Search

Hydroxychloroquine is a disease-modifying antirheumatic drug used for various rheumatological conditions. Its long-term use is well-known to have toxic effects on cardiac muscle cells. We present a biopsy-proven case of hydroxychloroquine-induced cardiotoxicity with detailed histopathological and imaging findings. The patient was referred to our heart failure clinic for concerns of reduction in left ventricular ejection fraction despite being on guideline-directed medical therapy. She had been diagnosed with rheumatoid arthritis, pulmonary hypertension and then subsequently heart failure with reduced ejection fraction 5 years ago. The evaluation included right heart catheterisation, cardiac MRI and endomyocardial biopsy. Light and electron microscopy showed myocyte hypertrophy and vacuolar change, abnormal mitochondria, myeloid bodies and curvilinear bodies. These findings were specific for hydroxychloroquine-induced cardiomyopathy. This case highlights the importance of clinical monitoring, early suspicion and consideration of drug-induced toxicities as a culprit for heart failure.

Severe hyponatraemia in setting of cardiac tamponade is very rare and only few case reports have been reported so far. This case report highlights pericardial tamponade as a rare but easily treatable cause of severe hyponatraemia. Pertinent literature is also reviewed. A 70-year-old woman presented to the emergency department with altered mental status. She was tachycardic and hypotensive with cardiomegaly on a chest X-ray. Serum sodium was severely low at 109 mmol/L and was identified as the likely cause for her abnormal mentation. She was also in acute renal failure with serum creatinine of 4.1 mg/dL. A transthoracic echocardiogram was done that showed a large pericardial effusion with evidence of tamponade physiology. She underwent emergent pericardiocentesis with rapid improvement in clinical picture and blood pressure. Her serum sodium level rapidly improved and was normal in 48 hours.