Jhawar, N

Ischemic symptoms may be explained by a multitude of coronary pathologies, including coronary artery tortuosity, atherosclerosis, fibromuscular dysplasia, vasculitis, coronary vasospasm, or microvascular disease. We present an unusual case of coronary kinking in a patient presenting with exertional jaw pain in the absence of atherosclerotic risk factors. Multimodality imaging, coronary imaging, and coronary physiology helped establish the diagnosis and guide management.

AbstractBackgroundAmyloidosis is a systemic disorder of abnormal protein folding and deposition resulting in a range of symptoms including neuropathy, heart failure, renal disease, and dermatologic findings. The two most common types of amyloidosis that affect the heart are transthyretin (ATTR) amyloidosis and light chain (AL) amyloidosis, which vary in clinical presentation. Skin findings such as periorbital purpura are considered more specific for AL amyloidosis. However, there are rare cases of ATTR amyloidosis causing the same dermatologic findings.Case SummaryA 69-year-old female presented for evaluation of amyloidosis after cardiac imaging done at the time of a recent atrial fibrillation ablation showed signs of infiltrative disease. On examination, she had periorbital purpura which she reportedly had for years without receiving a diagnosis, as well as macroglossia with teeth indentation. These exam findings, in addition to her transthoracic echocardiogram showing apical sparing, are typically considered characteristic of AL amyloidosis. Subsequent workup revealed the presence of hereditary ATTR (hATTR) amyloidosis with a heterozygous pathogenic variant in the TTR gene producing the p.Thr80Ala mutation.ConclusionSpontaneous periorbital purpura is thought to be pathognomonic for AL amyloidosis. However, we describe a case of hereditary ATTR amyloidosis with the Thr80Ala TTR genetic variant presenting initially with periorbital purpura, the first case documented in the literature to our knowledge.

Abstract Background: Prescribing physicians must be aware of drug-drug interactions and exercise caution to prevent life-threatening electrolyte abnormalities. Here, we present a case of hyperkalemia-induced cardiac arrest in a patient treated with lisinopril with underlying chronic kidney disease and a recent course trimethoprim-sulfamethoxazole. We emphasize the need for awareness and vigilance when reconciling medications to thwart life-threatening consequences of even seemingly benign drug interactions. Case presentation: A 55-year-old male was brought to the emergency room after being found unresponsive and pulseless for an unknown period due to cardiac arrest. Resuscitative efforts were successful in achieving return of spontaneous circulation after 15 minutes. In the emergency department, he was found to have a potassium level of 6.9. Further history obtained from the medical proxy revealed that the patient recently completed a course of trimethoprim-sulfamethoxazole, and he had underlying past medical history of chronic kidney disease and hypertension requiring treatment with lisinopril. The patient was subsequently transferred to the intensive care unit for neuroprognostication after arrest, continuous renal replacement therapy, and pressor support. Workup to investigate other causes of his arrest was unremarkable, leaving drug-induced hyperkalemia as the leading diagnosis made by exclusion. Conclusions: We underscore the need to recognize drug interactions when prescribing new medications and the potential complications they may have in patients with particular risk factors. In this case, our patient had underlying chronic kidney disease and hypertension requiring management with lisinopril. The addition of TMP-SMX precipitated life-threatening hyperkalemia which caused his cardiac arrest. We underscore the importance of preventing dangerous arrhythmias through detailed medication reconciliations and diligence when prescribing new medications to prevent adverse interactions.