Effect of Ventricular Pacing on Coronary Blood Flow in Patients with Normal Coronary Arteries

Although ventricular pacing is thought to produce impairment of left ventricular function by altering the sequence of ventricular activation and AV dyssynchrony, little is known about the effect of ventricular pacing on coronary blood flow. We measured coronary blood flow and coronary flow reserve in the left anterior descending coronary artery during sinus rhythm, and during both atrial and ventricular pacing at a rate of 100 ppm in 14 patients with normal coronary arteries. The double product increased significantly during both types of pacing. Coronary arterial diameter during ventricular pacing significantly increased compared to that during both sinus rhythm and atrial pacing. Coronary flow velocity during ventricular pacing was significantly lower compared to that during both sinus rhythm and atrial pacing. Coronary blood flow increased significantly during atriai pacing (30.7%± 12.1%; P < 0.001), but not significantly during ventricular pacing (23.6%± 47.0%; P = ns). While coronary flow re-serve during both atrial (3.9 ± 1.3) and ventricular pacing (3.8 ± 0.9) was lower compared to its value during sinus rhythm (4,5 ± 1.5), the difference was not significant. There was a significant positive correlation between the coronary flow reserve during sinus rhythm and the increase of coronary blood flow during ventricular pacing (R²= 0.78; P < 0.001). We concluded that an increase in coronary blood flow during ventricular pacing is not a common finding regardless of the increase in metabolic demand. The increase of coronary blood flow during ventricular pacing was less in patients with a reduced coronary flow reserve. These findings suggest that preservation of AV synchrony and the presence of a normal sequence of ventricular activation may play an important role in preserving coranary blaod flow in this subset of patients.     

Short-Term Atrioventricular Sequential Pacing Does Not Adversely Affect Collateral Blood Flow: A Study During Angioplasty

Altered sequence of ventricular activation sequence results in marked derangements in mechanical events. In the present study, we investigated the comparative effects of atrial and AV sequential pacing on collateral blood flow during angioplasty. Twenty-eight patients with stable angina and left anterior descending artery disease undergoing balloon angioplasty were studied. Collateral flow was determined during balloon inflation from the distal flow velocity of the ipsilateral artery (17 patients) or from the increase of the maximal diastolic blood flow velocity (Vc) of the contralateral artery (11 patients). Flow measurements were made using the Doppler flow guidewire. The relative resistance in the collateral vascular bed (RRj also was estimated in the latter group of patients. After the first balloon inflation, two similar consecutive balloon inflations were done under atrial and AV sequential pacing, at a rate of 15 beats/min higher than the sinus rate, in the absence ofvasoactive medication. One minute after the initiation of pacing, the second and third balloon inflations were begun and the pacing continued until the balloon inflations were completed. In the ipsilateral group, average peak velocity was 84.6 t 24.2 mm/s during atrial pacing and 82.7 ± 29.7 mm/s during AV sequential pacing (P = NS). In the contralateral group. Vc was l8%± 12% during atrial pacing and 17%± 14% during AV sequential pacing, and the RR was 4.5 ± 4.7 and 4.9 ± 6.4, respectively (both P = NS). The coronary wedge/mean blood pressure was similar during the two tested balloon inflations. Short-term AV sequential pacing at rest does not adversely affect collateral blood flow and resistance in patients with left anterior descending artery disease.     

Modulation of the Arterial Coronary Blood Flow by Asynchronous Activation with Ventricular Pacing

