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Patient: Male, 32Final Diagnosis: Pericardial effusion related to the consumption of herbal productSymptoms: DyspneaMedication: Horse chestnut (Aesculus hippocastanum L)Clinical Procedure: Pericardial and pleural effusions were drained through a pericardiopleural windowSpecialty: CardiologyObjective:Unusual clinical courseBackground:There are many well-known causes of pericardial effusion, such as cancer metastasis, bacterial or viral pericarditis, and uremic pericarditis; however, no reports exist in the literature demonstrating a pericardial effusion that led to cardiac tamponade following consumption of an herbal remedy.Case Report:A 32-year-old male patient was referred to our cardiology outpatient clinic with a complaint of dyspnea. The patient’s medical history was unremarkable; however, he had consumed 3 boxes of horse chestnut (Aesculus hippocastanum L) paste over the previous 1.5 months. His chest x-ray examination revealed an enlarged cardiac shadow and bilateral pleural effusion. On transthoracic echocardiographic examination, his ejection fraction was found to be 55% with circumferentially extended pericardial effusion that reached 3.9 cm at its maximal thickness. No growth had been detected in the pericardial and pleural biopsies or blood samples; there was no evidence of an infectious process in the physical examination. Based on this information, we diagnosed pericarditis resulting from the use of herbal remedies. This is the first report to demonstrate that herbal remedy consumption may cause this type of clinical condition.Conclusions:Besides other well-known causes, pericardial effusion related to the consumption of herbal remedies should always be considered when treating patients with pericardial effusion caused by unclear etiologies.

Objective: The use of the radial approach in coronary angiography or percutaneous coronary intervention has increased owing to its advantages over the femoral approach such as rapid patient mobilization and improved patient comfort. However, radial artery spasm (RAS) that occurs during the procedure is a crucial factor in transradial approach failure and access site switch. Asymmetric dimethylarginine (ADMA) is a naturally occurring, modified amino acid that inhibits nitric oxide (NO) production. High ADMA levels may reduce arterial elasticity especially in small arteries like the radial artery. This study aimed to evaluate the relationship between ADMA levels and RAS in radial artery access. Methods: This study included 155 patients (89 males and 66 females) who underwent transradial coronary angiography between January 2016 and June 2016. The ADMA level in the plasma was determined using a quantitative sandwich enzyme immunoassay technique. Results: RAS was observed in 16 of the 155 patients (10.1%). The RAS was found to be more frequent in female patients (17.9% for women vs. 4.4% for men, p=0.019). The plasma concentration of ADMA in the RAS group was significantly higher than that in the control group [22.1 ng/mL (12.1–37.8) vs. 9.2 ng/mL (5.9–14.8), p<0.001]. Moreover, the plasma concentration of ADMA was significantly higher in patients with RAS among female patients [20.4 ng/mL (12.1–44.9) vs. 9.9 ng/mL (6.2–16.6); p=0.002] and among male patients [25.2 ng/mL (13.7–35.4) vs. 8.2 ng/mL (5.9–12.8); p=0.007]. Binary logistic regression analysis of all patients showed that ADMA concentration was the only predictor for RAS (odds ratio=1.142; 95% confidence interval=1.061–1.228; p<0.001). Conclusion: It was found that the ADMA concentration of the patients in the RAS group was elevated compared to that of controls. The findings indicated that elevated ADMA concentrations could predict RAS that may occur. (Anatol J Cardiol 2020; 23: 228-32)

Objective: Identification of the asymptomatic target organ damage (AOD) helps to stratify the overall risk of cardiovascular (CV) diseases and guides a treatment decision in hypertensive patients without a symptomatic CV or renal disease. The endothelial-cell-specific molecule 1 (endocan) is regarded as a novel marker of endothelial dysfunction. Its release is increased in hypertensive patients, especially those with symptomatic CV and renal disease. In the present study, we aimed to evaluate the endocan levels in asymptomatic hypertensive patients with or without AOD. Methods: The study included 132 asymptomatic hypertensive patients, and 101 of who had at least one AOD. Results: Serum endocan levels did not differ between patients with and without AOD (3.81±0.78 vs. 3.83±0.63 ng/mL, p=0.88). An analysis according to the presence of any specific AOD did not show any difference between groups. No significant correlation was found between serum endocan levels and any of the continuous variables related to AOD, such as the pulse pressure, carotid intimae-media thickness, cardio-ankle vascular index, ankle-brachial index, left ventricular mass index, Sokolow–Lyon index, Cornell voltage-duration product, and estimated glomerular filtration rate. Conclusion: Endocan may not serve as a useful biomarker at asymptomatic vascular stages of hypertension, despite its role in indicating disease severity and inflammatory activation in advanced symptomatic CV and renal disease.