A Totally Occluded Right Coronary Artery Presenting with a Normal Electrocardiogram

The surface electrocardiogram (ECG) is usually the first diagnostic test a patient with chest pain receives upon arriving to the emergency department (ED). The manifestation of regional myocardial ischemia or injury is dependent upon the distance of the culprit vessel from interrogating leads of the surface ECG, the time the ECG was obtained relative to the acute occlusion of the culprit artery, the mass of myocardium involved, and the lead arrangement used.3,6,7 An acutely occluded right coronary artery (RCA) usually manifests on surface electrocardiogram with ST-segment elevation in the inferior leads II, III, and avf sometimes extending to the lateral precordial leads V4-V6. This is the first report of a totally occluded proximal RCA presenting with a normal ECG. Case Report. A 47-year-old Caucasian male firefighter presented with 2 days of intermittent anginal-type chest discomfort while performing fire-fighting exercises. The pain is located at the top of his sternum radiating to both arms medially. There was associated diaphoresis but no dyspnea, nausea or vomiting. Coronary risk factors include smoking, family history and male gender. ECG shows sinus rhythm and a SR notching pattern in leads II, III, and avf. There was no ST-elevation or T-wave abnormality (Figure 1). Initial cardiac enzymes show a CPK of 154 IU (44–204 units/L), CK-MB of 6 ng/ml ( Discussion. Classic ST-elevation is seen in 81% of patients with an acute myocardial infarction (MI).10 In the cardiac catheterization lab, with transient balloon occlusion of the RCA, ST-elevation was seen in 92% of patients.9 The overall sensitivity of ECGs to diagnose myocardial infarction regardless of age, location, thickness, or presence of more than 1 infarct is 69%.6 The sensitivity of ECG rises to 75% when used to detect an AMI.6 If clinical factors are included along with the ECG criteria, the sensitivity rises to 81%.7 However, 45% of all patients with acute coronary syndromes (ACS) presenting to the ED do not exhibit the typical ECG changes of ACS and AMI.7 Moreover, 3.7% of patients with an AMI can have an entirely normal ECG and show on cardiac catheterization no occlusion of a major epicardial vessel.8 A totally occluded left anterior descending artery presenting with a persistently normal ECG has been reported.3 This patient failed to show the typical ECG changes seen with an obstructed RCA. This case, therefore, is the first report of a completely and proximally occluded RCA presenting with a persistently normal ECG. The mechanisms by which normal ECG waveforms can be preserved with a totally occluded major epicardial coronary vessel are multiple. The location of the myocardial infarct, its distance from the surface electrocardiogram, nontransmural necrosis, the size of infarcted muscle, history of previous MIs, the presence of dense collaterals, and the timing of the ECG with respect to the timing of vessel occlusion are all factors involved in the absence of ECG abnormalities in the context of an AMI.3 The inferior wall can directly be interrogated by the surface electrocardiogram and is not “hidden” as the left circumflex is. A threshold 3% of myocardium must become necrosed before changes become evident on surface electrocardiogram.8 Certainly in this patient, almost the entire inferior wall was in jeopardy since the RCA was occluded proximally. The initial ECG often precedes the complete occlusion of the epicardial artery and therefore appears normal. The concept of the pre-infarction ECG is not operative in this case because the patient had anginal symptoms 2 days prior to admission. The RCA was either completely occluded or critically stenosed before he presented to our ED. The very presence of collateral circulation to the RCA territory substantiates this supposition. Only during the actual reopening of the artery did the patient exhibit ST-elevation, which also quickly resolved. This and the previous case report3 demonstrate that a normal ECG in the context of clinical symptoms consistent with acute coronary syndromes should not lull the clinician into proceeding with an initially conservative approach. The fact that this patient failed to show any ECG abnormality even with crescendo anginal symptoms suggests a mechanism of perfusion not visible angiographically. Gibson et al. suggests the importance of establishing flow not just at an epicardial level but also a subepicardial level by examining TIMI frame counts during an acute MI and using the TIMI frame count as a prognostic indicator after successful reperfusion post-thrombolysis.2 Stone et al. also describe myocardial blush as a prognostic indicator for successful reperfusion post-angioplasty for acute myocardial infarction patients.1 In the absence of epicardial coronary flow, subepicardial flow, however measured, does not exist. This patient maintained at least minimal perfusion to the inferior wall (e.g. normal ECG) in the context of an already occluded RCA. Since this patient had minimal epicardial coronary flow at presentation, it is unlikely that subepicardial coronary flow is a major mechanism of alternate perfusion. The faint collateral circulation does not appear to provide enough perfusion other than allowing for myocardial hibernation. It is also possible we are underestimating