This study aims to test the assumptions that: (1) coronary arterial flow is attenuated in an early activated region by ventricular pacing; (2) asynchronous mechanical activation caused by ventricular pacing under controlled perfusion pressure and intact coronary tone is associated with reduced coronary flow compared to atrial pacing; and (3) abolishment of vascular tone under controlled perfasion pressure diminishes the expected difference in blood flow between atrial and ventricular pacing. Blood flow velocity (BFV) in the left anterior descending (LAD) and the left circumflex arteries (CFX) and a wall thickening index were measured in 14 open-chest dogs under normal conditions, and constant perfasion pressure. Four pacing sites were used: right atrium (RAJ, mid-right ventricle (RVyJ, mid-left ventricle (LVp), and left ventricular apex (Apex. Pacing modes were either sequential ventriculoatrial (VA) (protocol A, n = 7), or sequential atrioventricalar (AV) (protocol B, n = 7), with a shorter AV difference (30 msec) than normal. Residis: BFV was decreased in the LAD during HV and Apex, pacingby 9.7%-12.9% versas LV^p and by 1.6%-14.6% versus LV^p (P < 0.05). No BFV variations were observed in the CFX. Flow velocity conductance (FVC = mean blood flow velocity divided by the mean aortic pressure) was higher by 16%-28% in the CFX for the three ventricular pacing sites versus the airial pacing, and higher by 14.1%± 6.1% only in LV_p versus RA_p pacing in the LAD (P < 0.05). Wall thickening index reduced during ventricular pacing in all three ventricular sites by 50%-64% (P < 0.05) compared to atrial pacing. Under constant perfusion pressure, LAD blood flow decreased with ventricular pacing as compared to right atrial pacing; this was particularly pronounced during the diastolic phase (16.6%?45.5%, P < 0.02). Normalized oscillatory flow amplitude (OFA.J was reduced in RVy, pacing compared to RA_p and LV_p pacing (16.2 ± 3.5 and 21.7%± 4.1%, respectively, P < 0.03). The variations in blood flow and OFAn disappeared with adenosine-mediated maximum vasodilatation. Summary; (1) Mean and phasic flows are reduced in the early activated LAD region by ventricular pacing (RV_p, Apex. (2) Under controlled perfusion pressure and intact vascular tone, ventricular pacing compromises blood flow compared with atrial pacing. (3) This effect disappears when vascular tone is eliminated by intracoronary injection of adenosine, suggesting that the coronary autoregulation is responsible for some of the effects.     

Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial-Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy

HETTRICK, D.A., et al .: Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy. The role of atrial lead location in cardiovascular function in the presence of impaired ventricular dysfunction is unknown. We tested the hypothesis that left atrial (LA) and left ventricular (LV) hemodynamics are affected by alterations in AV delay and are influenced by atrial pacing site in dogs with dilated cardiomyopathy. Dogs   (n = 7)   were chronically paced at 220 beats/min for 3 weeks to produce cardiomyopathy and then instrumented for measurement of LA, LV end diastolic pressure (LVEDP) and mean arterial pressure (MAP), LA volume, LV short-axis diameter, and aortic and pulmonary venous blood flow. Hemodynamics were measured after instrumentation and during atrial overdrive pacing from the right atrial appendage (RAA), coronary sinus ostium (CSO) and lower LA lateral wall (LAW). The AV node was then ablated, and hemodynamics were compared during dual chamber AV pacing (right ventricular apex) from each atrial lead location at several AV delays between 20 and 350 ms. Atrial overdrive pacing from different sites did not alter hemodynamics. Cardiac output (CO), stroke volume, LVEDP, MAP and +dLVP/dt demonstrated significant (P < 0.05) variation with AV delay during dual chamber pacing. CO was higher during LAW pacing than RAA and CSO pacing (   2.3 ± 0.4   vs   2.1 ± 0.3   vs   2.0 ± 0.3 l/min   , respectively) at an AV delay of 120 ms. Also, MAP was higher in the LAW than RAA and CSO (   65 ± 9   vs   59 ± 9   vs   54 ± 11 mmHg   , respectively) at an AV delay of 350 ms. Atrial lead location affects indices of LV performance independent of AV delay during dual chamber pacing in dogs with cardiomyopathy. (PACE 2003; 26[Pt. I]:853–861)     

Evaluation of atrial thrombus formation and atrial appendage function in patients with pacemaker by transesophageal echocardiography

BACKGROUND: Physiologic pacing is claimed to be superior to ventricular pacing in as much as it entails lower risk of atrial fibrillation, stroke, and atrial remodeling. There are few data on the relation between atrioventricular (AV) synchrony and atrial clot formation. Utilizing transesophageal echocardiography (TEE), this study sought to evaluate the effect of AV synchrony loss on left atrial physiology, atrial stasis, and clot formation. METHODS: We conducted a cross-sectional study on patients with both AV and ventricular pacing with left ventricular ejection fraction (LVEF) >30%. TEE enabled us to explore atrial and pacing leads thrombi and measure left atrial appendage (LAA) flow velocity. RESULTS: A total 72 patients (mean age, 65 +/- 11.7) were enrolled in the study. The pacing mode was VVI in 53% and AV sequential in 47% of patients. LVEF (mean +/- SD; %) was 53.3 +/- 6.2% in ventricular pacing mode and 52.2 +/- 6.6 in physiologic pacing mode. Thrombus formation on pacing lead (<10 mm in 97% of patients) was observed in 32% of all the patients (23% in patients with AV sequential pacing mode and 39% with VVI mode). Left atrial appendage flow velocity (LAA-FV) was significantly higher among the patients with AV sequential pacing mode (49.44 +/- 18 cm/s vs 40.94 +/- 19.4 cm/s, P value = 0.02). LAA-FV >40 cm/s was detected in 60% of the patients, 60% of whom were in physiologic mode. Left atrial size was significantly larger among the patients with VVI pacing mode (42.3 +/- 2.3 mm vs 37.79 +/- 4.5 mm, P = 0.001). Multivariate analysis showed no relation between LAA-FV and age, hypertension, diabetes mellitus, left atrial size, and left ventricular function. Only one patient had right atrial clot. There was no thrombus in the ventricles and atrial appendage. CONCLUSION: Long-term loss of AV synchrony induced by VVI pacing is associated with the impairment of LAA contraction. Thrombus formation in the LAA is not increased by VVI pacing in patients with relatively good left ventricular (LV) function and sinus rhythm.     

