Optimal sensed atrio-ventricular interval determined by paced QRS morphology

BACKGROUND: In cardiac resynchronization therapy (CRT), the atrio-ventricular (AV) and interventricular (VV) intervals have to be optimized. For maximal optimization, the paced and sensed AV intervals have to be determined. We hypothesized that the morphology of the paced QRS complex at the optimal paced AV interval (PAV) can be used to determine the optimal sensed AV (SAV) interval in patients with normal AV conduction. PATIENTS AND METHODS: In 16 patients with implanted CRT devices, the optimal PAV and V-V interval were determined by invasive measurement of left ventricle (LV) dP/dt(max). A 12-lead electrocardiogram (ECG) was recorded at the optimum setting. Subsequently, during atrial sensing ventricular pacing, the SAV interval was changed until the QRS morphology was identical to the morphology at the optimal PAV interval. The optimal SAV interval was verified by repeated measurement of LV dP/dt(max). RESULTS: By optimization of the PAV and VV interval, the LV dP/dt(max) increased from 639 +/- 204 to 789 +/- 223 mmHg/s (+23%; P = 0.0000002). The optimized PAV was 149 +/- 19 ms; the optimized SAV was 100 +/- 20 ms and the corresponding LV dP/dt(max) at this interval was 774 +/- 204 ms (+21%; P = 0.000004). LV dP/dt(max) at optimized SAV - 20 ms and optimized SAV + 20 ms was 747 +/- 213 mmHg/s (P = 0.00004) and 751 +/- 203 mmHg/s (P = 0.0000003), respectively. The mean difference in optimized PAV and optimized SAV was 49 +/- 17 ms, ranging from 20 to 80 ms. CONCLUSIONS: The QRS morphology at optimized PAV can be used as a template to determine the optimal SAV, provided that the patient has normal AV conduction.     

Invasive optimization of cardiac resynchronization therapy: role of sequential biventricular and left ventricular pacing

BACKGROUND: Aim of this invasive study was to characterize and quantify changes in left ventricular (LV) systolic function due to sequential biventricular pacing (BV) as compared to right atrial triggered simultaneous BV (BV(0)), LV, and right ventricular (RV) pacing in patients with congestive heart failure (CHF). METHODS: In 22 CHF patients, all in sinus rhythm, temporary multisite pacing was performed prior to implantation of a permanent system. LV systolic function was evaluated invasively by the maximum rate of LV pressure increase (dP/dt(max)). Sequential BV pacing was performed with preactivation of either ventricle at 20-80 ms. RESULTS: In comparison to RV pacing, LV and BV(0) pacing increased dP/dt(max) by 33.9 +/- 19.3% and 34.0 +/- 22.6%, respectively (P < 0.001). In 9 patients, optimized sequential BV pacing further improved dP/dt(max) by 8.5 +/- 4.8% compared to BV(0) (range 3.3-17.1, P < 0.05). In 10 patients exhibiting a PR interval < or =200 ms, LV pacing was either superior (n = 6) or equal to BV(0) pacing (n = 4). In these 10 patients, LV pacing yielded a 7.4 +/- 8.0% higher dP/dt(max) than BV(0) pacing (P < 0.05). CONCLUSIONS: Using sequential BV pacing, generally with LV preactivation, moderate improvements in LV systolic function can be achieved in selected patients. Baseline PR interval may aid in the selection of the optimum cardiac resynchronization therapy (CRT) mode, favoring LV pacing in patients with a PR interval < or =200 ms.     

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.     

Alterations in left ventricular diastolic function in conscious dogs with pacing-induced heart failure.

We investigated in conscious dogs (a) the effects of heart failure induced by chronic rapid ventricular pacing on the sequence of development of left ventricular (LV) diastolic versus systolic dysfunction and (b) whether the changes were load dependent or secondary to alterations in structure. LV systolic and diastolic dysfunction were evident within 24 h after initiation of pacing and occurred in parallel over 3 wk. LV systolic function was reduced at 3 wk, i.e., peak LV dP/dt fell by -1,327 +/- 105 mmHg/s and ejection fraction by -22 +/- 2%. LV diastolic dysfunction also progressed over 3 wk of pacing, i.e., tau increased by +14.0 +/- 2.8 ms and the myocardial stiffness constant by +6.5 +/- 1.4, whereas LV chamber stiffness did not change. These alterations were associated with increases in LV end-systolic (+28.6 +/- 5.7 g/cm2) and LV end-diastolic stresses (+40.4 +/- 5.3 g/cm2). When stresses and heart rate were matched at the same levels in the control and failure states, the increases in tau and myocardial stiffness were no longer observed, whereas LV systolic function remained depressed. There were no increases in connective tissue content in heart failure. Thus, pacing-induced heart failure in conscious dogs is characterized by major alterations in diastolic function which are reversible with normalization of increased loading condition.     

