A CASE OF CARDIOGENIC SHOCK DUE TO ISCHEMIA WITH NO OBSTRUCTIVE CORONARY ARTERY DISEASE (INOCA)

Document Type

Conference Proceeding

Publication Date

6-27-2024

Publication Title

J Gen Intern Med

Keywords

gadolinium, lactic acid, troponin, adult, artery embolism, blood clotting, cardiogenic shock, cardiovascular magnetic resonance, case report, clinical article, complication, computer assisted tomography, conference abstract, coronary angiography, coronary artery dissection, coronary artery spasm, coronary stenosis, diagnosis, differential diagnosis, drug therapy, echocardiography, electrocardiogram, electrocardiography, emergency ward, exertional dyspnea, heart catheterization, heart infarction, heart palpitation, heart ventricle function, high anion gap metabolic acidosis, human, hypertransaminasemia, hypokinesia, intravenous drug administration, invasive ventilation, ischemia, lung artery pressure, male, muscle contraction, nausea, non-obstructive coronary artery disease, obstructive coronary artery disease, prevalence, risk factor, sinus tachycardia, tachycardia, traffic accident, transesophageal echocardiography, traumatic brain injury, uremia, vomiting

Abstract

CASE: A 25-year-old white gentleman with a past medical history of a traumatic brain injury after a motor vehicle accident and previous tobacco use presented to the Emergency Department with a chief compliant of subacute dyspnea on exertion associated with palpitations and nausea with vomiting. He was initially found to be hemodynamically stable and tachycardic with workup showing an elevated BNP, mildly elevated troponins and electrocardiogram demonstrating sinus tachycardia. His transthoracic echocardiogram (TTE) revealed a newly decreased ejection fraction (EF) of 15%, a large 3.3 cm left ventricular (LV) thrombus, right ventricular dysfunction, and estimated pulmonary artery pressure of 33 mmHg. He quickly decompensated and required increasing oxygen supplementation and invasive ventilation, as well as vasopressor and inotropic support. His labs were suggestive of end-organ dysfunction including high anion gap metabolic acidosis, azotemia, transaminitis, abnormal coagulation profile, severely elevated BNP and elevated lactate. Following stabilization, he underwent a Cardiac MRI (cMRI) that showed a severely dilated and hypokinetic LV, decreased perfusion of the basal anterior wall, transmural late gadolinium enhancement in the basal anterior and antero-septal wall with central low sign suggesting acute necrosis and/or microvascular obstruction. Due to these results, he underwent a left heart catheterization, which showed non-obstructive coronary artery disease and no signs of an acute plaque rupture or thrombus. IMPACT/DISCUSSION: INOCA is caused by a lack of perfusion into the myocardium with normal or near normal coronary arteries shown in coronary angiography. This condition has several potential etiologies including coronary vasospasm, spontaneous coronary artery dissection, microvascular dysfunction and coronary artery embolism (CE). CE is a rare cause of INOCA and has a prevalence of around 3%. According to the criteria proposed by Shibata et al, this would be a case of probable CE based on two minor criteria: less than 25% of coronary artery stenosis and evidence of embolic source based on TTE, transesophageal echocardiography, computed tomography, or cMRI. CONCLUSION: Myocardial infarction or ischemia in the absence of obstructive coronary artery disease (INOCA) is still under-diagnosed, and its complications can be devastating. CE is a rare cause of INOCA, and should be part of the differential diagnosis, especially in the presence of embolic risk factors.

Volume

39

First Page

S215

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