The end of an electrocardiographic dogma: a prominent R wave in V1 is caused by a lateral not posterior myocardial infarction--new evidence based on contrast-enhanced cardiac magnetic resonance--electrocardiogram correlations

Since 1964, a tall and broad R wave in V1–V2, in the absence of right ventricular hypertrophy, complete right bundle-branch block, or Wolff–Parkinson–White syndrome, has been considered the sign of a posterior myocardial infarction (MI).1 According to this theory, the basal segment of the left ventricular (LV) inferior wall (formerly called posterior) bends upwards in the living subject, as a true posterior wall, so that an MI of this wall generates a necrosis vector directed forward. Thus, a prominent R wave in V1–V2 has been considered a mirror image of a Q wave in posterior leads (Figure 1). However, the study by Perloff1 that defines the most frequently used electrocardiogram (ECG) criteria for posterior MI assessed 20 patients, with autopsy verification in only 4 of them. At autopsy, the heart is evaluated outside of the chest, in a position (antero-posterior) completely different from the usual orientation of the heart inside the thorax, an approach usually referred to as St. Valentine's.2 The anatomical relationships between heart and thorax are better evaluated in vivo using cardiac magnetic resonance (CMR). Using this method, the basal segment of the LV inferior wall follows a straight alignment with respect to the other segments of this wall in more than two-thirds of subjects. In a small number of cases, the basal segment of the inferior wall bends upward, and only in rare cases of very lean subjects, the heart is in a more vertical position, with the entire inferior wall being more posterior.3,4 Original drawing of true posterior infarction with the QRS morphology according to Perloff.1 Already in the 1950s,5 it was demonstrated by pathologic correlations that the prominent R wave in V1 that appears in post-MI patients is due to a lateral LV-free wall necrosis. Later in the 1980s, Ward et al.6 demonstrated that the post-MI patients with a prominent R wave in V1 present a lateral MI at pathology, while Roark et al.7 showed that an MI of the basal inferior wall (formerly called posterior) does not originate any prominent R wave in V1. Contemporarily, a prominent R wave in right precordial leads was strongly associated with wall motion abnormalities of the basal lateral wall of the left ventricle at radionuclide angiography,8 although asynergies of adjacent inferior and lateral segments were common. In this study, a prominent R wave in V1 exhibited a very high specificity and a low sensitivity (36%) in diagnosing lateral MI. Despite this evidence, a prominent R wave in V1 in post-MI patients is still considered synonymous with posterior MI in current European and American guidelines.9,10 Cardiac magnetic resonance imaging with delayed contrast enhancement precisely detects MI and is the new gold standard technique for determining MI location, size, and transmural extent in vivo.11 In various studies, MI location by CMR has been correlated with electrocardiographic morphology in patients with Q-wave MI. We will present the most relevant data showing that a prominent R wave in right precordial leads is caused by a lateral rather than posterior MI. In studies performed at four different centres, MI location by CMR has been correlated with electrocardiographic features in patients with Q-wave MI (Figures 2–4).12–19 Pooling the data of the different studies together, a total of 237 patients with inferior, lateral, or infero-lateral MI were studied by ECG and CMR. Inclusion criteria were having had a previous first Q-wave MI and being in stable clinical condition. We excluded, patients with multiple MIs, or patients with contraindications to the magnetic resonance imaging (MRI). We also excluded patients with inadequate image quality of the MRI scan or with any condition that could have altered QRS shape, such as Wolff–Parkinson–White syndrome, advanced intraventricular conduction blocks, left anterior or posterior hemiblock or bundle-branch block, or severe LV hypertrophy. Finally, we excluded patients with evidence of MI involving the anterior or anteroseptal segments. Electrocardiographic and cardiac magnetic resonance images of an inferior infarct. Despite the clear infero-basal location of infarction at contrast-enhanced cardiac magnetic resonance (left-hand panel, between