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.     

AV Pacing and LV Performance

Five patients with impaired left ventricular function (LV) and implanted AV sequential pacemakers underwent serial radionuclide angiograms. The goal was a non-invasive evaluation of the rapid changes in left ventricular performance elicited by rate, pacing mode and AV interval manipulation. End diastolic volume, end systolic volume, stroke volume and cardiac output were increased by AV sequential pacing in comparison with ventricular pacing at 70 beats per minute. No significant change in ejection fraction and blood pressure were noted with changing AV sequential pacing rates at usual pacing rates. Our data suggest that a short A V interval (150 ms) improved LV performance more than a long AV interval (250 ms). A non-invasive technique to optimize left ventricular performance on an acute basis by varying heart rate, AV interval and pacing mode with the implanted AV sequential pacemaker is feasible and may be useful in selective clinical situations.     

Rate Modulated Pacing Based on Right Ventricular dP/dt: Quantitative Analysis of Chronotropic Response

Right ventricular contractility increases in response to catecholamine stimulation and greater ventricular preload, factors that increase with exercise workload. Thus, the maximum systolic dP/dt may be a potentially useful sensor to control the pacing rate of a permanent pacing system. The present study was designed to test the long-term performance of a permanent pacemaker that modulates pacing rate based on right ventricular dP/dt and to quantitatively analyze the chronotropic response characteristics of this sensor in a group of patients with widely varying structural heart diseases and degrees of hemodynamic impairment. A permanent pacing system incorporating a high fidelity pressure sensor in the lead for measurement of right ventricular dP/dt was implanted in 13 patients with atrial arrhythmias and AV block, including individuals with coronary artery disease, hypertension, severe obstructive pulmonary disease with prior pneumonectomy, atrial septal defect, dilated cardiomyopathy, restrictive cardiomyopathy, and mitral stenosis. Patients underwent paired treadmill exercise testing in the VVI and VVIR pacing modes with measurement of expired gas exchange and quantitative analysis of chronotropic response using the concept of metabolic reserve. The peak right ventricular dP/dt ranged from 238–891 mmHg/sec with a pulse pressure that ranged from 19–41 mmHg. There was a positive correlation between the right ventricular dP/dt and pulse pressure (r = 0.70, P = 0.012). The maximum pacing rate and VO_2max were 72 ± 6 beats/min and 12.61 ± 4.0 cc O₂/kg per minute during VVI pacing and increased to 124 ± 18 beats/min and 15.89 ± 5.9 cc 0₂/kg per minute in the VVIR pacing mode (P < 0.0003 and P < 0.002, respectively). The integrated area under the normalized rate response curve was 96.7 ± 45.7% of expected during exercise and 100.1 ± 43.4% of expected during recovery. One patient demonstrated an anomalous increase in pacing rate in response to a change in posture to the left lateral decubitus position. Thus, the peak positive right ventricular dP/dt is an effective rate control parameter for permanent pacing systems. The chronotropic response was proportional to metabolic workload during treadmill exercise in this study population with widely varying forms of structural heart disease.     

Positive inotropic and vasodilator actions of milrinone in patients with severe congestive heart failure. Dose-response relationships and comparison to nitroprusside

