Diagnostic Significance of a Small Q Wave in Precordial Leads V2 or V3

Background: An abnormal Q wave is usually defined as an initial depression of the QRS complex having a duration of ≥40 ms and amplitude exceeding 25% of the following R wave in any contiguous leads on the 12‐lead electrocardiogram (ECG). However, much smaller Q waves are sometimes recorded on the ECG. This study investigated the diagnostic value of the small Q wave recorded in precordial leads V₂ or V₃ on the ECG. Methods: We investigated 807 consecutive patients who underwent coronary angiography. A small Q wave was defined as any negative deflection preceding the R wave in V₂ or V₃ with <40‐ms duration and <0.5‐mV amplitude, with or without a small (<0.1‐mV) slurred, spiky fragmented initial QRS deflection before the Q wave (early fragmentation). ECG and coronary angiographic findings were analyzed. Results: The small Q wave was present in 87 patients. Multiple logistic regression analysis revealed that presence of a small Q wave was a strong independent predictor of any coronary artery stenosis or left anterior descending artery (LAD) stenosis (odds ratio = 2.706, 2.902; P < 0.001, < 0.001, respectively). Conclusion: A small Q wave (<40‐ms duration and <0.5‐mV amplitude) in V₂ or V₃ with or without early fragmentation significantly predicted the presence of CAD and, especially, significant stenosis in the LAD. Ann Noninvasive Electrocardiol 2010;15(2):116–123     

Conventional Electrocardiogram in Arrhythmogenic Right Ventricular Dysplasia-Cardiomyopathy and Idiopathic Right Ventricular Outflow Tract Tachycardia

Objective: Arrhythmogenic right ventricular dysplasia up to now is a rare cardiomyopathic entity with certain difficulties in clinical definition of diagnostic criteria. In 42 patients with major and minor criteria of arrhythmogenic right ventricular dysplasia and 25 patients with idiopathic ventricular arrhythmia, the role of conventional ECG in the diagnosis of arrhythmogenic right ventricular dysplasia was reevaluated. Methods: In standard 12-lead ECG, QRS duration was measured in limb lead D₁, and in V₁-V₆. A ratio of the sum of right (V₂+ V₃) and left (V₄+ V₅) was calculated. T wave inversions, Epsilon wave, and mechanisms of advancing right bundle branch block were analyzed. Results: In 39 out of 42 patients (93%) with the diagnosis of arrhythmogenic right ventricular dysplasia, a ratio of right and left precordial QRS duration of >1.2, a maximum right precordial QRS duration of > 100 ms in 10 cases (26%) and >110 ms in 29 cases (74%) could be found. Incomplete right bundle branch block with right precordial T inversions was found in one case. The ECG in two patients revealed a precordial R/S transition in V₁ or V₂; in all other cases, R/S transition was localized in V₃ or V₄. R peak time was normal (< 0.04 s) in all cases, a “notching” or “slurring” of the S wave was striking in 16 cases. T wave inversions were found in 27 cases and definite Epsilon wave in only one case. Although incomplete right bundle branch block and certain preforms could also be disclosed in four patients with idiopathic right ventricular outflow tract (RVOT) tachycardia, localized right precordial QRS prolongation could be excluded in all but one of these cases. Localized right precordial QRS duration prolongation in one case was probably due to a rotation of the heart with a precordial R/S transition between V₁ and V₂. Conclusion: Localized right precordial QRS prolongation in a normal precordial R/S transition: (a) seems to be the most important aspect of arrhythmogenic right ventricular dysplasia at conventional ECG, with a sensitivity of 93% and a specificity of 96% in order to distinguish idiopathic RVOT tachycardia; (b) can appear with (64%) or without (36%) secondary T wave inversions; and (c) is due to a “parietal” block sparing the specialized conducting system.     

