ABSTRACT
Background Fulminant myocarditis can cause biventricular dysfunction with a mortality rate over 40%. We report a case with severe biventricular failure due to fulminant myocarditis that was successfully supported by left and right ventricular assist devices. Case A 65-year-old woman presented with chest pain, abdominal pain and diarrhea. She was hypotensive and labs revealed elevated troponin-T of 13.5 ng/mL and lactate of 4.3 mmol/L. She was positive for COVID by antigen testing. She was started on multiple vasopressor infusions and admitted to the intensive care unit. Echocardiogram revealed a severely reduced left ventricular ejection fraction of 15% and severe global hypokinesis. The following day, she developed a wide complex tachycardia that was refractory to amiodarone, lidocaine and multiple defibrillation attempts. She was transferred emergently to the cardiac cath lab where coronary angiography revealed an isolated 70% stenosis of the distal left circumflex artery. A Swan-Ganz catheter was placed that yielded a cardiac index by Fick of 1.2 L/min/m2, systemic vascular resistance of 1270 dynesseccm-5 and mixed venous oxygen saturation of 35%. Decision was made to emergently insert an Impella CP device. That evening, she developed complete heart block and transvenous pacing wire was inserted. Due to frequent suction alarms, decision was made to insert ProtekDuo device, which resulted in hemodynamic stabilization. A temporary coronary sinus pacing lead for atrial capture was inserted to improve atrioventricular synchrony. After several days of monitoring, repeat echocardiogram showed complete recovery of biventricular function and Impella CP and ProtekDuo devices were removed. Decision-making The decision of early implantation of ProtekDuo device was made to provide adequate blood flow to the left ventricular assist device for hemodynamic support. In addition, increased atrioventricular synchrony via insertion of temporary coronary sinus pacing wire improved cardiac output. Conclusion Fulminant myocarditis involving biventricular dysfunction can be supported by the use of simultaneous left and right ventricular assist devices.Copyright © 2023 American College of Cardiology Foundation
ABSTRACT
Introduction: This case identifies vagal tone as a paradoxical cause of coronary artery spasm, coinciding with complete heart block. It will additionally identify proper management in these cases. Clinical Presentation: A 53 year old male with a medical history of HIV not of ART, acute, infectious COVID-19 and late, latent syphilis admitted for malaise, found to have DLBCL. Following a routine blood draw the patient experienced acute chest and abdominal pain. Minutes later, while having a bowel movement he experienced syncope with heart rates in the 30s. EKG showed ST elevations in leads II, III, and aVF. Troponin-T was elevated to 0.15. Echocardiogram showed inferior wall hypokinesis. Coronary angiography showed non-obstructive right coronary disease. Cardiac MRI demonstrated no evidence of infiltrative disease or myocarditis. The patient experienced a similar episode the following morning, during blood draw, EKG and telemetry demonstrated complete heart block with ST elevations (image). This suggested vagal mediated AV block with coronary artery spasm (CAS). He was started on the anticholinergic hyoscyamine and amlodipine for vasodilation. Following initiation of therapy, the patient had no further episodes of chest pain or bradycardia. Discussion(s): While acetylcholine causes vasodilation via endothelial NO, interestingly, it can also lead to CAS. In the setting of vascular smooth muscle cell (VSMC) hyper-reactivity or high vagal tone, VSMC muscarinic receptors are activated leading to vasoconstriction. Vagal tone can cause both CAS with resulting STEMI as well as AV blockade resulting in high degree heart block (image). When ischemic symptoms are accompanied by AV block in the setting of high vagal tone, consider vagal mediated CAS. Calcium channel blockers such as amlodipine are used to manage CAS. When the suspected mechanism is vagal tone, management includes avoidance of precipitating factors and or anticholinergic premedication.