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.
This study aimed to evaluate the antioxidative and oxidative status of patients with ascending aortic dilatation using malondialdehyde, an oxidative stress marker, and paraoxonase-1 activity, an antioxidant enzyme. Methods: This cross-sectional study was conducted between August and December 2020. It included 56 consecutive patients (mean age 55.3 ± 8.6 years; range 31 to 67 years; 26 males, 30 females) with ascending aortic dilatation and 33 sex-and age-matched controls (mean age 54.5 ± 10.5 years; range 32 to 67 years; 13 males, 20 females) with normal aortic diameters. All participants were evaluated using transthoracic echocardiography. Malondialdehyde was analyzed using the thiobarbituric acid assay. Paraoxonase-1 activity was measured manually using a spectrophotometer. The relation of ascending aortic dilatation with malondialdehyde levels and paraoxonase-1 activity was identified with correlation analyses. Results: The patient group had significantly higher mean malondialdehyde than the control group (2.5 ± 1.9 µmoL/mL and 1.7 ± 0.3 µmoL/mL, respectively; p < 0.001). The patient group had significantly lower mean activity of paraoxonase-1 than the control group (18.5 ± 12.9 U/mL vs.30 ± 17.6 U/mL, respectively; p < 0.002). Serum malondialdehyde was negatively correlated with ascending aortic diameter (r = 0.293, p = 0.009). A significant negative correlation was found between the activity of serum paraoxonase-1 and ascending aortic diameter (r = -0.364, p = 0.001). Malondialdehyde levels and paraoxonase-1 activity were independent predictors of ascending aortic dilatation.
Conclusion:The results are in line with the notion that increased malondialdehyde levels indicate lipid peroxidation, and decreased paraoxonase-1 activity indicates impaired antioxidant defense. Using them may help protect against the pathophysiology of ascending aortic dilatation.
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