Hemodynamic benefits of right ventricular outflow tract pacing: comparison with right ventricular apex pacing

To assess optimal hemodynamics in relation to stimulation site during right ventricular pacing, 17 consecutive patients who underwent cardiac catheterization were studied. In all patients, right ventricular apex and right ventricular outflow tract stimulation was performed at 85, 100, and 120 beats/min. Cardiac index at both pacing sites was compared using the left ventricular outflow tract continuous wave Doppler technique. Comparison of the two stimulation sites demonstrated that right ventricular outflow tract pacing resulted in a higher cardiac index at 85 beats/min (2.42 +/- 1.2 vs 2.04 +/- 1.0 L/min per m2, P < 0.002) at 100 beats/min (2.78 +/- 1.4 vs 2.35 +/- 1.1 L/min per m2, P < 0.001) and 120 beats/min (3.00 +/- 1.5 vs 2.61 +/- 0.9 L/min per m2, P < 0.001). From a total of 51 paired observations, 45 showed an increase in cardiac index during outflow tract pacing as compared to apex pacing. Right ventricular outflow tract pacing at 120 beats/min resulted in a lower cardiac index than right ventricular apex pacing in patients with significant coronary artery disease and/or impaired left ventricular function (ejection fraction < or = 50%), whereas right ventricular outflow tract pacing produced higher cardiac indices in the absence of these abnormalities. Right ventricular outflow tract pacing resulted in higher cardiac indices as compared to apex pacing in all other subgroups at all other pacing sites tested. It is concluded that stimulation of the right ventricular outflow tract offers a significant hemodynamic benefit during single chamber pacing as compared to conventional apex pacing, particularly in the absence of significant coronary artery disease and/or left ventricular dysfunction.     

Physical training alters the pathogenesis of pacing-induced heart failure through endothelium-mediated mechanisms in awake dogs

BACKGROUND: Beneficial effects of exercise training on cardiovascular function in chronic heart failure (CHF) have been suggested previously, but the underlying mechanisms are unknown. We tested whether daily exercise training improves systemic hemodynamics and preserves endothelium-mediated vasodilator function during development of heart failure. METHODS AND RESULTS: Fifteen dogs were surgically instrumented for hemodynamic measurements. One group of dogs underwent 4 weeks of cardiac pacing (210 bpm for 3 weeks and 240 bpm during week 4), and another group underwent pacing plus daily exercise training (4.4+/-0.3 km/h, 2 h/d). Pacing-alone dogs developed CHF characterized by typical hemodynamic abnormalities, blunted endothelium-mediated vasodilator function in coronary and femoral circulations, and decreased gene expression of endothelial constitutive nitric oxide synthase (ECNOS, normalized to GAPDH expression; normal, 1.15+/-0.31 versus CHF, 0.29+/-0.08, P<.05). Exercise training preserved normal hemodynamics at rest, endothelium-mediated vasodilator function, and gene expression of ECNOS (0.72+/-0.16 versus normal, P=NS). Inhibition of NO synthesis (nitro-L-arginine) in exercise-trained dogs abolished the preserved endothelium-mediated vasodilation of epicardial coronary arteries and elevated left ventricular end-diastolic pressure (7.7+/-0.3 to 19+/-3.4 mm Hg, P<.05), suggesting that the preservation of resting hemodynamics was in large part due to preserved endothelial function concealing the underlying CHF state. CONCLUSIONS: Long-term exercise training altered the natural history of heart failure due to rapid cardiac pacing. One of the underlying mechanisms is through the preservation of endothelial vasodilator function.     

Prevention of recurrent atrial fibrillation with chronic dual-site right atrial pacing

