Europace Advance Access originally published online on January 5, 2006
Europace 2006 8(3):151-156; doi:10.1093/europace/euj019
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Impact of intraventricular conduction delay on coronary haemodynamics: a study with intracoronary Doppler in patients with bundle branch blocks and normal coronary arteries
1 Department of CardiologyUniversity Duisburg-EssenHufelandstr. 55, D-45122 Essen Germany; 2 Department of CardiologyMedisch Spectrum TwenteEnschede The Netherlands; 3 Second University Cardiology DepartmentAttikon University HospitalAthens Greece
Manuscript submitted 29 July 2004. Accepted after revision 14 August 2005.
* Corresponding author. Tel: +49 201 723 4404; fax: +49 201 723 5837. E-mail address: heinrich.wieneke{at}uni-essen.de
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Abstract |
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Aims The impact of right bundle branch block (RBBB) and left bundle branch block (LBBB) on myocardial perfusion is not completely understood as data are often blurred by underlying cardiac disease. The present study investigates whether conduction delays per se affect coronary perfusion-an indirect measure of myocardial oxygen demand.
Methods and results Intracoronary Doppler and ultrasound were performed in 8 patients with RBBB, 10 patients with LBBB, and 10 control subjects. All patients had angiographically normal coronary arteries and normal left ventricular function. Baseline (bAPV) and adenosine-induced hyperaemic average flow velocity and coronary flow velocity reserve (CFVR) were measured in left anterior descending arteries. Intravascular ultrasound showed no difference in lumen cross-sectional area and plaque burden between groups. Patients with RBBB and LBBB had higher bAPV values than controls (19.0±4.9, 21.9±5.1, and 14.6±2.4 cm/s, respectively; ANOVA P=0.003). There was no difference between patients with LBBB and RBBB compared with controls in CFVR (2.8±0.5, 3.0±1.0, and 3.4±0.7, respectively; ANOVA P=0.21).
Conclusion Bundle branch blocks, in particular LBBB, are associated with an increased coronary flow velocity, which indicates enhanced myocardial oxygen demand on the basis of mechanoenergetic disturbance. This may contribute to the unfavourable outcome of patients with intraventricular conduction delay.
Key Words: Coronary flow, Doppler, Right bundle branch block, Left bundle branch block
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Introduction |
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Left bundle branch block (LBBB) and, to a lesser extent, right bundle branch block (RBBB) are associated with an adverse outcome, which is independent of underlying cardiac diseases.1
Long-term observations suggest that LBBB and RBBB account for an annual reduction of left ventricular ejection fraction by 7 and 2%, respectively, which cannot be attributed to other underlying cardiac disorders.2 The mechanism by which these conduction disturbances impair myocardial function is not completely understood.
Increased blood flow velocity has been reported in a variety of disorders that are associated with enhanced cardiac workload, such as hypertrophic cardiomyopathy,3 arterial hypertension,4,5 and aortic stenosis.6 Observations in the experimental setting suggest that an increase in coronary flow velocity (CFV) reflects an increase in oxygen demand and may, therefore, serve as a sensitive indicator of increased myocardial workload.7,8 There is indirect evidence of an increased myocardial energy demand in patients with LBBB, as resynchronization therapy in patients with dilated cardiomyopathy and LBBB modestly lowers energy costs,9 whereas in patients with RBBB data are lacking. At this point, it is unclear how intraventricular conduction delays, such as LBBB or RBBB, may affect coronary perfusion.
The aim of our study with intracoronary Doppler (icD) and intravascular ultrasound (IVUS) was to evaluate whether conduction delays per se affect coronary perfusion-an indirect measure of myocardial oxygen demand. To exclude factors that may affect coronary perfusion, only patients with unobstructed coronary arteries and normal left ventricular function were examined.
