stemi or stemi mimic? that is the question
24-year-old male with no past medical history presents to the ER with left-sided chest pain since 7 AM. The pain started while he was riding his bike, reliably when his heart rate was above 130 on self-monitoring. He reports pain then radiated to his left shoulder and arm. Some associated nausea, but no vomiting. Patient felt more short of breath and sweaty than normal on his routine 20-mile bike ride. Patient has had worsening symptoms over the past 3 bike rides. No chest pain at rest. Pain is now 2 out of 10. Denies any recent fevers or URI symptoms. Pain does radiate to the back. No medications prior to arrival.
EKG read as STEMI by machine however appears more J-point elevation. ASA ordered. CTA ordered to rule out aortic dissection. A repeat EKG showed worsening ST elevation in lead III and AVF along with V4 and the consulted cardiologist agreed to take the patient to the cath lab. After CTA ruled out aortic dissection verapamil, heparin, and nitro were given. Troponin returned negative and the chest pain resolved after nitro.
As his first description of chest pain was typical for angina, he had urgent angiography performed. Heart angiography showed normal coronary arteries with extensive myocardial bridging in the first obtuse marginal artery, the left circumflex is non-dominant artery with a large segment of severe (greater than 75%) myocardial bridging. He was discharged with exercise restrictions until seen in cardiology clinic for follow-up.
Exam and Vitals
Myocardial Bridging is a congenital cardiac anomaly in which one of the major coronary arteries, which normally course over the epicardium, has a segment that tunnels through the myocardium. The heart muscle overlying the intramyocardial coronary segment is the myocardial “bridge”. Myocardial bridging most often occurs with the middle segment of the left anterior descending artery.
The prevalence of myocardial bridging varies, with estimations depending on the diagnostic modality employed. One study using results from 1,056 autopsies, found myocardial bridging in samples with a mean of 25%. The estimated prevalence of myocardial bridging decreases significantly when diagnosed by coronary angiography, as compared to autopsy. One retrospective study looked at 25,982 patients undergoing coronary angiograms and found a myocardial bridging prevalence of 1.22% in this population. The prevalence of myocardial bridging, as determined by coronary angiography, in patients with hypertrophic cardiomyopathy or heart transplantation was 30%, which is much higher than the general population. Utilizing coronary computed tomographic angiography (CCTA) found prevalence rates similar to those found by autopsy, with one study discovering a prevalence of 30.5%.
Clinical Significance and Diagnosis
Most patients with myocardial bridging are asymptomatic and live normal lives. It is usually the more severe cases of myocardial bridging that present symptomatically. For the small percentage of patients that do present with symptoms, they will typically present with chest pain and ischemic EKG changes, mimicking an acute coronary syndrome (ACS) presentation. Symptomatic myocardial bridging is caused by the intramuscular portion of the coronary artery becoming compressed during systole to such a degree that distal branches are functionally occluded. Differentiating between ACS and symptomatic myocardial bridging is nearly impossible, though suspicion for symptomatic myocardial bridging should increase in young patients without typical risk factors for atherosclerotic disease. Patients with hypertrophic cardiomyopathy or prior heart transplantation are also at increased risk for experiencing symptomatic myocardial bridging.
As myocardial bridging is not an ED diagnosis, chest pain should be worked up to rule out ACS and other significant causes. Typically, it is not until coronary angiography for ACS concern that a diagnosis of myocardial bridging is made. Further workup outside the ED by cardiology utilizing cardiac CT and doppler-flow catheters is required to confirm the diagnosis.
If a proper ACS workup is done and there is a high suspicion for myocardial bridging based on presentation, risk factors, and cardiac catheterization, most cases can be treated effectively prior to definitive diagnosis with beta blockers or non-dihydropyridine calcium channel blockers (CCB) although there have not been many studies regarding this topic and much of the treatment is based in theory. In theory, these medications reduce the heart rate and decrease contractility thus lessening the compression of the intramuscular portion of the coronary artery affected. One case study showed that two years of CCB treatment was effective in the treatment of myocardial bridging. Of note, nitroglycerin should be avoided as it can worsen the compression of the coronary artery. For patients who have symptoms that do not respond to medical therapy or demonstrate ischemia, surgical revascularization via dissection of the affected coronary artery with combination bypass grafting has been shown to be effective. Otherwise, patients will typically receive lifestyle modifications such as smoking cessation, exercise training that doesn’t provoke symptoms, and dietary adjustments.
Differential Diagnoses of ACS Mimics
- Variant or prinzmetal angina
- Cocaine abuse
- Myocardial Bridging
- Spontaneous coronary artery dissection
- Coronary vasospasm
- Hypertrophic cardiomyopathy
- Pulmonary embolism
- Symptomatic myocardial bridging is a rare mimic of ACS, usually in younger patients, caused by compression of a coronary artery that tunnels through the myocardium.
- Risk factors include hypertrophic cardiomyopathy and prior heart transplant.
- Diagnosis is typically made via coronary angiography during an ACS work-up.
- Treatment with beta blockers or CCBs have theoretical benefit and nitroglycerin is thought to worsen compression.
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Aaron Wolfe,DO,FACEP, Director of Education for Emergency Medical Minute and Clinical Associate Faculty for Rocky Vista University College of Osteopathic Medicine
Jack Spartz MSIV at Tulane
Josh Wahba MSIV at Tulane
Peter Haskins MSIV at Tulane