Prevalence of cardiovascular dysfunction and its association with outcome in patients with acute pancreatitis
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Abstract
Background
Organ failure (OF) is the most important predictor of outcome in severe acute pancreatitis (SAP). Cardiovascular failure (CVSF) occurs in a variable proportion of patients with SAP. We aimed to study myocardial dysfunction in acute pancreatitis (AP) and its impact on the outcome.
Methods
In this prospective study between January 2011 and July 2012, consecutive eligible patients of AP were enrolled. Myocardial function was assessed by measuring CK-MB (creatine phosphokinase isoenzyme) and echocardiography at admission. Electrocardiography (ECG) findings at admission were noted. Patients were managed in a high dependency unit using a step-up approach and followed up during hospital stay for their outcome. The outcome variables were computed tomography severity index (CTSI), the severity of AP, infection, need for intervention, length of hospital stay, and mortality.
Results
Of the 65 patients (mean age 39.55 ± 13.14 years; 67.7% males; etiology: alcohol 47.7%, gallstone disease 43.1%, and others 3%), 28 (43%) had organ failure. Respiratory failure was present in 21 (32.3%) patients, acute kidney injury (AKI) in 11 (16.9%) patients, and cardiovascular dysfunction was present in 4 (6.2%) patients. ECG changes were present in 26 (40%) patients with ST segment depression with T wave inversion being the most common (n = 22, 85%). Elevated CK-MB level (more than two times normal) was seen in 18 (27.7%) patients and was associated with increased necrosis (odds ratio = 2.44, 95% confidence interval = 0.5–12.3, p = 0.021), CTSI (7.7 ± 2.7 vs. 5.0 ± 3.0, p = 0.002), severity of AP (p = 0.05), CVSF (p = 0.005), hospital stay (19.3 ± 12.3 vs. 12.3 ± 7.0, p = 0.006), and mortality (odds ratio = 6.42, 95% confidence interval = 1.0–38.9, p = 0.045). Left ventricular systolic dysfunction (left ventricular ejection fraction [LVEF] < 55%) was seen in 9 (13.8%) patients, all of whom had mild systolic dysfunction and left ventricular diastolic dysfunction (LVDD) was seen in 17 (26.2%) patients. There was no association between poor LVEF or LVDD and necrosis, severity of AP, infection, need for intervention, duration of hospital stay, and mortality.
Conclusion
Elevated CK-MB levels were associated with increased necrosis, higher CTSI, the severity of AP, cardiovascular failure, prolonged hospital stay, LVDD, and mortality. Echocardiographic findings namely left ventricular systolic and diastolic dysfunctions were not associated with severity or outcome of AP.
Keywords
Acute pancreatitis Creatine phosphokinase Echocardiography Electrocardiography Myocardial dysfunction Organ failureNotes
Compliance with ethical standards
Conflict of interest
RP, ND, AB, TDY, and RK declare that they have no conflict of interest.
Ethical approval
All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.
Informed consent
Informed consent was obtained from all individual participants included in the study.
References
- 1.Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013;62:102–11.CrossRefPubMedGoogle Scholar
- 2.Yegneswaran B, Kostis JB, Pitchumoni CS. Cardiovascular manifestations of acute pancreatitis. J Crit Care. 2011;26:225 e11–8.CrossRefGoogle Scholar
- 3.Wilson PG, Manji M, Neoptolemos JP. Acute pancreatitis as a model of sepsis. J Antimicrob Chemother. 1998;41Suppl A:51–63.Google Scholar
- 4.Saulea A, Costin S, Rotari V. Heart ultrastructure in experimental acute pancreatitis. Rom J Physiol. 1997;34:35–44.PubMedGoogle Scholar
