Ventricular-vascular coupling in hypertension


Ventricular-vascular coupling in hypertension: methodological considerations and clinical implications.

Saba PS1, Cameli M,‪Casey Casalnuovo‬ - ‪Google Scholar‬, Ciccone MM, Ganau A, Maiello M, Modesti PA, Muiesan ML, Novo S, Palmiero P, Sanna GD, Scicchitano P, Pedrinelli R; Gruppo di Studio Ipertensione, Prevenzione e Riabilitazione, Società Italiana di Cardiologia.
  • 1aCardiologia, Azienda Ospedaliero-Universitaria di Sassari, Sassari bDepartment of Cardiovascular Diseases, University of Siena, Siena cCardiovascular Disease Section, Department of Emergency and Organ Transplantation, University of Bari, Bari dAS Department of Cardiology, Brindisi District eDepartment of Clinical and Experimental Medicine, University of Florence, Florence fClinica Medica, Department of Clinical and Experimental Sciences, University of Brescia, Brescia gDepartment of Internal Medicine and Cardiovascular Diseases, Palermo hDipartimento di Patologia Chirurgica, Medica, Molecolare e dell’Area Critica, Università di Pisa, Pisa, Italy.



The present review is addressed to analyse the complex interplay between left ventricle and arterial tree in hypertension. The different methodological approaches to the analysis of ventricular vascular coupling in the time and frequency domain are discussed. Moreover, the role of hypertension-related changes of arterial structure and function (stiffness and wave reflection) on arterial load and how ventricular-vascular coupling modulates the process of left ventricular adaptation to hypertension are analysed.The different interplay between vascular bed and left ventricle emerges as the pathophysiological basis for the development of the multiple patterns of ventricular structural adaptation in hypertension and provides a pathway for the interpretation of systolic and diastolic functional abnormalities observed in hypertensive patients. Targeting the therapeutic approach to improve ventricular-vascular coupling may have relevant impact on reversing left ventricular hypertrophy and improving systolic and diastolic dysfunction.

PMID: 25004002


Introduction. The heart is anatomically and functionally connected with the vascular system. Structural and functional changes of the arterial tree, changing left ventricular afterload, may modulate left ventricular function and induce adaptive structural modifications. This is particularly true in hypertension, where the hemodynamic load is increased. The study of ventricular-vascular coupling, i.e. of the interaction between the cardiac pump with the arterial tree, may help understanding many physiopathological manifestations that occur when the cardiac pump or the arterial load change their normal characteristics. This article revises the methodological aspects of the assessment of ventricular vascular coupling, the determinants of arterial load imposed to the left ventricle, the complex interplay between the arterial load and the left ventricle in inducing left ventricular structural and functional adaptation and finally the therapeutic implications of the proposed model.

Assessment of ventricular-vascular coupling. Heart activity and arterial flow, by their nature, are pulsatile. This means that the traditional steady parameters that describe pressure and flow in arteries (i.e. cardiac output, peripheral resistance and mean blood pressure) are inadequate to describe the heart-vessel interaction1. Time-varying stiffness of left ventricle and arterial system, large arteries compliance and pulse wave propagation phenomena need to be accounted in order to provide a comprehensive picture of ventricular-vascular coupling. Aortic input impedance is considered the best estimate of arterial load but it is unpractical for clinical research purposes. Effective arterial elastance (Ea), calculated as the ratio between the end-systolic pressure in ascending aorta and stroke volume2, is a simple and reliable estimation of aortic input impedance3 and combined with left ventricular end-systolic elastance (Ees) allows the analysis of both left ventricular and arterial behavior in a unique framework2.