Milrinone is a potent positive inotropic and vascular smooth muscle-relaxing agent in vitro, and therefore, it is not known to what extent each of these actions contributes to the drug's hemodynamic effects in patients with heart failure. In 11 patients with New York Heart Association class III or IV congestive heart failure, incremental intravenous doses of milrinone were administered to determine the dose-response relationships for heart rate, systemic vascular resistance, and inotropic state, the latter measured by peak positive left ventricular derivative of pressure with respect to time (dP/dt). To clarify further the role of a positive inotropic action, the relative effects of milrinone and nitroprusside on left ventricular stroke work and dP/dt were compared in each patient at doses matched to cause equivalent reductions in mean arterial pressure or systemic vascular resistance, indices of left ventricular afterload. Milrinone caused heart rate, stroke volume, and dP/dt to increase, and systemic vascular resistance to decrease in a concentration-related manner. At the two lowest milrinone doses resulting in serum concentrations of 63 +/- 4 and 156 +/- 5 ng/ml, respectively, milrinone caused significant increases in stroke volume and dP/dt, but no changes in systemic vascular resistance or heart rate. At the maximum milrinone dose administered (mean serum concentration, 427 +/- 11 ng/ml), heart rate increased from 92 +/- 4 to 99 +/- 4 bpm (P less than 0.01), mean aortic pressure fell from 82 +/- 3 to 71 +/- 3 mmHg (P less than 0.01), right atrial pressure fell from 15 +/- 2 to 7 +/- 1 mmHg (P less than 0.005), left ventricular end-diastolic pressure fell from 26 +/- 3 to 18 +/- 3 (P less than 0.005), stroke volume index increased from 20 +/- 2 to 30 +/- 2 ml/m2 (P less than 0.005), stroke work index increased from 14 +/- 2 to 21 +/- 2 g X m/m2 (P less than 0.01), and dP/dt increased from 858 +/- 54 to 1,130 +/- 108 mmHg/s (P less than 0.005). When compared with nitroprusside for a matched reduction in mean aortic pressure or systemic vascular resistance, milrinone caused a significantly greater increase in stroke work index at the same or lower left ventricular end-diastolic pressure. Milrinone caused a concentration-related increase in dP/dt (32% increase at maximum milrinone dose), whereas nitroprusside had no effect. These data in patients with severe heart failure indicate that in addition to a vasodilating effect, milrinone exerts a concentration-related positive inotropic action that contributes significantly to the drug's overall hemodynamic effects. The positive inotropic action occurs at drug levels that do not exert significant chronotropic or vasodilator effects.     

Atrioventricular delay optimization by doppler-derived left ventricular dP/dt improves 6-month outcome of resynchronized patients

BACKGROUND: Atrioventricular (AV) interval optimization, ensuring the best filling and the abolishment of presystolic mitral regurgitation, is crucial for the efficacy of cardiac resynchronization therapy (CRT). The methods proposed to optimize AV delay have many limitations. The maximum left ventricular pressure derivative (LV dP/dt)--an index of cardiac performance--could provide a clue for AV optimization. DP/dt can be calculated by the Doppler curve of mitral regurgitation jet and it is related to micromanometer-derived dP/dt. AIM: The aim of this study was to assess whether optimal AV delay, defined as the highest noninvasive dP/dt, may provide clinical and functional benefits in CRT patients. METHODS: Of 41 consecutive patients, 23 echo Doppler recordings were obtained at AV delays of 60, 80, 100, 120, 140, 160, 180 ms (Group I). Three patients were discarded because of suboptimal Doppler signal. In 15 patients an empiric AV delay of 120 ms was chosen (Group II). Both groups were programmed to atriosynchronous pacing mode and synchronous VV stimulation. RESULTS: In Group I optimal AV delay was 60 ms in one patient, 80 ms in 6, 100 in 6, 120 in 8, 140 in 2. At 6 months follow-up, Group I showed a significantly lower NYHA class (2.1 +/- 0.1 vs 3 +/- 0.2 P < 0.01) and higher LV ejection fraction (LVEF): 32.1 + 1 versus 27.5 +/- 1.6% (P < 0.05) as compared to Group II. CONCLUSIONS: Doppler-derived dP/dt for AV delay optimization determines better functional class and LVEF at 6 months follow-up relative to an empiric AV delay program.     

