A Common Electrocardiographic Finding in an Uncommon Presentation

ABSTRACT: Anterior ST-segment elevation is the hallmark electrocardiographic finding of acute anterior left ventricular infarction that is caused by occlusion in one of the branches of the left coronary artery. We report a case of marked ST-segment elevation in the precordial leads, with concomitant inferior ST-segment elevation that was caused by acute occlusion of the marginal branches of the right coronary artery (RCA) causing an isolated right ventricular myocardial infarction (RVMI) during coronary angioplasty. Isolated occlusion of the marginal branches of the RCA appears to be extremely rare. In the case presented, this was caused by an iatrogenic spiral dissection with subsequent stenting of the RCA. This case illustrates that diffuse ST-segment elevation in the precordial leads may occur due to the occlusion of the RCA or its branches. It is important to recognize this scenario, since the treatment of left ventricular myocardial infarction differs from that of RVMI, where maintaining adequate preload and avoiding vasodilators to preserve right ventricular stroke volume is crucial.

J INVASIVE CARDIOL 2011;23:E142–E144

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Anterior ST-segment elevation is the hallmark electrocardiographic finding of acute anterior left ventricular infarction that is caused by occlusion in one of the branches of the left coronary artery. We report a case of marked ST-segment elevation in the precordial leads, with concomitant inferior ST-segment elevation that was caused by acute occlusion of the marginal branches of the right coronary artery (RCA), causing an isolated right ventricular myocardial infarction (RVMI) during coronary angioplasty.

Isolated occlusion of the marginal branches of the RCA appears to be extremely rare. In our case, this was caused by an iatrogenic spiral dissection with subsequent stenting of the RCA. This case illustrates that diffuse ST-segment elevation in the precordial leads may occur due to the occlusion of the RCA or its branches. It is important to recognize this scenario, since the treatment of left ventricular myocardial infarction (LVMI) differs from that of RVMI, where maintaining adequate preload and avoiding vasodilators to preserve RV stroke volume is crucial.

Case Report. A 42-year-old woman with hypertension presented with 8 months of typical angina. She was referred for an outpatient coronary angiography. The right dominant coronary artery showed no significant disease (Figure 1). Shortly after engagement of the left coronary artery, she developed chest pain, hypotension and new ST-segment elevation in both the precordial and inferior leads. Left coronary angiogram revealed TIMI 3 flow without any evidence of complications, including dissection or thrombosis. Left ventriculogram showed normal left ventricular ejection fraction (LVEF) without any wall motion abnormalities. Symptoms and ST-segment elevation persisted. Repeat RCA angiogram showed an extensive spiral dissection extending from the ostium to the distal RCA, with flow-limiting occlusion in the 3 marginal branches (Figure 2). The dissection was successively treated with direct stenting with 3 bare-metal stents (Figure 3).

The patient left the catheterization laboratory with minimal residual chest discomfort and significant resolution of the ST-segment elevation. Two-dimensional echocardiography showed normal LVEF with no evidence of right or left ventricular wall motion abnormality.

Three hours after the initial procedure, the patient went into cardiac arrest due to ventricular fibrillation. Post-arrest electrocardiogram showed ST-segment elevation in both the precordial and inferior leads (Figure 4). Emergency repeat coronary angiography was performed. Left coronary angiogram was normal and RCA angiogram showed no evidence of residual dissection with TIMI 3 flow, but the 3 marginal branches remained occluded (Figure 5).

A repeat echocardiogram showed no significant changes compared to the previous study. The patient’s chest discomfort resolved and electrocardiogram showed complete resolution of the ST-segment elevation without residual Q-waves (Figure 6).

We report a case of ST-segment elevation in the precordial and inferior leads in a patient with an isolated RVMI that resulted from occlusion of the marginal branches of the RCA.

