A case of infective endocarditis caused by an uncommon agent with atypical manifestations is presented. A 42-year-old woman previously had rheumatic heart disease, presented with the symptoms of fever and chills that resolved within 3 days under antibiotherapy. She was diagnosed with endocarditis due to. Despite culture-directed antibiotics being administered in the first admission, her symptoms and also blood culture growth relapsed 3 weeks later. She was successfully treated with antimicrobial therapy and surgical intervention including aorta and mitral valve replacement. This case demonstrates that should be considered as a causative organism of endocarditis particularly in the presence of atypical symptoms and should be followed up carefully in terms of relapses and complications.

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Objective Delayed revascularisation in patients with ST‐segment elevation myocardial infarction (STEMI) is associated with poor prognosis. The aim of this study is to investigate how the timeline in STEMI treatment was affected during the Covid‐19 outbreak. Method Consecutive 165 STEMI patients were enrolled in the study during the Covid‐19 pandemic period (Pandemic period) and the prepandemic period (Control period). The time period until patients' leaving their current position after the onset of pain (home delay), the time from the onset of pain to the first medical contact (FMC delay), door‐to‐balloon time, procedure time and hospitalisation time were recorded. Results A total of 165 patients, 82 in the Pandemic period and 83 in the Control period, were included in the study. When compared with the control period, home delay [30 (5‐6912) minutes vs 165 (10‐360) minutes, P < .001] and FMC delay [61 (20‐6932) minutes vs 190 (15‐3660) minutes, P < .001] were significantly prolonged during the pandemic period. In addition, non‐IRA PCI rate (8.8% vs 19.3% P = .043) and hospitalisation time [71 (15‐170) vs 74.2 (37‐329) hours, P = .045] were decreased. Conclusion During the Covid‐19 pandemic period, prolonged prehospital time parameters were observed in STEMI patients. Therefore, additional measures may be required to prevent unfavourable delays in STEMI patients during the outbreak.

Background Pulmonary hypertension (PH) is one of the complications of human immunodeficiency virus (HIV) infection. Despite the emergence of effective therapies, pulmonary arterial hypertension is commonly seen, especially at advanced stages. At the time of diagnosis, a majority of patients are at New York Heart Association‐Functional Class III or IV. Many of the current screening modalities are dependent on detecting a rise in pulmonary arterial pressure (PAP). However, high capacitance of the pulmonary circulation implies that early microcirculation loss is not accompanied by a change in resting PAP. Therefore, we aimed to demonstrate early changes in pulmonary vascular disease in HIV‐infected patients with a new echocardiographic parameter, called as pulmonary arterial stiffness (PAS). Methods and Results Thirty‐six HIV‐infected patients and 36 age‐ and sex‐matched healthy control subjects were enrolled in this study. PAS was calculated echocardiographically by using maximal frequency shift and acceleration time of the pulmonary artery flow trace. There was no significant difference in diastolic functions, right ventricular diameters, systolic PAP, inferior vena cava widths, right atrial area, and tricuspid annular plane systolic excursion values between the two groups. However, PAS was calculated as 24.3 ± 6.4 Hz/msn in HIV‐infected patients and 19.3 ± 3.1 Hz/msn in healthy control group (P < 0.001). Increase in PAS was correlated with duration of HIV infection (P < 0.05). Conclusion Our results suggest that HIV infection affects pulmonary vascular bed starting early onset of disease and this can be demonstrated by an easy‐to‐measure echocardiographic parameter.

Background and Objectives: The mean platelet volume (MPV) represents a possible marker of platelet activation. There is an association between the platelet count (PC) and inflammation and platelet reactivity. We assessed the association between the MPV/PC ratio and circadian alterations in blood pressure (BP). Material and Methods: One hundred and twenty subjects in total, 80 hypertensive subjects and 40 healthy subjects (controls), were enrolled in the study group. Twenty four hour ambulatory BP monitoring (ABPM) was applied to all subjects. According to ABPM results, the hypertensive subjects were separated into two groups, such as dippers (n = 40) and non-dippers (n = 40). In all subjects, the collection of venous peripheral blood samples was performed on admission for PC and MPV measurements. Results: The two groups exhibited similar clinical baseline characteristics. A significantly higher MPV/PC ratio was determined in non-dippers compared to that in dippers and normotensives. The higher MPV/PC ratio was observed in non-dippers in comparison with that in dippers and normotensives (0.046 ± 0.007 to 0.032 ± 0.004 fL/[109/L]; 0.046 ± 0.007 to 0.026 ± 0.004 fL/[109/L], p < 0.001, respectively). A receiver operating characteristic (ROC) curve analysis showed that the optimum cut-off value of the MPV/PC ratio for predicting non-dipping patterns in hypertensive patients was 0.036 (area under the curve [AUC]: 0.98, p < 0.001). According to the cut-off value, sensitivity and specificity were found to be 95% and 95%, respectively. Conclusions: The higher MPV/PC ratio was determined in non-dipper hypertensive subjects in comparison with that in dipper hypertensive subjects. An elevation of platelet activity and an increase in thrombus burden are reflected by an increase in the MPV/PC ratio. The MPV/PC ratio may underlie the increase in cardiovascular risk in non-dippers compared to that in dippers.