Stimulation rate and the optimal interventricular interval during cardiac resynchronization therapy in patients with chronic atrial fibrillation

Background: Optimization of cardiac resynchronization therapy (CRT) with respect to the interventricular (V‐V) interval is mainly limited to pacing at a resting heart rate. We studied the effect of higher stimulation rates with univentricular and biventricular (BiV) pacing modes including the effect of the V‐V interval optimization. Methods: In 36 patients with heart failure and chronic atrial fibrillation (AF), the effects of right ventricular (RV), left ventricular (LV), simultaneous BiV, and optimized sequential BiV (BiVopt) pacing were measured. The effect of the pacing mode and the optimal V‐V interval was determined at stimulation rates of 70, 90, and 110 ppm using invasive measurement of the maximum rate of left ventricular pressure rise (LV dP/dt_max). Results: The average LV dP/dt _max for all pacing modalities at stimulation rates of 70, 90, and 110 ppm was 781 ± 176, 833 ± 197, and 884 ± 223 mmHg/s for RV pacing; 893 ± 178, 942 ± 186, and 981 ± 194 mmHg/s for LV pacing; 904 ± 179, 973 ± 187, and 1052 ± 206 mmHg/s for simultaneous BiV pacing; and 941 ± 186, 1010 ± 198, and 1081 ± 206 mmHg/s for BiVopt pacing, respectively. In BiVopt pacing, the corresponding optimal V‐V interval decreased from 34 ± 29, 28 ± 28, and 21 ± 27 ms at stimulation rates of 70, 90, and 110 ppm, respectively . In two individuals, LV dP/dt_max decreased when the pacing rate was increased from 90 to 110 ppm. Conclusion: In patients with AF and heart failure, LV dP/dt_max increases for all pacing modalities at increasing stimulation rates in most, but not all, patients. The rise in LV dP/dt_max with increasing stimulation rates is higher in biventricular (BiV and BiVopt) than in univentricular (LV and RV) pacing. The optimal V‐V interval at sequential biventricular pacing decreases with increasing stimulation rates.     

Cardiovascular effects of haemorrhagic shock in spleen intact and in splenectomized dogs

Summary. Cardiac performance was evaluated during haemorrhagic shock in 27 dogs with spleens intact, 24 splenectomized, and 23 splenectomized transfused dogs that were given a volume of packed red blood cells simulating splenic contraction. Contractile changes were evaluated by calculating dP/dt at 20 mmHg developed pressure (dP/dt DP20), and by relating stroke work to left ventricular end-diastolic volume measured by biplane cinefluorography. Although heart rate increased comparably during early shock, cardiac output, stroke volume, maximal dP/dt, dP/dt DP20, and arterial blood pressure decreased more in splenectomized and splenectomized transfused dogs than in those with spleens intact. During shock dP/dt DP20 was more depressed in the splenectomized and splenectomized transfused dogs than in those with spleens intact. In addition, an increase in left ventricular end-diastolic volume was accompanied by an increase in left ventricular stroke work in dogs with spleens intact. In contrast, stroke work remained depressed in both splenectomized groups despite increased left ventricular volume. Progressive acidosis and decreased left ventricular blood flow were similar in all dogs during haemorrhage. The greater reduction in left ventricular performance during haemorrhagic shock in the splenectomized and splenectomized transfused dogs was not related to excess lactate, changes in plasma volume, or red blood cell mass. Decreased left ventricular performance, despite improved ventricular filling, indicates greater cardiac dysfunction during haemorrhagic shock. This study suggests that, in dogs, the spleen maintains left ventricular performance during haemorrhage by mechanisms other than autotransfusion.     

Morphology of the RV electrogram during LV pacing is related to the hemodynamic effect in cardiac resynchronization therapy

Background: Biventricular (BiV) pacing and left ventricular (LV) pacing both improve LV function in patients with heart failure and LV dyssynchrony. We studied the hemodynamic effect of the atrioventricular (AV) interval and the associated changes in the right ventricular (RV) electrogram (EGM) during LV pacing and compared this with the hemodynamic effect of optimized sequential BiV pacing.
Methods: In 16 patients with New York Heart Association (NYHA) class II to IV, sinus rhythm with normal AV conduction, left bundle branch block (LBBB), QRS > 130 ms, and optimal medical therapy, the changes in RV EGM during LV pacing with varying AV intervals were studied. The hemodynamic effect associated with these changes was evaluated by invasive measurement of LVdP/dt_max and compared with the result of optimized sequential BiV pacing in the same patient.
Results: All patients showed electrocardiographic fusion during LV pacing. The morphology of the RV EGM showed changes in the RV activation that indicated a shift in the extent of fusion from LV pacing. These changes were associated with significant changes in LVdP/dt_max. Baseline LV dP/dt_max was 734 ± 177 mmHg/s, which increased to 927 ± 202 mmHg/s (P<0.0001) with optimized LV pacing and to 920 ± 209 mmHg/s (P<0.0001) with optimized sequential BiV pacing.
Conclusion: The RV EGM is a proper indicator for intrinsic activation over the right bundle during LV pacing and reveals the transition to fusion in the RV EGM that is associated with a decrease in LVdP/dt_max. The hemodynamic effect of optimized LV pacing is equal to optimized sequential BiV pacing.     