Effects of Increasing Heart Rate Induced by Efferent Sympathetic Neuronal Stimulation, Isoproterenol or Cardiac Pacing on Myocardial Function and Oxygen Utilization

The effects of increasing heart rate by six different methods on cardiac /unction were investigated in 17 open-chest anesthetized dogs. Heart rate was increased approximately 30% by (1) right interganglionic nerve stimulation, (2) atrial pacing, (3) ventricular pacing, (4) atriovenfricular sequential pacing, (5) right stellate ganglion stimulntion, and (6) isoproterenoi administration. During heart rate increases induced by atrial pacing left ventricular intramyocardial pressure, coronary Wood flow, oxygen delivery per unit of myocardial oxygen consumption, and myocardial efficiency were unchanged. Ventricular pacing reduced left ventricular cavity and septal intramyocardial pressure, while circumflex coronary flow increased, resulting in reduced oxygen delivery relative to myocardial oxygen consumption. Similarly, atrioventricu-lar sequential pacing increased circumflex coronary artery flow and myocardial oxygen consumption, and decreased septal intramyocardial pressure and oxygen delivery per unit of myocardial oxygen consumption. Right stellate ganglion stimulation and isoproterenol increased left anterior descending and circumflex coronary artery blood flow, intramyocardial pressure, and myocardial oxygen consumption. Estimated myocardial efficiency (left ventricle) was decreased by ventricular pacing and isoproterenol, and was unchanged by atrial pacing and right interganglionic nerve stimulation. Increases in heart rate induced by right interganglionic nerve stimulation did not alter myocardial oxygen consumption, or the index of cardiac efficiency. It is concluded that augmentation of heart rate by either ventricular or atrioventricular pacing impairs myocardial function so that there is a decrease of left ventricular efficiency, and isoproterenol augments chronotropism and myocardial force relative to cardiac external work so there is a reduction in cardiac efficiency. In contrast, atrial pacing or right interganglionic nerve stimulation augments chronotropism such that myocardial oxygen consumption and efficiency are unchanged.     

The Hemodynamic Importance of Atrial Systole: A Function of the Kinetic Energy of Blood Flow?

The relative importance of atrial systole on left ventricular filling was investigated at rest and during exercise in 25 patients with dual chamber pacemakers. The mean blood flow velocity over the atrial valve, the velocities of the rapid filling phase (E), the active filling phase (A), and the E/ A ratio were determined for pulsed Doppler-echocardiography. The patients were first examined at rest during AV sequential pacing (DVI) at 70 and 104 beats/mm. The investigation was subsequently repeated during atrial synchronous pacing (VDD) at rest and during supine submaximal exercise at workloads adjusted to achieve heart rates corresponding to those during DVI pacing. The mean blood flow velocity at rest did not differ between DVI and VDD pacing at 70 beats/mm (0.46 vs 0.49 m/sec). When (he resting heart rate was increased to 104 beats/min (DVI) the mean blood flow velocity increased to 0.56 msec (P < 0.001). At a corresponding heart rate during exercise (VDD) the velocity increased to 0.70 msec (P < 0.001). At a resting heart rate of 70 beats/min the E/A ratio (n = 14) did not differ significantly between DVI and VDD pacing. With an increased resting heart rate (DVI) the E/A ratio decreased from 0,94 ± 0.45 to 0.78 ± 0.18; NS. When the heart rate increased during exercise (VDD) the E/A ratio increased from 0.75 ± 0.14 to 0.97 ± 0.16; P < 0.001. There was a positive correlation between the increase of the mean blood flow velocity and the increase of the E/A ratio during exercise (r = 0.69, P < 0,01). No such correlation was found when the heart rate was changed at rest. Thus, the importance of atrial systole on ventricular filling diminishes during exercise in accordance with increasing blood flow velocity, which by physical principles is related to the kinetic energy. The relative importance of atrial systole is hence inversely correlated to the kinetic energy of the blood flow.     