The characteristics of a 12-lead electrocardiogram measuring premature ventricular contractions originating from the tricuspid annulus using the clock position method

Objective

This study aimed to analyze the conventional surface electrocardiogram (ECG) characteristics of premature ventricular contractions (PVCs) originating from the tricuspid annulus and to investigate the efficacy of locating their origins according to ECG results.

Methods

Eight patients who underwent radiofrequency ablation in the First Hospital of Shanxi Medical University (China) were included in the study. Pace mapping (PM) was used to analyze the characteristics of the PVCs originating from the tricuspid annulus recorded via 12-lead body surface ECGs.

Results

An R-wave was found in leads I, V₅, and V₆. The QRS wave was narrower when the PVCs originated from the septum and shifted in lead V₃ (R-wave amplitude/S-wave amplitude in the precordial lead—1). The QRS wave was broadest when the PVCs originated from the 7 to 9 o'clock position. The augmented vector left lead showed RS, QS, or RSR-type waves with a low amplitude when the PVCs originated from the upper part of the annulus. When the PVCs originated from the lower part of the annulus, the augmented vector right lead reflected multidirectional and QS-type waves.

Conclusion

The ECG-lead characteristics related to the origin of PVCs in the tricuspid annulus indicate some level of significance and can be used to formulate a specific diagnosis.     

Electrocardiogram mimics of acute ST-segment elevation myocardial infarction: insights from cardiac magnetic resonance imaging in patients with tako-tsubo (stress) cardiomyopathy

An important subset of patients (10%) with chest pain and ST-segment elevation on initial electrocardiogram (ECG) do not have acute coronary occlusion. In our experience, 5% of women presenting with chest pain and ST-segment elevation are proven to have the newly recognized syndrome of tako-tsubo (stress) cardiomyopathy (TC). Patients with TC present with clinical and electrocardiographic features mimicking ST-segment elevation anterior myocardial infarction due to left anterior descending (LAD) occlusion. The initial and subsequent ECG findings in TC are therefore of clinical importance. Thirty-three consecutive patients with TC were identified from within a single institution community-based cardiology practice. All were female aged 32 to 90 years (mean, 68 years) with acute chest pain associated with an emotional or physical stressful event, and akinesia of the mid-distal left ventricle but without significant atherosclerotic coronary artery obstruction. All patients with TC presented with anterior ST-segment elevation most marked in leads V₁ to V₅, maximal in leads V₂ and V₃. Distribution of ST-segment elevation was similar to 44 female control patients with acute (LAD) occlusion. ST-segment elevation magnitude was less in patients with TC (1.4 ± 1.5 mm) than in patients with LAD occlusion (2.4 ± 2.2 mm) (P < .001) but with considerable overlap. Left ventricular ejection fraction (LVEF) was significantly lower in TC patients (29% ± 9%) than in patients with LAD occlusion (42% ± 13%) (P < .05). Peak troponin T was significantly lower in patients with TC (0.64 ± 0.86 ng/mL) than in patients with LAD occlusion (3.88 ± 4.9 ng/mL) (P < .0001). Cardiovascular magnetic resonance imaging detected myocardial necrosis in 1 patient with TC. At follow-up, LVEF returned to normal (> 50%) in all patients with TC. In patients with TC, ECG evolution was characterized by resolution of ST-segment elevation, appearance of T-wave inversion (most marked in precordial leads V₃-V₆ and limb leads aVL, I, and −aVR), QTc interval prolongation (378 ± 60 milliseconds [initial] vs 470 ± 72 milliseconds [follow-up], P < .05), and reappearance of precordial R waves. In conclusion, patients with TC frequently present with anterior ST-segment elevation, which cannot be reliably distinguished from that of acute LAD occlusion. In TC, the combination of minimal troponin release, absent delayed hyperenhancement on cardiac magnetic resonance imaging (in most of patients), and return to normal LVEF is consistent with the presence of significant myocardial stunning. The ECG evolution of progressive T-wave inversion, QTc interval lengthening, and R-wave reappearance could be the electrophysiologic manifestation of an underlying stunned myocardium in this condition.     

