In the majority of cases, rupture of coronary artery plaques resulting in thrombotic occlusions is responsible for the pathogenesis of acute MI. Plaque disruption is thought to be an interplay between factors intrinsic to the plaque and extrinsic forces.2
Evidence suggests that plaque rupture reflects local plaque instability attributable to spontaneous or triggered disruption of a vulnerable plaque site that is manifested angiographically or pathologically as a single complex lesion. However, the pathophysiologic factors that are believed to precede plaque rupture—whether as a result of primary weakening of the fibrous cap attributable to inflammation, or as a result of the extrinsic influences of intraluminal mechanical forces modulated by sympathetic tone and catecholamines—may reasonably be expected to exert their effects in a widespread pattern throughout the coronary vasculature.3,4
Systemic alterations in platelet aggregation and clotting factors implicated in triggering acute MI would also be expected to increase the thrombogenic potential of eroded and vulnerable plaque sites throughout the coronary arteries.5
Because of the potentially widespread effect of these factors that adversely influence plaque lesions, as well as the typical diffuse nature of coronary atherosclerosis, plaque instability may develop in a multifocal pattern, resulting in multiple complex and unstable plaque lesions in anatomically different sites. Any one of these lesions may progress to total occlusion of a vessel that may result in MI.6
An acute inferior or inferoposterior transmural MI presents with ST elevations in leads II, III, aVF, and possibly V5 to V9. Reciprocal ECG changes that can be seen in up to 70% of inferior and 30% of anterior infarctions are observed occasionally during the initial period of acute infarction, presenting as ST segment depression in leads V1 to V3, I, and aVL. ST segment depressions of >1 mm in lead aVL were found to be highly sensitive and specific for diagnosing right ventricular infarction, with high positive and negative predictive value and high diagnostic accuracy.7
The absence of ST elevation in aVL and of ST depression in leads II, aVF, and III immediately excludes an occlusion in a proximal part of the LAD.
ST segment elevations in the right sided precordial leads, especially in V4R, of
1 mm have been shown to be a reliable marker of right ventricular involvement and a strong predictor of poor outcome.8–10
This has been observed in 60–90% of patients with right ventricular infarction; however, it is important to recognise the transient nature of this right sided ST segment elevation and the resolution of ECG changes within 10 h. In patients with occlusion of the RCA proximal to the first right ventricular branch, no ST segment elevation in lead V4R can occur in cases of concomitant posterior wall involvement.11
In such patients the incidence of right ventricular involvement may be underestimated on the basis of the ST segment elevation in V4R.
Right ventricular infarction is most commonly associated with infarction of the inferior or inferoposterior wall of the left ventricle, occurring in more then one third of such cases. Its electrocardiographic signs may be misinterpreted or even missed, especially when the damage to the lower portion of the right ventricle is small and a typical clinical picture is lacking. Acute MI involving only the right ventricle is rare. If the damage to the right ventricle is large enough, the serious clinical picture of right ventricular failure with hypotension and jugular neck vein distention, all in the presence of clear lung fields, is present. These patients are at increased risk of death, shock, and arrhythmias, due more so to the presence of the right ventricular myocardial involvement itself rather than to the extent of left ventricular myocardial damage.8,9,12
ST segment elevations in left precordial leads associated with right ventricular infarction may be misleading and can be erroneously interpreted as abnormalities associated with infarction of the anterior wall of the left ventricle.13,14
Two potential mechanisms may explain these observations. The anterior ST elevation is associated with a minimal inferior and a lack of posterior injury with a predominance of right ventricular injury, and results in ST elevations in leads V1–V4. In comparison to a large inferior MI with right ventricular involvement, ST elevations in V1–V4 are counteracted by the dominant electrical forces of the posterior injury.15
However, acute right ventricular injury and dilatation as a result of proximal RCA occlusion may lead to injury of a larger part of the right ventricular free wall; thus, the electrical forces are directed anteriorly and ST elevation may therefore be seen in leads V1–V4.16,17
Correct interpretation is facilitated by recognition of the following ECG evidence. First, evaluate the QRS vector of the precordial leads to distinguish anterior from inferior MI; the QRS vector of the precordial leads is right sided and reflects the right ventricular infarct. The clue that these are right sided precordial leads is that the QRS vector in V6 is opposite from QRS vectors of leads I and aVL. In the left sided precordial leads, the QRS in leads I, aVL, and V6 should look similar because these leads face the heart from analogous angles. Second, right ventricular infarction should be suspected when the mean ST segment vector is directed more than 90° to the right in the frontal plane. This axis orientation produces downward displacement of the ST segment in lead I and anteriorly, and ST segment elevation in leads V1–V4. The probability of right ventricular infarction increases as the mean ST vector becomes directed more and more to the right and anteriorly. In contrast, if there is an infarct of the anteroseptal region of the left ventricle, the mean ST segment vector resulting from epicardial injury is usually located from −30° to −90° to the left in the frontal plane, which produces an elevation of the ST segment in lead I. Therefore, the frontal plane axis of the mean ST segment vector separates the two infarct types, although the elevated ST segments are oriented anteriorly in both right ventricular and anteroseptal infarction.18–20
Proximal RCA occlusion compromising right ventricular branch perfusion commonly results in right ventricular ischaemic dysfunction. In some cases with proximal RCA culprits, collaterals or spontaneous reperfusion preserve right ventricular performance.21
Acute MI with simultaneous ST segment elevation in the precordial and inferior leads can also be caused by a wrapped LAD, defined as an LAD extending around the apex to supply part of the inferior wall of the left ventricle. The clinical presentation is usually benign because there is occlusion of the LAD distal to at least one diagonal branch, which in turn leads to a small mass of ischaemic anterior myocardium.22
Patients with simultaneous ST segment elevation resulting from non-wrapped LAD occlusion usually demonstrate ST segment elevation of
2 mm and a sum of inferior ST segment elevation of >11 mm. Following angiography, the majority of these patients have multivessel and severe obstructive disease with preexisting dependent collaterals. These patients usually present with serious clinical symptoms and exhibit unfavourable clinical outcomes.23
In our patient, there was clear evidence of an acute inferior wall MI with ST elevations in II, III, aVF, V5 and V6 accompanied by reciprocal changes in I and aVL (). In this clinical case, ST segment elevations in V1–V4 were due to right ventricular involvement, which was confirmed by coronary angiography, with typical clinical signs of right ventricular ischaemia.
- ST segment elevation in V1–V4 may be caused by right ventricular infarction.
- ST segment elevations in the right sided precordial leads, especially in V4R, of 1 mm is a marker of right ventricular involvement and a strong predictor of poor outcome.
- The absence of ST elevation in aVL and of ST depression in leads II, aVF, and III immediately excludes an occlusion in a proximal part of the left anterior descending coronary artery.