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International Journal of Bioelectromagnetism
Vol. 5, No. 1, pp. 130-131, 2003.

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Right Ventricular MI

Rory Childers

University of Chicago Medical Center, Chicago IL, USA


The ECG in RV MI shows relatively short-duration ST segment elevation over the right ventricular wall; it has the following unique features;

a)   the ST elevation in V1>V2 or V3[1]; and spatially projects a rightward anterior vector in the frontal plane. Since most cases show also acute inferior MI, this rightward influence often makes the frontal axis of the ST segment approximate 120o; the STiii > STii

b)   the ST is elevated in leads V3R and V4R[2]. Besides being diagnostic of RV infarction [sensitivity=88%; specificity=78%] ST elevation in V4R independently predicts a higher incidence of pace-requiring AV block, ventricular arrhythmias, cardiogenic shock and a greater in-hospital mortality: 31% vs. 6%[3]

c)   V3R and V4R may also show pathologic Q waves; these respective leads normally register an rS or rSr prime deflection in 99-100% and 91% of cases[4].

d)   Although the enzymes show a diagnostic rise, the ST elevations return to normal without further T wave change

e)   Catheterization will show occlusion in the RCA, if dominant, or in the RV branch of a diminutive RCA

f)    In many cases the function of the right ventricle improves sufficiently quickly to suggest reversible ischemia as opposed to muscle necrosis. In similar fashion the Q waves in V3R and V4R, having appeared sooner than is the case with LV MI, disappear rapidly also, seldom seen after 2 months.

g)   while most right ventricular infarctions show transmural inferior MI, evidence for the latter is occasionally lacking

h)   atrial infarction is seen if 3o AV nodal block permits scrutiny of the elevated STa wave

i)    RV coronary insufficiency during exercise is also suggested by stress-induced elevation of ST in V4R[5] (occasionally V1). In other words, while nonocclusive angina, or stress induced myocardial ischemia in the LV, is expressed as ST depression, nonocclusive ischemia, proximal RCA or RV branch PTCA, and acute RV MI, all uniquely cause ST elevation over the RV, optimally in V4R. Thus the RV does not exhibit a physiologically separable subendocardium

In RV MI the ST elevation in V1 has a dome-like character, while ST is normal or even depressed in V2. In isolated RV MI [i.e. without left ventricular ischemia] the ST elevations in V1-V3 may resemble entirely an acute ASMI, except no Q waves develop and the ST’s rapidly normalize.

The very early appearance of both ST and QS in right precordial leads and their rapid disappearance (generally within 10 hours) make the expression RV ischemia[6] more appropriate than infarction. The literature, trying to explain these RV peculiarities, emphasizes the lower O2 needs of a ventricle with less myocardial mass, less squeeze of intramural vessels, lower preload and afterload, in which coronary flow takes place in both systole and diastole, with 30% from the left coronary system. But there are other reasons for differential behavior of the two ventricles in the face of ischemia. In 1995 the Antzelevitch group had already[7] noted that there were marked differences between the endocardium and epicardium in terms of a) the impact of cycle length change on action potential [AP] duration, b) the morphologic characteristics of the AP in these two regions which were a function of the strength of the transient outward current [Ito]. In further papers these authors noted that the presence of Ito in a tissue layer rendered it more sensitive to ischemia[8]. Of specific relevance to the subject at hand, the canine right ventricular epicardium was very much more sensitive to ischemia than the epicardium of the left ventricle[9]. The action potential typifying Ito shows a ‘spike and dome’. It is probably no coincidence that the ST elevations seen in the V1 of RV ischemia are described as “dome-like”. Thus the RV is more sensitive to ischemia, shows the classic features of same [ST elevation and Q waves] much sooner. Of signal importance: Ito is maximally expressed at slow heart rates or long cycle lengths, explaining why the bradycardia of AV nodal block is so severe a complication, responding well to RV pacing.


References

1. Geft PL, Shah PK, Rodriguez L : ST elevation in leads V1-V5 may be caused by right coronary artery occlusion and acute right ventricular infarction. Am J Cardiol 1984; 53: 991-6.

2. Kulbertus HE, Rigo P, Legrabd V: Right ventricular infarction: Pathophysiology, diagnosis, clinical course, and treatment. Mod. Concepts Cardiovasc. Dis 1985; 54:

3. Zehender M, Kasper W, Kauder E, Schonthaler M et al.: Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. N Engl J Med 1993;328:981-8

4. Morgera T, Alberti E, Silvestri F, Pandullo C, Delle Mea MT, Camerini F: Right precordial ST and QRS changes in the diagnosis of acute right ventricular infarction. Am Heart J 1984; 108:13-18.

5. Bratt SH, Kingma H, Brugada P, Wellens HJJ: Value of lead V4R in exercise testing to predict the proximal stenosis of the right coronary artery: J Am Coll Cardiol 1985;5:1308-11

6. Goldstein JA J AM Coll Cardiol 2002;40:841-53

7. Litovsky SH, Antzelevitch C Transient outward current prominent in canine ventricular epicardium but not endocardium. Circ Res 1988;62:116-126

8. Lukas A, Antzelevitch C: Differences in the electrophysiological response of canine ventricular epuicardium and endocardium to ischemia. Role of the transient outward current Circulation 1993;88:2903-2915

9. Di Diego JM, Zhuo-Qian Sun, Antzelevitch C: Ito and action potential notch are smaller in left vs, right canine ventricular epicardium. Am J Physiol 1996;271: Heart Circ Physiol 40: H548-H561.

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