Coronavirus disease 2019 re-infection: first report from Turkey.

There are concerns about the possibility of SARS-CoV-2 reinfection and recently, a patient with SARS-CoV-2 re-infection (or COVID-19) confirmed by epidemiological, clinical, serological and genomic analyses have been published. We have noticed another patient with SARS-CoV-2 re-infection based on clinical and laboratory studies: A 23-year-old woman presented to her hospital with fever (39°C), chills, fatigue, cough, headache, sore throat, muscle and joint pain on April 9, 2020. On examination, oropharynx was mildly hyperemic, and chest auscultation was normal. SARS-CoV-2 PCR from nasopharyngeal specimen was ordered. She was given isotonic saline and acetaminophen and prescribed azithromycin and acetaminophen and sent home for isolation. SARS-CoV-2 PCR was reported positive and she was given hydroxychloroquine for five days. She improved in 10 days and PCR studies on April 22, and April 27 remained negative. On 4 August 2020, she was re-admitted with fever (38.7°C), chills, fatigue, loss of appetite, taste and smell loss, muscle and joint pain. On examination, oropharynx and chest auscultation were normal. SARS-CoV-2 PCR was reported positive and she was prescribed hydroxychloroquine, acetaminophen and sent home for isolation again. She improved in one week (taste-smell loss improved in 10 days) and on follow-up visit after 14 days, she was doing well. PCR was negative on 17 August 2020. Her anti-SARS-CoV-2 antibodies were negative on 17 August 2020 and slightly positive (2.14 signal-to-cutoff) on 29 August 2020. Previous report from To et al. [Clin Infect Dis. 2020;ciaa1275. doi:10.1093/cid/ciaa1275] showed that viral genomes from first and second episodes belonged to different clades/lineages. They described second episode of asymptomatic infection occurred 142 day after the first symptomatic one. Our patient is the first report, describing two symptomatic episodes 116 days apart. We conclude that as the patients recovered from COVID-19 increases, increased awareness may delineate the characteristics of re-infection.

Investigation of the relationship between non-alcoholic fatty liver disease and coronary artery disease.

AIMS: The purpose of the study was to examine the association between visceral adiposity form of non-alcoholic fatty liver and coronary artery disease severity and also to investigate the relationship between the epicardial adipose tissue thickness and non-alcoholic fatty liver disease with clinical and anthropometric measurements. MATERIALS AND METHODS: This study included 105 patients (mean age of patients were 57 ± 11, 82 of them male) who were hospitalized for coronary angiography because of chest pain. Nonalcoholic fatty liver disease was investigated by using ultrasonography. Thickness of the epicardial adipose tissue was measured by transthorasic echocardiography to right ventricular free wall adjacent to the parasternal long and short axis images. Gensini score was used for the severity of coronary artery disease. RESULTS: In patients with non-alcoholic fatty liver disease, right ventricular free wall epicardial adipose tissue thickness average of parasternal long and short axis were thicker than those who do not have non alcholic fatty liver disease (0,90 ± 0,19 cm; 0.58 ± 0.18 cm, p<0.001). Also, in patients with severe coronary artery disease, right ventricular free wall parasternal long and short axis average thickness of epicardial fat tissue was thicker than those of patients without severe coronary stenosis (0.86 ± 0.21 cm; 0,66 ± 0.26 cm, p=0.001). For predictability of coronary artery disease, Receiver Operating Characteristic analysis of the area under the curve was found to be 0.60 (50.2 to 74.7, 95% Confidence Limits). CONCLUSIONS: Not only the fatty tissue which surrounds the heart effects the coronary arteries but also other visceral organs adiposity effects the coronary arteries atherosclerotic process.

The prevalence of the metabolic syndrome and its impact on the left ventricular systolic function in the patients with non-diabetic first ST elevation myocardial infarction.

OBJECTIVE: Metabolic syndrome (MS) is common among the patients with myocardial infarction. The degree of the left ventricular systolic dysfunction is shown to be associated with poor prognosis after myocardial infarction. The aim of this study was to evaluate the prevalence of MS and its impact on the left ventricular systolic function in non-diabetic patients suffering first ST elevation myocardial infarction (STEMI). MATERIAL AND METHODS: This study was conducted prospectively in three centers. We included patients presenting with non-diabetic first acute STEMI. The systolic functions of the left ventricle were assessed through the ejection fraction, the wall motion score index (WMSI) and tissue Doppler myocardial S wave velocities. The diagnosis of MS was done based on the Adult Treatment Panel III clinical definition of the MS. RESULTS: Among the 240 patients, 90 patients (37.5%) had MS but 150 patients (62.5%) were free of the MS. The patients in the MS group were older and the prevalence was higher among the females. Mean myocardial S wave velocities were significantly lower in the patients with the MS in comparison to the patients without the MS (6.70 +/- 1.68 vs. 7.39 +/- 1.64; p < 0.01). LVEF and WMSI were similar in two groups. CONCLUSIONS: MS was highly common in nondiabetic patients with acute STEMI and left ventricular systolic function were more severely impaired in these patients. Our observations suggest that more severely impaired left ventricular systolic function after acute STEMI may contribute to the higher morbidity and mortality seen in the patients with MS after acute STEMI.

