Coronary microvascular dysfunction is common in patients hospitalized with COVID‐19 infection

Abstract

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.

Association of vasopressors with mortality in critically ill patients with COVID-19: A systematic review and meta-analysis

“…In COVID-19, the progressive hypoxemia initially increases cardiac output and capillary recruitment, which maintain microcirculatory oxygen-extraction capacity by increasing red blood cell availability (silent hypoxia) [66][67][68]. However, microcirculatory flow decreases proportionally to the increasing inflammation, hypercoagulation, and thrombosis, resulting in multi-organ failure at later stages [66,[69][70][71]. In the study by Mesquida et al, patients showed alterations in systemic microcirculatory status, and the degree of these alterations correlated with the severity of the respiratory disease [24].…”

“…These agents may be associated with a significant increase in survival. A possible explanation for the association of vasopressors with mortality may lie in the microcirculation [65][66][67][68][69][70][71]. The physiological pulsatile shear stress from normal laminar flow maintains the normal endothelial cell functions and the expression of ACE2s and other anticoagulant/antithrombotic and antioxidant substances [72].…”

Familial hypercholesterolemia: The nexus of endothelial dysfunction and lipoprotein metabolism in COVID-19

“…This study concluded that COVID-19 patients had infection-triggered mechanisms, which ultimately resulted in the development of CMD. Although this finding has been confirmed in several studies, especially in hospitalized patients with COVID-19, the severity of CMD among COVID-19 patients appears to vary partly because of the virus variant that caused the disease [34–39]. Importantly, a very recent study in the United Kingdom identified microangiopathic thrombosis as a common cause of myocardial injury in hospitalized COVID-19 patients with troponin elevation [40].…”

Coronary microcirculatory dysfunction in hypercholesterolemic patients with COVID-19: potential benefit from cholesterol-lowering treatment

“…More than a decade ago CMD was reported in patients with acute respiratory distress syndrome and influenza A (H1N1) [ 15 ]. This year an echocardiographic coronary flow velocity reserve analysis revealed that CMD is common in patients hospitalized with SARS-CoV-2 infection [ 16 ]. In a very comprehensive study of patients who had recently recovered from COVID-19, patients with classic hypertrophic cardiomyopathy and healthy controls were compared using vasodilator stress cardiovascular magnetic resonance examination for the evaluation of myocardial perfusion reserve (MPR) [ 17 ].…”