Clinical Significance of QS Complexes in V1 and V2 without Other Electrocardiographic Abnormality

Background: In the absence of other electrocardiographic (ECG) abnormalities, QS deflections simultaneously in both of the leads V₁–V₂ may have multiple possible causes. Despite much information in the literature indicating that this is an unlikely pattern for pure septal infarction, such an ECG diagnosis is frequently given. Methods: Ninety‐nine cases having QS deflections in both leads V₁ and V₂ but no other ECG abnormality were compared to 99 other patients with entirely normal ECGs, to whom they were matched by age, gender, and the presence or absence of septal Q waves. Retrospective analysis of medical records was performed to determine the nature of any cardiovascular disease in these two groups, and to find a possible explanation for the ECG abnormality. Results: Because of its intermittence in subjects with multiple ECGs, QS deflections in leads V₁–V₂ appeared most often to be an artifact of precordial lead placement. Prior myocardial infarction, or presence of clinical coronary disease was present in only about 20% of the cases. Neither the intermittence of Q wave in V₂ on repeated ECGs nor the absence of septal Q waves was useful in distinguishing between those with and without coronary heart disease. Conclusions: This ECG pattern is a sign of prior myocardial infarction in only a minority of cases, and in the latter, infarction limited to the interventricular septum is exceptional. This ECG finding should be interpreted as a nonspecific QRS abnormality with multiple possible causes. Clinical correlation and repeat tracings with attention to lead placement will help to clarify its significance.     

New algorithm for the localization of accessory atrioventricular connections using a baseline electrocardiogram

Objectives. In this study, we propose a new algorithm for accessory atrioventricalar pathway localization using a 12-lead electrocardiogram (ECG).Background. Radiofrequency catheter ablation produces a very discrete lesion, and ECG localization based en surgical dissection is obsolete.Methods. Stepwise discrimination analysis was used to assess the relation of 18 pro-excited ECG (QRS duration >100 ms) variables to the site of successful ablation in 93 patients. The most discriminating variables were combined to form rules for each location. The ECGs were retested by these rules to determine predictive accuracy.Results. If the precordlal QRS transition was at or before lead V₁, the pathway had been ablated on the left side. If it was after lead V₂, the pathway had been ablated on the right side. If the QRS transition was between leads V₁and V₂or at lead V₂, then if the R wave amplitude in lead I was greater the S wave by ≥1.0 mV, it was right-sided; otherwise, It was left-sided (p < 0.0001, sensitivity 100%, specificity 97%). Right-sided pathways. If the QRS transition was between leads V₂and V₃, the pathway was right septal; if after lead V₄, it was right lateral. If it was between leads V₃and V₄, then if the delta wave amplitude in lead II was ≥1.0 mV, it was right septal; otherwise, it was right lateral (p < 0.0001, sensitivity 97% specificity 95%). In right lateral locations, if the delta wave frontal axis was ≥0 °, or if it was <0 ° but the R wave amplitude in lead III was ≥0 mV, it was anterolateral; otherwise, it was pesterolateral (p < 0.0001, sensitivity 100%, specificity 87.3%). Anteroseptal pathways had two or more positive delta waves in leads II, III and aVF (p < 0.0001, sensitivity 100%, specificity 100%). Postereseptal pathways (two or more negative inferior lead delta waves) were less well discriminated from right midseptal pathways (inferior wave sum ≤1≥−1) (p < 0.0001, sensitivity 76.5%, specificity 71%).Leftsided pathway. Two or more positive delta waves in the inferior leads or the presence of an S wave amplitude in lead aVL greater than the R wave, or both, discriminated left anterolateral pathways from posterior pathways (p < 0.001, sensitivity and specificity 100%). If the R wave in lead I was greater than the S wave by ≥0.8 mV, and the sum of inferior delta wave polarities was negative, the location was posteroseptal; otherwise, It was posterolateral (p < 0.05, sensitivity 71.4%, specificity 100%).Conclusions. Using the algorithm derived, a right-sided accessory pathway can be reliably distinguished from one that is left-sided, right free wall from right septal, right anterolateral from posterolateral and anteroseptal from other right septal pathways. Left anterolateral pathways can be distinguished from left posterior pathways and left posterolateral pathways from left posteroseptal pathways.     

