Table of Contents  
ORIGINAL ARTICLE
Year : 2015  |  Volume : 8  |  Issue : 2  |  Page : 196-198  

Electrocardiographic changes in patients with acute pancreatitis


1 Department of Internal Medicine, Findikli State Hospital, Agri, Rize, Turkey
2 Department of Cardiology, Sakarya University Faculty of Medicine, Sakarya, Turkey
3 Department of Internal Medicine, Taslicay State Hospital, Agri, Rize, Turkey
4 Department of Internal Medicine, Sakarya University Faculty of Medicine, Sakarya, Turkey
5 Department of Gastroenterology, Sakarya University Faculty of Medicine, Sakarya, Turkey

Date of Web Publication13-Mar-2015

Correspondence Address:
Selcuk Yaylaci
Department of Internal Medicine, F?nd?kl? State Hospital, Rize
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-2870.153159

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  Abstract 

Background and Aims: Multiple organ system dysfunctions especially cardiovascular manifestations are frequently seen in severe acute pancreatitis (AP). The aim of this study was to investigate the frequency and type of electrocardiographic (ECG) abnormalities present in patients with AP. Materials and Methods: Patients with AP admitted to our hospital, the National Tertiary Referral Center, from January 2009 to December 2010 were included in the study. The diagnosis of AP was made by acute abdominal pain and tenderness, elevated serum enzymes and typical findings detected by abdominal ultrasonography and/or contrast-enhanced computed tomography. A 12-lead derivation ECG was recorded, and serum electrolytes were performed on admission in all cases. ECG abnormalities were recorded. ECG findings were summarized in terms of frequencies, means, and standard deviations. Results: A total of 64 AP cases 19 males (29, 7%), 45 females (70, 3%) were included into the study. Among patients included in the study, 42 (65.7%) were biliary, 20 (31.2%) were idiopathic, and 2 (3.1%) were drug-related. There were 42 (65.6%) patients with one or more serum electrolyte disturbances. 56.3% of the patients with AP had normal sinus rhythm, 43.7% had changes in ECG; and the T-wave negativity was the most frequent ECG abnormality. Twenty-five (89.2%) of the 28 patients with ECG abnormalities had one or more electrolyte abnormalities. Conclusion: The study results suggested that ECG changes may be observed frequently in patients with AP, and more attention should be paid to the cardiac patients with electrolyte imbalance.

Keywords: Acute pancreatitis, 64 cases, electrocardiographic abnormalities


How to cite this article:
Yaylaci S, Kocayigit I, Genc AB, Cakar MA, Tamer A, Uslan MI. Electrocardiographic changes in patients with acute pancreatitis. Med J DY Patil Univ 2015;8:196-8

How to cite this URL:
Yaylaci S, Kocayigit I, Genc AB, Cakar MA, Tamer A, Uslan MI. Electrocardiographic changes in patients with acute pancreatitis. Med J DY Patil Univ [serial online] 2015 [cited 2023 May 31];8:196-8. Available from: https://journals.lww.com/mjdy/pages/default.aspx/text.asp?2015/8/2/196/153159


  Introduction Top


Acute pancreatitis (AP) is a common inflammatory disorder of the pancreas which presents with severe upper abdominal pain, nausea, or vomiting accompanied by elevated pancreatic enzymes (amylase and lipase) in serum. The incidence of AP ranges between 5 and 80/population of 100,000. [1] Multiple organ system dysfunctions especially cardiovascular manifestations are frequently seen in severe AP. [2]

The cardiovascular system can be affected alone or with other systems in AP. Hypovolemia and metabolic disturbances including hyperkalemia, hypomagnesemia, and hypophosphatemia during AP may cause cardiac rhythm and contractility disorder. These conditions are generally associated with electrocardiographic (ECG) abnormalities including arrhythmias, ST-T-wave changes, and intraventricular conduction disturbances. [3],[4],[5]

Several studies have been reported to demonstrate the ECG abnormalities in AP, however, the data are still limited and lacking. [4],[6],[7] The aim of this study was to investigate the frequency and type of ECG abnormalities present in patients with AP.


