Sudden Cardiac Death Following Acute Myocardial Infarction With Obstructive and Nonobstructive Coronary Arteries in Brazilian Patients Receiving Tirzepatide (Mounjaro®): Exploring the Convergence of Plaque Destabilization, Coronary Vasomotor Dystunction, Microvascular Ischemia, Prothrombotic Remodeling, and Cardiometabolic Transition Through a Multimodal Mechanistic Case Report
Authors/Creators
- 1. MD/ Family Medicine UCM Carlos J Finlay, Cuba; General Cardiology, Diplomate in Cardiovascular Diseases/ American College of Cardiology (FACC), USA; Postdoctoral Research Fellow Stem Cell and Patient Care, Harvard Medical School; Associate Professor of European Society of Preventive Cardiology; Medical Office Manager Professional Certificate Johopkins University, USA; EanEmergency & Critical Care
Description
Purpose To investigate sudden cardiac death following acute myocardial infarction with obstructive and nonobstructive coronary arteries in Brazilian patients receiving tirzepatide, examining the interplyy of plaque destabilization, coronary vasomotor dysfunction, microvascular ischemia, and prothrombotic remodeling within the context of cardiometabolic transition.
Methods A multimodal mechanistic case report was conducted, integrating coronary angiography and physiology assessment, cardiac magnetic resonance and coronary computed tomography imaging, microvascular function testing, and circulating biomarker profiling in two Brazilian patients on tirzepatide therapy to evaluate structural, functional, and biochemial mechanisms underlying sudden cardiac death risk.
Results Both cases presented with acute myocardial infarction and subsequent sudden cardiac death; one with obstructive coronary artery disease demonstrating unstable plaque rupture and thrombotic occlusion, and one with nonobstructive coronary arteries exhibiting severe coronary vasomotor dysfunction and microvascular ischemia, elevated thrombogenic markers, and evidence of prothrombotic remodeling.
Tirzepatide use was associated with marked cardiometabolic transition including improved insulin sensitivity and weight loss, yet persistent endothelial dysfunction and heightened thrombotic risk were observed. Multimodal data revealed convergence of microvascular ischemia, autonomic imbalance, and inflammatory/prothrombotic pathways as potential mechanistic drivers.
Conclusion This case series highlights that tirzepatide-mediated cardiometabolic transition may coincide with increased vulnerability to plaque destabilization and vasomotor dysfunction in susceptible Brazilian patients, underscoring that sudden cardiac death risk can arise in both obstructide and nonobstructive coronary artery scenarios. Findings emplasize the need for vigilance in monitoring coronary microvascular health and thrombotic status in patients on tirzepatide, and call for further investigation of GLP-1/GIP dual agonism effects on coronary stability.