OBJECTIVES: We investigated 1) the feasibility, safety and efficacy of multisite right atrial pacing for prevention of atrial fibrillation (AF); and 2) the ability of atrial pacing in single- and dual-site modes to increase arrhythmia-free intervals in patients with drug-refractory AF. BACKGROUND: We recently developed and applied a novel technique of dual-site right atrial pacing in an unselected group of consecutive patients with AF requiring demand pacing. A prospective crossover study design was used to evaluate single- and dual-site right atrial pacing modes. METHODS: The frequency of AF during the 3 months before pacemaker implantation was analyzed. Consecutive consenting patients underwent insertion of two atrial leads and one ventricular lead with a DDDR pulse generator. Patients were placed in a dual-site pacing mode for the first 3 months and subsequently mode switched to single site pacing for 3 months. Mode switching was repeated at 6-month intervals thereafter. RESULTS: Atrial pacing resulted in a marked decline in AF recurrences (p < 0.001). During dual-site pacing with an optimal drug regimen, there was no AF recurrence in any patient compared with five recurrences in 12 patients during single-site pacing (p = 0.03). The mean (+/-SD) arrhythmia-free interval before pacing (14 +/- 14 days) was prolonged with dual- (89 +/- 7 days, p < 0.0001) and single-site pacing (76 +/- 27 days, p < 0.0001). Symptomatic AF episodes showed a declining trend during dual- and single-site pacing compared with those during the preimplantation period (p = 0.10). Mean antiarrhythmic drug use for all classes declined from 4 +/- 1.9 drugs before implantation to 1.5 +/- 0.5 (p < 0.01) drugs after implantation. Twelve (80%) of 15 patients remained in atrial paced rhythm at 13 +/- 3 months. CONCLUSIONS: We conclude that multisite right atrial pacing is feasible, effective and safe for long-term application. Atrial pacing significantly prolongs arrhythmia-free intervals in patients with drug-refractory paroxysmal AF. Dual-site right atrial pacing may offer additional benefits and should be considered either as the primary mode or in patients unresponsive to single-site pacing.     

Lifestyle and 15-year survival free of heart attack, stroke, and diabetes in middle-aged British men

BACKGROUND: Arrhythmogenic right ventricular dysplasia (ARVD) is characterized by local or diffuse wall motion abnormalities in the right ventricle (RV), associated with recurrent ventricular tachycardia (VT) of RV origin. Brain natriuretic peptide (BNP) was first isolated from a porcine brain extract. In humans, BNP is expressed predominantly in the ventricles of failing hearts, and its expression has been observed primarily in myocytes in the interstitial fibrous area in dilated cardiomyopathy. We hypothesized that BNP is increasingly secreted from the residual myocytes within the atrophic tissue in patients with ARVD. METHODS AND RESULTS: Plasma BNP levels were measured in 17 patients with ARVD, 12 patients with idiopathic RV outflow tract tachycardia (RVOT), and 120 control subjects. We performed cardiac catheterization, RV endomyocardial biopsy, electron- beam CT, and biventricular endomyocardial mapping in the ARVD patients. There was a significant increase in plasma BNP levels in the ARVD patients compared with the RVOT patients and control subjects (61.4+/-59.6 pg/mL versus 8.3+/-5. 5 pg/mL and 9.3+/-5.8 pg/mL; P<0.0001, respectively). The plasma BNP levels had no correlation with any of the hemodynamic data, but they had a significant correlation with the RV ejection fraction (r=-0. 588, P=0.025) and with the fractionated-area scores (r=0.705, P=0. 005). Light microscopic immunohistochemistry showed strong BNP immunoreactivity in residual myocytes with fibrofatty replacement. CONCLUSIONS: These results suggest that plasma BNP levels were not increased in RVOT patients but were increased in ARVD patients, and that the increased BNP levels indicate the severity of both the RV dysfunction and the arrhythmogenic substrate.     

Results of postmortem examination of psittacine birds with cardiac disease: 26 cases (1991-1995)

OBJECTIVE: To characterize prevalence and type of cardiac disease evident in psittacine birds during postmortem examination. DESIGN: Retrospective study. ANIMALS: 26 psittacine birds with gross and histologic evidence of cardiac disease. PROCEDURE: Records of postmortem examinations of psittacine birds necropsied during a 4-year period were reviewed. Data on gross and histologic evidence of cardiac disease were analyzed. Birds identified included those in which congestive heart failure (CHF) was considered the primary cause of death and those in which substantial cardiac disease was evident, despite a lack of postmortem findings supportive of CHF. RESULTS: Of 269 psittacine birds necropsied, 26 (9.7%) had evidence of cardiac disease. In 15 (58%) birds with cardiac disease, changes consistent with CHF were evident and were sufficiently severe as to be considered the cause of death. The remaining 11 birds had cardiac lesions secondary to other systemic diseases; cardiac lesions were considered to be an incidental finding in these birds, and CHF was not evident. Of the 15 birds with CHF, 10 had evidence of right ventricular or biventricular failure, whereas only 5 had evidence of left ventricular failure. CLINICAL IMPLICATIONS: Prevalence of cardiac disease in the psittacine birds reported here was similar to that seen clinically in other companion animals. The high incidence of right ventricular or biventricular heart failure in psittacine birds was similar to that for poultry in which lesions of right-sided heart failure predominate.     