Mechanisms of abnormal Q waves in hypertrophic cardiomyopathy assessed by intracoronary electrocardiography

INTRODUCTION: To clarify the mechanisms of abnormal Q waves in hypertrophic cardiomyopathy (HCM), local epicardial electrical activities were assessed by intracoronary electrocardiography (ECG). METHODS AND RESULTS: Unipolar intracoronary ECG was recorded by introducing a guide wire for angioplasty into the left anterior descending artery (LAD) in 20 patients with HCM and 10 control subjects. Intracoronary ECG showed no Q waves in any control subjects. Intracoronary ECG showed no Q waves in 8 HCM patients without abnormal Q waves on surface ECG. In 12 HCM patients with abnormal Q waves on surface ECG, 4 showed Q waves on intracoronary ECG associated with regional wall-motion abnormalities, suggesting Q waves are formed by loss of electrical forces due to transmural myocardial fibrosis. The remaining 8 patients, who did not have Q waves on intracoronary ECG, showed greater thickening of the basal free wall than the apical free wall, with no wall-motion abnormalities. Intracoronary ECG was characterized by increased R or R' waves and prolonged R peak times at the proximal LAD, suggesting Q waves are formed by increased electrical forces of hypertrophied basal septal and/or ventricular free wall, unopposed by apical forces. CONCLUSION: The study findings provide evidence for two mechanisms of abnormal Q waves in HCM: (1) loss of electrical forces due to transmural myocardial fibrosis, and (2) altered direction of resultant initial QRS vector due to increased electrical forces of disproportionate hypertrophy of the basal septal and/or ventricular free wall, unopposed by apical forces.     

Concordance of distinguishing electrocardiographic features during sinus rhythm with the location of accessory pathways in the Wolff-Parkinson-White syndrome

Knowledge of the location of accessory pathways in patients with Wolff-Parkinson-White (WPW) syndrome is pertinent to patient management. Despite the recognition that features of delta waves present during maximal preexcitation reflect ventricular activation at different sites around the anulus fibrosus, the value of electrocardiographic patterns observed during sinus rhythm, when ventricular preexcitation is often not maximal for identifying accessory pathway locations, has not been determined. In this study, 12-lead electrocardiograms recorded during sinus rhythm from 66 patients with WPW syndrome were analyzed for delta-wave polarity, QRS axis in the frontal plane, the pattern of precordial R-wave transition, and concordance between electrocardiographic patterns and the site of the accessory pathway determined using catheter and intraoperative computer mapping. Electrocardiograms from patients with left lateral sites showed negative delta waves in leads I or aVL, a normal QRS axis and early precordial R-wave transition (20 of 24 patients); left posterior sites manifested negative delta waves in II, III and aVF and a prominent R wave in V1 (14 of 16 patients); posteroseptal sites had negative delta waves in II, III and aVF, a superior QRS axis and an R less than S in V1 (all 16 patients); right free wall locations manifested negative delta waves in aVR, a normal QRS axis, and R-wave transition in V3-V5 (6 of 6 patients); and anterior septal sites had negative delta waves in V1 and V2, a normal QRS axis, and R-wave transition in V3-V5 (4 of 4 patients). Characteristic electrocardiographic patterns were not observed in 5 patients because of insufficient preexcitation. Each had a left lateral or left posterior pathway. Overall, the proposed electrocardiographic criteria derived during sinus rhythm identified correctly the accessory pathway location in 60 of 66 patients (91%). Thus, the electrocardiogram provides the physician with a reliable noninvasive means of regionalizing the location of accessory pathways in patients with WPW syndrome.     