  Materials and Methods Top


Patients with AP admitted to our hospital, the National Tertiary Referral center, from January 2009 to December 2010 were included in the study. The diagnosis of AP was made by acute abdominal pain and tenderness, elevated serum enzymes (≥3-fold increase in amylase and/or lipase), and typical findings detected by abdominal ultrasonography and/or contrast-enhanced computed tomography.

Exclusion criteria were determined as younger than 18 or older than 70 years, known heart disease (coronary artery disease and/or valvular heart disease), diabetes mellitus, uncontrolled arterial hypertension, and arrhythmias such as atrial fibrillation, chronic renal failure, and cirrhosis. The severity of AP was assessed according to the Atlanta criteria. A 12-lead derivation ECG was recorded, and serum electrolytes were performed on admission in all cases. Normal serum electrolyte values were 136-145 mEq/L for sodium, 3.6-5.5 mEq/L for potassium, 2.2-4.3 mEq/L for phosphorus, and 8.4-10.2 mg/dL for calcium. The calcium levels were corrected by serum albumin levels. ECG abnormalities were recorded.

Electrocardiogram assessment

A 12-lead derivation ECGs were recorded in all patients at 25 mm/s. QT intervals were measured using a caliper by two experienced cardiologists as described previously, unaware of any other data. The QT interval was measured in each lead from the beginning of the depolarization of the QRS complex to the end of the T-wave, defined as a return to the T-P baseline. Three consecutive cycles were measured by visual inspection in each lead, and the mean value was calculated. The results were averaged. The dispersion of the QTc interval was defined as the difference between the maximum and minimum of the measured corrected QT intervals (in milliseconds) in any of the measured ECG leads. All QTc were calculated by dividing QT intervals by the square roots of the R-R intervals (Bazett formula). Prolonged QTc interval was defined as QTc. 440 ms. Corrected QT dispersion (QTcd) equal to or exceeding 70 ms was considered abnormally increased.

Statistical analysis

Electrocardiogram findings were summarized in terms of frequencies, means, and standard deviations. Electrolyte and pancreatic enzyme levels were summarized as medians. The SPSS (version 15) software was used.


  Results Top


A total of 64 AP cases 19 males (29, 7%), 45 females (70, 3%) were included into the study. Among patients included in the study, 42 (65.7%) were biliary, 20 (31.2%) were idiopathic, and 2 (3.1%) were drug-related. [Table 1] shows the distribution of characteristics of patients.
Table 1: Characteristics of patients

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[Table 2] and [Table 3] show the distribution of ECG parameters and abnormal findings. There were 42 (65.6%) patients with one or more serum electrolyte disturbances. In a descending order of frequency, these were: Hypokalemia (55%), hyponatremia (45%), hyperphosphatemia (21%), hypocalcemia (17%), hypophosphatemia (12%), and hypernatremia (5%). Eight patients had only one-electrolyte abnormality, and 36 patients had two or more abnormalities. 25 (89.2%) of the 28 patients with ECG abnormalities had one or more electrolyte abnormalities.
Table 2: Summary of electrocardiographic parameters

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Table 3: Electrocardiographic findings

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  Discussion Top


Various tachyarrhythmias and bradyarrhythmias, atrial flutter and fibrillation, supraventricular premature contractions, shortened PR interval, QRS prolongation, various bundle-branch blocks (such as left bundle-branch block, right bundle-branch block, and left anterior hemiblock), nonspecific changes in repolarization, decreased T-wave voltage, T-wave changes, and ST-segment abnormalities are often seen (approximately 50% of patients). Most frequently associated changes with AP are T-wave inversion and ST-segment depression. AP can be associated with atrial fibrillation and flutter, which disappear with treatment of AP. [4],[5],[8]