Effects of renin inhibition compared to angiotensin converting enzyme inhibition in conscious dogs with pacing-induced heart failure

OBJECTIVE: To compare the effects of angiotensin converting enzyme inhibition (ACEI) (captopril 1 mg/kg i.v.) to direct renin inhibition (CP80794 3 mg/kg i.v.) on left ventricular and systemic hemodynamics and peripheral blood flows in advanced congestive heart failure (CHF). METHODS: Conscious chronically instrumented dogs (n = 14) were treated with captopril, 1 mg/kg, i.v., or CP80794, 3 mg/kg, i.v., before and after development of advanced CHF induced by 4-7 weeks of rapid ventricular pacing. After advanced CHF, comparisons between the inhibitors were made at equihypotensive doses. RESULTS: In advanced CHF, both agents caused comparable reductions in mean arterial pressure (MAP) (-22% from 79 +/- 4 mmHg) and comparable increases (P < 0.01) in cardiac output (CP80794, 1.4 +/- 0.3 to 1.8 +/- 0.1 l/min; captopril, 1.4 +/- 0.1 to 1.9 +/- 0.1 l/min). Neither agent had a significant effect on LV contractility. In contrast, CP80794 caused a greater (P < 0.05) increase in renal blood flow (66 +/- 6% from 64 +/- 5 ml/min) compared to captopril (33 +/- 4% from 66 +/- 7 ml/min). CONCLUSIONS: Renin inhibition with CP80794 and ACEI with captopril caused comparable hemodynamic effects in advanced CHF. However, CP80794 caused significantly greater increases in renal blood flow and suppressed renin activity to a greater degree than captopril.     

Effects of pulsatile perfusion on human saphenous vein vasoreactivity: a preliminary report

The present study examined alterations in left atrial diameter (LAD) and diastolic left ventricular diameter (LVDd) in 37 patients (72.2 +/- 9.8 years old) who received physiological pacemakers; 22 with atrioventricular (AV) block and 15 with sick sinus syndrome (SSS). After pacemaker implantation, LAD and LVDd were serially measured using echocardiography, and their diameters were expressed per body surface area (LADI and LVDdI; mm/m2). Pulmonary capillary wedge pressure (PCWP) and cardiac output (CO) were measured in ten patients with SSS and ten with AV block during both right ventricular and AV sequential pacing. After AV sequential pacing, CO increased in 19 of 20 patients (3.2 +/- 0.9 L/min to 3.9 +/- 1.0 L/min; P < 0.001). LADI decreased from 24.9 +/- 4.2 mm/m2 to 21.8 +/- 4.4 mm/m2 (P < 0.001) in 22 patients with AV block and from 24.1 +/- 3.4 mm/m2 to 20.4 +/- 3.8 mm/m2 (P < 0.001) in 15 SSS patients. However, LVDdI did not change significantly in either group of patients. The changes in LAD after the implantation of a physiological pacemaker occurred rapidly, i.e., LAD began to decrease within 1 minute after the procedure, and then reached a plateau. This plateau phase continued for at least 7 days during physiological pacing. There was a positive correlation between the changes in LADI after pacemaker implantation and those in PCWP observed during the AV sequential pacing performed prior to the implantation (r = 0.86; P < 0.001). The reduction in LAD following pacemaker implantation was rapid and seemed to be accompanied by improvement of cardiac function. Thus, it is suggested that the serial measurement of LADI is useful to predict the efficacy of physiological pacemaker implantation.     

Enhanced susceptibility for acquired torsade de pointes arrhythmias in the dog with chronic, complete AV block is related to cardiac hypertrophy and electrical remodeling

BACKGROUND: Chronic, complete AV block (CAVB) in the dog leads to ventricular hypertrophy, which has been described as an independent risk factor for arrhythmias. In this model, we examined (1) whether the short- and long-term electrical adaptations predispose to acquired torsade de pointes arrhythmias (TdP) and (2) the nature of the structural and functional adaptations involved. METHODS AND RESULTS: We determined (1) endocardial right (RV) and left (LV) ventricular APD, DeltaAPD (LV APD-RV APD), presence of EADs at 0 weeks (acute: AAVB), and CAVB (6 weeks) and inducibility of TdP by pacing and d-sotalol (n=10); (2) steady-state and dynamic LV hemodynamics at 0 and 6 weeks (n=6); (3) plasma neurohumoral levels in time (n=7); (4) structural parameters of the LV and RV of CAVB dogs (n=6) compared with sinus rhythm (SR) dogs (n=6); and (5) expression of ventricular mRNA atrial natriuretic factor (ANF) in CAVB (n=4) and SR (n=4) dogs. Compared with AAVB, CAVB led to nonhomogeneous prolongation of LV and RV APD and different sensitivity for d-sotalol, leading to EADs (4 of 14 versus 9 of 18, P<0.05), increased DeltaAPD (45+/-30 versus 125+/-60 ms, P<0.05), and induction of TdP in most dogs (0% versus 60%, P<0.05). CAVB led to biventricular hypertrophy, whereas LV function was similar in AAVB and CAVB. The neurohumoral levels were transiently elevated. The LV and RV collagen and the capillary/fiber ratio remained normal, whereas ventricular ANF mRNA was not detectable. CONCLUSIONS: The electrical remodeling occurring after CAVB predisposes the heart to acquired TdP, whereas the structural changes (hypertrophy) are successfully aimed at maintaining cardiac function.     

