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36 Journal of The Association of Physicians of India ■ Vol. 64 ■ September 2016 Original Article Etiology and Left Ventricular Functions in Left Bundle Branch Block- A Prospective Observational Study Rajeev Bhardwaj Editorial Viewpoint Abstract Purpose of study: Left bundle branch (LBBB) is common ECG finding. Common causes of LBBB are coronary artery disease (CAD), hypertension and dilated cardiomyopathy (DCM). Purpose of the study was to find out the etiology and left ventricular function in patients coming to a territory care hospital. Material and methods: All consecutive patients coming to our hospital as indoor or outdoor patients with ECG suggestive of LBBB were studied. The detail history and examination was done. Echocardiography was done in all patients. Results: 132 patients with LBBB were studied. Mean age was 61.65±13.02 yrs. 70 were male (53.03%) and 62 were female (44.97%). 40 patients presented with dyspnea ((30.3%) and 34 with chest pain ((24.24%). 23 patients were asymptomatic (17.4%). 63 were hypertensive (47.7%) and 6 were diabetic (4.5%). Left ventricular hypertrophy (LVH) was present in 42 patients (31.8%), with 33 having diastolic and 9 systolic dysfunction. 33 patients had DCM (25%) and 31 patients had evidence of myocardial infarction (23.48%). 20 patients had normal echocardiography (15.15%). 75 patients had systolic dysfunction (56.8%) Conclusion: Commonest presentation in patients wih LBBB was dyspnea followed by chest pain. Majority had hypertension. LVH was the commonest echocardiographic finding followed by global hypokinesia and regional wall motion abnormality. More than 50% patients had left ventricular systolic dysfunction. L eft bundle branch block (LBBB) is essentially an electrocardiographic (ECG) diagnosis and so it’s true incidence in general population is difficult to assess. Incidence in patients referred to ECG department was found to be 1%. 1 We studied the left ventricular (LV) functions in patients with ECG evidence of LBBB. Material and Methods 132 consecutive patients with ECG evidence of complete LBBB coming to our hospital with various complaints were studied. Detailed h i s t o r y wa s t a k e n . T h o r o u g h physical examination was carried out. All were subjected to detailed echocardiography. Special • Commonest presentation of LBBB was dyspnea and chest pain. • C o m m o n e c h o c a r d i o graphy findings were LVH, global hypokinesia and regional wall motion abnormality. attention was given for wall motion abnormality. Depending upon the presentation, some were admitted and some were followed on OPD basis. The treatment as per diagnosis was started. Coronary angiography (CAG) was done in patients when there was doubt about the etiology, especially to differentiate dilated cardiomyopathy (DCM) from ischemic LV dysfunction. CAG was also done in patients undergoing primary PTCA or patients having angina. Acute MI was diagnosed when patient came with chest pain suggestive of myocardial infarction (MI), new LBBB, rise in troponin levels and presence of new regional wall motional abnormality(RWMA). AMI in presence of preexisting LBBB was diagnosed by chest pain suggestive of MI, rise in troponins and by ECG evidence of one or more of (1) ST segment elevation ≥ 1mm and with concordant QRS complex (2) ST depression ≥ 1mm Professor, Department of Cardiology, Indira Gandhi Medical College, Shimla, Himachal Pradesh Received: 04.11.2014; Revised: 07.01.2015; Re-revised: 09.11.2015; Accepted: 23.03.2016 37 Journal of The Association of Physicians of India ■ Vol. 64 ■ September 2016 Table 1: Clinical characteristics of the patients Total patients Male Female Mean age Hypertensive Diabetic Symptoms Dyspnea Chest pain Syncope Palpitation Asymptomatic 132 70(53.03%) 62(46.97%). 61.65±13.02 yrs 63(47.7%) 11 (8.33%). 40(30.3%) 34(25.76%) 03((2.27%) 04(3%) 23(17.4%) Table 2: Echocardiographic findings Total patients 132 Left ventricular hypertrophy 42(31.8%) Diastolic dysfunction 33 Systolic dysfunction 9 DCM 33(25%) Coronary artery disease 31(23.48%) Old MI 20 Acute MI 11 Intermittent complete heart 03(2.27%) block Misc. 03(2.27%) Normal cardiovascular system 20(15.15%) Systolic dysfunction 75(56.8%) Table 3 : Age distribution of LBBB patients Age (yrs) 18-40 40-49 50-59 60-69 70-79 >80 Male 1 6 11 25 20 7 Female 4 7 16 21 9 5 Total 5 13 27 46 29 12 in leads V1, V2,V3 (3) ST elevation of ≥ 5mm and discordant with QRS complex and new RWMA. In cases of doubt, CAG was done. Coronary artery disease was diagnosed by presence of acute MI, old records of MI or old CAG report, record of PTCA or bypass grafting. Duration of QRS was measured