Acute effects of left ventricular asynchronous activation in normal hearts.

• Type: Summary of Presentation in an International Conference
• Date: 2005

Authors

Vasconcelos M (Author) Other; Santos M (Author) FMUP; Brandão-Nogueira A (Author) Other; Henriques-Coelho T (Author) FMUP; Leite-Moreira AF (Author) FMUP

Conference proceedings International

Title: European Journal of Heart Failure

Initial page: 189

ESC Annual Congress 2005

Stockholm, Sweden , 03 a 07 de Setembro de 2005

Scientific classification

FOS: Medical and Health sciences > Other medical sciences

Other information

Resumo (PT): Background: Asynchronous electromechanical activation (AEA) of the left ventricle in patients with left branch block or right ventricular pacing leads to asymmetric distribution of load with differences in local blood flow and metabolism. In the long-term this process induces asymmetrical hypertrophy and ventricular enlargement leading to heart failure progression. The aim of this study was to investigate the acute effects of AEA on LV haemodynamics. Methods: Male Wistar rats (n=12; 303-4-20g) were instrumented with pressure tip micromanometers in the LV and pacing wires in the RV free wall. Animals were randomly assigned to two experimental protocols: (i) RV pacing during 2h at a rate less than 5% above baseline (n=6); (ii) sham group (n=6). In both groups hemodynamic parameters were registered at the beginning and at the end of protocol, with the pacemaker turned-on (Pc) and turned-off. Systolic (Pmax) and end-diastolic (EDP) pressures, dP/dtmax and dP/dtmin and time constant of isovolumetric relaxation tau were measured. Results presented in table 1 as mean 4- SEM (*p<0.05 vs 0 min; # p<0.05 vs Pc0min). Results: Turning on the pace resulted in an impairment of the indices of systolic function (Pmax and dP/dtmax), which improved progressively during the 2 hours the pacemaker was turned on. This increased myocardial contractility was still observed when the pacemaker was turned-off. Concerning diastolic function we observed increased EDP and a faster relaxation rate (tau decreased) immediately after turning on the pacemaker, an effect that remained during the rest of the experimental protocol. Table 1 0rain Pc 0rain Pc f20min f20min Pmax (mmHg) 80.2±6.4 78.9±7.0 92.0± 1.3 86.3±9.4 dP/dtmax (mmHg/s) 3478±799 3279±669 4335±966 * # 4455±867 # dP/dtmin (mmHg/s) -2185±466 -2109±412 -2827±622 # -3019±702 # EDP (mmHg) 0.0±7.7 0.8±9.5 1.9±9.9 * # 1.8±9.i * tau (ms) 29.2±7.7 22.1±2.3 * 21.9±2.4 * 22.1±2.0 * Conclusion: In normal hearts, asynchronous LV activation induced transitory systolic dysfunction, followed by activation of compensatory mechanisms that lead to increased contractility and faster relaxation.

Language: English

Type (Professor's evaluation): Scientific

Notes: ESC Annual Congress 2005, published in journal, European Journal of Heart Failure, 2005; Vol.4(Suppl.1):189-189.