Results of atrioventricular synchronous pacing with optimized delay in patients with severe congestive heart failure

To verify that atrioventricular (AV) synchronous pacing (DDD) with short AV delay improves the condition of patients with severe congestive heart failure, we implanted DDD pacemakers in 10 patients with severe heart failure (New York Heart Association [NYHA] class III to IV). One day after pacemaker implantation, the AV delay was optimized by Doppler echocardiographic measurements over the aortic outflow tract. Patients were evaluated regarding NYHA class, stroke volume, cardiac output, ejection fraction, and quality of life at 1, 3, and 6 months after pacemaker implantation. Although the optimized AV delay was associated with short-term improvement in stroke volume and cardiac output (baseline stroke volume = 22 +/- 7 ml, day 1 = 28 +/- 12 ml; p = 0.03: baseline cardiac output = 1.9 +/- 0.6 L/min, day 1 = 2.2 +/- 1.1 L/min; p = 0.10), the mean stroke volume, cardiac output, NYHA class, and ejection fraction did not change significantly after 1, 3, and 6 months of pacing compared with baseline values. Three patients improved in NYHA class during the follow-up. A consistent improvement in stroke volume, cardiac output, NYHA class, and ejection fraction was observed in only 1 patient. In conclusion, we found no beneficial effects of AV-synchronous pacing with optimized AV delay in patients with severe heart failure.     

Reversibility of changes in left and right ventricular geometry and hemodynamics in pulmonary hypertension. Echocardiographic characteristics before and after pulmonary thromboendarterectomy

Pulmonary thromboendarterectomy (PTE) leads to an acute decrease of right ventricular (RV) afterload in patients with chronic thromboembolic pulmonary hypertension. We investigated the changes in right and left ventricular (LV) geometry and hemodynamics by means of transthoracic echocardiography. The prospective study was performed in 14 patients (8 female, 6 male; age 55 +/- 20 years) before and 18 +/- 12 days after PTE. Total pulmonary vascular resistance and systolic pulmonary artery pressure were significantly decreased (PVR: preoperative 986 +/- 318, postoperative 323 +/- 280 dyn x s/cm5, p < 0.05; PAP preoperative 71 +/- 40, postoperative 41 +/- 40 mm Hg + right atrial pressure, p < 0.05). End diastolic and end systolic RV area decreased from 33 +/- 12 to 23 +/- 8 cm2, respectively, from 26 +/- 10 to 16 +/- 6 cm2, p < 0.05. There was an increase in systolic RV fractional area change from 20 +/- 12 to 30 +/- 16%, p < 0.05. RV systolic pressure rise remained unchanged (516 +/- 166 vs. 556 +/- 128 mm Hg/sec). LV ejection fraction remained within normal ranges (64 +/- 16 vs. 62 +/- 12%). Echocardiographically determined cardiac index increased from 2.8 +/- 0.74 to 4.1 +/- 1.74 l/min/m2. A decrease in LV excentricity indices (end diastolic: 1.9 +/- 1 vs. 1.1 +/- 0.3, end systolic: 1.7 +/- 0.6 vs. 1.1 +/- 0.4, p < 0.05) proved a normalization of preoperatively altered septum motion. LV diastolic filling returned to normal limits: (E/A ratio: 0.62 +/- 0.34 vs. 1.3 +/- 0.8; p < 0.05); Peak E velocity: 0.51 +/- 0.34 vs. 0.88 +/- 0.28 m/sec, p < 0.05; Peak A velocity: 0.81 +/- 0.36 vs. 0.72 +/- 0.42 m/sec, ns; E deceleration velocity: 299 +/- 328 vs. 582 +/- 294 cm/sec2, p < 0.05; Isovolumic relaxation time: 134 +/- 40 vs. 83 +/- 38 m/sec, p < 0.05). We could show a marked decrease in RV afterload shortly after PTE with a profound recovery of right ventricular systolic function--even in case of severe pulmonary hypertension. A decrease in paradoxic motion of the interventricular septum and normalization of LV diastolic filling pattern resulted in a significant increase of cardiac index.     