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Methods |
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Study population
The cohort was derived from patients who were referred to the West German Heart Centre for suspected coronary artery disease between 1997 and 2003. All patients showed angiographically normal coronary arteries (i.e., coronary arteries with an angiographically smooth silhouette). Patients with RBBB (n=8) and LBBB (n=10) and patients without conduction delay as controls (n=10) were included in the study. Patients with valvular heart disease, hypertrophic obstructive cardiomyopathy, dilated cardiomyopathy, or myocarditis were not considered for this study. The study complies with the Declaration of Helsinki and all patients signed a written informed consent form.
Electrocardiography
Resting electrocardiograms were evaluated by two experienced cardiologists. RBBB was defined as a QRS duration >120 ms, a second R-wave in the precordial leads (rsr', rsR', or rSR'), and a wide S-wave in the left sided leads (I, V5, and V6). LBBB was defined as a QRS duration >120 ms, broad monophasic R-waves and absent Q-waves in leads I, V5, and V6, and displacement of ST-segments and T-waves in the opposite direction from the main QRS complex.10
Doppler measurements
Intracoronary Doppler measurements were performed with a 0.014 in. Doppler wire (FloWireTM, Cardiometrics, Inc.), as validated and described in detail by Doucette et al.11 ECG, coronary ostial pressure, instantaneous spectral peak velocity, and time average spectral peak flow velocity were recorded on-line. Heart rate (obtained from the ECG) and blood pressure (obtained from the guiding catheter) were recorded simultaneously with the Doppler flow velocity measurement. For off-line analysis, angiography and Doppler measurements were recorded on CD and videotape, respectively. The positions of the Doppler wire and IVUS catheter were documented in a picture-in-picture mode using the Echomap-SystemTM (Siemens, Erlangen, Germany) and saved in DICOM3 format (Fig. 1).12
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Coronary flow velocity measurements were performed after routine coronary angiography. All patients received 5000 I.E. heparin and 0.2 mg intracoronary nitroglycerine before angiography. A 6F or 8F guiding catheter without side holes was inserted into the left coronary artery ostium without damping of the arterial pressure signal. The Doppler wire was advanced into the target segment of the vessel; baseline parameters were recorded when a stable and high quality baseline signal without significant artefacts could be obtained. Then an intracoronary bolus of adenosine (18 µg) was injected and further measurements were obtained under peak hyperaemic conditions. Doppler measurements were made in the left anterior descending (LAD) (28 patients) and in the left circumflex artery (LCX) (26 patients). In two patients (LBBB-group), no stable Doppler signal could be obtained in the circumflex artery. The coronary flow velocity reserve (CFVR) was calculated as the ratio of hyperaemic average peak velocity and baseline average peak velocity (bAPV).13
All measurements were performed twice, and mean values were calculated from two consecutive measurements. Spatially averaged flow velocity was calculated as V=APV/2.14 Coronary flow for a certain vessel was calculated as Qvessel=VxA, where V is the average peak velocity and A the lumen area as measured by IVUS. Ejection fraction, left ventricular endsystolic, and end-diastolic volume were measured using ventriculo-graphic projections.
IVUS imaging protocol
IVUS imaging was performed with two commercially available IVUS systems during continuous recording of the electrocardiogram. The first IVUS system was a mechanical sector scanner (Boston Scientific Corporation, San Jose, CA, USA) incorporating a 30 MHz single-element bevelled transducer rotating at 1800 rpm. The second system was a solid-state electronic device (Endosonics, Rancho Cordova, CA, USA). With both systems, the transducer was first withdrawn through the entire vessel at a speed of 0.5 mm/s; the pullback was started as distal as possible, and the entire artery was imaged to the aorto-ostial junction. Consecutively, exact positioning of the IVUS probe at the site of icD measurement was achieved using the Echomap picture-in-picture imaging system.12 IVUS measurements were performed in the proximal coronary segments of the LAD on end-diastolic frames.15
Echocardiography
Images were taken with patients in the left lateral position with simultaneous electrocardiogram recording. Echocardiography was obtained in 25 of 28 patients. The echocardiographic examination was performed according to the Guidelines of the American Society of Echocardiography.16 Interventricular septum end-diastolic diameter and posterior wall end-diastolic diameter were measured M-mode in the parasternal short axis and myocardial muscle mass was calculated using the method described by Devereux and Reichek as LVM=1.04x[(LVEDD+IVSEDD+PWEDD)3–LVEDD3]–13.6, where LVEDD is the left ventricular end-diastolic diameter, IVSD the interventricular septum end-diastolic diameter, and PWEDD the posterior wall end-diastolic diameter.17
Statistics
Body mass index (BMI) was calculated as body weight (kg)/[body height (m)]2. Linear regression analyses were performed by the use of standard methods. Continuous variables were compared with the two-tailed (unpaired) Student's t-test. If more than two groups were compared, one-way ANOVA was used for comparison of intergroup differences. Post hoc testing was performed using Student's t-test.
