Health & Medical Cardiovascular Health

Myocardial Contractility in the Stress Echo Lab

Myocardial Contractility in the Stress Echo Lab

Abstract and Introduction

Abstract


Up-regulation of Ca entry through Ca channels by high rates of beating is involved in the frequency-dependent regulation of contractility: this process is crucial in adaptation to exercise and stress and is universally known as force-frequency relation (FFR). Disturbances in calcium handling play a central role in the disturbed contractile function in myocardial failure. Measurements of twitch tension in isolated left-ventricular strips from explanted cardiomyopathic hearts compared with non-failing hearts show flat or biphasic FFR, while it is up-sloping in normal hearts. Starting in 2003 we introduced the FFR measurement in the stress echo lab using the end-systolic pressure (ESP)/End-systolic volume index (ESVi) ratio (the Suga index) at increasing heart rates. We studied a total of 2,031 patients reported in peer-reviewed journals: 483 during exercise, 34 with pacing, 850 with dobutamine and 664 during dipyridamole stress echo. We demonstrated the feasibility of FFR in the stress echo lab, the clinical usefulness of FFR for diagnosing latent contractile dysfunction in apparently normal hearts, and residual contractile reserve in dilated idiopathic and ischemic cardiomyopathy. In 400 patients with left ventricular dysfunction (ejection fraction 30 ± 9%) with negative stress echocardiography results, event-free survival was higher (p < 0.001) in patients with ΔESPVR (the difference between peak and rest end-systolic pressure-volume ratio, ESPVR) ≥ 0.4 mmHg/mL/m. The prognostic stratification of patients was better with FFR, beyond the standard LV ejection fraction evaluation, also in the particular settings of severe mitral regurgitation or diabetics without stress-induced ischemia. In the particular setting of selection of heart transplant donors, the stress echo FFR was able to correctly select 34 marginal donor hearts efficiently transplanted in emergency recipients. Starting in 2007, we introduced an operator-independent cutaneous sensor to monitor the FFR: the force is quantified as the sensed pre-ejection myocardial vibration amplitude. We demonstrated that the sensor-derived force changes at increasing heart rates are highly related with both max dP/dt in animal models, and with the stress echo FFR in 220 humans, opening a new window for pervasive cardiac heart failure monitoring in telemedicine systems.

Introduction


The assessment of left ventricular contractility (usually obtained in the daily routine through gross proxies such as ejection fraction and regional wall motion) is an old dream for the cardiologist, but until recently it has also been a methodological nightmare. The pressure-volume relationship is a conceptually immaculate way to assess contractility and is extensively used in the experimental setting for animal studies, but only rarely in the clinical arena, and then only for research purposes in complex, technically demanding studies requiring invasive cardiac catheterization and maneuvers in the cath lab, with the attending risks of invasivity, contrast injection and radiation exposure. In the last 10 years, left ventricular contractility was brought into the noninvasive stress imaging lab, and particularly in the stress echo lab, where with minimal extra-computing time and virtually no extra-imaging time, left ventricular contractility can be measured at baseline and during stress with simple raw measurements of end-systolic pressure (by tonometry or cuff sphygmomanometer) and end-systolic volume (by 2D or, even better, real time 3-D echo). In this way, left ventricular contractility no longer "cuts the airy way" of pathophysiology but has entered the real world of clinical cardiology. This review will discuss the pathophysiological basis, experimental evidence, and clinical data supporting a more extensive use of contractile reserve in key diagnostic domains such as identification of coronary artery stenosis, myocardial viability and initial occult cardiomyopathy.



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