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We investigated 2 hypotheses: (1) a relationship between platelet indices and stable coronary artery disease (CAD) and acute ST-segment elevation myocardial infarction (STEMI) and (2) a relationship between platelet indices on admission and thrombolysis outcomes in patients with STEMI. A total of 260 patients were enrolled. The white blood cell (WBC) and platelet distribution width (PDW) were found to be increased in patients with STEMI (P for both < .001). White blood cell and PDW were independent predictors of acute STEMI. Mean platelet volume (MPV) and PDW were significantly higher in the thrombolysis failure group than in the thrombolysis success group (9.9 ± 1.8 vs 9.2 ± 1.5 fL, P = .021 and 17.7 ± 1.0 vs 16.4 ± 2.1 fL, P < .001, respectively). Mean platelet volume and PDW were independent predictors of thrombolysis failure. Patients with acute STEMI had higher PDW than did patients with stable CAD. In addition, higher PDW and MPV seem to correlate with thrombolysis failure in patients with STEMI.

We have shown that patients with coronary artery ectasia have an increased prevalence of varicocele compared to those with coronary artery disease. The mechanism underlying coronary artery ectasia might further increase the prevalence of varicocele in susceptible patients.

Objective:We recently described the CHA2DS2-VASc-HS score as a novel predictor of coronary artery disease (CAD) severity in stable CAD patients. We aimed to assess the accuracy of the CHA2DS2-VASc-HS score in the determination of CAD severity and complexity and its availability in the risk stratification of in-hospital major adverse cardiovascular events (MACE) in non-ST elevation acute coronary syndrome (NSTE-ACS) patients.Methods:We prospectively analyzed the clinical and angiographic data of consecutive NSTE-ACS patients in our clinic. Patients were classified into three tertiles according to their SYNTAX score (SS): tertile 1 had an SS of 0–22; tertile 2 had an SS of 23–32; and tertile 3 had an SS of >32. There were no specific exclusion criteria except for previous coronary artery bypass grafting (CABG) because SS was validated for only native coronary arteries for this study. We used the following analyses: χ2 or Fisher’s exact tests, one-way analysis of variance or Kruskal–Wallis tests, Pearson’s or Spearman’s tests, the receiver operating characteristics (ROC) curve analysis, the area under the curve (AUC) or C-statistic, and pairwise comparisons of the ROC curves.Results:A total of 252 patients were enrolled. There were 131 patients in tertile 1, 79 in tertile 2, and 42 in tertile 3. The number of diseased vessels was correlated with the Global Registry for Acute Coronary Events (GRACE) (p<0.001), Thrombolysis in Myocardial Infarction (TIMI) (p<0.001), and CHA2DS2-VASc-HS (p<0.001) scores. In the ROC curve analyses, the cut-off value of the CHA2DS2-VASc-HS score in the prediction of in-hospital MACE was >5 with a sensitivity of 69.6% and specificity of 90.3% (AUC: 0.804, 95%: CI 0.750–0.851, p<0.001). We also compared the diagnostic accuracy of the CHA2DS2-VASc-HS score with the TIMI and GRACE risk scores in the determination of the in-hospital MACE and found no differences.Conclusion:The CHA2DS2-VASc-HS score was positively correlated with the severity and complexity of CAD. We also found that CHA2DS2-VASc-HS was comparable with other risk scores for the risk stratification of the in-hospital MACE of NSTE-ACS patients. Therefore, it may play an important role as a predictive model of NSTE-ACS patients in clinical practice. (Anatol J Cardiol 2016; 16: 742-8)

Background: Autonomic dysfunction may occur during the acute phase of COVID-19.Heart rate variability (HRV) is a useful tool for the assessment of cardiac sympathetic and parasympathetic balance. We aimed to evaluate cardiac autonomic function by using HRV in subjects after recovery from COVID-19 who had previously symptomatic and were followed outpatiently. Methods: The study group composed of 50 subjects with a confirmed history of COVID-19 and the control group composed of 50 healthy subjects without a history of COVID-19 and vaccination. All the study participants underwent 2-dimensional, pulsed-and tissue-Doppler echocardiographic examinations and 24-hour Holter monitoring for HRV analysis. Results: Time domain parameters of SDNN, SDANN, SDNNi, RMSSD, pNN50, and HRV triangular index were all decreased in the study group when compared with the control group. Frequency domain parameters of TP, VLF, LF, HF, and HFnu were also decreased in the study group in comparison with the control group. LFnu was similar between groups. Nonlinear parameters of HRV including α 1 and α 2 decreased in the study group. By contrast, Lmax, Lmean, DET, REC, and Shannon entropy increased in the study population. Approximate and sample entropies also enhanced in the study group. Conclusions:The present study showed that all three domain HRV significantly altered in patients after recovery from COVID-19 indicating some degree of dysfunction in cardiac autonomic nervous system. HRV may be a useful tool for the detection of preclinical autonomic dysfunction in this group of patients.

Persistent left superior vena cava (PLSVC) is a congenital anomaly of the thoracic venous system resulting from the abnormal persistence of an embryological vessel that normally regresses during early fetal life. This anomaly is often discovered incidentally during surgery, cardiovascular imaging or invasive cardiovascular procedures. In most cases, a PLSVC drains into the right atrium through the coronary sinus. In the remainder of cases, it enters directly or through the pulmonary veins into the left atrium. A dilated coronary sinus on echocardiography should always raise the suspicion of a PLSVC as it has important clinical implications. The diagnosis should be confirmed by saline contrast echocardiography. We report a patient with persistent left superior vena cava with an enlarged coronary sinus and normal right superior vena cava.

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Our study has shown that LA mechanical functions and volumes are impaired in BD. These results may be an early form of subclinical cardiac involvement in patients with BD who have no clinical evidence for cardiovascular disease.