A Case of Cardiac Arrest Due to Transcatheter Aortic Valve Infolding.

Prosthetic valvular infolding during transcatheter aortic valve implantation (TAVI) is an under-recognized yet significant complication that can occur. Here, we describe the case of a 61-year-old male with a history of heart failure with reduced ejection fraction (HFrEF) and low-flow, low-gradient severe aortic valve stenosis of a bicuspid aortic valve who presented to undergo TAVI. During the procedure, repositioning of the valve resulted in prosthetic valvular infolding and resultant severe aortic regurgitation (AR), culminating in cardiac arrest. Swift balloon valvuloplasty corrected the valve geometry and eliminated any AR, allowing hemodynamic recovery and completion of the procedure. Our case and review highlight methods, both angiographic and echocardiographic, to recognize prosthetic valvular infolding the moment it presents, as well as strategies to correct the infolding with minimal detriment to the patient.

Naltrexone-Associated Non-ST-Elevated Myocardial Infarction.

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.

COVID-19-Associated Acute Limb Ischemia in a Patient on Therapeutic Anticoagulation.

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).

Marked Sinus Bradycardia Associated With Remdesivir in COVID-19: A Case and Literature Review.

Remdesivir has seen extensive use during the coronavirus disease-2019 pandemic given its clinically proven efficacy against severe acute respiratory syndrome coronavirus type 2. There has been little cited regarding adverse effects. Here we present the case of a patient with marked sinus bradycardia that began acutely on initiation of remdesivir and resolved almost immediately on cessation of the drug. (Level of Difficulty: Beginner.).

Incomplete Trifascicular Block and Mobitz Type II Atrioventricular Block in COVID-19.

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.