Electrocardiographic abnormalities caused by acute pancreatitis

Abstract

A 51-year-old man presented with severe acute upper abdominal pain and elevated serum levels of pancreatic enzymes due to acute pancreatitis associated with alcohol consumption. On admission, his heart rate was 60 beats per min, blood pressure was 90/65 mmHg, and temperature was 37.1°C. There were no signs of right-sided heart failure. The heart sounds were normal, no murmurs, and no pericardial friction rubs were heard. The electrocardiogram (ECG) on admission (Fig. 1) demonstrated sinus rhythm, normal axis, normal conduction and generalised aspecific ST-segment abnormalities. The ST-segment abnormalities were not limited to a specific coronary territory. Serum electrolytes and cardiac markers were normal. Transthoracic echocardiography demonstrated a normal left ventricular function, without valvular abnormalities or pericardial effusion. Coronary angiography was normal. The patient received general supportive care including fluid administration and pain control. After 4 days the electrocardiogram had substantially improved (Fig. 2).Previous studies have described the association between pancreatitis and ECG abnormalities; up to 50% of patients hospitalised for acute pancreatitis have nonspecific ST-T changes, diffuse T-wave inversions or STsegment elevation [1,2]. Transient wall motion abnormalities may also be present in patients with acute pancreatitis in the absence of coronary artery disease [1]. Potential pathophysiological mechanisms are circulating proteolytic enzymes, a vagally mediated reflex or systemic inflammatory response [1][2][3][4].

Diastolic dysfunction, prolonged QTc interval and pericardial effusion as predictors of mortality in acute pancreatitis

“…In its more severe form, involvement of any organ system is possible. The effect of pancreatitis on cardiovascular system has received comparatively little attention …”

“…Acute pancreatitis has a wide spread effect involving multiple organ systems and involvement of the cardiovascular system has also been observed. The cardiovascular changes include hemodynamic alterations, electrocardiographic (ECG) changes and pericardial alterations . The hemodynamic changes described include increased cardiac index, tachycardia, myocardial depression, regional wall motion abnormalities, diastolic dysfunction, and decreased peak blood flow velocity .…”

“…The hemodynamic changes described include increased cardiac index, tachycardia, myocardial depression, regional wall motion abnormalities, diastolic dysfunction, and decreased peak blood flow velocity . Similarly a wide range of ECG changes including arrhythmias, bradycardia, T‐wave changes, intraventricular conduction disturbances, and ST‐segment elevation (pseudo‐infarction) have also been described . Also pericardial changes like pericardial effusion, chylous pericardial effusion and fibrinous constrictive pericarditis have been described in patients with acute pancreatitis .…”

Acute Pancreatitis Simulating Myocardial Infarction: A Challenging Case

“…We have tabulated acute pancreatitis-induced cardiovascular complications in The pathophysiology of acute pancreatitis-induced MI is complex and not fully understood. It is thought to involve a combination of direct and indirect effects on the heart, including damage to the blood vessels, hypercoagulability, and changes in cardiac function [13]. Several risk factors can increase the likelihood of developing AMI in this setting, which include advanced age, any previous heart disease, and a history of smoking [8].…”

Acute Pancreatitis Masquerading as Inferior Wall Myocardial Infarction: A Review

“…Although ischemic ECG findings have been known to present in pancreatitis from the 1930s, these generally lacked 12-lead ECG data and standardized nomenclature [3, 4]. Since Bauerlein and Stobbe in 1954 [5], 36 instances of such mimicry have been noted, as shown in Table 1,Table 2, and Table 3 [5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38] (clinical course, diagnostic testing, and patient outcome was not specified in one report and was omitted in the prevalence values for the respective categories). An inferior wall infarction pattern appears to be the most frequent (44.4%, or 16/36 cases).…”