the density of his collaterals because of inadequate force of injection or not staying on cine long enough to visualize the full extent of collaterals. However, dense collateral circulation, if present, would become visible in its entirety on at least one of the many cine runs during the diagnostic catheterization procedure. Therefore, we feel that this patient may have a nascent subendocardial perfusion that allowed him to not only preserve his inferior wall providing minimal perfusion at rest, but also allows for the maintenance of “normal” electrical milieu at prevent even minor repolarization abnormalities or ectopy to develop. In fact, this patient started having classical ECG ST-segment elevation current of injury only when epicardial flow was re-established. The presence of ST-elevation and regional ischemia during balloon inflation is a known phenomenon.9 However, this phenomenon is not applicable in this case because his RCA was totally occluded prior to the start of the procedure. It was the sudden re-opening of the RCA that caused the ST-changes and angina. This suggests embolization of microthrombi (that were unavoidably dislodged with introduction of wires and balloon catheters) causing interruption of flow in this critical microvascular network. The use of GP IIb/IIIa inhibitor successfully prevented the normal platelet aggregation thereby preventing microthrombi from getting lodged in this microvascular network, thus facilitating their clearance.4 This critical interruption of platelet function is probably the reason this patient’s ECG returned to normal 18 hours after the intervention. To date, we could not find in the medical literature any mention of subendocardial microvascular network (using Medline search). Such a theory of microvascular subendocardial network would be difficult to prove without first identifying it anatomically. Without some microvascular network providing even minimal perfusion, however, it is difficult to explain how this patient escaped a large myocardial area of injury with an occluded proximal RCA and minimal collaterals. Even several months later, the stress and rest cardiolyte images showed a small fixed inferior wall defect without any wall motion abnormalities on gated imaging. Because the fixed inferior wall perfusion defect is not associated with a corresponding wall motion abnormality, the defect is more likely due to diaphragmatic attenuation than a transmural myocardial infarction. Moreover, the inferior wall shows equal thickening as the other walls of the left ventricle. Even a non-transmural myocardial infarction of the inferior wall would at the very least cause a wall motion abnormality or decreased thickening of the inferior wall. Therefore, the myocardial necrosis, if present, is not extensive enough to show any functional impairment of wall motion or contractility. This patient probably represents the rare person with such a nascent rich plexus of subendocardial microvascular coronary circulation that he was able to maintain a normal appearing ECG even with a major epicardial coronary vessel totally occluded. We recommend further study to identify and better describe this subendocardial microvascular network. Acknowledgment. We would like to express our sincere gratitude to John Osecki for his assistance in the monographs used in this article.

1. Stone GW, Peterson MA, et al. Impact of normalized myocardial perfusion after successful angioplasty in acute myocardial infarction. J Am Coll Cardiol 2003;39:591–597. 2. Gibson CM, Murphy S, et al. Determinants of coronary flow after thrombolytic administration. J Am Coll Cardiol 1999;34:1403–1412. 3. Arjomand H, Mascarenhas D, et al. Normal electrocardiogram with total occlusion of the left anterior descending coronary artery. J Invas Cardiol 1999;11:500–502. 4. Neuman FJ, Blasini R, Schmidt C, et al. Effect of glycoprotein IIb/IIIa receptor blockade on recovery of coronary flow and left ventricular function after placement of coronary artery stents in acute myocardial infarction. Circulation 1998;98:2695–2701. 5. The EPISTENT Investigators. Randomized placebo-controlled and balloon angioplasty-controlled trial to assess safety of coronary stenting with use of platelet glycoprotein IIb/IIIa blockade. Lancet 1998;352:87–92. 6. Parker A, Waller B, et al. Usefulness of 12-lead electrocardiogram in detection of myocardial infarction: Electrocardiographic-anatomic correlations — Part I. Clin Cardiol 1996;19:55–61. 7. Parker A, Waller B, et al. Usefulness of 12-lead electrocardiogram in detection of myocardial infarction: Electrocardiographic-anatomic correlations — Part II. Clin Cardiol 1996;9:141–148. 8. Caceres L, Cooke D, et al. Myocardial infarction with an initially normal electrocardiogram-angiographic findings. Clin Cardiol 1995;18:563–568. 9. Berry G, Zaleswski A, et al. Surface electrocardiogram in the detection of transmural myocardial ischemia during coronary artery occlusion. Am J Cardiol 1989;63:21–26. 10. Rude R, Poole K, et al. Electrocardiographic and clinical criteria for recognition of acute myocardial infarction based on analysis of 3,697 patients. Am J Cardiol 1983;52:936–942. 11. Wohlgelerhter D, Cleman M, et al. Regional myocardial dysfunction during coronary angioplasty: Evaluation by two-dimensional echocardiography and 12-lead electrocardiography. J Am Coll Cardiol 1986;7:1245–1254.