Pancreatitis with Electrocardiographic Changes Mimicking Acute Myocardial Infarction

Abstract

A 64-year-old woman with mild acute pancreatitis presented with epigastric pain, nausea and vomiting while undergoing hemodialysis for chronic renal insufficiency. Serial electrocardiograms revealed new onset ST segment elevations in leads V2 to V4 mimicking an anterior myocardial infarction, followed by diffusely inverted deep T waves. No cardiac pathology was demonstrated by echocardiography or coronary angiography. A review of the literature and possible pathophysiological mechanisms of electrocardiographic changes in acute pancreatitis, such as metabolic abnormalities, hemodynamic instability, vasopressors, pericarditis, myocarditis, a cardiobiliary reflex, exacerbation of underlying cardiac pathology, coagulopathy and coronary vasospasm, are discussed.

T-wave depletion and bradycardia possibly secondary to acute pancreatitis: Review of the literature

“…In one case, there were concomitant wall motion abnormalities in echocardiography examination (5). In some patients, the coronary angiogram was normal, thus totally excluding the coexistence of CAD (5)(6)(7)(8). Undoubtedly, in such cases, there is a considerable diagnostic and therapeutic challenge for the clinician.…”

“…Electrocardiography changes mimicking acute myocardial infarction (AMI) in patients with acute pancreatitis have been reported in the literature (1,(5)(6)(7)(8). In these cases, cardiac-specific enzymes remained within normal levels, suggesting that ST-segment elevation was not due to AMI.…”

“…Various hypotheses have been formulated for the underlying mechanism of electrocardiography abnormalities and/or myocardial damage in acute pancreatitis (7)(8)(9)(10). These include toxic effects of the pancreatic proteolytic enzymes on the myocardium, autonomic imbalance with vagal predominance, coronary artery spasm, metabolic and electrolyte abnormalities, prothrombotic derangements, hemodynamic instability, and systemic inflammatory response-induced cardiac damage.…”

QT interval changes and reversibility of QT dispersion in patients with acute pancreatitis

“…Although the exact mechanism of cardiovascular changes remain topics of continued research, various hypotheses have been speculated for the underlying mechanism of electrocardiographic changes during the course of AP, including toxic effects of the pancreatic proteolytic enzymes such as myocardial depressant factor and kinins on the myocardium, autonomic imbalance with vagal predominance, coronary artery spasm, metabolic and electrolyte abnormalities, prothrombotic derangements, hemodynamic instability, and systemic inflammatory response-induced cardiac damage (22)(23)(24)(25).…”

Abnormal Cardiovascular Findings in Acute Pancreatitis: Are They Associated with Disease Severity?

“…Mechanisms such as myocardial ultrastructural disturbances 10 , release of pancreatic proteolytic enzymes 11 , hypovolemia, cytokines 4 , electrolyte disturbances 3,4 , and hemodynamic instability have been previously proposed 12 .…”