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Results |
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Descriptive electrocardiographic parameters
In all patients, icD and IVUS were performed without complications. Baseline characteristics of the patients are given in Table 1. Analysis of variance revealed no statistical difference for the variables age, weight, and BMI. Patients with LBBB and RBBB showed a significantly longer QRS-duration than normals (145.1±10.7, 127.2±5.9, and 92.2±9.6, respectively; ANOVA P<0.0001). Mean QRS-duration was significantly longer in patients with LBBB than in patients with RBBB (P=0.001). Analysis of echocardiography data showed that there were no differences with respect to IVSD (normal: 1.03±0.18 cm; RBBB: 0.94±0.18 cm; LBBB: 1.16±0.23 cm; ANOVA P=0.12), PWEDD (normal: 1.0±0.26 cm; RBBB 1.0±0.19 cm; LBBB: 1.1±0.14 cm; ANOVA P=0.33), and muscle mass (normal: 260±62 g; RBBB: 219±55 g; LBBB: 301±80 g; ANOVA P=0.08).
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IVUS parameters
There was no significant difference in mean lumen area between patients with RBBB (14.0±3.2 mm2), patients with LBBB (13.8±2.6 mm2), and controls (15.2±4.0 mm2). Both plaque burden (control: 1.9±2.1 mm2; RBBB: 2.6±2.1 mm2; LBBB: 3.6±2.7 mm2) and lumen area stenosis (control: 10.9±12.0%; RBBB: 14.0±9.1%; LBBB 18.3±12.6%) indicate that the extent of atherosclerotic alterations was similar in the three groups. There was no significant relation between lumen area and resting CFV (r=0.08) or between lumen area stenosis and resting CFV (r=0.25) in the LAD.
Haemodynamic parameters
In all patients, left ventricular ejection fraction was >50%; however, mean ejection fraction was significantly lower in patients with LBBB than in controls (ANOVA P=0.02). Left ventricular endsystolic volume (ANOVA P=0.05), but not left ventricular end-diastolic volume (ANOVA P=0.11), was higher in patients with LBBB compared with patients with no conduction disturbance. No differences were observed in patients with RBBB (Table 2). Patients with LBBB showed higher systolic blood pressure values than patients with RBBB. No significant difference with respect to diastolic blood pressure, heart rate, and pressure-rate-product was observed (Table 2).
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Baseline average peak velocity in the LAD was significantly increased in patients with RBBB (19.0±4.9 cm/s, P=0.02) and LBBB (21.9±5.1 cm/s, P<0.001) compared with the control group (14.6±2.4 cm/s) (Fig. 2). In the LCX, only patients with LBBB showed a significantly increased bAPV when compared with controls (controls: 13.9±2.8 cm/s; RBBB: 18.0±7.2 cm/s; LBBB: 19.7±2.9 cm/s; P<0.001 LBBB vs. controls). After intracoronary administration of 18 µg adenosine, a significant increase in flow velocity occurred in all three groups in the LAD and LCX. However, there was no significant difference in hyperaemic average flow velocity between the groups either in the LAD (controls: 49.8±12.3 cm/s; RBBB: 53.2±8.7 cm/s; LBBB: 62.7±20.4 cm/s; ANOVA P=0.16) (Fig. 2) or in the LCX (controls: 43.4±9.4 cm/s; RBBB: 46.8±8.8 cm/s; LBBB: 56.0±15.1 cm/s; ANOVA P=0.20). In controls, baseline average peak velocity of the LAD was closely related to pressure-rate-product (r=0.7, P=0.02), whereas this relation was not observed over the whole study population (r=0.07, P=0.69).