- 5.Lefer AM, Glenn TM, O'Neill TJ, Lovett WL, Geissinger WT, Wangensteen SL. Inotropic influence of endogenous peptides in experimental hemorrhagic pancreatitis. Surgery. 1971;69:220–8.PubMedGoogle Scholar
- 6.Altimari AF, Prinz RA, Leutz DW, Sandberg L, Kober PM, Raymond RM. Myocardial depression during acute pancreatitis: fact or fiction? Surgery. 1986;100:724–31.PubMedGoogle Scholar
- 7.Jambrik Z, Gyongyosi M, Hegyi P, et al. Plasma levels of IL-6 correlate with hemodynamic abnormalities in acute pancreatitis in rabbits. Intensive Care Med. 2002;28:1810–8.Google Scholar
- 8.Meyer A, Kubrusly MS, Salemi VM, et al. Severe acute pancreatitis: a possible role of intramyocardial cytokine production. JOP. 2014;15:237–42.Google Scholar
- 9.Malmstrom ML, Hansen MB, Andersen AM, et al. Cytokines and organ failure in acute pancreatitis: inflammatory response in acute pancreatitis. Pancreas. 2012;41:271–7.Google Scholar
- 10.Buch J, Buch A, Schmidt A. Transient ECG changes during acute attacks of pancreatitis. Acta Cardiol. 1980;35:381–90.PubMedGoogle Scholar
- 11.Yu AC, Riegert-Johnson DL. A case of acute pancreatitis presenting with electrocardiographic signs of acute myocardial infarction. Pancreatology. 2003;3:515–7.CrossRefPubMedGoogle Scholar
- 12.Rubio-Tapia A, Garcia-Leiva J, Asensio-Lafuente E, Robles-Diaz G, Vargas-Vorackova F. Electrocardiographic abnormalities in patients with acute pancreatitis. J Clin Gastroenterol. 2005;39:815–8.CrossRefPubMedGoogle Scholar
- 13.Pezzilli R, Barakat B, Billi P, Bertaccini B. Electrocardiographic abnormalities in acute pancreatitis. Eur J Emerg Med. 1999;6:27–9.PubMedGoogle Scholar
- 14.Ro TK, Lang RM, Ward RP. Acute pancreatitis mimicking myocardial infarction: evaluation with myocardial contrast echocardiography. J Am Soc Echocardiogr. 2004;17:387–90.CrossRefPubMedGoogle Scholar
- 15.Gyongyosi M, Takacs T, Czako L, et al. Noninvasive monitoring of hemodynamic changes in acute pancreatitis in rabbits. Dig Dis Sci. 1997;42:955–61.CrossRefPubMedGoogle Scholar
- 16.Variyam EP, Shah A. Pericardial effusion and left ventricular function in patients with acute alcoholic pancreatitis. Arch Intern Med. 1987;147:923–5.CrossRefPubMedGoogle Scholar
- 17.Pezzilli R, Billi P, Bertaccini B, Gullo L. Pericardial effusion and left ventricular function in acute pancreatitis. Am J Gastroenterol. 1996;91:997–1000.PubMedGoogle Scholar
- 18.Nadkarni N, Bhasin DK, Rana SS, et al. Diastolic dysfunction, prolonged QTc interval and pericardial effusion as predictors of mortality in acute pancreatitis. J Gastroenterol Hepatol. 2012;27:1576–80.Google Scholar
- 19.Albrecht CA, Laws FA. ST-segment elevation pattern of acute myocardial infarction induced by acute pancreatitis. Cardiol Rev. 2003;11:147–51.CrossRefPubMedGoogle Scholar
- 20.Korantzopoulos P, Pappa E, Dimitroula V, et al. ST-segment elevation pattern and myocardial injury induced by acute pancreatitis. Cardiology. 2005;103:128–30.CrossRefPubMedGoogle Scholar
- 21.Karachaliou I, Papadopoulou K, Karachalios G, Charalabopoulos A, Papalimneou V, Charalabopoulos K. An increase in creatine kinase secondary to acute pancreatitis: a case report. Int J Clin Pract Suppl. 2005;147:40–2.CrossRefGoogle Scholar
- 22.Thandassery RB, Choudhary N, Bahl A, Kochhar R. Characterization of cardiac dysfunction by echocardiography in early severe acute pancreatitis. Pancreas. 2017;46:626–30.CrossRefPubMedGoogle Scholar
- 23.Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH. Acute pancreatitis: value of CT in establishing prognosis. Radiology. 1990;174:331–6.CrossRefPubMedGoogle Scholar
- 24.Knaus WA, Draper EA, Wagner DP, Zimmerman JE. APACHE II: a severity of disease classification system. Crit Care Med. 1985;13:818–29.CrossRefPubMedGoogle Scholar
