We report the case of a 30-year old man who came to the emergency department of our hospital with acute left heart failure, and was diagnosed with a rare congenital anomaly (cor triatriatrum sinister), which can mimic a severe mitral stenosis. Cor triatriatum sinister is a rare anomaly (0.1% of all cases of congenital heart disease) that is seldom diagnosed in adult patients. The hallmark of this congenital defect is the presence of a fibromuscular membrane that divides the left atrium (LA) into two chambers: a postero-superior chamber into which the pulmonary veins drain and an infero-anterior chamber (true LA) containing the mitral valve and atrial appendage. Both chambers communicate through a membrane in which one or more drain holes can be found. When the hole is significantly obstructive, it results in increased venous and arterial pressures. Even though the definitive treatment of cor triatriatum is the surgical excision of the membrane, we present a balloon dilatation case with a good response to percutaneous therapy, both initially and in the ensuing months.Heart failure † Cor triatriatum sinister † Percutaneous repair Cor triatriatum sinister is a rare anomaly accounting for 0.1% of all cases of congenital heart disease. It is seldom diagnosed in adult patients.
Case reportWe report a case of a 30-year-old male who presented to the Emergency Department complaining of fatigue, shortness of breath, and cough on exertion. The patient had been developing progressive symptoms over the past 6 weeks. During the past week the cough had worsened and he had also observed that expectoration was frequently stained with blood. His past medical history and family history were unremarkable. He worked as an information technology technician until he became ill.Shortly after arrival, the patient suffered a witnessed episode of large volume haemoptysis estimated to be . 250 mL of fresh blood. On physical examination, he appeared uncomfortable and in distress, and continued to cough up small amounts of blood. Vital signs were notable for a blood pressure of 101/60 mmHg, a regular pulse rate of 120 b.p.m., a respiratory rate of 36 breaths/ min, and an oxygen saturation of 93% on 100% oxygen via a highflow face mask. The cardiac exam demonstrated tachycardia, a normal S1, and an increased S2, probably in the context of pulmonary hypertension; however, the murmur was clearly diastolic, most probably in relation to the obstructive nature of the membrane.The lungs were notable for the presence of bilateral low-pitched rhonchi predominantly on the right side. Extremities were slightly cool, without cyanosis, clubbing, or oedema.The patient underwent immediate endotracheal intubation in order to secure the airway and was transferred to the Intensive Care Unit.The electrocardiogram showed sinus tachycardia and left atrial enlargement. Chest X-ray showed pulmonary artery enlargement and signs of venous hypertension. Transthoracic echocardiography (TTE) demonstrated the presence of a thin echo-bright membrane attached medially to ...
The benefits obtained with cardiac resynchronization therapy are directly related to the occurrence of continuous biventricular pacing. We report a case of intermittent loss of biventricular pacing due to ventricular oversensing that worsened the functional status of the patient.
A 64-year-old man with history of hyperlipidemia and type 2 diabetes mellitus presented with sudden onset of atypical chest pain and dyspnea at rest. He denied palpitations or dizziness. Examination revealed blood pressure of 132/ 81 mm Hg and a heart rate of 153 bpm. The ECG showed a wide-QRS-complex tachycardia compatible with a sustained monomorphic ventricular tachycardia ( Figure 1). An amiodarone drip was started, and the tachycardia abruptly terminated during the infusion. In the ECG performed shortly after (Figure 2), normal sinus rhythm with T-wave inversion (transient) in the lateral leads (I, aVL) was evident, probably related to cardiac memory phenomenon. There was no evidence of further arrhythmias while the patient was maintained on oral amiodarone treatment. A chest x-ray showed moderate cardiomegaly and an abnormal left mediastinal contour owing to a bulge in the surface of the left ventricle ( Figure 3A and 3B). A transthoracic echocardiogram was performed, demonstrating a normal-size left ventricle, with mild septal hypertrophy, normal systolic function of both ventricles, and no pericardial effusion. A coronary angiography excluded any occlusive disease but revealed a cardiac mass with multiple "feeding" collaterals from the left anterior
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