Assessment of right ventricular function and interstitial fibrosis in idiopathic dilated cardiomyopathy: hemodynamic correlates and prognostic value

BACKGROUND: Right ventricular (RV) function and morphometric quantitation of interstitial fibrosis in idiopathic dilated cardiomyopathy (IDC) have not been the subject of specifically designed clinical observations. In particular, their role in routine assessment and prognostic evaluation of patients (pts) with IDC remains to be settled. METHODS: Eighty-one consecutive IDC patients (63 M, 18 F; mean age 52 +/- 11 yrs) with left ventricular (LV) systolic dysfunction (angiographic ejection fraction - EF - < 55%), normal coronary arteries and no histologic evidence of myocarditis were studied. Cardiac catheterization and endomyocardial biopsy (EMB) were routinely performed in all cases. RV volumes and EF were obtained by angiography according to Ferlinz' method and interstitial fibrosis was quantitated by computer-assisted morphometric analysis. These data were analyzed in order to study correlations with hemodynamic parameters and to assess their prognostic value in a long-term follow-up. RESULTS: In the study population, right ventricular EF was significantly lower than in normal controls (35 +/- 11% vs 53 +/- 6%, p < 0.0001) and showed a significant positive correlation with LV EF (r = 0.54; p < 0.0001), and a weak but significant negative correlation with fibrosis (r = -0.29; p = 0.03). RV volumes, but not EF, were significantly related to mean pulmonary pressure. At multivariate analysis, RV end-diastolic volume (EDV) and EF were the two independent predictors of severe heart failure (NYHA class III-IV). After a mean follow-up of 64 +/- 36 months, 20 pts died and 9 had heart transplantation, for a 63% transplant-free survival rate (TFS). Multivariate analysis identified three independent predictors of TFS: LV stroke work index (p < 0.0001), RV stroke work index (p = 0.02) and RV EDV (p = 0.03). Fibrosis was predictive of survival only in the subgroup with LV EF < 20%. CONCLUSIONS: Assessment of RV function provides useful information in the evaluation of hemodynamic profile and prognosis of pts with IDC. Quantitation of interstitial fibrosis by morphometry provides little additional data.     

Evaluation of pulmonary arterial trunk on frontal chest radiograph in patients with atrial septal defects

Atrial septal defect (ASD) is one of the most common congenital cardiac anomalies encountered in adulthood. The evaluation of the pulmonary hypertension in ASD is clinically important for operative indication and prognosis. The pulmonary vasculature in chest radiographs in patients with ASD is characterized as dilatation of the central pulmonary arteries and increase of the peripheral pulmonary vessels in patients without pulmonary arterial hypertension (PH) and constriction of the peripheral pulmonary arteries in those with pulmonary hypertension. While the dilatation of the main pulmonary artery occurs in the patients both with and without pulmonary hypertension, its precise radiographic evaluation with regard to the morphological and hemodynamic change of the right ventricle and pulmonary arteries has not been reported. This study was to determine if the contour of the main pulmonary artery segment of the cardiac silhouette in the conventional frontal chest radiograph could be used 1) as indicators of PH or raised right ventricular pressure and 2) as a reliable base for evaluation of the size of the right ventricule (RV) in ASD. The intersection of the line (line A) drawn tangentially to the lateral lower margin of the main pulmonary artery segment to the horizontal line at the left hemidiaphragm is closely related to the apex of RV as measured by right ventricular angiography in supine position. The ratios of the distance of the intersection from the midline of the frontal chest radiograph to the internal diameter of the left hemithorax in normal subjects were 0.50 +/- 0.08 (mean +/- standard deviation) for male and 0.54 +/- 0.09 for female. The ratio increased with increasing left-to-right shunt [0.59(Qp/QS < 2), and 0.71 (Qp/QS > 2)] and shows a tendency of decrease with raised right ventricular systolic pressure (0.52-0.64 in normal subjects and patients with mild raised right ventricular systolic pressure and 0.43 in patients with severe raised right ventricular systolic pressure). The measurement of the angle of the line A from the vertical line tends to show increasing decrease with raised pulmonary arterial and right ventricular systolic pressure (20.1 degrees +/- 4.9 in mild PH and 10.3 degrees +/- 4.1 in moderate to severe PH). The decrease of the angle of the line A to the vertical line was well correlated with conventional radiographic criteria of the right and left central pulmonary arteries of PH.(ABSTRACT TRUNCATED AT 400 WORDS)     

Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans

Ten patients with preserved inotropic function having a dual-chamber (right atrium and right ventricle) pacemaker placed for complete heart block were studied. They performed static one-legged knee extension at 20% of their maximal voluntary contraction for 5 min during three conditions: 1) atrioventricular sensing and pacing mode [normal increase in heart rate (HR; DDD)], 2) HR fixed at the resting value (DOO-Rest; 73 +/- 3 beats/min), and 3) HR fixed at peak exercise rate (DOO-Ex; 107 +/- 4 beats/min). During control exercise (DDD mode), mean arterial pressure (MAP) increased by 25 mmHg with no change in stroke volume (SV) or systemic vascular resistance. During DOO-Rest and DOO-Ex, MAP increased (+25 and +29 mmHg, respectively) because of a SV-dependent increase in cardiac output (+1.3 and +1.8 l/min, respectively). The increase in SV during DOO-Rest utilized a combination of increased contractility and the Frank-Starling mechanism (end-diastolic volume 118-136 ml). However, during DOO-Ex, a greater left ventricular contractility (end-systolic volume 55-38 ml) mediated the increase in SV.     

QRS duration widening: reduced synchronization of endocardial activation or transseptal conduction time?

Antegrade activation of the His-Purkinje system (HPS) results in synchronized activation of the right ventricular (RV) and left ventricular (LV) endocardia forming normal, narrow QRS duration (QRSD). An alteration in septal activation and transseptal conduction time have been reported to be the causes for QRSD widening seen with bundle branch block. However, reduced synchronization of activation of RV and LV endocardia as another potential mechanism for QRSD widening has not been systematically studied. Fifteen consecutive patients underwent radiofrequency ablation (RFA) for treatment of supraventricular tachycardia. After RFA, mean QRSD in normal sinus rhythm was 86 +/- 8 ms with mean HV interval of 40 +/- 5 ms. Right atrial (RA), coronary sinus (CS), simultaneous (S) RA-CS, RV apex (RVA), LV apex (LVA), and SRVA-LVA pacing were performed. Mean QRSD with RA, CS, SRA-CS pacing was similar to normal sinus rhythm (87 +/- 7, 87 +/- 8 and 88 +/- 8 ms respectively). Mean QRSD was significantly longer with SRVA-LVA and either RVA or LVA pacing alone compared to normal sinus rhythm (106 +/- 8, 146 +/- 12 and 157 +/- 13 ms, respectively). However, QRSD was significantly shorter with SRVA-LVA pacing compared to either RVA or LVA pacing alone (P < 0.0001). We conclude that shorter QRSD with SRVA-LVA pacing compared to either RVA or LVA pacing alone is due to elimination of transseptal conduction delay; longer QRSD with SRVA-LVA pacing compared to sinus or atrial paced rhythm is due to reduced synchronization of endocardial activation secondary to ectopic entry of impulses into the HPS network and inability to take advantage of the branching structure of the HPS. Therefore, in addition to transseptal conduction delay, reduced synchronization of endocardial activation is another potential mechanism for QRSD widening.     

Vertebral artery injury in C1-2 transarticular screw fixation: results of a survey of the AANS/CNS section on disorders of the spine and peripheral nerves. American Association of Neurological Surgeons/Congress of Neurological Surgeons

