No abstract

Cardiac sarcoidosis (CS) can be silent in most patients with extrapulmonary sarcoidosis. Atrioventricular (AV) block is the most common clinical presentation, but it can also present as fatal ventricular arrhythmias and sudden cardiac death. Endomyocardial biopsy is the gold standard; however, it is not sensitive since CS can involve the myocardium in a patchy distribution. Our case depicts a female who presented with syncope; however, her hospital course was complicated by multiple cardiac arrests. Her initial laboratory tests, including an autoimmune workup, were unremarkable. Cardiac magnetic resonance and fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging revealed intramyocardial delayed enhancement of the basal anteroseptal (non-ischemic distribution) and patchy foci of increased uptake in the anteroseptal and inferior myocardial region, respectively. The patient was started on intravenous methylprednisolone, and her condition slowly improved. Post-discharge, the patient followed in the outpatient clinic with a repeat FDG-PET scan revealing resolution of myocardial FDG uptake. She also underwent bronchoscopy with lymph node biopsy showing granulomas and endobronchial biopsy confirming pulmonary sarcoidosis.

Anomalous aortic origin of coronary arteries from the opposite sinus (AAOCA) is a rare finding which, when discovered, raises questions regarding its approach and management. Modern imaging techniques can help us to identify certain anatomical features of the anomalous coronary arteries to further classify them as benign or malignant anomalies. We present a case of a 64-year-old male who had an incidental finding of AAOCA with the left anterior descending artery arising from the right coronary cusp from an ostium anterior to the one that gave rise to both the left circumflex artery and right coronary artery (RCA). The patient was managed with a percutaneous coronary intervention for an obstructive disease of the RCA and was discharged with regular follow-ups.

Thrombocytopenia is defined as a condition where the platelet count is below the lower limit of normal (<150 G/L), and it is categorized as mild (100–149 G/L), moderate (50–99 G/L), and severe (<50 G/L). We present here a 79-year-old man who developed severe thrombocytopenia with a platelet count of 6 G/L, less than 24 hours after intravenous tirofiban infusion that was given to the patient during a percutaneous transluminal coronary angioplasty procedure with placement of 3 drug-eluting stents. The patient's baseline platelet count was 233 G/L before the procedure. Based on the timeline of events during hospitalization and laboratory evidence, it was highly likely that the patient's thrombocytopenia was the result of tirofiban-induced immune thrombocytopenia, a type of drug-induced immune thrombocytopenia (DITP) which occurs due to drug-dependent antibody-mediated platelet destruction. Anticoagulant-mediated artefactual pseudothrombocytopenia was ruled out as no platelet clumping was seen on the peripheral blood smears. The treatment of DITP includes discontinuation of the causative drug; monitoring of platelet count recovery; or treatment of severe thrombocytopenia with glucocorticoids, IVIG, or platelet transfusions depending on the clinical presentation. The most likely causative agent of this patient's thrombocytopenia—tirofiban—was discontinued, and the patient did not develop any signs of bleeding during the remainder of his hospital stay. His platelet count gradually improved to 24 G/L, and he was discharged on the sixth hospital day.

A 66-year-old female presented to the emergency room with an episode of chest pain that lasted for a few minutes before resolving spontaneously. Electrocardiogram showed a left bundle branch block, left ventricular hypertrophy, and T wave inversions in the lateral leads. Initial cardiac troponin level was 0.15 ng/ml, with levels of 4 ng/ml and 9 ng/ml obtained 6 and 12 hours later, respectively. The peak blood pressure recorded was 195/43 mmHg. Echocardiogram with DEFINITY showed a small left ventricular cavity with apical hypertrophy, and coronary angiogram showed no stenotic or occluding lesions in the coronary arteries. The patient was admitted for a type 2 myocardial infarction with hypertensive crises. She was diagnosed with having apical hypertrophic cardiomyopathy, which is a variant of hypertrophic cardiomyopathy (HCM) in which the hypertrophy predominantly involves the apex of the left ventricle resulting in midventricular obstruction, as opposed to the left ventricular outflow tract obstruction seen in HCM. Patients with apical HCM may present with angina, heart failure, myocardial infarction, syncope, or arrhythmias and are typically managed with medications like verapamil and beta-blockers for those who have symptoms and antiarrhythmic agents like amiodarone and procainamide for treatment of atrial fibrillation and ventricular arrhythmias. An implantable cardioverter defibrillator (ICD) is recommended for high-risk HCM patients with a history of previous cardiac arrest or sustained episodes of ventricular tachycardia, syncope, and a family history of sudden death.