Is This a True STEMI ECG? Typical and Atypical Findings


Morton Kern, MD, Clinical Editor, Chief Cardiology, Long Beach Veterans Administration Hospital; Associate Chief Cardiology, University California Irvine; Professor of Medicine, UCI
Orange, California;


We recently had a very unusual “STEMI” patient. His presentation, ECG and cath results demonstrated one end of the patient spectrum that the cath lab call team may encounter. 

The atypical case

A 26-year-old man complained of chest pain beginning at midnight and persistent for at least 6 hours. He had no prior history of chest pain and had no coronary artery disease risk factors. He had used alcohol and methamphetamines in the distant past, but none within the last 12 months. He smoked cigarettes. He had a “cold” last week. His physical exam was normal. His electrocardiogram (ECG) demonstrated acute ST-elevation myocardial infarction (STEMI) involving the lateral leads (Figure 1). Cardiac enzymes of CPK-MB (creatine phosphokinase-muscle band) and troponins were positive. The remainder of the lab was normal, without evidence of use of toxins.  Given his young age and lack of coronary artery disease risk factors, what is your differential diagnosis and how should we proceed? 

Before answering this question, let’s look at the more typical STEMI patient.

The typical case

More typical is the 59-year-old man who presented to the emergency department (ED) having experienced 2 hours of chest pain after returning from a day at Disneyland. He had been treated for high blood pressure and hyperlipidemia. The patient was brought to the emergency room. The ECG showed typical findings for inferior STEMI (Figure 2). The cath lab was activated. In this stable patient without hemodynamic or electrical instability, emergent percutaneous coronary intervention (PCI) is performed.  

To remind everyone of the usual order of business in the cath lab, we do the following: 

1) Carefully consider radial vs. femoral access, since there is lower bleeding risk with radial. If femoral access is chosen, quickly image the femoral artery to make proper plans for post procedure closure. 

2) Image the non-infarct related artery (in this case, the left coronary artery [LCA]).

3) Image the infarct-related artery to confirm the status of patency, the need for a special guide catheter, thromboaspiration catheter, and sufficient PCI back up.  

In this case, the right coronary artery (RCA) was totally occluded (Figure 3a). 

4) The patient undergoes PCI with thrombus aspiration followed by stenting, either with bare metal or drug-eluting stent(s). The details of these decisions will be the subjects of future discussion on these pages. After stent placement and reperfusion (Figure 3b), hemostasis is obtained (see point #1) and the patient returned to the cardiac care unit (CCU) for medical therapy for STEMI/coronary artery disease.

What are the causes of ST-segment elevation?

ST-segment elevation (STE) is the result of myocardial injury, showing elevation of the J point and continuation of the upward slope of the T wave on an ECG (Figure 4). Although STEMI is the most important association with STE on the ECG, there are other causes of STE1 (Table 1), the most common of which include early repolarization (benign), pericarditis, intraventricular conduction defects, paced rhythms, left ventricular hypertrophy and Brugada syndrome.

What kinds of myocardial infarctions exist?

According the Universal Definition of Myocardial Infarction review1, there are five types of myocardial infarctions. The most common MI we encounter in the cath lab is that of type I, plaque rupture of atherosclerosis. A type II MI is caused by increased myocardial demand, out of proportion to myocardial oxygen supply, coronary spasm, coronary dissection, coronary thromboembolus, or other rare causes of vasculitis. Type III is sudden death, presumed to be due to acute coronary thrombosis, and includes cardiac arrest and new left bundle branch block. Type IV is in the setting of PCI and includes MI resulting from in-stent thrombosis. Type V is MI in the setting of coronary artery bypass graft surgery. 

Our typical 59-year-old patient in Figure 2 had a RCA occlusion with STE of the leads II, III, and AVF reflecting injury current on the inferior left ventricular wall that involves not only the left ventricle, but also the inferior septum and portions of the right ventricular free wall. Note that some inferior MIs may not always show the typical STEMI in leads II, III, and AVF, but may have T wave changes with only a tall R wave in V1, suggesting a posterior MI. In the cath lab, remember that MIs involving the right ventricle may also produce hypotensive, elevated right heart pressures, and normal left-sided filling pressure (pulmonary capillary wedge pressure [PCWP] with clear lungs). This constellation of findings defines a clinical right ventricular infarction and will need volume resuscitation, possible inotropic support and avoidance of nitroglycerin, since the patient will need his preload to maintain cardiac output.