Effect of Short Atrioventricular Delay on Cardiac Output

RONASZEKI, A., ET AL.: Effect of Short Atrioventricular Delay on Cardiac Output. Short atrioventricular (AV) delay modifies late diastolic filling dynamics. The effect of this change on cardiac output [CO) was studied in closed chest, AV blocked canine preparations (N: 10), during AV sequential pacing (80 bpm). CO (thermodilution technique) and transmitral flow velocity (TMFV, pulsed-wave Doppler) were measured and compared (paired t-test) on the basis of TMFV pattern, when atrial contraction (A wave) started just after early diastolic transmitral flow deceleration [PR:219 ± 25 ms, mean ± SD) and when A wave occurred at the end of late diastole and shortened due to the next ventricular contraction (PR: 56 ± 11 ms). The short AV delay resulted in 12.0 ± 5.9% decrease of CO, reflecting the interrupted late diastolic atrial transport. Properly timed atrial contraction is necessary for optimal AV sequential pacing.     

The Importance of the Left Atrioventricular Interval during Atrioventricular Sequential Pacing

During atrioventricular (AV) sequential pacing from the right heart, the interval between the left atrium and ventricle may vary from the programmed AV interval depending on the position of the atrial and ventricular electrodes and interatrial and interventricular conduction. The aim of this study was to determine the hemodynamic effects of altering the left AV interval while keeping the programmed AV interval constant. Four male and 17 female patients, aged 49 ± 15 years were studied. The left AV interval was measured by a catheter in the coronary sinus. Stroke volume and mitral flow were measured by simultaneous echo Doppler during AV sequential pacing from the right atrial appendage and right ventricular apex at programmed AV intervals of 100. 60, and 6 ms. The atrial catheter was then positioned on the atrial septum and the measurements repeated. With the atrial catheter in the right atrial appendage, interatrial activation time (118 ± 20 ms) was similar to interventricular activation time (125 ± 21 ms) and the left AV interval was almost identical to the programmed right AV interval. There was a significant correlation between interatrial and interventricular activation times (r = 0.8; P < 0.001). Positioning the atrial electrode on the septum decreased interatrial activation time by 39 ± 12 ms and increased the left AV interval by a similar amount. At a programmed AV interval of 60 ms, the left AV interval increased from 67 ± 15 ms to 105 ± 17 ms after the atrial catheter was repositioned from the appendage to the septum (P < 0.001). Compared to pacing from the right atrial appendage, atrial septal pacing increased mitral A wave velocity integral (2.8 ± 1.4 vs 4.4 ±1.7 cm at a programmed AV interval of 60 ms, P < 0.01), decreased E wave velocity integral (8.1 ± 2.2 vs 6.1 ± 2.4 cm, P < 0.001) but did not alter stroke volume (44.8 ± 10.6 vs 44.9 ± 10.1 mL). In contrast, a 40 ms decrease in the programmed right AV interval from 100 to 60 ms decreased stroke volume from 48.0 ± 10.0 to 44.9 ± 10.2 mL (P < 0.001). There was a strong relationship between interatrial and interventricular conduction so that patients with prolonged interatrial conduction still had equivalent left and right AV intervals during atrioventricular sequential pacing from the right atrial appendage and right ventricular apex. Positioning the atrial electrode on the septum decreases interatrial activation time and increases the left AV interval by about 40 ms but has minimal hemodynamic effect in patients without heart failure.     

The Effect of Ventricular Activation Sequence on Cardiac Performance During Pacing

The aim of this study was to evaluate the importance of a normal ventricular activation pattern for cardiac performance. In nine mongrel clogs, atrial pacing was compared to AV synchronous pacing at three different A V delays (150, 100, and 60 nis). In six dogs, proximal septal AV synchronous pacing was compared to apical A V synchronous pacing at three different A V delays. AV synchronous pacing was performed after RF induced complete heart block. Hemodynarnics were evaluated by assessment of positive and negative dP/dt, cardiac output, and left ventricular and pulmonary pressures. Atrial pacing was superior to AV synchronous pacing with respect to positive and negative dP/dt and cardiac output. This difference was present at all AV delays. Proximal septal pacing was associated with a higher positive and negative dP/dl compared to apical pacing at all AV delays. Left ventricular activation time was significantly shorter during proximal septal pacing than during apical pacing (88 ± 4 vs 115 ± 4 ms, P < 0.001). We conclude that atrial and proximal septal pacing improves cardiac function and shortens the ventricular activation time compared to apical AV synchronous pacing independent of the AV interval.     