OBJECTIVES: The goal of this study was to investigate the possible role of transesophageal echocardiography in the evaluation of patients with clinical pacemaker syndrome. BACKGROUND: Several reports on transthoracic echocardiographic features of ventricular pacing were described; however, no previous study of transesophageal echocardiography has been undertaken in patients at the severe end of pacemaker syndrome who need reprogramming of dual-chamber pacing for symptom relief. METHODS: Twelve patients with ventricular-inhibited pacemakers (VVI) with clinical symptomatic pacemaker syndrome (group I) and 10 patients with VVI without pacemaker syndrome (group II) were prospectively studied. The two groups were pacemaker dependent and had persistent ventriculoatrial conduction. Transesophageal echocardiographic parameters were assessed in group II and within 6 hours before reprogramming to the DDD mode in group I. Follow-up transesophageal echocardiographic study was performed 28+/-5 days after reprogramming in group I. RESULTS: All patients in group I had subjective improvements of symptoms after DDD reprogramming. The atrial reverse flow velocities of pulmonary veins in group I before reprogramming were significantly higher in group II (39.3+/-11.4 versus 15.7+/-13.5 cm/sec, p < 0.0001). Spontaneous echo contrast in the descending aorta was detected in all patients from group I before reprogramming. The prevalence of significant mitral regurgitation (> or = moderate) was significantly higher in group I before reprogramming than in group II (67% versus 8%, p = 0.01). Significant mitral regurgitation and spontaneous echo contrast in the descending aorta in group I disappeared after reprogramming to the DDD mode. CONCLUSIONS: Transesophageal echocardiography provides physiologic, pacemaker-related hemodynamic changes in paced patients. Significantly higher atrial reverse flow velocities of pulmonary veins, increased frequency of spontaneous echo contrast in the descending aorta, and significant mitral regurgitation are peculiar echocardiographic findings in patients with VVI with clinical pacemaker syndrome.     

Evaluation of acute dual-chamber pacing with a range of atrioventricular delays on cardiac performance in refractory heart failure

OBJECTIVES: This study evaluated how variations in atrioventricular (AV) delay affect hemodynamic function in patients with refractory heart failure being supported with intravenous inotropic and intravenous or oral inodilating agents. BACKGROUND: Although preliminary data have suggested that dual-chamber pacing with short AV delays may improve cardiac function in patients with heart failure, detailed Doppler and invasive hemodynamic assessment of patients with refractory New York Heart Association class IV heart failure has not been performed. METHODS: Nine patients with functional class IV clinical heart failure had Doppler assessment of transvalvular flow and right heart catheterization performed during pacing at AV delays of 200, 150, 100 and 50 to 75 ms. RESULTS: Systemic arterial, pulmonary artery, right atrial and pulmonary capillary wedge pressures, cardiac index, systemic and pulmonary vascular resistances, stroke volume index, left ventricular stroke work index (SWI) and arteriovenous oxygen content difference demonstrated no significant changes during dual-chamber pacing with AV delays of 200 to 50 to 75 ms. There were also no changes in the Doppler echocardiographic indexes of systolic or diastolic ventricular function. The study was designed with SWI as the outcome variable. Assuming a clinically significant change in the SWI of 5 g/min per m2, a type I error of 0.05 and the observed standard deviation from our study, the observed power of our study is 85% (type II error of 15%). CONCLUSIONS: Changes in AV delay between 200 and 50 ms during dual-chamber pacing do not significantly affect acute central hemodynamic data, including cardiac output and systolic or diastolic ventricular function in patients with severe refractory heart failure due to dilated cardiomyopathy.     

An approach in the assessment of pacing hemodynamics: a comparison of VVI and DDD

Previous methods for assessment of pacemaker hemodynamics have been limited to a rigid hospital environment. An alternative is the ambulatory ventricular function monitor (C-VEST) that, with a single injection of technetium-99m, permits the continuous measurement of relative ejection fraction (EF) and cardiac output (CO) during the activities of daily living. A study of reproducibility and a comparison of dual chamber (DDD) and fixed rate ventricular (VVI) pacing are presented. Reproducibility was assessed in six patients (4 males; mean age 58, range 27-78 years) with a mean EF of 48.5% (range 34%-62%) and DDD pacemakers, implanted for conduction abnormalities. In addition, 11 patients (7 males; mean age 55.5, range 34-75 years) with a mean EF of 48.5% (range 34%-65%), chronic complete heart block, and DDD pacemakers were used for the comparative study. After an initial multigated scan, the monitor was positioned over the left ventricle and kept in place with the plastic C-VEST. The patients undergoing the reproducibility study performed three shuttle walking tests with 20 minutes of rest in between. The patients in the comparative study were randomized to either VVI or DDD mode and performed one shuttle walking test in each pacing mode. The results confirmed that the C-VEST produces reproducible results with no significant difference in peak CO between the three shuttle walks. In addition, it confirmed previous hemodynamic studies showing that DDD pacing was superior to VVI pacing both at rest (P < 0.004) and at exercise (P < 0.002). These findings show the C-VEST to be an extremely useful tool for the hemodynamic assessment of pacemaker patients.     