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In patients with LBBB, resting flow in the LAD was significantly increased compared with controls (92.3±32.2 mL/min vs. 66.4±20.6 mL/min, P=0.04), but not in patients with RBBB (79.5±32.2 mL/min vs. 66.4±20.6 mL/min, P=0.3). In all groups, there was a significant increase in flow after the administration of adenosine. However, there was no difference in hyperaemic flow between the groups (controls: 231.9±100.6 mL/min; RBBB: 215.8±69.6 mL/min; LBBB: 261.4±103.3 mL/min; ANOVA P=0.6) (Fig. 3).
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There was a non-significant trend for patients with LBBB and RBBB to have a decreased CFVR compared with normals in the LAD (controls: 3.4±0.7; RBBB: 2.9±0.9; LBBB 2.8±0.5; ANOVA P=0.14) as well as in the LCX (controls: 3.1±0.4; RBBB: 2.7±0.6; LBBB: 2.7±0.6; ANOVA P=0.13). CFVR was closely related to the resting flow velocity in all patients in the LAD (r=0.45, P<0.0001) and in the LCX (r=0.49, P<0.0001).
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Discussion |
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The main findings of the present study are, that both, LBBB and RBBB, led to a significant increase in baseline (resting) CFV in the LAD, whereas hyperaemic flow velocity remained unchanged. In patients with LBBB, this increase was more pronounced than in patients with RBBB and was also observed in the LCX. As there was no difference in coronary cross-sectional area between groups, absolute coronary flow was increased; however, this result was also only statistically significant in patients with LBBB.
Coronary flow velocity can be increased (1) in the presence of increased myocardial workload with consecutively increased oxygen demand, (2) in the presence of coronary stenosis, and (3) by the administration of drugs decreasing myocardial vascular resistance.18 As there was no significant difference in lumen area or plaque burden between patients with and without conduction disturbance, reduced coronary lumen area can be ruled out as a reason for the increased flow velocity. We could also find no differences in oral medication what could account for the increased resting flow. Therefore, the increase in coronary perfusion and partial exhaustion of coronary flow reserve that was observed in the present study indicate an increased myocardial oxygen demand, most likely, on the basis of mechano-energetic disturbance. This may contribute to the unfavourable outcome of patients with intraventricular conduction delay in the long-run.
Left bundle branch block
Intraventricular conduction delay is accompanied by an asynchronous activation of the ventricular myocardium. LBBB leads to an essential impairment of the mechanical efficiency of the left ventricle contraction with reduced left ventricular ejection fraction,19 mitral regurgitation,20 and diastolic dysfunction.21 In patients with LBBB, lateral wall contraction is delayed in comparison with the interventricular septum. The septal contraction against a relaxed left ventricle reduces septal workload;22 however, at the expense of a higher stress on the lateral wall due to late activation.23 These alterations induce ventricular remodelling and redistribution of myocardial perfusion in the experimental setting.24
To the best of our knowledge, there is only one study that previously investigated coronary haemodynamics in patients with LBBB. Skalidis et al.25 stratified patients with LBBB according to exercise perfusion defects in stress thallium-201 scintigraphy. In patients with perfusion defects, CFVR was significantly decreased compared with controls; however, in patients without perfusion defects no difference was observed. In our study, we observed only a trend towards a decreased flow velocity reserve in patients with LBBB. These results did not reach statistical significance, as we performed no further stratification with regard to perfusion defects in myocardial scintigraphy. In addition to coronary flow reserve, the present study was focused on baseline flow parameters like CFV and coronary flow, assessed by integrating IVUS-data of coronary lumen area. As other parameters like decreased coronary lumen area and differences in pressure-rate-product could be excluded as potential causes of increased coronary flow, our data strongly suggest that an enhanced oxygen demand evoked by the LBBB is responsible for the increased coronary flow.