Several case reports of patients who have AP demonstrate that findings consistent with acute coronary syndrome, including ST-segment elevation, T-wave inversions, and a new left bundle-branch block suggestive of acute myocardial infarction can occur. These patients had normal cardiac enzymes and normal coronary angiograms. [7],[9],[10]

Various hypotheses have been formulated for the underlying mechanism of ECG abnormalities and/or myocardial damage in AP. These include toxic effects of the pancreatic proteolytic enzymes on the myocardium, autonomic imbalance with a vagal predominance, coronary artery spasm, metabolic and electrolyte abnormalities, prothrombotic derangements, hemodynamic instability, and systemic inflammatory response-induced cardiac damage. [5]

Electrocardiographic abnormalities may be associated with AP. More than 50% of the patients with AP had ECG abnormalities, and these changes could be related to electrolyte alterations. [4] There was no significant relation between lateral early repolarization and echocardiographic findings in AP in a study. [11] Our study was based on ECG changes, so that we did not perform echocardiographic evaluation routinely.

In our study, 56.3% of the patients with AP had normal sinus rhythm, 43.7% had changes in ECG, and the T-wave negativity was the most frequent ECG abnormality. 83% of the patients had electrolyte abnormality, and the most common electrolyte abnormality was hypokalemia. A significant portion of patients with ECG abnormalities (89.2%) had electrolyte abnormality. Therefore, monitoring electrolyte in patients with AP is of great importance for the cardiac complications.


  Conclusion Top


The results of our study it was suggested that ECG changes may be observed frequently in patients with AP, and more attention should be paid to the cardiac patients with electrolyte imbalance.

 
  References Top

1.
Whitcomb DC. Clinical practice. Acute pancreatitis. N Engl J Med 2006;354:2142-50.  Back to cited text no. 1
    
2.
Horton JW, Burnweit CA. Hemodynamic function in acute pancreatitis. Surgery 1988;103:538-46.  Back to cited text no. 2
    
3.
Tejada JG, Hernández F, Chimeno J, Alonso MA, Martin R, Bastante T. Acute pancreatitis mimicking acute inferior myocardial infarction. Angiology 2008;59:365-7.  Back to cited text no. 3
    
4.
Rubio-Tapia A, García-Leiva J, Asensio-Lafuente E, Robles-Díaz G, Vargas-Vorácková F. Electrocardiographic abnormalities in patients with acute pancreatitis. J Clin Gastroenterol 2005;39:815-8.  Back to cited text no. 4
    
5.
Yegneswaran B, Kostis JB, Pitchumoni CS. Cardiovascular manifestations of acute pancreatitis. J Crit Care 2011;26:225.e11-8.  Back to cited text no. 5
    
6.
Mautner RK, Siegel LA, Giles TD, Kayser J. Electrocardiographic changes in acute pancreatitis. South Med J 1982;75:317-20.  Back to cited text no. 6
    
7.
Khairy P, Marsolais P. Pancreatitis with electrocardiographic changes mimicking acute myocardial infarction. Can J Gastroenterol 2001;15:522-6.  Back to cited text no. 7
    
8.
Pezzilli R, Barakat B, Billi P, Bertaccini B. Electrocardiographic abnormalities in acute pancreatitis. Eur J Emerg Med 1999;6:27-9.  Back to cited text no. 8
    
9.
Yu AC, Riegert-Johnson DL. A case of acute pancreatitis presenting with electrocardiographic signs of acute myocardial infarction. Pancreatology 2003;3:515-7.  Back to cited text no. 9
    
10.
Türkay C, Aydogan T, Karanfil A, Uyar ME, Selçoki Y, Kanbay M. T-wave depletion and bradycardia possibly secondary to acute pancreatitis: Review of the literature. Turk J Gastroenterol 2009;20:295-7.  Back to cited text no. 10
    
11.
Sökmen M, Bugdaci MS, Oztekin E. Electrocardiographic changes and importance of repolarization changes in cases with acute pancreatitis. Turk J Gastroenterol 2011;22:315-20.  Back to cited text no. 11
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3]


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