Relationship between myocardial performance index and aortic distensibility in patients with essential hypertension.

We aimed to investigate the association between aortic distensibility (AD) and left ventricle myocardial performance index (MPI) in patients with newly diagnosed hypertension (HT). We studied 49 patients with HT and 24 healthy control subjects. AD was calculated from the echocardiographically derived ascending aorta diameters. The MPI was calculated from both conventional flow Doppler echocardiography and tissue Doppler echocardiography recordings. Conventional Doppler E/A and tissue Doppler derived Ea/Aa were determined for all the subjects. Aortic distensibility was lower, and both conventional and tissue Doppler MPI values were higher (p<0.001 for all) in patient group compared with control group. AD was correlated with systolic blood pressure (SBP) (beta=-0.436, p=0.037), Ea/Aa (beta=0.228, p=0.038) and tissue derived MPI (beta=-0.302, p=0.043) in multiple linear regression analysis. Aortic distensibility was independently related to tissue derived MPI and Ea/Aa besides SBP.

Paraoxonase and arylesterase activities in coronary artery disease.

BACKGROUND: Paraoxonase-1 is an enzyme with three activities which are inversely related to cardiovascular diseases. Accordingly, the aim of the study was to investigate the paraoxonase, arylesterase activities and oxidative/anti-oxidative status in coronary artery disease (CAD) and their correlation with the extent of CAD. MATERIALS AND METHODS: Study populations of 193 patients with angiographically documented CAD, 83 patients with normal coronary angiograms (NCAD) and 55 healthy volunteers were included in the study. The patients with CAD were divided into three categories according to the number of diseased coronaries. Also, a Gensini score was calculated for each patient. Serum paraoxonase and arylesterase activities were measured spectrophotometrically. Oxidative and anti-oxidative status was evaluated by measuring serum lipid hydroperoxide (LOOH), total anti-oxidant status (TAS) and free sulfhydryl groups (-SH = total thiol). Lipid parameters were determined by routine laboratory methods. RESULTS: Serum paraoxonase and arylesterase activities, TAS and -SH levels were lower in the CAD group compared with the NCAD group and control group (P < 0.05, all). Serum LOOH levels of the CAD group were greater than those in both the control and NCAD groups (P < 0.05). The major decreases in paraoxonase, arylesterase activities, -SH and TAS levels and the major increase in LOOH levels were observed in the 3-vessels disease group. In multiple linear regression analysis, the Gensini score was independently correlated with paraoxonase activity (beta = -0.469, P < 0.001), -SH levels (beta = -0.232, P < 0.001), HDL levels and history of diabetes. CONCLUSIONS: Both paraoxonase activity and -SH levels are independently associated with the presence and extent of CAD. Reduced paraoxonase activity and -SH levels may play a role in the severity of coronary atherosclerosis.

The effects of 12 months of growth hormone replacement therapy on cardiac autonomic tone in adults with growth hormone deficiency.

OBJECTIVES: Growth hormone deficiency (GHD) in adults is associated with a cluster of cardiovascular risk factors. Some abnormalities of cardiac structure and function have been reported in adult patients with GHD, but there are few data related to cardiac autonomic tone. Non-invasive assessment of cardiac autonomic status can be achieved by heart rate variability (HRV), which can be measured by using time-domain or frequency-domain variables. To our knowledge, short-term (6 months) effects of GH replacement therapy (GHRT) on HRV in a limited number of patients have been evaluated prospectively in only two previous studies. The present study was therefore designed to investigate the effects of GHD and 12 months of GHRT on cardiac autonomic tone in a larger number of adult patients with severe GHD. PATIENTS AND METHODS: HRV measurement, by using time-domain variables, was performed in 22 patients with GHD (eight men, 14 women; mean age 45.4 +/- 2.4 years) and 22 healthy controls (nine men, 13 women; mean age 40.8 +/- 1.8 years) at baseline. The time-domain variables (sympathetically influenced parameters SDNN and SDANN and parasympathetically influenced parameters RMSSD and PNN50) were derived from 24-h electrocardiogram (ECG) recordings. In the patient group, cardiac autonomic tone was re-evaluated after 6 and 12 months of GHRT. RESULTS: Mean baseline values of SDNN and SDANN were significantly higher (higher values mean lower sympathetic activity) in GHD patients than in healthy controls (P < 0.05), but mean baseline values of RMSSD and PNN50 did not differ significantly in healthy controls and patients. After 6 and 12 months of GHRT, mean SDNN and SDANN were decreased significantly when compared with the baseline values before GHRT (P < 0.05). However, mean RMSSD and PNN50 did not differ significantly from baseline. When SDNN and SDANN measurements were evaluated individually for each patient, after 12 months of GHRT both of the sympathetically influenced parameters decreased in 90% of the patients. CONCLUSIONS: These data indicate that sympathetic tone is decreased in adult patients with severe GHD. Additionally, an increment in sympathetic activity and normalization of sympathovagal balance have been demonstrated after 6 and 12 months of GHRT. This result suggests that, at least at the doses used in this study, GHRT improves sympathetic tone, without an obvious arrhythmogenic effect.