Evaluation of very low amplitude intra-QRS potentials during the initial minutes of acute transmural myocardial ischemia

Introduction

Low-level electrocardiographic changes from depolarization wavefront may accompany acute myocardial ischemia. The purpose of this study was to assess the changes of microvolt amplitude intra-QRS potentials induced by elective percutaneous coronary interventions (PCI).

Methods

Fifty-seven patients with balloon inflation periods ranging from 3.1 to 7.3 minutes (4.9 ± 0.7 min) were studied. Nine leads continuous high-resolution ECG before and during PCI were recorded and signal-averaged. Abnormal intra-QRS at microvolt level (μAIQP) were obtained using a signal modeling approach. μAIQP, R-wave amplitude and QRS duration were measured in the processed ECG during baseline and PCI episodes.

Results

The mean μAIQP amplitude significantly decreased for each of the standard 12 leads at the PCI event respect to baseline. Left anterior descending artery (LAD) occlusion resulted in a decrease μAIQP in both the precordial leads and the limb leads, while right coronary (RCA) and left circumflex (LCx) arteries occlusions mainly affected limb leads. R-wave amplitude increased during PCI in RCA and LCx groups in lead III but decreased in the precordial leads, while the amplitude decreased in the LAD group in lead III. The average duration of the QRS augmented in groups RCA and LCx but not in the LAD group.

Conclusions

Abnormal intra-QRS potentials at the level of μV provide an excellent tool to characterize the very-low amplitude fragmentation of the QRS complex and its changes due to ischemic injuries. μAIQP shows promise as a new ECG index to measure electrophysiologic changes associated with acute myocardial ischemia.     

Relation between QRS changes and left ventricular function after coronary artery bypass grafting

Preoperative and serial postoperative electrocar-diograms (ECGs) were reviewed in 104 patients undergoing rest and exercise radionuclide angiocardiography before and 1 to 12 months after coronary artery bypass grafting (CABG). Five patient groups were defined by ECG findings before and after CABG: Group I—normal ECG before and no ECG change after CABG; Group II—prior myocardial infarction by ECG before but no QRS change after CABG; Group III—all patients with a minor QRS change (< 0.04-second Q wave, loss of R-wave amplitude) after CABG; Group IV—all patients with a major QRS change (≥ 0.04-second Q wave) after CABG; Group V—all patients without new Q waves or loss of R-wave amplitude but with a major QRS change (conduction disturbance) after CABG. Mean resting ejection fraction changed little after CABG in all groups, although the 0.03 increase in Group I was significant (p < 0.05). Group IV had the largest decrease in resting ejection fraction after CABG (0.04), but this was not statistically significant. Mean exercise ejection fraction increased significantly (p < 0.0001) in Groups I, II and III but not in Groups IV and V. QRS changes do not consistently reflect impairment of left ventricular (LV) function after CABG.     

不同心电图特征对特发性室性期前收缩右室流出道起源部位诊断价值比较

目的 比较体表心电图鉴别右室流出道室性期前收缩具体起源点的诊断价值。 方法 分析经射频导管消融治疗室性期前收缩靶点明确为右室流出道的139例患者（其中右室流出道间隔部起源的111例,游离壁起源的28例）的体表心电图特点,以室性期前收缩时Ⅰ导联主波形态、QRS波时限、胸前导联移行及下壁三肢体导联有无顿挫进行分析,评估其对鉴别右室流出道室性期前收缩具体起源点的准确性。 结果 以室性期前收缩的QRS波宽度≥140 ms判断为右室流出道游离壁起源的灵敏度为86%,特异度为58%;以下壁三肢体导联均有顿挫或切迹判断为游离壁起源的灵敏度为64%,特异度为91%;以Ⅰ导联主波向上判断游离壁起源的灵敏度为86%,特异度为73%。 结论 I导联主波方向及下壁三肢体导联有无顿挫能对鉴别游离壁还是间隔起源有较大实用价值。     

