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Transient ST-segment elevation during acute pancreatitis

Published:February 20, 2016DOI:https://doi.org/10.1016/j.ejim.2016.02.008

      1. Indication

      A 27-year-old-woman with history of insulin dependent diabetes mellitus, hypertriglyceridemia and recent laparoscopic cholecystectomy presented to the hospital with severe upper abdominal pain. Initial laboratory workup was pertinent for a lipase of 1163 units/L, triglyceride level of 5680 mg/dL, random blood sugar of 321 g/dL, anion gap of 19 without acetone in the blood and the liver and kidney functions were normal. Abdominal CT scan was consistent with acute pancreatitis. An electrocardiogram (ECG) revealed ST-segment elevation (STE) in V4–V6 without pathological Q waves or reciprocal ST-segment depression (STD). She had denied any chest pain and had no prior history suggestive of coronary artery disease. Serial cardiac markers including troponin and CKMB were normal. An immediate echocardiogram showed normal left ventricular systolic function and no regional wall motion abnormalities (RWMA). Interestingly, repeat ECG 2 h later showed resolution of STE. The patient ultimately required plasmapheresis for hypertriglyceridemia-induced pancreatitis which was well tolerated with decrease of triglycerides to 203 mg/dL and was discharged on fenofibrate 160 mg and pravastatin 40 mg daily in stable condition. (See Fig. 1.)
      Figure thumbnail gr1
      Fig. 1panel a: ST-segment elevation (convex or tombstone pattern) in leads V4–V6 without reciprocal ST-segment depression.
      Panel b: Repeat ECG 2 h later revealing resolution of ST-segment elevation and anterior precordial ST-segment depression.
      What is the diagnosis?

      2. Diagnosis

      In the presented case, a woman with a negative history of cardiovascular disease developed transient STE during hypertriglyceridemia-induced pancreatitis. In our case the absence of chest pain, the pattern of STE without reciprocal STD and the absence of RWMA and normal cardiac markers argue against myocardial infarction (MI). Also, the presentation argues against takotsubo cardiomyopathy due to the normal left ventricular systolic function. The majority of reported cases of pancreatitis and STE had no evidence of myocardial damage or occlusive coronary artery disease. Several postulations were offered to explain ECG abnormalities and/or myocardial damage in pancreatitis including coronary spasm, systemic inflammatory response-induced cardiac damage, electrolyte abnormalities, prothrombotic derangement, hemodynamic instability or from the effects of autonomic imbalance with vagal predominance [
      • Cafri C.
      • Basok A.
      • Katz A.
      • Abuful A.
      • Gilutz H.
      • Battler A.
      Thrombolytic therapy in acute pancreatitis presenting as acute myocardial infarction.
      ,
      • Khairy P.
      • Marsolais P.
      Pancreatitis with electrocardiographic changes mimicking acute myocardial infarction.
      ]. Awareness of this presentation would avoid the erroneous administration of thrombolytic agents – especially in hospitals not equipped with catheterization suites – which may have fatal consequences [
      • Main G.
      • Heath D.
      • Candlish W.
      • Imrie C.W.
      • Hutton I.
      Dangers of thrombolysis.
      ]. In our case coronary angiography was not performed as the presentation was not felt to be due to MI but the exact pathophysiology remains elusive. STE in pancreatitis is a diagnostic dilemma that has prompted invasive coronary evaluation or even thrombolytic therapy. If there is any concern of myocardial injury in a patient with acute pancreatitis with evident STE and coronary evaluation is deemed necessary, then coronary angiography is the test of choice and thrombolytic therapy should be avoided.

      Conflict of interest

      There are no conflicts of interest to disclose.

      Acknowledgments

      We have received no funding for this report. All authors have read and approved the final submitted manuscript.

      References

        • 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 May; 49: 279-281
        • Khairy P.
        • Marsolais P.
        Pancreatitis with electrocardiographic changes mimicking acute myocardial infarction.
        Can J Gastroenterol. 2001 Aug; 15: 522-526
        • Main G.
        • Heath D.
        • Candlish W.
        • Imrie C.W.
        • Hutton I.
        Dangers of thrombolysis.
        BMJ. 1990; 300: 811