in each patient. Inclusion Criteria: All consecutive patients coming to our OPD/ admitted in our hospital with ECG changes of complete LBBB. Exclusion Criteria: Patients with ECG showing incomplete LBBB. Patients who did not report for echocardiography. Table 4: Age distribution of etiology of LBBB Etiology HT with LV dysfunction Coronary artery disease DCM Heart block Misc. Normal 18-39 (N 5) 0 2 2 40-49 (N 13) 4 1 2 1 50-59 (N 27) 9 7 8 1 5 3 Results Overall 132 patients were studied. Table 1 shows the clinical characteristics of the patients. Mean age was 61.65±13.02 yrs. 70 were male and 62 were female. C o m m o n e s t p r e s e n t a t i o n wa s dyspnea, in 40 patients; 34 patients presented with chest pain and 3 patients presented with syncope. 23 patients had LBBB without symptoms. 20 of these had referral for ECG changes after preanesthetic check up before surgery or other interventions. Table 2 shows the diagnosis after echocardiography and other investigations. Commonest abnormality in echocardiography was left ventricular hypertrophy (LVH) seen in 42 patients, 33 of whom had diastolic dysfunction and 9 had systolic dysfunction. 33 patients had coronary artery disease (CAD) w i t h LV s y s t o l i c d y s f u n c t i o n . 20 of these had old myocardial infarction (MI) and 11 had acute MI. One patient had rheumatic heart disease with severe mitral regurgitation (MR) with severe aortic regurgitation (AR), with severe LV dysfunction; one had calcific aortic valve with severe AR with mild LV dysfunction and one had hypertrophic cardiomyopathy. Three patients presenting with syncope were found to have intermittent complete heart block. Left ventricular systolic dysfunction was present in 75 patients (56.8%); mild in 10 patients (13.3%), moderate in 16 patients (21.3%) and severe in 49 patients (65.3%). Twenty patients were found to 60-69 (N 46) 18 9 10 1 2 6 70-79 (N29) 12 8 7 >80 (N 12) 5 1 3 1 1 3 have normal cardiovascular system. Out of 23 asymptomatic patients, 20 were found to have normal echocardiography while 3 had DCM with mild LV dysfunction. Table 3 shows the age distribution of LBBB patients. It can be seen that it is more common in older age group. Most of the patients were between 50-70 yrs of age. Ta b l e 4 s h o w s t h e a g e w i s e distribution of etiology of LBBB. It can be seen that in less than 40yrs of age, CAD and DCM are more common causes. After 40 yrs of age hypertensive heart disease, CAD and DCM are the common causes, in almost equal proportion. Mean QRS duration was 131±9.11ms. I n p a t i e n t s w i t h m i l d LV dysfunction, QRS duration was 125±5.86ms, with moderate LV dysfunction it was 132±6.28ms and in patients with severe LV dysfunction, it was 137±10.20ms. Coronary angiography was done in 15 patients due to various reasons. S e ve n h a d n o r m a l c o r o n a r i e s . Single vessel disease was present in 3 patients, two vessel disease in 2 patients and three vessel disease in 3 patients. Two patients underwent primary angioplasty and one patient underwent coronary artery bypass grafting. Discussion The association between LBBB a n d c a r d i o va s c u l a r m o r b i d i t y has been investigated, but given conflicting results, controversy regarding the prognosis of LBBB persists. Fahy et al observed a higher rate of developing overt c a r d i o va s c u l a r d i s e a s e a m o n g 38 Journal of The Association of Physicians of India ■ Vol. 64 ■ September 2016 people with isolated LBBB. 2 Azadani et al followed 1688 individuals without cardiovascular disease or heart failure for 6 years. 2.5% had LBBB on baseline ECG. In multivariable logistic regression analysis adjusting for potential confounders, participants with baseline LBBB remained nearly three (2.85) times more likely to develop CHF. Unadjusted mortality r a t e f r o m c a r d i o va s c u l a r a n d cardiac diseases was higher among patients with LBBB compared to those without LBBB. In bivariate analysis, patients with LBBB had 4.34 times greater odds of dying from cardiovascular disease. 3 E ve n i n p a t i e n t s w i t h h e a r t failure, LBBB carries a poorer prognosis. In a cohort of 5517 p a t i e n t s w i t h c o n g e s t i ve H F , 4 patients with LBBB (n = 1391) showed a higher 1-year all-cause mortality and sudden death than controls free of LBBB. An unfavorable prognosis of LBBB was also observed in a cohort of patients with acute HF one year after admission. 