A study evaluating the impact of permanent right ventricular pacing showed that disturbance of ventricular conduction causes alterations in coronary perfusion.26 In this setting, the authors also observed that CFVR was significantly reduced in patients with right ventricular pacing. Differing data have been presented by Kolettis et al.,27 who reported that right ventricular pacing caused a significant decrease in resting CFV and an increase in CFVR. On the first glance, these data seem to be in conflict with our findings, as we observed an increased baseline flow velocity in patients with LBBB. However, the effect of LBBB and right ventricular pacing on ventricular contraction may differ: right ventricular pacing leads to a ‘kind of artificial LBBB’ and also produces right ventricular dyssynchrony, whereas natural LBBB leads to a (pathophysiological) delayed excitation of the right ventricular myocardium.
Right bundle branch block
The prognosis of RBBB depends on the patient population investigated. While in patients with established coronary artery disease an increased mortality rate has been reported,28 in young asymptomatic persons, no impact on long-term survival was found.29 Evaluation of patients with dilated cardiomyopathy revealed that right ventricular dyssynchrony has the same impact on long-term prognosis as left ventricular dyssynchrony.30 Beside these effects on prognosis, RBBB directly influences left and right ventricular performance. A study that used radionuclide ventriculography found a decreased left ventricular ejection fraction in patients with RBBB.31 In addition, there is an association between RBBB and an increased prevalence of coronary artery disease and left ventricular contraction abnormalities.32
To the best of our knowledge, there are, thus far, no studies investigating the impact of RBBB on coronary haemodynamics. In this study, we observed an increased resting flow velocity in patients with this conduction disturbance compared with control subjects; however, this increase was less pronounced in patients with RBBB than in those with LBBB. Our data suggest that RBBB might be mechanoenergetically less unfavourable than LBBB. This hypothesis may be supported by the observation that left ventricular pacing (a kind of artificial RBBB) is haemodynamically more advantageous than right ventricular pacing.33
Study limitations
All patients in this study were referred to our hospital for suspected coronary artery disease. Although neither with angiography nor with IVUS was a relevant extent of plaque burden seen, these patients may not be considered to be free of any underlying cardiac disease.34 However, as there was no significant difference in the extent of minimal atherosclerotic changes between the three groups, the early stages of atherosclerotic plaque formation may not affect our study.
Coronary flow is determined by myocardial workload and myocardial mass.35 Although there was no difference in pressure-rate-product as a measure of instantaneous myocardial workload and global left ventricular muscle mass in this study, we cannot rule out potential differences between the study groups in myocardial mass supplied by the LAD. However, studies that investigated global myocardial perfusion showed that muscle mass is not related to flow velocity but to vessel area (which we examined with IVUS).18
Although the impact of pacing at different pacing sites on coronary haemodynamics would have been of major interest, performing these procedures in addition to IVUS and Doppler in two separate coronary vessels would have led to a prolongation of the examination to an extent, which would have hardly been accepted by the patients.
Clinical implication
Our data in patients with bundle branch blocks suggest that intraventricular conduction delay (in particular in LBBB) is associated with an increase in coronary perfusion and partial exhaustion of coronary flow reserve. This may reflect increased myocardial oxygen demand, caused by a mechanically ineffective left ventricular contraction which may contribute to the unfavourable outcome of patients with intraventricular conduction delay. As CFV can readily be assessed by Doppler echocardiography,36 further studies might evaluate whether flow velocity is eligible for the assessment of resynchronization therapy in patients with congestive heart failure intraventricular conduction delay.