Systolic and Diastolic Function with Alternate and Combined Site Pacing in the Right Ventricle

We hypothesized that pacing at two ventricular sites simultaneously would activate the myocardium more rapidly and improve ventricular function. We studied the effect of pacing at the right ventricular outflow tract (RYOT) and the RV apex (EVA) on systolic and diastolic function. In 14 patients with a reduced systolic ejection fraction < 40% (mean EF 32%±4%)we measured RV pressures, left ventricular pressures, EF, cardiac output, peak dP/dt, peak negative dP/dt, and the time constant of relaxation, Tau, during intrinsic rhythm, atrial pacing and DVI pacing at the RVA, the RVOT, and both RV sites combined in random order. Repeated measures analysis of variance showed no significant differences in any of these parameters. The highest absolute values of dP/dt were observed during sinus rhythm and the lowest with RVA pacing. This parameter tended to improve progressively with pacing in the RVOT and at both sites. Peak negative dP/dt showed a similar nonsignificant trend. Conclusion: These data suggest that in patients with poor LV function, there may be subtle improvements in diastolic and systolic function with pacing in the RVOT and at combined sites in the RV compared to traditional RVA pacing.     

Role of ventriculovascular coupling in cardiac response to increased contractility in closed-chest dogs.

While both dobutamine and pacing tachycardia augment left ventricular (LV) contractility, whether overall cardiovascular response to these stimuli is comparable is not known. To address this question we studied seven dogs previously instrumented with three LV diameter gauges and LV pressure manometers. After ganglionic blockade and sedation, caval occlusions were performed at heart rates of 120, 160, and 200 bpm before (C), and 160 and 200 bpm after administration of 10 micrograms/kg per min dobutamine, i.v. (D). The effective arterial elastance (Ea) went up from 14.2 +/- 4.5 mmHg/ml at C120 to 19.6 +/- 8.8 (P less than 0.025 vs C120) and 24.2 +/- 10.4 (P less than 0.001 vs C120) mmHg/ml at C160 and C200. Ees, the slope of the end-systolic pressure-volume relation, increased with pacing from 9.7 +/- 4.6 to 11.7 +/- 4.3 (P less than 0.02), and 13.2 +/- 5.7 (P less than 0.02) mmHg/ml at 160 and 200 bpm. With dobutamine infusion Ea went down, and Ees was further increased to 37.0 +/- 20.9 mmHg/ml at 160 bpm (P less than 0.002 vs C160), and 53.0 +/- 22.6 mmHg/ml at 200 bpm (P less than 0.002 vs C200). Comparison of stroke work and pressure-volume area from single beats with matched LV end-diastolic volumes showed that these were both increased by dobutamine, but not by pacing tachycardia. While increased heart rate after dobutamine markedly increased contractility, Ea was not changed, and neither stroke work nor pressure-volume was further increased. Thus, how well an increase in contractility is transmitted to the periphery is determined in part by arterial behavior. Assessment of both the arterial system and cardiac contractility is necessary to fully evaluate the overall impact of an inotropic stimulus.     

Hemodynamically optimized temporary cardiac pacing after surgery for congenital heart defects

