Etiologies of left bundle branch block and correlations with hemodynamic and angiographic findings

E and Rothberger1 introduced the concept of bundle branch block (BBB) 60 years ago in Vienna. The causes of left BBB are varied. Clinical2 and pathologic3 studies suggest systemic hypertension and coronary artery disease (CAD) as the most common causes.2–7 Cardiomyopathy, valvular heart disease, and several other less common causes have been described.7 It has also been known that some patients with left BBB have apparently normal hearts except for conduction system abnormalities.4 However, the true incidence of various etiologic groups needs further corroboration by a larger study.7 Therefore, this communication provides additional data in a large number of patients regarding the various etiologies of left BBB and correlates electrocardiographic and clinical observations with left ventricular (LV) functions and coronary angiocardiographic data. • • • A review of 25,522 patients who underwent cardiac catheterization during 8 years (1995 to 2002) revealed 550 patients aged 18 to 87 years (mean 56 14), of which 226 were women (41%) who had electrocardiographic criteria of left BBB (Figure 1). The criteria set by the Criteria Committee of the New York Heart Association8 used to interpret left BBB are: (1) QRS interval 120 ms; (2) slurred/notched wide and predominant R waves in leads I, aVL, V5, and V6; (3) slurred/notched and broad S waves in V1 and V2 with absent or small R waves; (4) midconduction delay defined as notching or a plateau in the mid-QRS wave; (5) ventricular activation time 50 ms at the onset of the QRS interval; (6) M-shaped QRS variants with occasionally wide R waves in V5 and V6; (7) no initial Q wave over the left precordium; and (8) absence of preexcitation. History, physical examination, 12-lead electrocardiograms, chest x-rays, pertinent laboratory findings, blood sugar, risk factors for CAD, electrolytes, complete blood counts, stress tests, and echocardiograms were evaluated. Hemodynamic studies in all 550 patients included left heart catheterization, selective cineangiography of coronary arteries, and left ventriculography. LV end-diastolic pressure was measured with fluid-filled catheters, and ejection fraction was calculated by the area-method technique. Techniques for coronary angiography were in accordance with those of Sones and Shirey9 or Judkins.10 LV cineangiograms were obtained in a 40° right oblique position and were followed by selective coronary angiograms recorded in multiple projections.9,10 Each x-ray film was reviewed by 2 observers, with particular attention to the details of calibers of coronary arteries, the degree of narrowing, the smallest opacified arteries, the extent of collaterals, and possible artifacts. The total pattern of contractility of the left ventricle, abnormal localized myocardial contraction,11 LV ejection fraction, and end-diastolic pressure were evaluated during left ventriculography. Coronary artery obstruction was measured at the maximal luminal diameter narrowing observed on the cine film. A lesion in the coronary artery was considered to be of significance if there was 50% narrowing of the internal diameter. The number of coronary arteries (left main, left anterior descending, right coronary, and circumflex) involved with significant disease was noted. Narrowing of coronary arteries was graded on the basis of the following score system previously defined12: grade 0, 25%; grade 1 , 25% to 50%; grade 2 , 50% to 75%; grade 3 , 75% to 95%; and grade 4 , 100% occlusion. In Table 1,grades 2 to 3 represent subtotal occlusion and grade 4 total occlusion. The main left coronary lesions were considered separately. Uncommon and rarer causes of left BBB included in this report had a well-proved diagnosis. The pattern of LV contraction was determined by reviewing the superimposition of end-diastolic and end-systolic silhouettes and using terminology as defined by Herman et al.11 LV contractility was classified as normal, hypokinetic, dyskinetic, or akinetic. Electrocardiographic data, width of the QRS, and largest width and mean axis of the QRS in the frontal plane were analyzed in detail. These data were correlated with clinical, roentgenologic, hemodynamic, and coronary cineangiographic findings in these patients and were independently reviewed by both the investigators. Statistical analyses were performed using analysis of variance and Student’s t test. Mean values are expressed as mean SD. Univariate, bivariate, and multivariate analyses were performed using Statistica software (version 6.0; Tulsa, Oklahoma). A p value 0.05 was considered significant. Subjects included in the study belonged to 6 etiologic groups (Figure 2): group 1 (12%) with normal hearts (Table 2); group 2 (49%) had a history of CAD (26% myocardial infarction and 23% angina pectoris; Figure 3); group 3 (8%) had systemic hypertension (Table 1); group 4 (9%) had valvular and congenital heart disease; group 5 (8.5%) had cardiomyopathy; and group 6 (18 patients, 3.5%) had uncommon and From the Department of Medicine, Section of Cardiology, West Virginia University School of Medicine, Robert C. Byrd Health Sciences Center, Morgantown, West Virginia. Dr. Mehta’s address is: Section of Cardiology, West Virginia University, 2203 Robert C. Byrd Health Sciences Center South, PO Box 9157, Morgantown, West Virginia 26506-9157. E-mail: mmehta@hsc.wvu.edu. Manuscript received December 27, 2002; revised manuscript received and accepted February 24, 2003.