Effect of Dual Chamber Atrioventricular Sequential Pacing on Coronary Flow Velocity in a Patient with Hypertrophic Obstructive Cardiomyopathy

Effects of dual chamber A V sequential pacing on coronary flow velocity, especially systolic reversal flow, were tested in a patient with hypertrophic obstructive Cardiomyopathy. AV sequential pacing with shorter AV delays reduced the systolic reversal flow in the coronary artery, and improved the pressure gradient of the left ventricular outflow tract.     

冠状动脉慢血流现象的冠状动脉血流成像分析

目的 应用冠状动脉血流成像(CFI)无创性评估冠状动脉慢血流现象患者的冠状动脉血流速度变化.方法 冠状动脉无明显狭窄且心肌梗死溶栓试验(TIMI)提示慢血流现象患者21例,冠状动脉造影无明显狭窄且TIMI血流正常者9例作为对照组.采用校正的TIMI血流计帧法(CTFC)评价冠状动脉血流速度.常规超声心动图测量左室舒张末期内径、收缩末期内径、左室射血分数、E峰、A峰、E/A值.CFI测量冠状动脉前降支远端舒张期峰值血流速度(Vmax)、舒张期平均流速(Vmean)和血流速度时间积分(VTI).结果 慢血流组前降支CTFC为(45.37±8.62)帧,对照组为(15.94±4.66)帧,二者差异有统计学意义(t=-9.596,P=0.000).慢血流组与对照组常规超声心动图测值差异均无统计学意义.慢血流组前降支Vmax为(22.86±3.04)cm/s,Vmean为(17.62±2.89)cm/s,VTI为(8.49±2.01)cm;对照组前降支Vmax为(31.78±9.28)cm/s,Vmean为(23.67±7.60)cm/s,VTI为(10.91±4.47)cm,两组差异均有统计学意义(P＜0.05).对照组及慢血流组前降支CTFC与Vmax和Vmean呈负相关,对照组前降支CTFC与VTI呈负相关,慢血流组前降支CTFC与VTI无相关性.结论 冠状动脉慢血流现象患者冠状动脉前降支远端血流速度减慢,CFI能够反映冠状动脉造影TIMI血流的变化,但诊断冠状动脉慢血流现象有局限.

Abstract：

Objective To non-invasive assess coronary blood flow velocity changes of patients with slow coronary flow phenomenon (SCFP) by coronary blood flow imaging (CFI).Methods Twenty-one patients who had no significant coronary artery stenosis but had thrombolysis in myocardial infarction (TIMI) slow-flow phenomenon were the experimental group,nine patients who has no significant coronary stenosis and TIMI flow normal were the control group.Using corrected TIMI frame count(CTFC) assess velocity of coronary artery.The left ventricular end diastolic diameter,end systolic diameter,ejection fraction,E peak velocity,A peak velocity,E/A ratio were measured by conventional echocardiography.The distal anterior descending coronary artery diastolic peak flow velocity(Vmax),mean velocity(Vmean) and blood flow velocity time integral(VTI) were measured by CFI.Results The corrected TIMI frame count (CTFC) of left anterior descending artery blood flow in slow blood group was (45.37 ± 8.62)frame,that in control group was (15.94± 4.66)frame,the difference was statistically significant (t = -9.596,P =0.000).The conventional echocardiographic measurements of two groups were not significantly different.The left anterior descending artery Vmax was (22.86 ± 3.04)cm/s,Vmean was (17.62 ± 2.89)cm/s,VTIwas (8.49± 2.01)cm in the slow blood flow group,the left anterior descending artery Vmax was (31.78 ± 9.28) cm/s,Vmean was (23.67 ± 7.60) cm/s,VTI was (10.91 ± 4.47) cm in the control group.The difference was statistically significant.The left anterior descending artery CTFC with Vmax and Vmean was negative correlation in the control group and the slow blood flow group.The left anterior descending artery CTFC was negatively correlated with VTI in the control group,there was no correlation between left anterior descending artery CTFC and VTI in the slow blood flow group.Conclusions Coronary artery flow velocity in the left anterior descending artery was declined.CFI can reflect changes in coronary TIMI flow,but in the diagnosis of coronary slow flow phenomenon CFI has limitations.     