Disturbance of normal AV synchrony and dyssynchronous ventricular contraction may be deleterious in patients with otherwise compromised hemodynamics. This study evaluated the effect of hemodynamically optimized temporary dual chamber pacing in patients after surgery for congenital heart disease. Pacing was performed in 23 children aged 5 days to 7.7 years (median 7.3 months) with various postoperative dysrhythmias, low cardiac output, and/or high inotropic support and optimized to achieve the highest systolic and mean arterial pressures. The following four pacing modes were used: (1) AV synchronous or AV sequential pacing with individually optimized AV delay in 11 patients with first- to third-degree AV block; (2) AV sequential pacing using transesophageal atrial pacing in combination with a temporary DDD pacemaker for atrial tracking and ventricular pacing in three patients with third-degree AV block and junctional ectopic tachycardia, respectively, who had poor signal and exit block on atrial epicardial pacing wires; (3) R wave synchronized atrial pacing in eight patients with junctional ectopic tachycardia and impaired antegrade AV conduction precluding the use of atrial overdrive pacing; (4) Atrio-biventricular sequential pacing in two patients. Pressures measured during optimized pacing were compared to baseline values at underlying rhythm (13 patients with first-degree AV block or junctional ectopic tachycardia) or during pacing modes commonly used in the given clinical situation: AAI pacing (1 patient with slow junctional rhythm and first-degree AV block during atrial pacing), VVI pacing (2 patients with third-degree AV block and exit block and poor sensing on epicardial atrial pacing wires) and dual-chamber pacing with AV delays set to 100 ms (atrial tracking) or 150 ms (AV sequential pacing) in 7 patients with second- to third-degree AV block and functional atrial pacing wires. Optimized pacing led to a significant increase in arterial systolic (mean) pressure from 71.5 +/- 12.5 (52.3 +/- 9.0) to 80.5 +/- 12.2 (59.7 +/- 9.1) mmHg (P < 0.001 for both) and a decrease in central venous (left atrial) pressure from 12.3 +/- 3.4 (10.5 +/- 3.2) to 11.0 +/- 3.0 (9.2 +/- 2.7) mmHg (P < 0.001 and < 0.005, respectively). In conclusion, several techniques of individually optimized temporary dual chamber pacing leading to optimal AV synchrony and/or synchronous ventricular contraction were successfully used to improve hemodynamics in patients with heart failure and selected dysrhythmias after congenital heart surgery.     

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)     

Effects of AV Sequential Versus Asynchronous AV Pacing on Pulmonary Hemodynamics

We studied the effects of various pacing modes on cardiac hemodynamics and pulmonary gas alterations in chronic heart blocked dogs. Changing the pacing mode from an atrioventricular interval of 100 ms (AV100) to a ventriculo-atrial interval of 100 ms (VA100) caused a significant fall in left ventricular pressure (117.64 +/- 11.91 to 95.60 +/- 16.58 mmHg) and cardiac output from 2.18 +/- 0.24 to 1.46 +/- 0.20 L/min. Following the change in pacing mode from AV100 to VA100, there was an increase in the alveolar-arterial O2 gradient from 23.28 +/- 6.97 to 28.74 +/- 8.43 mmHg and a decrease in the arterial CO2 tension from 32.42 +/- 3.22 to 29.42 +/- 3.22 mmHg. There was also a decrease in arterial CO2 tension when the AV100 pacing mode was compared to asynchronous ventricular pacing (32.42 +/- 3.22 versus 30.56 +/- 2.82 mmHg). The minute volume of O2 also decreased when the pacing mode was changed from AV100 to asynchronous ventricular pacing (0.134 +/- 0.01 versus 0.126 +/- 0.01 L/min) and decreased further at VA100 to 0.114 +/- 0.01 L/min. Other significant changes were also observed: the percent of expired CO2 decreased when the pacing mode was changed from AV100 to VA100 (3.68 +/- 0.13 versus 3.37 +/- 0.26%) or to asynchronous ventricular pacing (3.40 +/- 0.31%). The end-expiratory O2 increased and CO2 decreased when the pacing mode was changed from AV100 to VA100. The breath-by-breath correlation of end-expiratory O2 and CO2 with left ventricular systolic pressure showed an almost immediate increase in O2 and reduction in CO2 concentration associated with decreasing systolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Echo doppler assessment of left ventricular function in rats with hypertensive hypertrophy.

