Key result
COVID-19 hospitalization is linked to ~17% lower CFVR versus controls.
Why the study?
Direct evidence demonstrating coronary microvascular dysfunction in patients hospitalized with COVID-19 was missing despite hypotheses and evidence of microvascular dysfunction in other tissues.
Case-Control (n=79)
Absolute Event Rate: 2% vs 2.4%
p-value: p=< .001
Coronary microvascular dysfunction is common in hospitalized COVID-19 patients, correlates with disease severity and inflammatory biomarkers, and may explain cryptic myocardial injury.
Suggests microvascular dysfunction in hospitalized COVID-19; hypothesis-generating for its role in myocardial injury and requires prospective confirmation.
BACKGROUND AND AIMS: Microvascular disease is considered as one of the main drivers of morbidity and mortality in severe COVID-19, and microvascular dysfunction has been demonstrated in the subcutaneous and sublingual tissues in COVID-19 patients. The presence of coronary microvascular dysfunction (CMD) has also been hypothesized, but direct evidence demonstrating CMD in COVID-19 patients is missing. In the present study, we aimed to investigate CMD in patients hospitalized with COVID-19, and to understand whether there is a relationship between biomarkers of myocardial injury, myocardial strain and inflammation and CMD. METHODS: 39 patients that were hospitalized with COVID-19 and 40 control subjects were included to the present study. Biomarkers for myocardial injury, myocardial strain, inflammation, and fibrin turnover were obtained at admission. A comprehensive echocardiographic examination, including measurement of coronary flow velocity reserve (CFVR), was done after the patient was stabilized. RESULTS: Patients with COVID-19 infection had a significantly lower hyperemic coronary flow velocity, resulting in a significantly lower CFVR (2.0 ± 0.3 vs. 2.4 ± 0.5, p < .001). Patients with severe COVID-19 had a lower CFVR compared to those with moderate COVID-19 (1.8 ± 0.2 vs. 2.2 ± 0.2, p < .001) driven by a trend toward higher basal flow velocity. CFVR correlated with troponin (p = .003, r: -.470), B-type natriuretic peptide (p < .001, r: -.580), C-reactive protein (p < .001, r: -.369), interleukin-6 (p < .001, r: -.597), and d-dimer (p < .001, r: -.561), with the three latter biomarkers having the highest areas-under-curve for predicting CMD. CONCLUSIONS: Coronary microvascular dysfunction is common in patients with COVID-19 and is related to the severity of the infection. CMD may also explain the "cryptic" myocardial injury seen in patients with severe COVID-19 infection.
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Çalışkan et al. (2022) conducted a case-control in COVID-19 (n=79). COVID-19 infection vs. Control subjects was evaluated on Coronary flow velocity reserve (CFVR) (p=< .001). Patients hospitalized with COVID-19 had significantly lower coronary flow velocity reserve compared to control subjects (2.0 vs. 2.4, p < 0.001).
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