Evaluation of Asynchronous Left Ventricular Relaxation by Doppler Echocardiography During Ventricular Pacing with AV Synchrony (VDD): Comparison with Atrial Pacing (AAI)

The effect of right ventricular pacing on left ventricular relaxation was studied in 13 patients (age 62 ± 3 years), with the atrial sensing ventricular pacing mode (VDD). A control group of similar age (64 ± 4 years) consisted of 11 patients with atrial pacing (AAI). The timing of events was determined in both groups at similar R-R intervals (921 ± 77 ms vs 967 ± 37 ms). The loading conditions as estimated by peak systolic wall stress (afterload) and end-diastolic left ventricular dimensions (preload) were approximately the same in both groups. The ratio of late to early filling velocities were similar in both groups. Dominant changes were: increased preejection period (142 ± 13 ms vs 95 ± 15 ms); and higher velocities of isovolumic relaxation flow (60 ± 34 cm/s vs 25 ± 4 cm/s) in patients with ventricular pacing. The isovolumic relaxation time was longer in patients with VDD pacing (127 ± 14 ms vs 108 ± 12 ms). Anterior systolic interventricular septal motion (paradoxal motion) was recorded in nine patients with VDD pacing and in none of the patients with AAI pacing. Isovolumic relaxation flow was detected during atrial pacing in five (45%) patients and in 13 (100%) patients during atrial sensing ventricular pacing, indicating asynchronous left ventricular relaxation. This data shows that VDD pacing compared to atrial pacing resulted in an altered activation pattern of the left ventricle, associated with delayed onset, asynchronous contraction with interventricular septal motion abnormalities and prolonged asynchronous left ventricular relaxation with abnormal motion manifested by the presence of isovolumic relaxation flow.     

Is DDD Pacing Superior to VVI,R? A Study on Cardiac Sympathetic Nerve Activity and Myocardial Oxygen Consumption at Rest and During Exercise

Rate responsive ventricular pacing (VVI,R) has been demonstrated to equal atrial synchronous ventricular pacing (DDD) with regard to hemodynamics and exercise tolerance. Whether the two modes are also comparable, with regard to cardiac metabolic effects, is not yet dear. We assessed central hemodynamics, cardiac sympathetic nerve activity fcardiac norepinephrine overflow), and myocardial oxygen consumption in 16 patients treated with rate responsive atrial synchronous ventricular pacemakers (DDD,R), due to high degree AV block. The study was performed at rest and during supine exercise at two workloads (30 ± 12 and 68 ± 24 watts, respectively) during VDD and rate matched VVI pacing (VVI_m). Ventricular rates at rest and during both workloads were almost identical. Cardiac output at rest tended to be higher in the VDD mode, due to a slightly higher stroke volume. Central pressures including right atrial pressure and pulmonary capillary wedge pressure were similar in the pacing modes. The coronary sinus blood flow, the coronary sinus arteriovenous oxygen difference, and the myocardial oxygen consumption did not differ between the two pacing modes. Cardiac norepinephrine overflow was similar in the two pacing modes, at rest or during exercise. Thus, we found no significant differences between VDD and VVI_m pacing with regard to central hemodynamics, cardiac sympathetic nerve activity (cardiac norepinephrine overflow), or myocardial oxygen consumption either at rest or during moderate exercise.     

Hemodynamic Findings During Sinus Rhythm, Atrial and AV Sequential Pacing Compared to Ventricular Pacing In a Dog Model

The hemodynamic responses of atrial lAF], atrioventricu-lar sequential (AVP) and ventricuJar pacing (VP) were compared to sinus rhythm (SfiJ in seventeen anesthetized dogs with intact AV conduction. The atrium and/or ventricle were paced at fixed rates above the control sinus rate. An AV interval shorter than normal conduction was selected to capture the ventricle. The changes of pulmonary capillary wedge pressure (PCWP, mmHg). mean aortic pressure (MAP, mmHg), cardiac output (CO, L/min), systemic vascular resistance (SVR, dynes/s/cm⁻⁵), left ventricular stroke work index (SWI) and mean systolic ejection rate (MSER, ml/s) during sinus rhythm, atrial pacing and atrio-ventricular sequential pacing (expressed in percentages of the individual values during ventricular pacing) were:
The importance of atrial systole for cardiac performance was clearly demonstrated in dogs with normally compliant hearts. In both atrial and atrioventricular sequential pacing compared to ventricular pacing there was a reduction of pulmonary capillary wedge pressure (PCWP) (p < 0.01) and systemic vascular resistance (SVR) (p < 0.01) despite an increase in cardiac output (CO). The lesser mean systolic ejection rate (MSER) found during atrioventricular sequential pacing compared to sinus rhythm and atrial pacing may be explained by the abnormal ventricular depolarization in this pacing mode; nevertheless, the mean systolic ejection rate was still greater than that found during ventricular pacing (p < 0.05).     

