Brugada syndrome is a congenital channelopathy in cardiac ion transmembrane causing an alteration in the electrical conduction of the heart. ST-elevation, as well as right bundle-branch block in anterior precordial electrocardiography (ECG), is pathognomonic in this syndrome. The patient might be asymptomatic or with a history of syncope and prone to develop ventricular tachyarrhythmia which may spontaneously recover or degenerates to ventricular fibrillation, cardiac arrest and even sudden death. Nevertheless, this can be prevented by implantable cardioverter defibrillator implantation. Therefore, it is of paramount importance that clinical suspicion and identification, interpretation of its characteristic ECG pattern and risk stratification to be properly done to diagnose and to manage Brugada syndrome. The author has also done a systematic review (included in the article) for several noninvasive ECG parameters for risk stratification with promising results. Epicardial ablation is an emerging therapy that may “cure” Brugada syndrome.

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An 80-year-old male, who had undergone dual-chamber pacemaker implantation through left subclavian approach, developed tension pneumothorax of the left side. It caused a pseudoaneurysm-like contracting mass image on the chest X-ray. The diagnosis of pneumothorax was verified by chest computed tomography. Tube thoracostomy drainage was performed immediately without any sequel.

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Human immunodeficiency virus (HIV) infection is an independent predictor of ischemic stroke, especially in the younger age group. Approximately 1%–5% of HIV/acquired immunodeficiency syndrome patients develop stroke. A 16-year-old male presented with a decreased level of consciousness and a history of right-sided hemiparesis, fever, cough, and dyspnea. The patient was an intravenous drug user (IVDU). Examination revealed the following: blood pressure: 130/70 mmHg, heart rate: 124×/min, temperature 38.5°C, and respiratory rate: 26×/min. Electrocardiographic findings revealed the following: sinus tachycardia: 124×/min, right-axis deviation, incomplete right bundle branch block, and right ventricular hypertrophy. Laboratory findings were as follows: microcytic hypochromic anemia (7.33 g/dL), leukocytosis (32.2 × 10^3/μL) with shift to the left, hyponatremia (122 mmol/L), HIV was positive, and chest X-ray showed pneumonia. Echocardiography showed vegetation in the posterior mitral leaflet, mitral regurgitation, and tricuspid regurgitation with an intact interatrial septum. Computed tomography scan revealed ischemic stroke of the left parieto-occipital lobe. HIV-infected individuals are at 1.5 times increased risk of stroke compared to those without. This case involves an IVDU and a HIV-positive young male presenting with large ischemic stroke in large-vessel territory, suggestive of embolic origin. A part of vegetation on the left side of the heart of this patient dislodged and caused a cerebrovascular accident. There was also unconfirmed suspicion of pulmonary embolism from the right side of the heart. Empiric antibiotics should be started before tailoring to the result of blood culture. Endocarditis conveys a significant risk of cerebral embolism resulting in ischemic stroke and a potentially dismal prognosis.

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Acute aortic dissection is considered a potentially fatal condition. Neurologic manifestations such as paraplegia are quite rare. We report a case of acute paraplegia in a hypertensive smoker chronic obstructive lung disease patient. Transthoracic echocardiography revealed a dissection flap starting at the aortic annulus and extending to the descending thoracic aorta. Computed tomographic aortography confirmed the diagnosis with a dissection flap extended from the aortic annulus to the entire distal aorta. The patient was referred to another specialized cardiothoracic center, but unfortunately, he died during the surgery.

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A 62-year-old man with high fever, general fatigue, and history of transient ischemic attack was transferred to our cardiology clinic with high clinic suspicious of endocarditis. He had a history of mitral ring annuloplasty and coronary artery bypass grafting operation before many years ago and reoperation for aortic dissection as Bentall procedure about 3 months ago. Blood tests showed leukocytosis with massive elevation of C-reactive protein, modest elevation of troponin, marked elevation of International Normalized Ratio, mild anemia, and hypoalbuminemia. Transesophageal echocardiogram (TEE) revealed a 4-mm × 15-mm round mobile mass originating from the anterior part of the mitral annular ring. In addition, there were a sac surrounding aortic graft and surrounding aneurismal aorta suggests a separation of graft because of possible aortic perivalvular abscess. There was blood flow into the sac and extensive thrombus with mobile component was seen in it. Blood cultures were positive for Streptococcus pneumoniae. Vancomycin, gentamicin, and rifampicin were chosen as antibiotic regimen. Early surgery planned for endocarditis and drained abscess cavity. However, the patient was persistently refused the third heart surgery operation. Repeat TEE showed the absence of vegetation on mitral valve and evident shrinkage of thrombus. Chest X-ray showed large left pleural effusion. Computed tomography with contrast enhancement confirmed this finding and revealed that contrast leak to the periaortic area and spreading a path under pulmonary artery to adjacent of the anterior wall of left ventricle. Thoracentesis was performed. Fistula to left pleura was suspected but not clearly confirmed. At 6 weeks of hospitalization, he clinically deteriorated. Due to confusional state, informed consent was obtained from attending relatives. The patient was transferred to the operating room. Cardiopulmonary resuscitation was initiated and thoracotomy was performed. Dehiscence of the aortic valve was seen. Infected tissues were extracted and repair with new prosthesis aortic valve was performed. Despite all resuscitation efforts, the patient died.

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Self-limited bradyarrhythmias are commonly seen in postorthotopic heart transplantation patients. The most common cause of such bradyarrhythmias is sinus node dysfunction. Atrioventricular (AV) nodal blocks requiring pacemaker implantation remain distinctly uncommon. After ruling out reversible causes including dyselectrolytemia and drug toxicity, prolonged ischemia time of donor heart and transplant rejection should be considered as possible causes. The present case describes an uncommon occurrence of persistent high-grade AV block in postheart transplantation period ultimately requiring permanent pacemaker implantation.

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Cor triatriatum sinister is an extremely rare congenital heart defect. Very few cases have been reported for cor triatriatum associated with mitral regurgitation. We are reporting an exceptional case of cor triatriatum associated with calcified mitral valve resulting mitral stenosis. Preoperatively, mitral stenosis was underestimated due to the presence of restricted communication between two chambers of the left atrium. The patient was operated for cor triatriatum repair with mitral valve replacement.

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Objective: The objective of this study was to determine nebivolol's inhibitory effect on endothelial dysfunction in hyperhomocysteinemic rats, based on heart pathology and biochemical analysis of serum samples. Methods: Male Wistar albino rats weighing between 200 g and 450 g were randomly divided into four groups of equal number (n = 7) as follows: control group, nebivolol group, methionine group, and methionine + nebivolol group. After 28 days, homocysteinemia (Hcy), asymmetric dimethylarginine (ADMA), malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), and catalase (CAT) levels were measured in blood samples and compared between groups. Each rat's hearts were dissected to observe cardiomyocyte degeneration; findings were compared between groups. Results: Moderate hyperHcy (hHcy) (Hcy 35.62 ± 7.60 μmol/L) was noted in methionine group (P < 0.001). The levels of the antioxidant molecules CAT, GSH, GPx, GR, and SOD were lower, and the levels of the oxidant molecules ADMA, Hcy, and MDA were higher in methionine group (P < 0.001). A decrease in antioxidants and also increase in oxidants did not occur in the methionine + nebivolol group (P < 0.001). Cardiomyocyte degeneration was more severe in methionine group (P = 0.01). Conclusion: Endothelial dysfunction induced through short-term hHcy can be prevented through the administration of nebivolol. Nebivolol can prevent elevation of the Hcy levels, and hHcy might cause cardiomyocyte degeneration.

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