the white arrows), lead V1 does not show a prominent R wave but an rS morphology. Electrocardiographic and cardiac magnetic resonance images of a lateral infarct. A tall R wave in V1 corresponds to a lateral infarct at contrast-enhanced cardiac magnetic resonance (lower central and right-hand panels). Of note, the infero-basal segment (segment 4) does not present any sign of necrosis (lower left and right panels). Electrocardiographic and cardiac magnetic resonance images of an infero-lateral infarct. Q waves of necrosis are present in leads II, III, and aVF (inferior necrosis); an R ≥ S morphology is present in lead V1 (lateral necrosis). Contrast-enhanced cardiac magnetic resonance (four-chamber, long-, and short-axis views) clearly shows an infero-lateral necrosis. A 12-lead ECG was recorded on the same day as the MRI, at a speed of 25 mm/s and a voltage of 10 mm/mV. The cardiologists who analysed the ECG tracings were blinded to the clinical and CMR data. In each patient, the location and size of MI were evaluated by contrast-enhanced CMR. The LV myocardium was divided according to a 17-segment model.20 A segment was considered involved if contrast enhancement occupied >10% of the segment. All these 237 patients showed areas of delayed contrast enhancement at CMR. A total of 30 patients had a prominent R wave in right precordial leads: none of them showed an MI in the infero-basal segment (formerly called posterior) and only one of them showed a small subendocardial area of delayed contrast enhancement located in the mid-inferior segment; all the remaining 29 patients showed a lateral MI at CMR (i.e. true positives = 29; false positives = 1). Conversely, 119 of 207 patients without a prominent R wave in right precordial leads showed lateral involvement at contrast-enhanced CMR (i.e. true negatives = 88; false negatives = 119). Thus, the specificity of the R/S > 1 pattern in the diagnosis of lateral MI was very high (98.9%, 88/89), as well as the positive predictive value (96.7%, 29/30). On the other hand, the sensitivity of the R/S > 1 pattern was low (19.6%, 29/119), as well as the negative predictive value (42.5%, 88/207). From a practical point of view, a prominent R wave in V1 is a very specific sign for lateral wall involvement in post-MI patients, but its absence does not rule out a lateral MI. This pattern can be isolated or associated with an inferior MI if Q waves of necrosis are present in leads II, III, and VF. Thus, pathology,5–7 radionuclide,8 and CMR studies12–19 show that a prominent R wave in V1 appearing in post-MI patients is due to lateral involvement. The involvement of the basal segment of the inferior wall is not the origin of this pattern, as already accepted in some books.21,22 Although a prominent R wave in V1 is a specific sign of a lateral MI, its sensitivity is limited (ranging from 18 to 30%).12–19 It is well-known that there are cases of lateral MI with near normal ECG or only with a qr or a small r in lateral leads. One possible explanation for the limited sensitivity of the prominent R wave in V1 pattern in detecting a lateral MI is that a large MI is needed to generate a prominent R wave, in line with the observation that a large MI (either in terms of size or circumferential extent)23,24 is needed to generate Q waves of necrosis. In one study,16 the height, width, and surface (height × width) of R waves in V1 or V2 showed strong correlations with lateral MI size and were more predictive of lateral MI size. Figure 5 shows global MI size, infarct extent in the lateral and inferior LV walls and transmural infarct extent in a group of 50 patients with inferior and/or lateral MI.18 Myocardial infarction size was measured according to a semiautomatic validated method.25 In each contrast-enhanced short-axis image, the endocardial and epicardial borders of the left ventricle were manually drawn. The areas of delayed contrast enhancement inside LV boundaries were automatically identified using a fuzzy clustering method. The latter classifies signal intensity of each pixel in two classes corresponding to the remote non-infarcted myocardium and to hyper-enhanced areas. This approach identifies different tissues without the use of an explicit threshold. The computer-generated results were corrected by the user when needed. The sum of contrast-enhanced areas among all images was considered to reflect MI size and was expressed as percentage of the entire LV myocardium. Top panel: Global myocardial infarct size, and infarct size in the lateral and inferior walls in 50 patients with inferior and/or lateral myocardial infarction according to the presence or absence of a prominent R wave in V1.18 Patients with this pattern (blue histograms) have a higher global infarct size and infarct size in the lateral wall, despite a similar infarct size in the inferior wall, than do patients without (red histograms). Lower panel: Transmural extent of myocardial infarction in patients with inferior and/or lateral infarcts according to the presence or absence of a prominent R wave in V1. In patients with a prominent R wave in V1 (blue histograms), the infarction has a greater transmural extent. The transmural extent of the MI in each segment was scored according to a 4-point scale, where 1 corresponds to <25% of LV myocardial thickness, 2 is between 26 and 50%, 3 between 51 and 75%, and 4 corresponds to an extent >75% of LV thickness. Infarct transmural extent was calculated as the mean score in the segments with contrast-enhanced myocardium. These data show that a prominent R wave in V1 corresponds to a larger, more transmurally extended infarction in the lateral wall than in the patients without this pattern, despite a similar infarct size in the inferior wall.18 From an electrophysiological point of view, the myocardium of the basal inferior segment depolarizes late (40 ms after the beginning of the QRS complex),26 while the Q wave starts with the beginning of the QRS. Such a late activation of the basal inferior segment (within the QRS complex) would make it difficult for a lateral infarction to generate Q waves of necrosis or prominent R waves in V1–V2 as a mirror image. Finally, the necrosis vector generated by the infero-basal segment (formerly called posterior) would be directed towards V3–V4, while the necrosis vector generated by the lateral wall is directed toward V1 (Figure 6). Transverse plane of the thorax at cardiac magnetic resonance. The infarction vector produced by involvement of the wall formerly termed posterior (blue arrow) is directed towards V3–V4, while the infarction vector generated by the lateral wall (yellow arrow) is directed towards V1. The electrocardiographic diagnosis of a chronic lateral MI requires that other conditions also presenting a tall R wave in right precordial leads be excluded. These conditions include right ventricular hypertrophy, complete right bundle-branch block, Wolff–Parkinson–White syndrome, hypertrophic cardiomyopathy, severe chronic obstructive pulmonary disease, and normal variants of extreme laevorotation. Although the data supporting our ECG interpretation were collected in four different centres and the findings were consistent, the number of patients enrolled was limited, and studies on larger patient populations would be desirable. From a clinical point of view, the presence or absence of a prominent R wave in V1 has several implications. In patients with right coronary dominance, the LV inferior wall is perfused by the right coronary artery, while the lateral wall is usually perfused by the left circumflex artery. Myocardial infarction location with respect to the infarct-related artery should be taken into account when patients undergo myocardial revascularization. A prominent R wave in right precordial leads identifies patients with larger infarctions than when this pattern is absent. Lateral MIs more frequently undergo cardiac rupture than do inferior MIs.27 Inferior MIs are more frequently complicated by arrhythmic sudden cardiac death and papillary muscle dysfunction leading to acute mitral regurgitation than are lateral MIs.28 For decades, a tall and broad R wave in right precordial leads has been considered the sign of a posterior MI. This conclusion has been accepted as dogma, but it is now time to move on. In the absence of conditions with modified QRS shape, such as right ventricular hypertrophy, complete right bundle-branch block, or Wolff–Parkinson–White syndrome, the appearance of a prominent R wave in V1 in the course of acute coronary syndromes reflects a lateral MI, usually larger and more transmurally extended than when a prominent R wave in right precordial leads is absent. Thanks to this evidence, we propose incorporating these considerations in the standards of scientific guidelines. Conflict of interest: R.J.K. is an inventor on a US patent describing delayed-enhancement CMR, which is owned by Northwestern University.