Differential considerations in the atypical STEMI patient

Now back to the 26-year-old male with lateral STEMI, denoted by STE in leads I, AVL, V5, and V6. In young patients with a STEMI ECG, what are the possible causes of STE that may not be true plaque rupture? Atherosclerotic plaque is rare in young people without juvenile diabetes mellitus. The most common causes of STE in this age group are coronary spasm and coronary dissection. Coronary thromboembolus, coronary anomalies, extension of an aortic dissection into the coronary artery and possibly vasculitis could also cause this presentation. Myopericarditis is not usually associated with such localized STE and was very low on our list of STE in this patient. Surprise!

Before rushing to the cath lab, we obtained an echocardiogram that showed decreased segmental wall motion abnormality with an ejection fraction of 40-45%, normal aortic root without dissection, and no intracardiac masses (which excludes endocarditis or myxoma associated with thromboebolism). Because of possible coronary spasm, the patient was treated with several doses of sublingual nitrates without change in his pain or ECG. His chest x-ray and lab values were normal except for CPK-MB/troponins. Upon further questioning, a viral syndrome that lasted all week with cough and congestion was reported.

Because we could not exclude a coronary artery occlusion due to coronary artery disease (unlikely), spasm or dissection (likely), or another critical and probably rare problem, we performed cardiac catheterization from the right radial artery without problems. The coronary arteries were normal (Figure 5); the LV function, as shown on the echocardiogram, and had global mild hypokinesis with a left ventricular end diastolic pressure (LVEDP) of 20mmHg.

After excluding all obstructive coronary mechanisms, we finally gave him a diagnosis of myocarditis and treated him with beta blockers, aspirin (ASA), analgesics, and afterload reduction.  

ECG changes of myopericarditis

STE in all leads except AVR and V1 (Figure 6) are the classic ECG of pericarditis, an inflammation of the pericardium and associated injury of the epicardial, but not endocavity, surfaces. Pericarditis can be confused for a myocardial infarction, which usually has more acute complaints and ST-elevations that are limited to the infarct area. ECG findings in pericarditis evolve over the course of illness and include the following findings, depending on the stage of the illness. Early: ST elevation in all leads with P-T segment depression (depression between the end of the P-wave and the beginning of the QRS-complex); mid course: normalization of the ST segment; late course: inverted T-waves; resolution: normalization of the ECG. Similarly, the ECG findings most commonly seen in myocarditis alone are diffuse T wave inversions and in some cases, saddle-shaped ST-segment elevations similar to those seen in our 26-year-old patient. These changes may also be present in pericarditis. This case was highly unusual in the finding of distinctly localized STE, suggesting local myocardial injury rather than a diffuse process.

It also very useful to recall the causes of elevated troponins in the absence of true myocardial ischemia. Troponins can be present in myopericarditis and a number of other non-STEMI conditions1 (Table 2).

Bottom line for STE ECG changes

When suspecting an atypical STE ECG presentation, always review the clinical story, physical exam, chest x-ray, echocardiogram, and lab data. In some centers, for patients with very low likelihood of true type I myocardial infarction, a non-invasive computed tomography angiography (CTA) may be helpful. Ultimately, the answer may be revealed in the clinical data, but many times, confirmation of STEMI (or not) must be made by angiography.  


  1. Thygesen K, Alpert JS, White HD, et al. Universal definition of myocardial infarction. Circulation. 2007; 116: 2634-2653.

Letter to the Clinical Editor

Dear Dr. Kern,

I enjoyed your article on hemodynamic calculations in the April issue of Cath Lab Digest.

I wanted to add one thought to your article on the use of Benadryl. Our cath lab at Maine Medical Center in Portland, Maine has not been using Benadryl routinely for cardiac caths for several years now. In addition to the reasons that you mentioned for not utilizing this drug on a routine basis, I believe there is one more important reason — Benadryl can cause spasm of the urethra, which may then become a real issue, especially for males with enlarged prostate glands.

 Donna Gagne, RCIS, Level IV, Maine Medical Center, Portland, Maine,

Dear Donna,

Thanks for this.  I’d never thought of it. My compliments and appreciation.



Add new comment