Discussion. Precordial ST-segment elevation is classically seen in cases of anterior wall myocardial infarction secondary to an occlusion in the left anterior descending coronary artery or its branches. In this case, acute occlusion of the large marginal branches of the RCA caused isolated RVMI that presented with ST-segment elevations in the precordial and inferior leads with reciprocal ST-segment depressions in the lateral leads (I and aVL). This is an uncommon and under-recognized cause of precordial ST-segment elevation.

Geft et al demonstrated that precordial ST-segment elevation can result from isolated RVMI in a canine model.¹ Van der Bolt et al showed that acute occlusion of the marginal branches after angioplasty could be associated with ST-segment elevations in the precordial leads.² Similar findings were reported by Sonoda et al when ST-segment elevation in the precordial leads occurred in a reproducible manner when the balloon occluded the marginal branches of the RCA.³

Isolated RVMI accounts for 0.4–2.4% of acute ST-segment elevation myocardial infarction.⁴ This can occur in any of the following situations: isolated acute occlusion of RV marginal branch during percutaneous coronary intervention,⁵ acute occlusion of a non-dominant RCA,⁶ or acute occlusion of the proximal RCA, with a patent graft protecting the distal vessel.⁷

RVMI usually occurs with simultaneous inferior wall infarction. The dominant electric forces generated by the ischemia of the inferior wall suppress the changes caused by the ischemia of the right ventricle. This is because the inferior wall has a larger mass of myocardium compared with the thin right ventricular wall; therefore, the precordial electrocardiographic manifestations of RVMI are absent in most patients.¹

Conclusion. This case highlights the fact that isolated RVMI can mimic anterior left ventricular infarction electrocardiographically, as both may present with ST-segment elevation in the precordial leads. The differential diagnosis of diffuse precordial ST-segment elevation following RCA intervention should include isolated RVMI in addition to anterior wall infarction. Early recognition of this scenario and subsequent initiation of the appropriate management may change the outcome of the disease.

References

1. Geft IL, Shah PK, Rodriguez L, et al. ST elevations in leads V1 to V5 may be caused by right coronary artery occlusion and acute right ventricular infarction. Am J Cardiol 1984;53:991–996.
2. Van der Bolt CL, Vermeersch PH, Plokker HW. Isolated acute occlusion of a large right ventricular branch of the right coronary artery following coronary balloon angioplasty: The only true ‘model’ to study ECG changes in acute, isolated right ventricular infarction. Eur J Heart 1996;17:247–250.
3. Sonoda M, Keigo T, Hizukuri K, et al. Transient but marked ST elevation in precordial leads caused by ischemia of the isolated right ventricular branch. Jpn Circ J 2001;65:129–131.
4. Antonelli D, Schiller D, Kaufman N, Barzilay J. Isolated right ventricular infarction: A diagnostic challenge. Cardiology 1984;71:273–276.
5. Koh TW, Coghlan JG, Lipkin DP. Anterior ST-segment elevation due to isolated right ventricular infarction during right coronary angioplasty. Int J Cardiol 1996;54:201–206.
6. Kircher T, Moothart R. Isolated right ventricular infarction with massive dilation: Acquired Uhl’s disease? Arch Pathol Lab Med 1982;106:385–387.
7. Muhammad KI, Kapadia SR. Anterior ST-segment elevation with right coronary artery occlusion: A unique case of isolated right ventricular infarction. Angiology 2008;59:622–624.

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From ¹the Department of Medicine, George Washington University, Washington, D.C., ²the Department of Medicine, St. Luke’s Hospital, Chesterfield, Missouri, and ³the Department of Medicine, Division of Interventional Cardiology, George Washington University, Washington, D.C.
The authors report no conflicts of interest regarding the content herein.
Manuscript submitted September 28, 2010, final version accepted October 25, 2010.
Address for correspondence: Amr Mohsen, MD, Department of Medicine, Ambulatory Care Center, Suite 5-441, 2150 Pennsylvania Avenue, NW, Washington, DC 22037. Email: Mohsen@gwu.edu