Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been found to cause multiple complications across several organ systems in patterns not typically observed in previous iterations of the virus. Hemostatic mechanisms have been noted to be significantly altered in particular, resulting in a disseminated intravascular coagulation (DIC)-like picture with elements of coagulopathy as well as hypercoagulability. A 65-year-old man with hypertension, hyperlipidemia, prior tobacco use, chronic kidney disease, and diabetes presented from a correctional facility with hypoxia. The diagnosis of COVID-19 was confirmed. With his elevated D-dimer of >7,955 ng/mL (reference: 90-500 ng/mL) in the setting of COVID-19 and hypoxia, he was empirically started on therapeutic anticoagulation with enoxaparin. His oxygen requirements increased, mental status deteriorated, and platelets began falling, raising concern for heparin-induced thrombocytopenia versus DIC. Heparin products were discontinued in favor of a direct oral anticoagulant. He later became obtunded and unable to tolerate oral medications. Fondaparinux was initiated. Two days later, he was found to have acute limb ischemia of the right lower extremity. He underwent surgical thrombectomy but required an above-the-knee amputation the following day. Shortly after he died secondary to hypoxic respiratory failure. This case highlights the derangement of hemostatic mechanisms seen prominently in COVID-19 infection and raises questions as to appropriate anticoagulant choices to adequately prevent thrombosis. Thorough physical exams should be performed on all patients with COVID-19, taking into account this documented hypercoagulability. Further investigation is warranted into the use of heparin products as the anticoagulant of choice in these patients given observed deficiencies of antithrombin III (ATIII).

A 74-year-old female with a history of diabetes presented with chest pain and shortness of breath for two days. She was hypoxic to an oxygen saturation of 60% in the emergency department, requiring bilevel positive airway pressure (BiPAP) to maintain saturations. Chest X-ray demonstrated bilateral hazy opacities suspicious for viral pneumonia. Coronavirus disease 2019 (COVID-19) was confirmed. Right bundle branch block (RBBB) with left anterior fascicular block was noted on admission electrocardiogram (ECG). Cardiac enzymes and brain natriuretic peptide levels were within normal limits. After noting frequent pauses on telemetry, a repeat ECG was performed that demonstrated RBBB with left posterior fascicular block as well as second-degree atrioventricular block (Mobitz type II). Transcutaneous pacing pads were placed, and atropine was placed at the bedside. Cardiac enzymes remained negative. Interleukin-6 levels were elevated at 159 pg/mL. Hydroxychloroquine was deferred due to the patient's arrhythmia and prolonged QTc. Tocilizumab was deferred due to the patient's age. The patient's oxygen requirements and mental status continued to worsen. She continued to desaturate despite maximal BiPAP therapy and eventually died. Cardiac involvement in COVID-19, whether caused primarily by the virus, secondary to its clinical sequelae, or even due to its treatment, cannot be ignored. Further high-quality research is needed to clarify the cardiac pathophysiology. Thorough cardiac exams with electrocardiographic correlation should be performed on all patients with COVID-19. Clinicians should not hesitate to consult cardiovascular services in the event of abnormality.

Medications for opioid use disorder (MOUD) and opioid agonist therapy (OAT) are the mainstays of treatment in opioid use disorder. Significant caution is encouraged upon initiation to reduce the precipitation of opioid withdrawal. Cardiac events in the setting of opioid withdrawal are rare and incompletely understood. A 46-year-old woman with a history of opioid-use disorder, hypertension, hyperlipidemia, diabetes, tobacco-use disorder, and rheumatoid arthritis presented with nausea, vomiting, and lightheadedness after taking naltrexone following buprenorphine. She was found to be hypertensive and tachycardic in the emergency department, with a troponin of 0.38 ng/mL (reference: 0.00-0.30 ng/mL) and an electrocardiogram (ECG) without ST or T-wave changes. She was admitted for a non-ST-elevation myocardial infarction (NSTEMI) and hypertensive emergency in the setting of opioid withdrawal. Her blood pressure was controlled, and she received full-dose aspirin and high intensity atorvastatin. Afterwards she was started on a modified OAT regimen of buprenorphine 8 mg daily. Her cardiac enzymes down-trended and her condition became stable after which she was discharged home. Cardiac events are an uncommon yet lethal occurrence in opioid withdrawal. The likely etiology of NSTEMI in our patient was demand ischemia induced by opioid withdrawal, augmented by her various other cardiac risk factors. Practitioners should be aware of these possible adverse events, especially in those with preexisting cardiac disease. Meticulous efforts should be made to instruct patients as to the proper dosing schedule when initiating opioid therapy, and when initiating MOUD/OAT in order to prevent poor outcomes.

INTRODUCTION: Takotsubo cardiomyopathy (TCM) is characterized by transient systolic dysfunction resulting in hallmark apical ballooning/hypokinesis without the presence of coronary artery disease.1 The pathophysiology entails extreme stress, which generates a sudden and massive surge of catecholamines which then markedly deranges cardiac contractility.1 One source of the catecholamine surge is pheochromocytoma: a catecholamine secreting tumor of the chromaffin cells.2 We present the case of patient who presents with both TCM and a suspected pheochromocytoma. CASE PRESENTATION:A 56-year-old female with history of both STEMI and NSTEMI presented with chest pain, nausea, vomiting, and lightheadedness. Blood pressure was 197/119 mmHg on admission. Cardiac enzymes were normal, however ECG demonstrated new lateral ST elevations in V4-V6. TTE showed apical and anterolateral akinesis with a markedly reduced EF of 18%. Nitroglycerin infusion was initiated, and patient was transferred emergently for cardiac catheterization. Patent coronary vessels were found, no intervention was performed, and medical management was pursued. Echocardiographic and catheterization findings were consistent with TCM. Further chart review showed multiple similar prior episodes plus a prior CT scan which demonstrated a 2 cm adrenal mass. Given clinical suspicion, workup for pheochromocytoma was initiated. Plasma and spot-urine metanephrines, plus spot-urine normetanephrines and 24-hour urine metanephrines were within normal limits. Plasma normetanephrines, 24-hour urine normetanephrines, epinephrine, norepinephrine, and dopamine were elevated at 731.7 pg/mL, 1538 ug/24 hours, 83 pg/mL, 4213 pg/mL, and 1020 pg/mL respectively.The patient's blood pressure was eventually controlled with oral medications. She was initiated on goal-directed medical therapy for her newly reduced EF and discharged home with endocrinology follow-up.DISCUSSION: Detection of pheochromocytoma is elusive and largely depends on elevated catecholamines in urine or blood samples via 24-hour collection. The difficulty lies in the fact that the secretion is intermittent. Measurement of VMA in urine can be done yet despite a high specificity (95%) there is a low sensitivity (64%).3 Pheochromocytoma can result in mass catecholamine release with systemic manifestations, affecting cardiac contractility.CONCLUSIONS: Our patient presented with TCM from a suspected pheochromocytoma. This diagnosis was reached via a combination of echocardiographic imaging showing apical and anterolateral akinesis, not consistent with any single coronary distribution, a clean coronary catheterization, and several lab panels demonstrating elevated levels of catecholamines/ metanephrines in both the blood and urine.

No abstract