- 25.Puleo PR, Meyer D, Wathen C, et al. Use of a rapid assay of subforms of creatine kinase-MB to diagnose or rule out acute myocardial infarction. N Engl J Med. 1994;331:561–6.CrossRefPubMedGoogle Scholar
- 26.Kleiman NS, Lakkis N, Cannon CP, et al. Prospective analysis of creatine kinase muscle-brain fraction and comparison with troponin T to predict cardiac risk and benefit of an invasive strategy in patients with non-ST-elevation acute coronary syndromes. J Am Coll Cardiol. 2002;40:1044–50.CrossRefPubMedGoogle Scholar
- 27.Folland ED, Parisi AF, Moynihan PF, Jones DR, Feldman CL, Tow DE. Assessment of left ventricular ejection fraction and volumes by real-time, two-dimensional echocardiography. A comparison of cineangiographic and radionuclide techniques. Circulation. 1979;60:760–6.CrossRefPubMedGoogle Scholar
- 28.Paulus WJ, Tschope C, Sanderson JE, et al. How to diagnose diastolic heart failure: a consensus statement on the diagnosis of heart failure with normal left ventricular ejection fraction by the Heart Failure and Echocardiography Associations of the European Society of Cardiology. Eur Heart J. 2007;28:2539–50.CrossRefPubMedGoogle Scholar
- 29.Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantification: a report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr. 2005;18:1440–63.CrossRefPubMedGoogle Scholar
- 30.Kumar S, Gautam SK, Gupta D, Agarwal A, Dhirraj S, Khuba S. The effect of Valsalva maneuver in attenuating skin puncture pain during spinal anesthesia: a randomized controlled trial. Korean J Anesthesiol. 2016;69:27–31. CrossRefPubMedPubMedCentralGoogle Scholar
- 31.Hsu PC, Lin TH, Su HM, Lin ZY, Lai WT, Sheu SH. Acute necrotizing pancreatitis complicated with ST elevation acute myocardial infarction: a case report and literature review. Kaohsiung J Med Sci. 2010;26:200–5.CrossRefPubMedGoogle Scholar
- 32.Mautner RK, Siegel LA, Giles TD, Kayser J. Electrocardiographic changes in acute pancreatitis. South Med J. 1982;75:317–20.CrossRefPubMedGoogle Scholar
- 33.Randeva HS, Bolodeoku J, Mikhailidis DP, Winder AD, Press M. Elevated serum creatine kinase activity in a patient with acute pancreatitis. Int J Clin Pract. 1999;53:482–3.PubMedGoogle Scholar
- 34.Eisenberg MJ. Magnesium deficiency and sudden death. Am Heart J. 1992;124:544–9.CrossRefPubMedGoogle Scholar
- 35.Cafri C, Basok A, Katz A, Abuful A, Gilutz H, Battler A. Thrombolytic therapy in acute pancreatitis presenting as acute myocardial infarction. Int J Cardiol. 1995;49:279–81.CrossRefPubMedGoogle Scholar
- 36.Lieberman JS, Taylor A, Wright IS. The effect of intravenous trypsin administration on the electrocardiogram of the rabbit. Circulation. 1954;10:338–42.CrossRefPubMedGoogle Scholar
- 37.Kellner A, Robertson T. Selective necrosis of cardiac and skeletal muscle induced experimentally by means of proteolytic enzyme solutions given intravenously. J Exp Med. 1954;99:387–404.Google Scholar
- 38.Aundhakar S, Mahajan S, Agarwal A, Mhaskar D. Acute pancreatitis associated with elevated troponin levels: whether to thrombolyse or not? Ann Med Health Sci Res. 2013;3Suppl 1:S50–2.Google Scholar
- 39.Landesberg G, Gilon D, Meroz Y, et al. Diastolic dysfunction and mortality in severe sepsis and septic shock. Eur Heart J. 2012;33:895–903.CrossRefPubMedGoogle Scholar
- 40.Landesberg G, Levin PD, Gilon D, et al. Myocardial dysfunction in severe sepsis and septic shock: no correlation with inflammatory cytokines in real-life clinical setting. Chest. 2015;148:93–102.Google Scholar
- 41.Bradley EL, Hall JR, Lutz J, Hamner L, Lattouf O. Hemodynamic consequences of severe pancreatitis. Ann Surg. 1983;198:130–3.CrossRefPubMedPubMedCentralGoogle Scholar