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[1] Hesse B, Diaz LA, Snader CE, Blackstone EH, et al. Complete bundle branch block as an independent predictor of all-cause mortality: report of 7,073 patients referred for nuclear exercise testing. Am J Med 2001; 110: 253–9.[CrossRef][Web of Science][Medline]
[2] Lee SJ, McCulloch C, Mangat I, et al. Isolated bundle branch block and left ventricular dysfunction. J Card Fail 2003; 9: 87–92.[CrossRef][Web of Science][Medline]
[3] Misawa K, Nitta Y, Matsubara T, et al. Difference in coronary blood flow dynamics between patients with hypertension and those with hypertrophic cardiomyopathy. Hypertens Res 2002; 25: 711–6.[CrossRef][Web of Science][Medline]
[4] Wieneke H, Haude M, Ge J, et al. Corrected coronary flow velocity reserve: a new concept for assessing coronary perfusion. J Am Coll Cardiol 2000; 35: 1713–20.
[5] Nitenberg A and Antony I. Epicardial coronary arteries are not adequately sized in hypertensive patients. J Am Coll Cardiol 1996; 27: 115–23.[Abstract]
[6] Petropoulakis PN, Kyriakidis MK, Tentolouris CA, et al. Changes in phasic coronary blood flow velocity profile in relation to changes in hemodynamic parameters during stress in patients with aortic valve stenosis. Circulation 1995; 92: 1437–47.
[7] Krivokapich J, Huang SC, Schelbert HR. Assessment of the effects of dobutamine on myocardial blood flow and oxidative metabolism in normal human subjects using nitrogen-13 ammonia and carbon-11 acetate. Am J Cardiol 1993; 71: 1351–6.[CrossRef][Web of Science][Medline]
[8] McGinn AL, White CW, Wilson RF. Interstudy variability of coronary flow reserve. Influence of heart rate, arterial pressure, and ventricular preload. Circulation 1990; 81: 1319–30.
[9] Nelson GS, Berger RD, Fetics BJ, et al. Left ventricular or biventricular pacing improves cardiac function at diminished energy cost in patients with dilated cardiomyopathy and left bundle-branch block. Circulation 2000; 102: 3053–9.
[10] Harrigan RA, Pollack ML, Chan TC. Electrocardiographic manifestations: bundle branch blocks and fascicular blocks. J Emerg Med 2003; 25: 67–77.[Medline]
[11] Doucette JW, Corl PD, Payne HM, et al. Validation of a Doppler guide wire for intravascular measurement of coronary artery flow velocity. Circulation 1992; 85: 1899–911.
[12] Baumgart D, Haude M, Ge J, et al. Online integration of intravascular ultrasound images into angiographic images. Cathet Cardiovasc Diag 1996; 39: 328–9.[CrossRef][Web of Science][Medline]
[13] Bache RJ and Cobb FR. Effect of maximal coronary vasodilation on transmural myocardial perfusion during tachycardia in the awake dog. Circ Res 1977; 41: 648–53.
[14] Ofili EO, Kern MJ, St Vrain JA, et al. Differential characterization of blood flow, velocity, and vascular resistance between proximal and distal normal epicardial human coronary arteries: analysis by intracoronary Doppler spectral flow velocity. Am Heart J 1995; 130: 37–46.[CrossRef][Web of Science][Medline]
[15] Ge J, Erbel R, Gerber T, et al. Intravascular ultrasound imaging of angiographically normal coronary arteries: a prospective study in vivo. Br Heart J 1994; 71: 572–8.
[16] Schiller NB, Shah PM, Crawford M, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr 1989; 2: 358–67.[Medline]
[17] Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E, Sachs I, et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol 1986; 57: 450–58.[CrossRef][Web of Science][Medline]
[18] Anderson HV, Stokes MJ, Leon M, et al. Coronary artery flow velocity is related to lumen area and regional left ventricular mass. Circulation 2000; 102: 48–54.
[19] Grines CL, Bashore TM, Boudoulas H, et al. Functional abnormalities in isolated left bundle branch block. The effect of interventricular asynchrony. Circulation 1989; 79: 845–53.[Medline]
[20] Breithardt OA, Sinha AM, Schwammenthal E, et al. Acute effects of cardiac resynchronization therapy on functional mitral regurgitation in advanced systolic heart failure. J Am Coll Cardiol 2003; 41: 765–70.
