Determinants of LV Performance

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The primary activity of the heart is the pump function with the aim to guarantee an adequate flow to all tissues and organs with a sufficient perfusion pressure. This activity is allowed by the perpetual sequence of relaxation (from Greek, diastole) and contraction (systole). Albeit traditionally distinct, left ventricular (LV) contraction, relaxation and early phase of diastolic filling share the need of a metabolic activation; moreover, an increased contractility is often associated with an enhanced rate of relaxation (lusitropic effect). Nevertheless, the evaluation of systolic function covers a specific role in several clinical scenarios, from post-infarction to congestive heart failure prognostic stratification, from surgical to thrombotic risk assessment (e.g. in atrial fibrillation), from congenital to valve diseases evaluation, in single patient follow-up, such as in clinical trials [1].


The intrinsic capacity of the heart to generate pressure and blood ejection is called contractility; it corresponds, at molecular level, to interaction of myofilaments (actine and myosin with the support of regulatory proteins) consequently to calcium delivery and is affected by several factors such as exercise, adrenergic stimulation and other inotropic agents. The contractility of myocardial cell can be expressed as the maximal velocity of contraction in absence of loading condition (V max) as derived from the force-velocity curve (figure 1); however, it cannot be measured in vivo because the impossibility to obtain a free-loading condition. The best approach to estimate the myocardial contractility derives from the pressure-volume curve. In particular the ratio of end-systolic pressure and volume (Es) indicates the contractile behaviour of LV; even if loading conditions of that ventricle change with related modification of the pressure-volume loop, the Es slope remains unchanged [2] (figure 2).


Figure 1. The force-velocity curve describes the inverse relationship between shortening force and contraction velocity of the myocardium. The Vmax is the maximal theoretical velocity with null afterload of a specific left ventricle; it corresponds to the intercept of the curve with the velocity-axis and its value is a measurement of myocardial contractility. Despite the upward shift of the curve by increased preload, the intercept with the Y-axis remains unchanged.


The force, which stretches the myocardial fibres at end-diastole, is called the preload; it reflects the venous filling pressure, the load before the contraction starts. Preload is related to LV performance depending on Frank-Starling’s law; it states that, within physiologic limits, the larger is LV end-diastolic volume, the greater the energy of contraction and the stroke volume; moreover, at this positive inotropic effect corresponds an increased lusitropic activity [3]. More precisely, preload is the wall stress at end-diastole; however it is difficult to measure wall stress in vivo because the complexity three-dimensional shape of LV.


Figure 2. The pressure-volume curve describes the cardiac cycle with its four phases, where the end-systole is expression of myocardial contractility. As shown in the figure, with different load changes the end-systolic pressure-volume ratio remains unchanged and the relative points on the cardiac loop (A, A’and A’’) lye in the same half-line (Es).


The load encountered by the ventricle during contraction is named afterload; it is determined by peripheral resistance, arterial compliance and peak intraventricular pressure. A more exact definition of afterload is the wall stress during LV ejection. It can be expressed in a very simplified manner by the Laplace law, as follows:

wall stress (T) = P x R/2h

where P is intraventricular pressure, R is ventricular radius and h is the myocardial wall thickness. As corollary of this equation, the larger is the LV cavity, the greater the wall stress and so the myocardial oxygen uptake even with the same endocavitary pressure. Additionally Laplace’s law explains the compensatory mechanism of concentric hypertrophy in chronic pressure overload as realizes aortic valve stenosis or systemic arterial hypertension; at least during the first stages of ventricular concentric remodelling, the myocardial wall stress is balanced by the increased myocardial thickness.

Heart rate

An increased heart rate leads to an augmented contractility, probably because the reduced time for calcium uptake by sarcoplasmatic reticulum pumps (it is the Bowditch staircase phenomenon). Since left ventricle needs a physiologic period for ventricular filling, so the optimal heart rate in humans is a balance between heart rate acceleration and diastolic time.

Non-invasive systolic function evaluation

Since the importance of systolic function evaluation, the echocardiography developed several methods to answer this question. Starting from M-mode with the shortening fraction, the 2D echo allowed a good appraisal of left ventricular performance through the ejection fraction. Both M-mode shortening and 2D ejection fraction are limited by the single line and single- or biplanar measurement with geometric assumptions on ventricular shape; the recent development of 3D echocardiography allows the real calculation of ejection fraction in a more accurate way. All these parameters reflect, at the global level, the shortening of the single myocardial fibre but they don’t represent the myocardial contractility per se, instead are mirror of the global left ventricular performance. The echocardiographic technology through the more sophisticated techniques of tissue Doppler and speckle tracking imaging allows an assessment of systolic function, virtually independent from loading conditions [4].

  1. Opie LH and Hasenfuss G. Mechanism of Cardiac Contraction and Relaxation. In: Braunwald’s Heart Disease. A textbook of Cardiovascular Medicine. 9th ed. Elsevier Saunders. Philadelphia, 2012.
  2. Sagawa K, Suga H, Shoukas AA, Bakalar KM. End-systolic pressure/volume ratio: a new index of ventricular contractility. Am J Cardiol 1977; 40:748-753.
  3. Opie LH. Heart Physiology, From Cell to Circulation. 4th ed, Lippincott Williams & Wilkins, Philadelphia, 2004.
  4. Goncalves A, Marcos-Alberca P, Sogaard P, Zamorano JL. Assessment of systolic function. In: Galiuto L, Badano L Fox K, Sicari R, Zamorano JL. The EAE Textbook of Echocardiography. Oxford University Press, London, 2011.
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