A Fatal Consequence: Amiodarone-Induced Multiorgan Toxicity.

Amiodarone is commonly used nowadays for the treatment of atrial fibrillation (AF). The wide use of this medication has led to the occurrence of adverse events, including pulmonary toxicity, hepatotoxicity, thyroid dysfunction, and many others. Higher doses of Amiodarone of ≥400 mg/day have been linked to increased complications. We present a case of a 70-year-old male with multivessel coronary artery disease (CAD) with ischemic cardiomyopathy and severe peripheral artery disease (PAD) who underwent an elective left femoral to posterior tibial bypass surgery followed by percutaneous coronary intervention (PCI) complicated by new-onset AF. The patient was loaded with 150 mg of intravenous (IV) Amiodarone followed by 360 mg infusion over six hours for chemical cardioversion. The patient was then maintained on oral Amiodarone 400 mg/day until the day of presentation when he complained of progressive dyspnea. Imaging was significant for diffuse ground glass opacities and interstitial thickening. The echocardiogram revealed an improved ejection fraction (EF) of 40% from 20%. The patient had worsening oxygenation despite adequate IV diuresis and developed severe acute respiratory distress syndrome (ARDS) requiring mechanical ventilation (MV). A bronchoscopy with bronchoalveolar lavage (BAL) showed diffuse alveolar hemorrhage (DAH) with a high lymphocyte count and negative infectious disease testing. Lab tests revealed elevated liver enzyme levels. There were also changes in thyroid function from baseline with elevated free T4 at 1.83 ng/dL (0.8-1.4 ng/dL), suppressed thyroid stimulating hormone (TSH) at 0.109 mIU/mL (0.4-4 mIU/mL), negative anti-thyroglobulin (TG) antibodies, and anti-thyroid peroxidase (TPO) antibodies indicating a type 2 Amiodarone-induced thyrotoxicosis. Unfortunately, the patient's condition deteriorated further despite appropriate treatment, and it was ultimately followed by his demise. Severe, fatal cases of Amiodarone toxicity are scarce, but more reports are being seen. We strongly believe clinicians should have a high index of suspicion for Amiodarone-related adverse events in elderly males with cardiopulmonary comorbidities. It is imperative to have an increased understanding, greater vigilance, and closer monitoring of pulmonary function tests (PFTs), laboratory tests, and imaging studies.

A Novel Case of Acquired Isolated Left Ventricular Non-compaction in a Primigravida: Revisiting the Diagnostic Criteria of Left Ventricular Non-compaction.

Left ventricular non-compaction (LVNC) is rare cardiomyopathy characterized by the presence of a two-layered myocardium with prominent trabeculations. It has high rates of mortality and morbidity. Clinical presentation could vary from asymptomatic patients to developing ventricular arrhythmias, thromboembolism, heart failure, and even sudden cardiac death. We present a 23-year-old primigravida with a childhood history of dilated cardiomyopathy secondary to post-viral myocarditis presenting at 32 weeks gestation with dyspnea on exertion. Initial 2-D echocardiogram revealed a mildly dilated left ventricle with apical trabeculation and a 2-layer distinction between compacted and noncompacted myocardium indicating non-compaction of the left ventricle. This case presents a peculiar confluence of cardiac genetics, normal physiology, and infection. We describe a rare form of acquired LVNC that transformed from another type of cardiomyopathy to LVNC during pregnancy drawing attention to the causality pathways of LVNC.

Acute myocarditis in bodybuilder from coxsackievirus and thyrotoxicosis.

A 25-year-old male with no past medical history presented with 1 day of chest pain. The patient had exercised with high intensity for a bodybuilding competition. He had fever, malaise, sore throat, and cough 1 week before presentation. He was tachycardic and tachypneic. Cardiac examination was unremarkable. Electrocardiogram showed diffuse ST segment elevation. Laboratory results showed leukocytosis, creatinine kinase 3078 unit/L, and troponin I 78.06 ng/mL. Coronary angiography revealed no occlusion. Echocardiogram showed ejection fraction of 45% with global hypokinesis. The next day, the patient became dyspneic, hypoxic, and hypotensive. Chest X-ray showed pulmonary edema requiring intubation for respiratory failure. Inotropic support and intra-aortic balloon pump were started. A viral panel was ordered and antibody titer of coxsackievirus B type 4 was ≥1:640. On obtaining further history, it was found that he took liothyronine 75 mcg daily for 3 weeks. Thyroid-stimulating hormone was 0.015 U/mL and free T3 was 4.4 ng/mL. Burch-Wartofsky score was 75. Methimazole and hydrocortisone were started. Cardiac magnetic resonance imaging showed diffuse myocardial inflammation and edema. There was multifocal dense epicardial and midmyocardial necrosis in all segments. The patient was discharged on metoprolol and enalapril. The patient was instructed to refrain from supplements. .