[21] Xiao HB, Lee CH, Gibson DG. Effect of left bundle branch block on diastolic function in dilated cardiomyopathy. Br Heart J 1991; 66: 443–7.
[22] Prinzen FW, Hunter WC, Wyman BT, et al. Mapping of regional myocardial strain and work during ventricular pacing: experimental study using magnetic resonance imaging tagging. J Am Coll Cardiol 1999; 33: 1735–42.
[23] Kawaguchi M, Murabayashi T, Fetics BJ, et al. Quantitation of basal dyssynchrony and acute resynchronization from left or biventricular pacing by novel echo-contrast variability imaging. J Am Coll Cardiol 2002; 39: 2052–8.
[24] Vernooy K, Verbeek XA, Peschar M, et al. Left bundle branch block induces ventricular remodelling and functional septal hypoperfusion. Eur Heart J 2005; 26: 91–8.
[25] Skalidis EI, Kochiadakis GE, Koukouraki SI, et al. Phasic coronary flow pattern and flow reserve in patients with left bundle branch block and normal coronary arteries. J Am Coll Cardiol 1999; 33: 1338–46.
[26] Skalidis EI, Kochiadakis GE, Koukouraki SI, et al. Myocardial perfusion in patients with permanent ventricular pacing and normal coronary arteries. J Am Coll Cardiol 2001; 37: 124–29.
[27] Kolettis TM, Kremastinos DT, Kyriakides ZS, et al. Effects of atrial, ventricular, and atrioventricular sequential pacing on coronary flow reserve. Pacing Clin Electrophysiol 1995; 18: 1628–35.[Medline]
[28] Freedman RA, Alderman EL, Sheffield LT, et al. Bundle branch block in patients with chronic coronary artery disease: angiographic correlates and prognostic significance. J Am Coll Cardiol 1987; 10: 73–80.[Abstract]
[29] Rotman M and Triebwasser JH. A clinical and follow-up study of right and left bundle branch block. Circulation 1975; 51: 477–84.
[30] Fauchier L, Marie O, Casset-Senon D, et al. Interventricular and intraventricular dyssynchrony in idiopathic dilated cardiomyopathy: a prognostic study with Fourier phase analysis of radionuclide angioscintigraphy. J Am Coll Cardiol 2002; 40: 2022–30.
[31] Allen MR, Gibbons RJ, Zinsmeister AR. Sex differences in ventricular function in patients with right bundle branch block. Am Heart J 1998; 136: 418–24.[CrossRef][Web of Science][Medline]
[32] Haft JI, DeMaio SJ Jr, Bartoszyk OB. Coronary arteriographic findings in symptomatic right bundle branch block. Am J Cardiol 1984; 53: 770–3.[CrossRef][Web of Science][Medline]
[33] Breithardt OA, Stellbrink C, Franke A, et al. Pacing therapies for congestive heart failure study group; guidant congestive heart failure research group. Acute effects of cardiac resynchronization therapy on left ventricular Doppler indices in patients with congestive heart failure. Am Heart J 2002; 143: 34–44.[CrossRef][Web of Science][Medline]
[34] Wieneke H, Schmermund A, Ge J, et al. Increased heterogeneity of coronary perfusion in patients with early coronary atherosclerosis. Am Heart J 2001; 142: 691–7.[CrossRef][Web of Science][Medline]
[35] Wieneke H, von Birgelen-C, Haude M, et al. Determinants of coronary blood flow in humans: quantification by intracoronary Doppler and ultrasound. J Appl Physiol 2005; 98: 1076–82.
[36] Bartel T, Yang Y, Muller S, Wenzel RR, et al. Noninvasive assessment of microvascular function in arterial hypertension by transthoracic Doppler harmonic echocardiography. J Am Coll Cardiol 2002; 39: 2012–8.
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