Simultaneous ST-segment elevation in lead V1 and depression in lead V2

Journal of Electrocardiology Vol. 27 No. 3 1994

S i m u l t a n e o u s ST-Segment Elevation in Lead and Depression in Lead V2 A Discordant ECG Pattern Indicating Right Ventricular Infarction

K. H. Mak, MRCP(UK),*

B. L. C h i a , F R A C P , FACC,-I-

A. T. H. T a n , F R A C P , F A C C , * a n d A . J o h a n ,

FRACP, FACC*

Abstract: The major electrocardiographic change in right ventricular infarction (RVI) is ST-segment elevation in leads V4R--V6R. The authors describe a discordant electrocardiographic pattern of ST-segment elevation in lead V~ and STsegment depression in lead V2 in five patients presenting with acute transmural (Q wave) inferior infarction and RVI. There were 51 patients with transmural inferior infarction from a thrombolytic trial. In 25 patients, the ST-segment in the right-sided precordial leads was elevated by ~>I mm indicating the presence of RVI. In 5 of these 25 patients, simultaneous ST-segment elevation of 1.0-8.0 mm (mean, 2.8 -+ 2.9 mm) in lead V~ and ST-segment depression of 2.5 to 4.0 mm (mean, 3.3 + 0.6 mm) in lead V2 were also present. The discordant pattern of the ST-segments in leads V1 and V2 is an important and specific sign for RVI. K e y words: inferior, posterior, posterolateral, right ventricular infarction, right coronary artery.

responded to plasma fluid expansion. Autopsy in two patients revealed extensive infarction of b o t h the right and left ventricle. Up until the mid-1970s, no ECG abnormality specific for RVI was described. In 1976, Erhardt et al. 7 reported that -> 1 m m ST-segment elevation in lead CR4R (lead placed in the fifth intercostal space at the level of the mid-clavicular line) was a reliable sign of RVI, with a sensitivity of 70% and a specificity of 100%. Since then, the value of the right-sided precordial leads, V4R--V6R, for the diagnosis of RVI has b e e n well established, s We describe in this study a discordant pattern of ST-segment elevation in lead V~ and depression in lead V2. We believe that this pattern is a highly specific indicator of RVI in patients with acute inferior infarction.

Right ventricular infarction (RVI) has b e e n k n o w n to clinicians for m o r e t h a n 60 years. 1 About 40 years ago, attempts to m a k e an accurate diagnosis of RVI from the electrocardiogram (ECG) were unsuccessful. 2-4 Imerest in RVI gradually diminished with the assumption that d a m a g e to the right ventricle (RV) did not affect cardiac function significantly. 5 H o w ever, in 1974, C o h n et al. 6 reported six patients with acute myocardial infarction presenting with p r e d o m inant RV failure. These patients were in shock but

From the *Department of Cardiology, Singapore General Hospital and -{Department of Medicine, National University of Singapore, Singapore.

Reprint requests: Dr. K. H. Mak, Department of Cardiology, Tan Tock "Seng Hospital, Moulmein Road, Singapore i 130.

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Journal of Electrocardiology Vol. 27 No. 3 July 1994

Materials and Methods The patients were part of a research protocol on the use of the combination of streptokinase and recombinant tissue plasminogen activator (SK-rtPA) in an on-going study on acute transmural (Q wave) inferior infarction (TII). All patients presented with retrosternal chest pain typical of acute myocardial infarction. Serial creatine-kinase changes were also present. Patients with previous myocardial infarction clinically or electrocardiographically were excluded. Standard I2-1ead and right-sided precordial lead (V4R--V6R) ECGs were performed on admission to the coronary care unit. They were repeated regularly. Electrocardiograms were recorded on a simultaneous 3-channel, Hewlett Packard Page-writer. Paper speed was 25 ram/s, and Calibration was at 10 m m for i inV. ST-segment elevation in the right precordial leads was measured at 40 ms after the last nadir of the QRS complex using the PQ segment as the isoelectric line: The m e a n of three consecutive complexes was obtained wherever possible. Patients with QRS complexes more than 110 ms and coexisting ventricular conduction defects were excluded. Gated radionuclide ventriculography using in vivo labeling of the red blood cell with 20 mCi of technetium-99m was performed within 24 hours of admission. In addition, an echocardiogram and coronary arteriography with left ventriculography were also performed within 7 days of admission. All of these investigations were read by physicians independent of the other findings.