OBJECTIVE: This study attempted to establish echocardiographic measurements of left ventricular (LV) mass and LV systolic and diastolic function, particularly in rats with hypertensive heart. METHODS: M-mode LV echograms and Doppler mitral flow were obtained in Dahl salt-sensitive rats placed on 0.3% or 8% sodium chloride diet. Echo Doppler measurements were compared with catheterization and pathologic measurements in 54 rats for LV mass and in 45 rats for LV systolic and diastolic function. RESULTS: Echocardiographic measurement of LV mass correlated well with pathologic measurement (r = 0.94, P <.01, n = 54, SEE = 0.08 mg), independent of LV size, aging, and therapeutic intervention. Endocardial fractional shortening (FS) correlated with LV peak + dP/dt (r = 0.56, n = 45, P <.01), and the correlation was improved to r = 0.71 if 11 rats with marked LV hypertrophy were excluded. Midwall FS correlated well with LV peak + dP/dt (r = 0.72, n = 45, P <.01) even if rats with extremely thickened ventricular wall were included. If midwall FS was lower than 14%, LV systolic dysfunction was very likely (sensitivity 67%, specificity 91%). Association of mitral E/A ratio of 2.0 or greater with deceleration time of shorter than 35 ms was an accurate indicator of elevated LV end-diastolic pressure (sensitivity 82%, specificity 86%) and increased lung weight because of congestive heart failure (sensitivity 89%, specificity 96%) in rats with hypertension. CONCLUSION: LV mass, LV systolic function, and LV end-diastolic pressure were assessable with echo Doppler in rats with hypertensive heart.     

Depression of systolic and diastolic myocardial reserve during atrial pacing tachycardia in patients with dilated cardiomyopathy.

Previous reports have shown that increases in heart rate may result in enhanced left ventricular (LV) systolic and diastolic performance. To assess whether this phenomenon occurs in the presence of depressed LV function, the effects of pacing on LV pressure and volume were compared in seven patients with dilated cardiomyopathy (LV ejection fraction 0.19 +/- 0.11) and six patients with no or minimal coronary artery disease (LV ejection fraction 0.69 +/- 0.11). Patients with normal LV function demonstrated significant increases in LV peak-positive dP/dt, LV end-systolic pressure-volume ratio, LV peak filling rate, and a progressive leftward and downward shift of their pressure-volume diagrams, compatible with increased contractility and distensibility in response to pacing tachycardia. There was no change in LV peak-negative dP/dt or tau. Patients with dilated cardiomyopathy, in contrast, demonstrated no increase in either LV peak-positive dP/dt or the end-systolic pressure-volume ratio, and absence of a progressive leftward shift of their pressure-volume diagrams. Moreover, cardiomyopathy patients demonstrated no increase in LV peak-negative dP/dt or LV peak filling rate and a blunted downward shift of the diastolic limb of their pressure-volume diagrams. Tau, as determined from a derivative method, became abbreviated although never reaching control values. We conclude that patients with dilated cardiomyopathy may demonstrate little or no significant enhancement in systolic and diastolic function during atrial pacing tachycardia, suggesting a depression of both inotropic and lusitropic reserve.     

Comparison of Ventricular Function in Atrial Rate Adaptive Versus Dual Chamber Rate Adaptive Pacing During Exercise

The hemodynamic effects of two different pacing modes—rate adaptive atrial (AAIR) versus dual chamber (DDDR) pacing—were assessed in 12 patients with DDDR pacemakers during upright bicycle exercise first-pass radionuclide angiography using a multiwire gamma camera with tantalum-178 as a tracer. All patients had sinus node disease with intact AV conduction. Patients exercised to the same heart rate in random order in these two different pacing modes, AAIR and DDDR with AV delay (of 100 msec) selected to maintain 100% ventricular capture. Cardiac output in creased significantly above baseline values during exercise in both pacing modes: 154 ± 41% (mean ± SEM, P = 0.002) with AAIR, versus 95 ± 24% (P = 0.004) with DDDR (P = NS between the two modes). The peak filling rate, likewise, increased in both pacing modes (2.3 ± 0.21 end-diastolic volumes/sec to 3.8 ± 0.31 end-diastolic volumes/sec in AAIR [P = 0.0004] and 2.2 ± 0.18 end-diastolic volumes/sec to 3.4 ± 0.27 end-diastolic volumes/sec in DDDR [P = 0.0008]). LV ejection fraction was normal at rest (60 ± 4%, SEM) and did not significantly change with submaximal exercise in either pacing mode (both 56%, P = NS). No significant changes in end-diastolic volume or stroke volume indexes occurred with exercise in either pacing mode. Our study demonstrates that in patients with normal resting LV function, AAIR and DDDR pacing are equally effective in attaining appropriate increases in cardiac output and LV filling during exercise.