5 In 1979, the Framingham Study 6 (5,209 subjects, 55 with LBBB) showed a clear association between LBBB and main cardiovascular diseases, such as hypertension, cardiac enlargement, and coronary heart disease. Our study showed that around 48% patients with LBBB had hypertension, 25% had DCM and around 23% had CAD. Systolic dysfunction of LV was present in about 56% patients. Only about 15% patients had normal echocardiography. How many of these develop cardiovascular disease on follow up remains to be seen. Boyle and Fenton found that 69 % of patients with LBBB had CAD and /or hypertension. 7. 88% of their patients were aged 50yrs or more. Similar was the case with our study, where 87% patients were 50 yrs or older. 34% of their patients were 70yrs or older. Similarly 30% of our patients were 70yrs or older. LBBB may occur in asymptomatic individuals, patients with extensive myocardial infarction, and in those with heart failure, especially in dilated, nonischemic cardiomyopathies. In some patients, LBBB (sometimes rate dependent) may be the first manifestation of heart disease whereas the clinical presentation of a dilated cardiomyopathy develops only some years later.8 Early studies reported a mean survival of less than 5 years after documentation of LBBB. 9 The etiology of LBBB plays a role in determining the H-V interval. Nearly all patients with congestive (dilated) cardiomyopathy exhibited a prolonged H-V interval whereas in other groups, both normal and abnormal values occurred. 10 Seventy-five patients (56.8%) i n o u r s t u d y h a d LV s y s t o l i c dysfunction. Out of these 49 patients had severe LV systolic dysfunction. Patients of severe LV dysfunction had mean QRS duration 137±10.20ms as against 125±5.86 in patients with mild LV d y s f u n c t i o n . I n p a t i e n t s with dilated cardiomyopathy, a p r o g r e s s i ve i n c r e a s e i n Q R S duration and the presence of a L B B B p a t t e r n we r e r e l a t e d t o disease progression. 11 In 14 of 18 patients with congestive (dilated) cardiomyopathy, progression of disease was accompanied by a movement of the QRS frontal plane vector from a normal axis to left axis deviation which mainly occurred during the first 2 years after clinical manifestation of cardiomyopathy. From the prognostic point of view, increased QRS duration in patients with heart failure has been shown by several studies to be correlated to a poor prognosis. 12 Conclusion Prevalence of LBBB increases with age. Majority of patients of LBBB had cardiovascular disease. Hypertensive heart disease, DCM and CAD are the common causes. Majority have LV dysfunction. QRS duration was more in patients with severe LV dysfunction. So all cases of LBBB require proper management and follow up. References 1. K a t z L N a n d P i c k A . C l i n i c a l electrocardiography, Part I(1956). The arrhythmia. Lee and Fabiger, Philadelphia. 2. Fahy GJ, Pinski SL, Miller DP, et al. Natural history of isolated bundle branch block. Am J Cardiol 1996; 77:1185-1190. 3. Azadani PN, Soleimanirahbar A, Marcus GM, et al. Asymptomatic left bundle branch block predicts new-onset congestive heart failure and death from cardiovascular diseases. Cardiol Res 2012; 3:258-263. 4. Baldasseroni S, Opasich C, Gorini M, et al. Italian network on congestive heart failure investigators. Left bundle-branch block is associated with increased 1-year sudden and total mortality rate in 5517 outpatients with congestive heart failure: a report from the Italian Network on Congestive Heart Failure. Am Heart J 2002; 143:398–405. 5. Huvelle E, Fay R, Alla F, et al. Left bundle branch block and mortality in patients with acute heart failure syndrome: sub study of the EFICA cohort. Eur J Heart Fail 2010; 12:156–163. 6. Schneider JF, Thomas HE Jr, Kreger BE, et al. Newly acquired left bundle-branch block:The Framingham study. Ann Intern Med 1979; 90:303–310. 7. Boyle DM, Fenton SS. Left bundle branch block . Ulster Med J 1966; 35:93-99. 8. Breithardt G, Knieriem HJ, Kohler E, et al. Prognosis and possible presymptomatic manifestations of congestive cardiomyopathy (COCM). Postgraduate Medical Journal 1978; 54:451–461. 9. Smith S, Hayes WL. The prognosis of complete left bundle branch block. American Heart Journal 1965; 70:157–159. 10. Breithardt G, Kuhn H. Significance of His bundle recording in bundle branch block. In: Thalen HJT, Harthome JW, editors. To pace or not to pace. Controversial subjects on cardiac pacing. The Hague: Martinus Nijhoff Medical Division 1978; 3345. 11. Breithardt LK, Breithardt G, Seipel L, L o o g e n F. D i e B e d e u t u n g d e s Elektrokardiogramms für die Diagnose und Verlaufsbeobachtung von Patienten mit kongestiver Kardiomyopathie. Zeitschrift für Kardiologie 1974; 63:916–927. 12. Kashani A, Barold SS. Significance of QRS complex duration in patients with heart failure. Journal of the American College of Cardiology 2005; 46:2183–2192.