Single versus dual chamber pacing in the young: noninvasive comparative evaluation of cardiac function

The advantages of atrial synchrony over asynchronous ventricular pacing remain unclear in the young, chronically right ventricular (RV) - paced patient. This is in contrast to the older patient with inherent diastolic dysfunction who has been shown to benefit from atrial synchrony with dual chamber (DDD,R/VDD), over single chamber rate response (VVI,R) ventricular pacing. The goal of this study was to noninvasively assess cardiac function in a group of young, RV-paced patients before and after establishment of atrial synchrony. Echocardiographic data were retrospectively analyzed from 10 patients with congenital or acquired complete AV block, who were VVI,R paced for 10.2 +/- 2 years (mean age at study 19.2 +/- 8.9 years), and were subsequently converted to DDD,R/VDD pacing (mean age at study 20.7 +/- 9.5 years). Paired t-test analysis of left ventricular (LV) systolic and diastolic function during VVI,R versus DDD,R/VDD pacing did not result in any short-term difference in LV short axis fractional area of change or FAC (53% +/- 7.5% vs 56.8% +/- 8.7%) or mitral maximal velocity (E) normalized to mitral flow velocity time integral (VTI) (5.2/s +/- 1.5 vs 4.4/s +/- 1.5). A decrease in mitral flow E/A ratio was observed after short-term DDD,R/VDD pacing (2.2 +/- 0.5 vs 1.9 +/- 0.3). Atrial synchronous dual chamber pacing in young patients with complete AV block does not lead to any appreciable early change in global LV function over single-site RV pacing. Therefore, early establishment of atrial synchrony in the young asymptomatic VVI,R-paced patient with normal intrinsic ventricular function may not be warranted.     

The effects of atrial fibrillation on coronary blood flow and performance of ischaemic myocardium in dogs with coronary artery stenosis

1. Atrial fibrillation may impair coronary blood flow by tachycardia and reflex vasoconstriction. It has not been documented, however, whether in the presence of coronary stenosis atrial fibrillation exceeds the effects of rhythmic atrial tachycardia. 2. The effects of experimentally induced atrial fibrillation compared with atrial tachycardia, therefore, were tested in 22 anaesthetized dogs. Stenosis of the left anterior descending coronary artery was induced to reduce coronary blood flow by about 40%. 3. In the presence of coronary stenosis, atrial fibrillation (ventricular rate: 234 +/- 21 beats/min) reduced coronary blood flow from 58 +/- 7 to 44 +/- 8 ml min-1 100 g-1 (P less than 0.001, mean +/- SEM) and subendocardial segment shortening (ultrasonic crystals) from 12 +/- 2 to 4 +/- 2% (P less than 0.0025), and resulted in a lactate production of 30 +/- 11% (P less than 0.005 vs sinus rhythm). 4. Atrial tachycardia (heart rate: 216 +/- 21 beats/min, NS vs atrial fibrillation) did not significantly change coronary blood flow and reduced segment shortening to 7 +/- 3% (P less than 0.05 vs atrial fibrillation). Significant lactate production did not occur. 5. Since mean arterial pressure fell from 100 +/- 4 mmHg at sinus rhythm to 89 +/- 3 mmHg (P less than 0.01) during atrial fibrillation but not during atrial tachycardia, it was held constant in 13 dogs by a pressurized blood reservoir. Coronary blood flow, however, fell from 43 +/- 6 to 36 +/- 5 ml min-1 100 g-1 (P less than 0.0025). 6. Thus atrial fibrillation may reduce coronary blood flow and induce myocardial ischaemia in the presence of coronary stenosis in excess of atrial tachycardia.     

