J Cardiovasc Med. 2014 Nov;15(11):773-87.

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

Saba PS1, Cameli M, Casalnuovo G, 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.

Figure 1

Figure 1. Arterial components of left ventricular afterload. The figure shows the different arterial components of left ventricular afterload, their structural or functional determinants and, between parentheses, which parameters are available for measuring the specific characteristics. Y= Young’s elastic modulus, EP= Peterson’s elastic modulus, PWV= Pulse wave velocity, i-m= intima-media, Ea= Effective arterial elastance


Determinants of arterial load (Figure 1). Arterial load is influenced by several genetic, structural and hemodynamic factors that interfere with arterial stiffness, resistance and pulse wave propagation (Figure 1). Hypertension is characterized by total peripheral resistance elevation, increased operative stiffness and enhanced pressure wave reflection that, in turn, increase aortic input impedance.

Ventricular vascular coupling in hypertension and left ventricular structural and functional adaptation (Figure 2). The adaptation mechanisms of left ventricle to hypertension induced afterload changes is complex. The increased arterial load determines, as a primary consequence, an imbalance of the Ea/Ees ratio that is energetically unfavorable for left ventricular mechanics. However, enhanced wave reflection and increased operative arterial stiffness are stimuli for left ventricular hypertrophy and concentric geometric remodeling, respectively4,5. The main functional consequence of these structural changes is the increase of Ees which in turn tends to normalize the Ea/Ees ratio and left ventricular mechanical efficiency. The latter is mainly achieved because left ventricular hypertrophy and concentric geometry reduce the need of increasing inotropism (and thus oxygen consumption per muscle unit) in order to maintain the same stroke volume against an higher afterload. However, this structural adaptation actually increases overall left ventricular metabolic needs and is associated with fibrosis development . Thus, the adaptive mechanism, that is at least initially mechanically and energetically favorable, in the long term impairs diastolic function and leads to heart failure with preserved ejection fraction. Diastolic dysfunction may in turn impair mechanical efficiency which finally, in association with fibrosis and microvascular rarefaction, predisposes to the onset of systolic dysfunction.

Figure 2

Figure 2. Ventricular-vascular coupling and left ventricular adaptation in hypertension. The complex interplay between arterial load and left ventricular adaptive changes in hypertension is depicted. Left ventricular hypertrophy and concentric geometry are compensatory mechanisms that normalize ventricular-vascular coupling and preserve, in an initial phase, mechanical efficiency. However, in the long term, left ventricular hypertrophy promotes the occurrence of fibrosis and ischemia, predisposing to diastolic dysfunction and, at the end-stage, also to systolic dysfunction. Ea= Effective arterial elastance, Ees= End-systolic ventricular elastance, FSm= Mid-wall fractional shortening; HFpEF= Heart failure with preserved ejection fraction; HFrEF= Heart failure with reduced ejection fraction. *= Reduced oxygen consumption is intended for unit of muscular mass.


Therapeutic implication of ventricular-vascular coupling in hypertension. One of the most relevant consequences of pressure wave propagation is the so-called “pressure wave amplification phenomenon”6. This implies that blood pressure measured at brachial artery does not accurately represent the actual pressure acting in ascending aorta. Accordingly, due to this phenomenon, brachial systolic pressure is significantly higher than aortic pressure in young healthy subjects. Conversely, in the elderly and in hypertensive patients this phenomenon attenuates and brachial and aortic pressures tend to be similar. However, vasodilators (especially ACE-inhibitors) but not beta-blockers, reducing wave reflections tend to restore normal pressure wave amplification. This means that, for the same decrease of brachial systolic blood pressure, vasodilators reduce for a larger degree than beta-blockers the arterial load acting on left ventricle. This could explain why in hypertension trials the inhibitors of renin-angiotensin system obtained better results in reducing left ventricular mass7 and outcomes7,8 when compared with beta-blockers.

What is outstanding in this paper? This review systematically analyzes methods and terminology for defining components of arterial load and ventricular-vascular coupling in hypertension. It also provides a comprehensive framework for understanding structural and functional left ventricular adaptation to high blood pressure and its relation with pharmacological anti-hypertensive treatment.



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