Jhawar, Nikita

Abstract Cardiovascular disease is a major cause of mortality among oncologic patients. As cancer therapies continue to evolve and advance, cancer survival rates have been increasing and so has the burden of cardiovascular disease within this population. For this reason, cardio-oncology plays an important role in promoting multidisciplinary care with the primary care provider, oncology, and cardiology. In this review, we discuss the roles of different providers, strategies to monitor patients receiving cardiotoxic therapies, and summarize cancer therapy class-specific toxicities. Continued collaboration among providers and ongoing research related to cardiotoxic cancer therapies will enable patients to receive maximal, evidence-based, comprehensive care.

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.

A previously healthy person in their 60s with progressive shortness of breath and fatigue for the past 6 months presented to the emergency department with palpitations and shortness of breath. What is your diagnosis?

Abstract Testosterone therapy is commonly utilized to treat hypogonadism. After diagnosis with morning serum testosterone level in patients with symptoms of hypogonadism, therapy has been shown to improve symptoms. Research focusing on cardiovascular risks associated with testosterone therapy has produced contradictory statements. We review trials that have investigated the impact of testosterone supplementation on heart failure, coronary artery disease, and myocardial ischemia.

Abstract Transthyretin cardiac amyloidosis is a progressive disease known to cause heart failure, conduction anomalies, and arrythmias. Due to poor outcomes and mortality from severe cardiomyopathy, prevalence and incident rates are often underreported. As global longevity is increasing and rates of amyloidosis are also increasing, there is a need to improve diagnostic and therapeutic interventions. Previously, symptom management and transplantation were the mainstay of treatment for heart failure symptoms, but studies using RNAi and siRNA technologies have shifted the paradigm of therapeutic strategy in amyloid cardiomyopathy management. Additionally, early detection and clinical monitoring with numerous imaging and non-imaging techniques are being increasingly investigated. Here, we review the epidemiology, pathophysiology, diagnosis, and management of transthyretin amyloid cardiomyopathy.

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.