Results There were 51 patients with TII. Twenty-five (49%) had ECG evidence of RVI as reflected by STsegment elevation of -> 1 m m in any of the leads V4R--V6R. Five patients demonstrated the discordant pattern of the ST-segment in leads Vt and V2. In these patients, the m e a n of the peak creatine kinase was 4,000 (SD _+ 1,713) IU/L, and the m e a n serum potassium at admission was 3.9 (_+0.7) mmol/L. None of the other 26 patients with TII without RVI showed the discordant pattern. The ages of the five patients ranged from 35 to 59 years (mean, 46.0 _+ 9.8 years). Four were m e n and one was a woman. The ECGs were performed 1 - 7 hours after the onset of chest pain, with a m e a n of 3.0 ( _+3.0) and median of 1.5. The following changes were present:

Acute TII as reflected by ST-segment elevation in the inferior leads (II, III, and aVF) and reciprocal ST-segment depression in leads I and aVL was observed. The maximal change was in lead III, with ST-segment elevation ranging from 2.5 to 6.0 m m (mean, 3.8 + 1.4 mm). Subsequent ECGs showed evolution of TII and posterior or posterolateral infarction. Acute RVI as reflected by ST-segment elevation -->1.0 m m in at least one of the right-sided precordial leads V4R--V6R was observed. In three patients, the ST-segment elevation was -->2 mm. In addition, all five patients had 1.0-8.0 m m (mean, 2.8 +__ 2.9 mm) ST-segment elevation in lead V~, and 2 . 5 - 4 . 0 m m (mean, 3.3 +- 0.6 ram) STsegment depression in lead V2 (Figs. 1,2). In four of these patients, the ratio of ST-segment elevation in lead V~ to ST-segment depression in lead V2 was -< 1, and additional ST-segment depression in at least two of the leads V3-V6 was also present. In all of these patients, echocardiographic or radionuclide imaging studies showed changes consistent with RVI, and coronary angiograms showed lesions in the right coronary artery proximal to tile RV branch.

Discussion Erhardt et al. 7 found that I3 of the 18 patients w h o died of TII with postmortem evidence of RVI had ->1 m m of ST-segment elevation in the precordial lead CR4R. Using this ECG criterion, the sensitivity for detection of RVI was 70% and the specificity was I00%. Candell-Riera et al. 9 and Klein et al. *° subsequently described similar findings in lead V4R. Since then, ST-segment elevation has also been observed in the rest of the right-sided precordial leads V3R--VTR.11 Braat et al. 12 found that ST-segment elevation of -->1 m m in any of the leads V3R--V6• was a reliable sign of RVI. ~2 They also noted that lead V4R had the greatest sensitivity (93%) and predictive accuracy (93%). Croft et al. z3 showed that ST-segment elevation in one or more of the leads V4R--V6R was a highly sensitive (90%) and specific (91%) sign of acute RVI. Furthermore, the combination of these three leads was more sensitive and specific than any individual lead. On the contrary, later studies showed that the right lateral leads at V6R and VTR had the highest accuracy for the diagnosis of RVI. x4-16 In addition, they showed that the accuracy did not improve by combining these leads with more medial leads.

