Pancreatitis with electrocardiographic changes mimicking acute myocardial infarction

acute coronary syndrome is rarely a source of confusion, subsidiary studies such as serial electrocardiograms (ECGs) may be very helpful when signs and symptoms overlap. A problem arises, however, when pancreatitis presents with ECG changes in the absence of coronary artery disease or hemodynamic instability. Minor transient ECG abnormalities such as nonspecific ST segment depression and T wave inversions are well described in association with pancreatitis (1-8). Whether pancreatitis presents with major ECG changes such as ST segment elevation in the absence of underlying cardiac pathology remains a subject BRIEF COMMUNICATION


CASE PRESENTATION
While undergoing hemodialysis, a 64-year-old white woman with hypertensive end-stage renal failure presented with sudden onset of burning epigastric pain radiating to the chest and back, accompanied by nausea and vomiting.Five hours later, she returned to hospital with nonbloody diarrhea and persisting pain.She denied fever, chills, dyspnea, palpitations, orthopnea, pleuritic chest pain and alcohol consumption.She had no known cardiac disease but had a 45 pack/year smoking history, controlled hypertension and mild dyslipidemia.In addition to chronic renal failure hemodialyzed for two months, her past medical history was remarkable for a peptic ulcer with Helicobacter pylori eradication and a remote cholecystectomy.
On arrival at the intensive care unit, the patient remained largely asymptomatic, with the occasional recurrence of mild epigastric discomfort.Subsequent analysis revealed peak amylase and lipase levels of 1454 IU/L and 5750 IU/L, respectively.A peak creatine kinase level of 250 IU/L was seen 22 h after the onset of pain with an MB fraction of 5.0%, indicating borderline significance, but this ratio was unchanged from baseline (ie, 4.7%).Serial ECGs demonstrated the evolution of diffuse deep T wave inversions with persistent 1 to 2 mm ST segment elevations in V2 and V3 (Figure 2).No segmental wall motion abnormality, pericardial effusion, valvulopathy or diastolic dysfunction was seen on transthoracic echocardiography.The left ventricular ejection fraction was estimated at 60%, and mild concentric left ventricular hypertrophy was noted.No coronary artery lesions were visualized on angiography.
An abdominal computed tomography scan revealed a small focus of inflammation surrounding the pancreatic tail, with pericaudal fat infiltration and mild thickening of Gerota's fascia.There was an unsuccessful attempt at cannulating the common bile duct by endoscopic retrograde cholangiopancreatography.The patient was discharged on day 8 with the diagnosis of acute pancreatitis of uncertain etiology with persisting anterior ST segment elevations and diffuse, but less pronounced, T wave inversions (Figure 3).9) described the first case of acute pancreatitis associated with ECG changes compatible with myocardial ischemia.Subsequently, numerous reports and case series have documented nonspecific ST and T wave alterations associated with acute pancreatitis (3)(4)(5)7,8,(10)(11)(12)(13)(14)(15)(16)(17)(18)(19).Based on such observations, it is generally believed that pancreatitis, like several other inflammatory conditions such as bacterial shock (20), myocarditis (21), cholecystitis (22)(23)(24) or pneumonitis (24), may produce minor transient ECG changes most frequently involving T wave inversions or ST segment depression.
Several hypotheses may be proposed to explain the ECG changes in acute pancreatitis.Pancreatitis is often accompanied by such metabolic abnormalities as hypocalcemia, hyponatremia, hypokalemia, hypomagnesemia and insulininduced hypoglycemia (37,38).Although such electrolyte disturbances may affect myocardial repolarization, no change in our patient's baseline electrolytes was noted.Furthermore, ST segment elevation would not be an expected finding with electrolyte disturbances, which more characteristically produce QT prolongation, ST segment depression, U waves and low amplitude T wave changes (4).
