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

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.

Endothelial dysfunction in patients with acromegaly and It's association with Endocan.

OBJECTIVE: This study aims to assess endocan levels in patients with acromegaly who have active disease or disease in remission and to investigate a relation between endocan levels and endothelial dysfunction in these patients. DESIGN: The study is a case-control study. Study was conducted at Istanbul Medeniyet University Goztepe Training and Research Hospital between 2013 and 2019. Patients who were older than 18 years with acromegaly diagnosis were recruited if they agreed to participate. Patients with uncontrolled diabetes (DM), hypertension (HT), hyperlipidemia, decompensated heart failure, immune or infectious diseases, moderate-severe valve disease and stage 3 or more advanced chronic kidney disease were excluded. There were 30 healthy control subjects who agreed to participate to the study. Patients with acromegaly were divided into two groups as: disease active patients and patients in remission. Serum endocan levels were measured with enzyme linked immunosorbent assay (ELISA) method endothelial function was assessed with flow mediated dilatation (FMD). RESULTS: There were 85 patients included to the study. Twenty-three patients had active disease, 31 were in remission and 31 were healthy controls. FMD was higher in controls compared to patients in active disease and patients in remission (p < 0.001). There was no difference between patients with active disease for FMD and patients in remission (p = 0.088). There was statistically significant correlation between FMD and endocan and insulin like growth hormone-1 (IGF-1) levels of patients with acromegaly. As FMD increased endocan and IGF-1 decreased. A moderate negative relation between FMD and endocan was identified (p < 0.001, r:-0.409) as well as FMD and IGF-1 levels (p:0.011, r:-0.377). Along with endocan and IGF-1, DM, HT, sex, body mass index, age and uric acid were associated with changes in FMD. CONCLUSIONS: Endocan levels and endothelial function measured with FMD have an inverse relationship. Endocan may prove to be a marker for endothelial dysfunction in acromegaly.