittany Weber, MD, PhD, cardiologist at Brigham and Women’s Hospital and instructor in medicine at Harvard Medical School, and colleagues wrote. “SARS-CoV-2 infection has been shown to be associated with endothelial dysfunction, and these results may suggest an acceleration of endothelial dysfunction or even a progression of atherosclerosis that occurs in the setting of SARS-CoV-2 infection.”
For this study, researchers at Brigham and Women’s Hospital identified 34 patients with confirmed SARS-CoV-2 infection who underwent myocardial stress perfusion PET from April 2020 to July 2021 (median time to imaging, 4.6 months). Measures of myocardial perfusion and blood flow reserve were compared with 103 matched controls without prior SARS-CoV-2 infection who underwent myocardial stress perfusion PET during the same period.
The primary outcome was prevalence of coronary vasomotor dysfunction, defined as myocardial blood flow reserve less than 2 associated with a maximal myocardial blood flow of less than 1.8 mL/min/g.
CV risk factors such as obesity (67.7%), hypertension (91.2%), hyperlipidemia (91.2%) and diabetes (55.8%) were common among patients with confirmed SARS-CoV-2 infection.
Fifty-three percent of patients with COVID-19 had abnormal myocardial perfusion on N13- ammonia PET.
Researchers observed myocardial blood flow reserve less than 2 in 44% of the patients with confirmed SARS-CoV-2 infection compared with 11.7% of matched controls (P < .001). The difference remained significant when the analysis was restricted to patients with visually normal PET scans (P < .001). The researchers posited that these findings are not only related to epicardial CAD but may indicate an abnormal microcirculatory response to stress.
In addition, mean myocardial blood flow reserve was 19.4% lower in patients with confirmed SARS-CoV-2 infection compared with the control group (2 vs. 2.48; P < .001).
There was no difference in mean myocardial blood flow reserve among patients with confirmed SARS-CoV-2 infection requiring hospitalization compared with those who did not require hospitalization (P = .5).
“In survivors, the longer-term cardiovascular consequences of COVID-19 are unknown and important to delineate to inform therapeutic strategies for long-term sequelae beyond acute illness, including the risk of myocardial infarction and stroke from endothelial damage,” the researchers wrote. “The excess microvascular risk in this study supports a potential role for vascular endothelial damage and/or inflammation in driving coronary vasomotor abnormalities that might contribute to excess cardiovascular risk in this population.”
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