Pancreatic proteolytic enzymes such as trypsin 1 may have resulted in direct injury to the pericardium or myocyte membrane, leading to changes in cell permeability with possible necrosis and consequent electrical changes.Kellner and Robertson (39) demonstrated ECG changes after the intravenous injection of proteolytic enzymes that took two weeks to resolve.Several authors have speculated that such damage may lead to a transient local hyperkalemia sufficient to block depolarization, which is not corrected by normalizing the electrolytes (5).Others argue that electrical changes induced by proteolytic enzymes, lipases or phospholipolytic enzymes are not secondary to myocardial necrosis, but rather to sublethal damage (40) because ECG changes should be transient (41) and no histological evidence has demonstrated myonecrosis (19).Bradykinins are also increased in acute pancreatitis but have no known relationship to ECG abnormalities (24,42).In our patient, the initial concave upward ST segment elevations in leads V2 and V3 (Figure 1) may have suggested acute pericarditis.However, ST segment elevations in acute pericarditis are characteristically either diffuse or in 'epicardial' lateral leads (43), and T wave inversions are rarely seen before ST segments return to baseline (44).Furthermore, no pleuritic chest pain, pericardial friction rub or pericardial effusion was present in our patient.Several investigators have postulated the existence of a cardiobiliary reflex (22,23,(45)(46)(47), which may cause cardiac damage by direct action on the myocardium or by altering coronary blood flow (48,49).Although innervation to the heart and gallbladder arises from different spinal levels, Morrison and Swulim (49) evoked the possibility of a vagally mediated reflex, later shown to travel through intermediate neurons connecting these rami.This reflex has been cited as the presumed cause of T wave changes in acute cholecystitis and has also been suspected in pancreatitis, gastrointestinal hemorrhage and intracranial bleeds (22).Gilbert et al (50) demonstrated reduced coronary blood flow after abdominal stimulation, which they hypothesized to be secondary to the cardobiliary reflex.In a study of prolonged vagal stimulation in animals, Manning et al (48) reported T wave inversions and myocardial damage.Furthermore, the cardiobiliary reflex has been inhibited experimentally by atropine and vagotomy (51).Some studies, however, have reported vagally mediated ECG changes only in subjects with underlying coronary artery disease.Hodge et al (45) noted ECG changes with gallbladder distention in dogs only when experimentally induced coronary lesions were produced.A later study of 26 patients undergoing biliary tract surgery in whom the gallbladder and common bile duct were distended confirmed ECG changes only in the presence of underlying coronary artery disease (47).Furthermore, ST segment elevations secondary to the cardiobiliary reflex have not been previously documented.
Other possible mechanisms such as coronary vasospasm (20), exacerbation of underlying coronary artery disease (22), or coronary thrombus formation secondary to increased platelet adhesiveness or pancreatic enzymeinduced coagulopathy (41) are unlikely in our patient given the prolonged duration of ST segment elevation and the normal coronary angiogram.
In the era of thrombolysis, misdiagnosing acute myocardial infarction in the presence of abdominal pathology may lead to serious hemorrhagic complications.Our case report demonstrates that despite the absence of hemodynamic instability, underlying cardiac disease or the use of vasopressors, acute pancreatitis may mimic the ECG changes seen with myocardial infarction.In selected cases, complementary noninvasive and invasive studies may be required to establish a definitive diagnosis.Further studies are required to determine whether, in the absence of hemodynamic instability, ECG abnormalities seen in pancreatitis have etiological, prognostic or therapeutic implications.

Pancreatitis with ECG changes mimicking acute MI
Pancreatitis with ECG changes mimicking acute MI Can J Gastroenterol Vol 15 No 8 August 2001 523

Figure 1 )Figure 2 )Figure 3 )
Figure 1) Initial electrocardiogram with 1 to 3 mm ST segment elevations in precordial leads V2 to V4, and T wave inversions in the anterolateral leads

Figure 4 )
Figure 4) Baseline electrocardiogram demonstrating absence of repolarization abnormalities before the onset of pancreatitis