R- and S-wave amplitude changes with acute anterior transmural myocardial ischemia. Correlations with left ventricular filling pressures

The value of R- and S-wave amplitude changes as electrocardiographic (ECG) markers of myocardial ischemia and dysfunction was evaluated using coronary angioplasty as a model of acute transmural ischemia and ST segment elevation. Hemodynamic data and 12-lead ECGs were recorded at baseline and during coronary occlusion in 34 patients with left anterior descending artery angioplasty. In the precordial leads V1 through V4, the sum of R-wave amplitude increased in 17 patients, was unchanged in ten, and decreased in seven; the sum of S-wave amplitude decreased in 33 patients (including two patients with complete loss of S wave) and increased in one. Mean R-wave change was 2.7 +/- 6.2 mm, mean S-wave change was -12.9 +/- 9.0 mm, and mean precordial ST elevation was 12.5 +/- 8.7 mm. Absolute R-wave change correlated directly with ST elevations (p = .013), while S-wave change correlated inversely (p less than .007). Only ST elevations correlated with changes in pulmonary capillary wedge pressure (PW) (p less than .007). In the precordial lead with maximum ST elevations, only R-wave changes correlated with ST elevations (p = .002), and both R-wave changes and ST elevations correlated with changes in PW (R:p = .027; ST:p = .007). The presence of large increases in R waves or decreases in S wave, or of high-magnitude ST elevations identified patients with the highest elevations in PW. In conclusion, decreases in S waves and, less commonly, increases in R waves are seen with diagnostic ST elevations and may have some limited clinical value. The correlation between magnitude of acute anterior ST elevations and changes in left ventricular filling pressures may have important clinical consequence.     

右室流出道起源与主动脉窦起源室性早搏的分析

目的 探讨右室流出道起源与主动脉窦起源室性早搏心电图的主要区别.方法 回顾分析因频发室性早搏,心电图室性早搏胸前导联呈左束支传导阻滞,Ⅱ、Ⅲ、aVF导联QRS主波向上,行射频消融成功的患者126例,分为右室流出道（RVOT）起源组66例,主动脉窦（ASC）起源组60例.结果 V1、V2导联R波时限指数和R/S波幅指数ASC组高于RVOT组.胸前导联移行区指数RVOT组高于ASC组.ROC曲线分析胸前导联移行区指数鉴别室性早搏起源有较高价值.结论 心电图呈左束支传导阻滞且Ⅱ、Ⅲ、aVF导联QRS主波向上的室性早搏,分析V1、V2导联R波时限指数、R/S波幅指数和胸前导联移行区指数可判断RVOT起源与ASC起源,指导射频消融治疗.     

U Wave Variability in the Surface ECG

A 72‐year‐old man with heart failure, left ventricular dysfunction (ejection fraction 20%), prior ischemic stroke, COPD, and exacerbation of chronic renal failure was admitted in our unit. Serum potassium was 6.1 mmol/L, calcium concentration was at the lower normal range 2.15 mmol/L, and NT‐pro‐BNP was 28,900 pg/mL. The surface 12‐lead electrocardiogram (ECG) showed sinus rhythm at 60 bpm, PR interval 160 ms, QRS duration 115 ms, QT interval 460 ms, and left ventricular hypertrophy criteria. Negative T waves in leads I, II, aVL, and V₄–V₆ were also seen. In leads V₄–V₆, negative U waves were observed in concordance with negative T waves. In all precordial leads, beat‐to‐beat U‐wave polarity variability was observed as a polarity variation from negative to positive with associated and stable negative T waves, in a beat‐to‐beat alternate morphology.     

