ECG Revealed Acute Inferolateral MI

Editor: I would like to comment on the very fine article in “Cases in Electrocardiography” in which the diagnosis was acute myopericarditis. (“Symptoms: Elderly Woman with Chest ‘Muscle Tightness’,” 2004;26[9]:48.) I may have misunderstood the article, but I get the impression that the authors are arguing that myopericarditis is the most likely diagnosis. I would argue that in a 76-year-old with these symptoms and this ECG, the most likely diagnosis is acute inferolateral myocardial infarction (AMI) due to circumflex artery occlusion. First, the incidence of myopericarditis is dwarfed by the incidence of AMI. Sarda et al studied 1,280 patients with positive biomarkers. Only 2.7 percent were found to have myopericarditis; the rest had AMI. And this included all patients of all ages. The proportion of all patients with new ST elevation who have myopericarditis is probably higher because of those who have pericarditis only, without muscle (myo-) involvement; it is muscle involvement that produces positive biomarkers. Nevertheless, the proportion of patients with new ST elevation who have myopericarditis is very low. Thus, the pre-test probability of AMI in a 76-year-old with new ST elevation is far higher than it is for myopericarditis. Secondly, the ECG is as consistent with AMI as it is with myopericarditis. Upward concavity is seen very commonly in AMI. (Acad Emerg Med 2001;8:961; Acad Emerg Med 2003;10:516.) PR depression is a normal finding due to atrial repolarization, and is only suggestive of myopericarditis when >0.5mm, and only diagnostic when > 0.8 mm. (Arch Intern Med 1973;131:657.) PR elevation in aVR is only suggestive, not diagnostic, of myopericarditis. (Prog Cardiovasc Dis 1974;33:470.) Reciprocal ST depression in aVR also is found in inferior MI because aVR is 150 opposite lead II. While differentiating myopericarditis from benign early repolarization (BER) is comparatively straightforward, as described in the article, differentiating myopericarditis from AMI due to circumflex artery occlusion is nearly impossible. Both have greater ST elevation in lead II than III (as seen in this case), and both may lack the normal reciprocal ST depression in lead aVL, especially when ST elevation is manifest in lateral precordial leads V4-V6 (as in this case). (Am J Cardiol 2000;86:341.) Because of the absence of ST depression in aVL and some pleuritic component of the pain, thrombolytics would be ill advised prior to obtaining an echocardiogram. However, an immediate echocardiogram or, better, immediate angiography with PCI, is the correct course of action. Unfortunately, an echocardiographic wall motion abnormality also can be seen in localized myopericarditis, and for that reason, immediate angiography is the preferred choice. Additionally, the risks of pericardial bleeding after thrombolytics therapy in a patient with pericarditis are minimal. (The ECG in Acute MI: an Evidence-Based Manual of Reperfusion Therapy. Philadelphia: Lippincott Williams & and Wilkins, 2002:358.) Finally, if the patient were 25 or had a pericardial rub, then the diagnosis of myopericarditis would be most likely. That is not the case here. This case should be assumed to be ST elevation MI until proven otherwise. Stephen W. Smith, MD Minneapolis, MN