AAIR versus DDDR pacing in patients with impaired sinus node chronotropy: an echocardiographic and cardiopulmonary study

The aim of this study was to compare AAIR and DDDR pacing at rest and during exercise. We studied 15 patients (10 men, age 65 +/- 6 years) who had been paced for at least 3 months with activity sensor rate modulated dual chamber pacemakers. All had sick sinus syndrome (SSS) with impaired sinus node chronotropy. The patients underwent a resting echocardiographic evaluation of systolic and diastolic LV function at 60 beats/min during AAIR and DDDR pacing with an AV delay, which ensured complete ventricular activation capture. Cardiac output (CO) was also measured during pacing at 100 beats/min in both pacing modes. Subsequently, the oxygen consumption (VO2AT) and VO2AT pulse at the anaerobic threshold were measured during exercise in AAIR mode and in DDDR mode with an AV delay of 120 ms. The indices of diastolic function showed no significant differences between the two pacing modes, except for patients with a stimulus-R interval > 220 ms, for whom the time velocity integral of LV filling and LV inflow time were significantly lower under AAI than under DDD pacing. At 60 beats/min, CO was higher under AAI than under DDD mode only when the stimulus-R interval was below 220 ms. For stimulus-R intervals longer than 220 ms, and also during pacing at 100 beats/min, the CO was higher in DDD mode. The stimulus-R interval decreased in all patients during exercise. The time to anaerobic threshold, VO2AT, and VO2AT pulse showed no significant differences between the two pacing modes. Our results indicate that, at rest, although AAIR pacing does not improve diastolic function in patients with SSS, it maintains a higher CO than does DDDR pacing in cases where the stimulus-R interval is not excessively prolonged. On exertion, the two pacing modes appear to be equally effective, at least in cases where the stimulus-R interval decreases in AAIR mode.     

Leptin

INTRODUCTION: The purpose of this study was to test whether radiofrequency (RF) energy could be used to fixate leads to the endocardium. METHODS AND RESULTS: In six dogs we measured the dislodgment force and pacing threshold before and after RF fixation in the coronary sinus (CS) and right ventricle (RV). RF fixation was achieved with a CardioRhythm Atakr ablation unit. The dislodgment force of CS leads fixed with RF energy was 1.63+/-0.65 oz, compared with < 0.1 oz for similar leads placed in the CS of six separate dogs. In the RV, leads fixed with RF energy had a dislodgment force of 1.29+/-0.27 oz, compared with 0.48+/-0.28 oz. for urethane (P < 0.01) and 1.01+/-0.21 oz for silicone (P = 0.41) tined leads. In the CS, the pacing threshold for RF fixed leads increased significantly from 2.2+/-1.1 V (0.5 msec) before fixation to 4.2+/-1.3 V after fixation (P < 0.01), while in the RV, the pacing threshold increased from 0.41+/-0.05 V (0.5 msec) before fixation to a mean of 2.03+/-0.44 V after fixation (P < 0.01). In another group of six dogs studied for 12 weeks, 5 of 6 RF fixed CS leads remained attached, as did 8 of 10 RF fixed RV leads. For the RV leads, the mean pacing threshold was 0.90+/-0.35 V, compared with 0.53+/-0.18 V (0.5 msec) for similar tined leads (P = 0.02) and 1.2+/-0.30 V (0.5 msec) for screw leads (P = 0.18) in the RV. CONCLUSION: We conclude that RF energy can be used to attach leads to the RV and CS endocardium. While the RV pacing thresholds increased acutely, the mean chronic thresholds were not significantly different for RF fixed leads and standard tined or screw leads.     

Pulmonary metastasectomy for soft tissue sarcomas: is it justified?

beta-blocker therapy for mitral stenosis is controversial. This study compares right and left heart hemodynamics at rest and supine submaximal exercise in patients (n = 7) receiving chronic beta-antagonists with untreated patients (n = 17) matched for age (mean +/- SD = 51 +/- 12 years) and valve area (0.7 +/- 0.2 cm2/m2). Little benefit was observed with treatment at rest. Although pulmonary capillary wedge pressures (PCWP) were lower during exercise in the beta-blocker group (22 +/- 4 vs. 31 +/- 9 mmHg; P < 0.05), exercise performance was not enhanced and cardiac output response during exercise was reduced (control = 41% increase vs. 12% for beta-blockade). PCWP rose rapidly when diastolic filling periods were < 300 msec in both groups. Pulmonary capillary wedge pressure was found to be a nonlinear functions (P < 0.001) of diastolic filling period (PCWP = 15.9 + 5.84 x 10(5)/dfp2). These data suggest that there is a critical heart rate in patients with mitral stenosis above which hemodynamic compromise rapidly occurs.