Electrocardiographic criteria for predicting total occlusion of the proximal left anterior descending coronary artery in anterior wall acute myocardial infarction

BACKGROUND: Patients with occlusion of the left anterior descending coronary artery (LAD) proximal to both the first septal branch and the first diagonal branch may benefit most from early reperfusion therapy due to extensive area at risk. HYPOTHESIS: The aim of the study was to examine whether 12-lead electrocardiograms (ECGs) in the acute phase of acute myocardial infarction (AMI) could identify total occlusion of the LAD proximal to both the first septal and the first diagonal branch. METHODS: A 12-lead electrocardiogram was recorded on admission in 128 patients with anterior AMI within 12 h from symptom onset. Patients were divided into three groups according to the culprit lesion: 33 patients had total occlusion of the LAD proximal to both the first septal perforator and the first diagonal branch (Group P), in 51 it was proximal to either the first septal perforator or the first diagonal branch (Group D-a), and in 44 it was distal to both the first septal perforator and the first diagonal branch (Group D-b). RESULTS: Sensitivity and specificity of a greater degree of ST-segment depression in lead III than that of ST-segment elevation in lead aVL were 85 and 95%, respectively, which was better than the results derived by all other ECG criteria (p< 0.001). CONCLUSIONS: We conclude that a greater degree of ST-segment depression in lead III than that of ST-segment elevation in lead aVL is a useful predictor of proximal LAD occlusion in patients with anterior AMI.     

Transient prominent anterior QRS forces in the setting ST segment elevation coronary syndrome: Left septal fascicular block

Numerous successive publications have shown that transient prominent anterior QRS forces (PAF) in the setting of acute coronary syndrome (ACS) is suggestive of critical proximal obstruction of left anterior descending coronary artery (LAD) before its first septal perforator branch (S₁). Transient ischemia of the left septal fascicle resulting in left septal fascicular block has been proposed as the causative mechanism. We present a case of acute inferior ST-elevation myocardial infarction caused by acute proximal occlusion of the right coronary artery associated with proximal critical obstruction of the left anterior descending coronary artery.     

Electrocardiographic features differentiating dilated cardiomyopathy from hypertrophic cardiomyopathy

To determine the usefulness of electrocardiographic (ECG) features in differentiating between hypertrophic cardiomyopathy with features mimicking dilated cardiomyopathy (D-HCM) and true dilated cardiomyopathy (DCM), we compared ECGs of 52 consecutive patients (11 with D-HCM, 41 with DCM). Left atrial dimension, left ventricular internal dimension, and septal and posterior wall thickness were employed as echocardiographic indexes, while QRS duration, amplitude of RV₅ or V₆ + SV₁, number of abnormal Q waves, P-terminal force in V₁, and frontal plane QRS axis were used as ECG parameters. The patients with D-HCM demonstrated a larger number of abnormal Q waves (P < .0001), greater prolongation of QRS duration (P < .0001), and lower amplitude of RV₅ or V₆ + SV₁ (P < .0001). In all cases of D-HCM, atrial overload was observed and abnormal QRS axis in 9 (82%) of the 11 patients. These features were noted in 21 (51%) and 17 (41%), respectively, of the 41 DCM patients (P < .005 and P < .05, respectively). Despite significant differences in the echocardiographic parameters between D-HCM and DCM, excluding left ventricular end-diastolic dimension, ECG abnormalities were more significant between the two groups. The results indicate that ECG features are extremely useful in differentiation between DCM and D-HCM.     

Correlation of electrocardiographic and pathologic findings in anteroseptal infarction

