Naslov
Is there any connection between severity of acute pancreatitis and electrocardiographic changes?

Autori
Štimac, Davor ; Tomulić, V. ; Hauser, Goran ; Jakljević, T. ; Radić, M.

Izvornik
Journal of clinical gastroenterology (0192-0790) 40 (2006), 6; 559-560

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, pismo, stručni

Ključne riječi
acute pancreatitis; electrocardiographic changes

Sažetak
To the Editor: It was a great pleasure to read the article written by Rubio TA et al, 1 regarding electrocardiographic (ECG) abnormalities in patients with acute pancreatitis (AP). The authors concluded, among others, that severity of AP, determined by Atlanta criteria, and serum amylase and lipase levels do not correlate with changes in ECG. Based upon their results, the leading ECG abnormalities were nonspecific changes of repolarization defined as the presence of flat or inverted T waves in different leads. Authors explained the observed ECG changes with metabolic disbalance. We conducted a prospective study2 in which we aimed to investigate the connection of AP severity and ECG changes. Three hundred three patients with AP admitted to our clinic between February 2001 and December 2004 were enrolled. Two groups were defined according to Atlanta criteria of AP severity. There were 149 (49.2%) mild AP patients and 154 (50.8%) severe AP patients. Both groups were similar in demographic characteristics, etiology of AP, and serum potassium level. Our results strongly supported the association of AP severity and ECG changes. The groups were significantly different in heart rate (82.7± ; ; 19.3 vs. 88.0± ; ; 21.7 bpm ; P=0.0256), PQ interval (152.9± ; ; 36.2 vs. 140.7± ; ; 52.1 ms, P=0.0189), and ST segment depression or elevation (17, 11.4% vs. 41, 26.7% ; P=0.0012). Higher heart rate and shortening of PQ interval could be explained by stronger activation of sympathetic nervous system in severe AP.3 Cause of increased ST segment abnormalities in severe group remained unclear. Possible explanations could be increased level of catecholamines, preexisting latent ischemic heart disease or stronger activation of proinflammatory cytokines.

Izvorni jezik
Engleski

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