Discordant ECG Pattern in RVI

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Journal of Electrocardioiogy Vo[. 27 No. 3 July 1994

Amidst all of these observations in the right-sided precordial leads, Geft et al. I7 found that 8% of patients with ST-segment elevation in leads V~-V5 had occlusion of the right coronary artery instead of the left anterior descending artery. This "spillover" of ST-segment elevation from the right to left precordial leads was later verified by Coma-Canella et al. ~8They examined 72 patients who died from acute myocardia infarction and found that ST-segment elevation in leads V~-V3 was seen in about a quarter to a third of the patients with RVI. However, they concluded that the accuracy of this ECG abnormality was too low to be useful as a diagnostic criterion. To distinguish between anterior infarction and RVI, Reddy and Schamroth s pointed out that the ST-segment elevation in leads Vx-V5 of patients with RVI decreased from right to left. Apart from using right-sided precordial leads, there have also been attempts to evaluate the ECG signs on the standard 12-lead ECG for the diagnosis of RVI. Lew et al.~9 demonstrated that in patients with TII, the sensitivity and specificity for detecting concomitant RVI when the ST-segment depression in lead V2 was 50% or less than the magnitude of ST-segment elevation in lead aVF were 79 and 91% respectively. In another study, Andersen et al. 2° showed that in 24 autopsied patients with infer0posterior acute myocardial infarction on the ECG, the sensitivity and specificity for the diagnosis of RVI when ST-segment elevation in lead III exceeded that of lead II were 63-65% and 57-88% respectively. When Chou et al. 2~ demonstrated ST-segment elevation of at least 1 mm in lead V1 in 8 of their 1 l patients with RVI, they mentioned that 5 of them had ST-segment depression in the adjacent precordial leads. One of the eight ECGs, which was published in their study (case 6), clearly showed the discordant pattern of the ST-segments in leads V~ and V2. Similarly, when Morgera et al. 22 described the ST-segment and QRS changes in the right precordial leads in RVI, one of the ECGs published also showed this pattern. In 1990, Marriott 23 published two case studies showing the discordant pattern and for the first time highlighted that it was a reflection of RVI. However, in neither patient was the diagnosis confirmed by right-sided precordial leads, echocardiography, radionuclide study, or coronary angiography. From the results of our patients, it is reasonable to conclude that the simultaneous discordant pattern of ST-segment elevation in lead Vx and ST-segment depression in lead V2 is indeed an important ECG pattern for the diagnosis of RVI, with a sensitivity and specificity of approximately 20 and 100% respectively. In all five of our patients, the coronary

angiogram showed lesions in the right coronary artery that were proximal to the RV branch. Geft et al. 17 studied the infrequent occurrence of ST-segment elevation in the precordial leads in patients presenting with RVI and inferior myocardial infarction. Using a canine model, they found that suppression of the ECG manifestations of RV injury was due mainly to the dominant electrical forces of simultaneous inferoposterior injury of the left ventricle. Other studies suggested that TII with extension to the posterior or posterolateral regions could produce reciprocal ST-segment depression in the precordial leads. 24-28 For example, Lew et al. 29 demonstrated in 61 patients that inferior infarction, especially with concomitant left ventricular lateral wall involvement, depressed the ST-segments of the precordial leads. Most recently, Wong et al., 3° using intracoronary thallium-201, found that ST-segment depression in the anterior precordial leads during angioplasty of the right coronary artery was associated with a significantly greater extent of posterior ischemia of the left ventricle. On the other hand, RVI tends to elevate the ST-segments in the precordial leads, especially V~-V3.17,1s Coma-Canella et al. 18 found that in patients presenting with larger RVI and myocardial injury extending towards the anterolateral wall of the RV, there was a greater propensity for the ST-segment to be elevated in leads V~-V3. Our patients probably had extensive RVI that resulted in ST-segment elevation in both the rightsided precordial leads V4R--V6R and lead V~. The marked ST-segment depression in the precordial leads indicate that concomitant posterolateral involvement of the left ventricle was likely to be present as well. This "tug-of-war" between these two opposing forces probably resulted in the discordant pattern observed in our patients who may have a poorer prognosis due to the large amount of myocardial damage resulting from proximal right coronary artery occlusion. 3~,3x In conclusion, the discordant pattern of ST-segment elevation in lead V~ and ST-segment depression in lead V2 is another important and specific marker for acute RVI in the surface 12-lead ECG. At this time, the genesis of this ECG pattern is not entirely clear. However, we believe that it is most likely due to the combination of the simultaneous electrical forces of extensive acute RVI together with inferior, posterior, and lateral infarction of the left ventricle.

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Discordant ECG Pattern in RVI

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