The findings in the Wilson precordial leads and in the standard and Goldberger limb leads have been correlated with the pathologic findings in 161 cases in which myocardial infarction was definitely established and accurately localized at autopsy. The cases have been classified in accordance with the anatomic location of the infarct into the following seven groups: anteroseptal, large anterolateral, anteroposterior, septal, posterior, posterolateral, and lateral, When classification into more than one category was possible, because of the large size or multiplicity of the infarct found at autopsy, the lesion of principal electrocardiographic interest became the determining factor.This communication comprises a study of the electrocardiographic and pathologic findings in twenty cases of anteroseptal infarction. In the majority, the infarct was confined to a relatively narrow strip of the free anterior wall and the contiguous anterior portion of the interventricular septum. Serial electrocardiograms taken during the acute phase are presented in six cases and include a control tracing antedating the infarct in four cases, and one or more records after healing in four cases. Single electrocardiograms obtained during the stage of injury are presented in eight additional cases. The remaining six cases came under study after the infarct was completely healed.In fourteen cases, the infarct involved the apical one-third to two-thirds of the anteroseptal wall of the left ventricle. The electrocardiogram in eight of these cases was characterized by a normal initial R wave in Lead V₁ and an abnormal QR or QS complex in one or more of the next three leads (V₂, V₃, and V₄). The Q wave of a QR complex was considered abnormal when the time interval from its onset to nadir exceeded .02 second and when its amplitude was more than 25 per cent of the voltage of the succeeding R. The electrocardiogram in five of the fourteen cases displayed a QS complex in Leads V₁ and V₂, as well as an abnormal initial downward deflection in Lead V₃ or V₃ and V₄. In four of these five cases, the QS complexes in Leads V₁ and V₂ were accompanied by abnormal elevation of the RS-T segment and could be correlated with extension of the infarct into the septum. The electrocardiogram of the last case in the group displayed marked RS-T displacement in Leads V₂, V₃, and V₄ without significant abnormalities in the initial phase of the QRS complex. The registration of an R wave in place of a Q wave in these leads could be correlated with the patchy distribution of the infarct through the anteroseptal wall.In two cases, the infarct was centered in the middle one-third of the anteroseptal wall and did not reach either the apex or base. The tracing of one of these displayed a normal initial R wave in Lead V₁ and an abnormal QR or QS complex in the next three leads. Serial changes in the T waves of Leads V₂ and V₃ without significant QRS abnormalities were observed in the other case during the acute stage of an anteroseptal infarct, which subsequently proved to be small in size and intramural in location.The infarct was located in the basal one-third of the anteroseptal wall in the four remaining cases and was manifested by an abnormal QR or QS pattern together with abnormal RS-T displacement confined to the first two or three precordial leads. Extension of the infarct into the basal one-third of the interventricular septum was demonstrated in three of these cases and may have been partly or wholly responsible for the QRS-T abnormalities in Leads V₁ and V₂.Definitely abnormal Q waves were not found in Leads V₅ or V₆ in any case where the infarct was confined to the anteroseptal wall, but borderline QR complexes were recorded in these leads in two cases and were attributed to reference of the potential variations of the anteroseptal infarct toward the axilla as a result of clockwise rotation of the heart on its longitudinal and anteroposterior axes.Diagnostic signs of anterior infarction were found in the standard limb leads in only two of the twenty cases. These three leads, together with a single precordial lead, would have been inadequate for diagnostic purposes in the majority of the cases in this series and would have been insufficient for localizing purposes in all cases. On the other hand, multiple precordial leads furnished adequate evidence in all cases for a positive or presumptive diagnosis of myocardial infarction and for a clinically satisfactory prediction of the position of the lesion.     

Electrocardiographs criteria for the diagnosis of anterior myocardial infarction: Importance of the duration of precordial R waves

A systematic evaluation of a large number of electrocardiographic (ECG) variables that might be useful for diagnosing anterior myocardial infarction (MI) is reported. Previous anterior MI was shown to be present or absent by cardiac catheterization in 199 patients. The best discriminator between cases and noncases of anterior MI in most patients is the presence of a Q wave of any magnitude or an initial R wave < 20 ms in lead V₂. In patients with ECG evidence of associated left ventricular or type C right ventricular enlargement, the more stringent criterion of a Q wave of any magnitude in lead V₂ yielded the optimal combination of sensitivity and specificity for diagnosing anterior MI. The diagnostic performance of the proposed criteria for anterior MI is superior to that of more traditional criteria that use measurements of the absolute and relative amplitudes of precordial R waves.