The Effects of Rate-Adaptive Atrial Pacing Versus Ventricular Backup Pacing on Exercise Capacity in Patients with Left Ventricular Dysfunction

Background: Atrial rate-adaptive pacing may improve cardiopulmonary reserve in patients with left ventricular dysfunction.
Methods: A randomized, blinded, single-crossover design enrolled dual-chamber implantable defibrillator recipients without pacing indications and an ejection fraction ≤40% to undergo cardiopulmonary exercise treadmill stress testing in both atrial rate-adaptive pacing (AAIR) and ventricular demand pacing (VVI) pacing modes. The primary endpoint was change in peak oxygen consumption (VO₂). Secondary endpoints were changes in anaerobic threshold, perceived exertion, exercise duration, and peak blood pressure.
Results: Ten patients, nine males, eight with New York Heart Association class I, mean ejection fraction 24 ± 7%, were analyzed. Baseline VO₂ was 3.6 ± 0.5 mL/kg/min. Heart rate at peak exercise was significantly higher during AAIR versus VVI pacing (142 ± 18 vs 130 ± 23 bpm; P = 0.05). However, there was no difference in peak VO₂ (AAIR 23.7 ± 6.1 vs VVI 23.8 ± 6.3 mL/kg/min; P = 0.8), anaerobic threshold (AAIR 1.3 ± 0.3 vs VVI 1.2 ± 0.2 L/min; P = 0.11), rate of perceived exertion (AAIR 7.3 ± 1.5 vs VVI 7.8 ± 1.2; P = 0.46), exercise duration (AAIR 15 minutes, 46 seconds ± 2 minutes, 54 seconds vs VVI 16 minutes, 3 seconds ± 2 minutes, 48 seconds; P = 0.38), or peak systolic blood pressure (AAIR 155 ± 22 vs VVI 153 ± 21; P = 0.61) between the two pacing modes.
Conclusion: In this study, AAIR pacing did not improve peak VO_2, anaerobic threshold, rate of perceived exertion, or exercise duration compared to VVI backup pacing in patients with left ventricular dysfunction and no pacing indications.     

Effects of Different Pacing Modes on Left Ventricular Relaxation in Closed-Chest Dogs

Ventricular relaxation is an important determinant of ventricular filling; impaired relaxation may decrease cardiac output and stroke volume. Relaxation hos been shown to occur more quickly following beats with an increased extent of systolic fiber shortening. Since cardiac output and stroke volume are greater during atrioventricular (AV) sequential pacing than during ventricular pacing at identical heart rates, we reasoned that AV sequential pacing would improve relaxation. To assess this hypothesis we studied 11 dogs with chronic (1-3 months) complete heart block (CHB) induced by radiofrequency catheter ablation of the His bundle. Right and left heart pressures, thermodilution cardiac output, und single plane ventriculography were recorded during baseline rhythm (CHB), and VVI, and AV sequential pacing at a heart rate greater than the sinus rate. None had ventriculoatrial conduction. During AV sequential pacing, the AV interval was set at 150 msec. Cardiac output and stroke volume were significantly increased in the AV sequential compared to the VVI pacing mode. Left ventricular pressures, maximal positive and negative dP/dt, and the time constant (T) of isovolumic pressure decay were not different in the two modes. We conclude that despite increased stroke volume in the AV sequential pacing mode, relaxation is unchanged. We believe the lack of change in relaxation is due to nonuniform ventricular activation when depolarization is initiated at the right ventricular apex.     

Reduced coronary flow reserve in patients with congestive heart failure assessed by transthoracic Doppler echocardiography.

BACKGROUND: Although coronary flow reserve (CFR) has been reported to be restricted in various conditions, there has been no report of CFR for patients with congestive heart failure (CHF). The purpose of this study was to assess coronary flow characteristics for patients with CHF. METHODS: We studied 15 patients with CHF: 8 with dilated myocardiopathy and 7 with hypertensive heart disease. Phasic coronary flow velocities were obtained in the left anterior descending coronary artery at rest and during hyperemia (0.15 mg/kg/min adenosine triphosphate infusion intravenously) by transthoracic echocardiography before and after treatment of CHF. CFR was obtained from the ratio of hyperemic/baseline diastolic mean velocity. RESULTS: CFR was significantly restricted in the condition of CHF compared with that after improvement of CHF (1.5 +/- 0.2 vs 2.0 +/- 0.3, P < .01). Baseline diastolic mean velocity in the condition with CHF was significantly greater than that after improvement of CHF (41 +/- 13 cm/s vs 33 +/- 13 cm/s, P = .04), although maximal hyperemic diastolic mean velocity was not significantly different before and after improvement of CHF (63 +/- 20 cm/s vs 61 +/- 19 cm/s, P = .68). After improvement of CHF, heart rate, along with left ventricular end-diastolic volume and dimension, were significantly decreased, and deceleration time of transmitral early filling flow was increased compared with before treatment of CHF. Blood pressure and ejection fraction were not significantly different before and after treatment of CHF. CONCLUSIONS: Restriction of CFR is demonstrated during CHF because of the elevation of baseline resting flow velocity, which might be related to increase in left ventricular preload and heart rate.