Brief Article
Copyright ©2011 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Cardiol. Oct 26, 2011; 3(10): 322-328
Published online Oct 26, 2011. doi: 10.4330/wjc.v3.i10.322
Assessment of right ventricular afterload by pressure waveform analysis in acute pulmonary hypertension
Juan C Grignola, Enric Domingo, Lucía Devera, Fernando Ginés
Juan C Grignola, Lucía Devera, Fernando Ginés, Department of Pathophysiology. Hospital de Clínicas, Facultad de Medicina. Universidad de la República, 11600 Montevideo, Uruguay
Enric Domingo, Area del Cor. Hospital Universitari Vall d’Hebron. Passeig Vall d’Hebron 119-129, 08035 Barcelona, Spain
Enric Domingo, Department of Physiology, Universitat Autonoma Barcelona, 08193 Bellaterra (Cerdanyola del Vallès), Barcelona, Spain
Author contributions: Grignola JC participated in protocol development, data acquisition, data analysis and manuscript preparation; Domingo E contributed to the analysis and interpretation of data and manuscript preparation; Devera L participated in protocol development and data acquisition; Ginés F contributed to the the analysis and interpretation of data, and the drafting and the critical revision of the manuscript.
Supported by Comisión Sectorial de Investigación Científica, Universidad de la República and Programa de Desarrollo de las Ciencias Básicas
Correspondence to: Juan C Grignola, MD, Department of Pathophysiology, Hospital de Clínicas, Facultad de Medicina, Universidad de la República, Avda Italia s/n, Piso 15, 11600 Montevideo, Uruguay. jgrig@fmed.edu.uy
Telephone: +598-2487-1515 Fax: +598-2480-0244
Received: March 28, 2011
Revised: July 8, 2011
Accepted: July 15, 2011
Published online: October 26, 2011
Abstract

AIM: To characterize hydraulic right ventricle (RV) afterload by pulmonary arterial pressure waveform analysis in an acute pulmonary hypertension (PH) model.

METHODS: Pulmonary artery (PA) flow and pressure were recorded in six anesthetized sheep. Acute isobaric PH was induced by phenylephrine (active) and PA mechanical constriction (passive). We estimated the amplitude of the forward and reflected pressure waves according to the inflection point. In most cases the inflection pressure was smooth, thus the inflection point was defined as the time at which the first derivative of pulmonary arterial pressure reached its first minimum. We calculated the input and characteristic (ZC, time-domain Li method) impedances, the capacitance index (stroke volume/pulse pressure), the augmentation index (AI) (reflected pressure/pulse pressure), the fractional pulse pressure (pulse pressure/mean pressure) and the wasted energy generated by the RV due to wave reflection during ejection (EW).

RESULTS: Pulse pressure, fractional pulse pressure, AI and ZC increased and capacitance index decreased during passive PH with respect to control (P < 0.05). In contrast, ZC and the capacitance index did not change and EW and the AI decreased during active PH. Pulse pressure correlated with EW and ZC and the AI was correlated with EW (r > 0.6, P < 0.05).

CONCLUSION: PA pressure waveform analysis allows the quantification of the dynamic RV afterload. Prospective clinical studies will be necessary to validate this time-domain approach to evaluate the dynamic RV afterload in chronic PH.

Keywords: Pulmonary hypertension, Time-domain analysis, Augmentation index, Characteristic impedance, Reflected wave