Abstract
We aimed to assess surrogate markers for left ventricular (LV) myocardial power and efficiency in patients with isolated aortic stenosis (AS) and combined stenosis/regurgitation (AS/AR). In AS (n = 59), AS/AR (n = 21) and controls (n = 14), surrogates for LV myocardial power and circulatory/external myocardial efficiency were obtained from cardiac MRI. Median surrogate LV myocardial power was increased in AS, 7.7 W/m2 (interquartile range 6.0–10.2; p = 0.010) and AS/AR, 10.8 W/m2 (8.9–13.4; p < 0.001) when compared to controls, 5.4 W/m2 (4.2–6.5), and was lower in AS than AS/AR (p < 0.001). Surrogate circulatory efficiency was decreased in AS, 8.6% (6.8–11.1; p < 0.001) and AS/AR, 5.4% (4.1–6.2; p < 0.001) when compared to controls, 11.8% (9.8–16.9). Surrogate external myocardial efficiency was higher in AS, 15.2% (11.9–18.6) than in AS/AR, 12.2% (10.1–14.2; p = 0.031) and was significantly lower compared to controls, 12.2% (10.7–18.1) in patients with reduced ejection fraction (EF), 9.8% (8.1–11.7; p = 0.025). In 16% of all cases, left ventricular mass/volume indices and EF were within normal ranges, wheras surrogate LV myocardial power was elevated and patients were symptomatic. Although influenced by pressure/volume load, the myocardium is additionally affected by remodelling processes. Surrogates for circulatory efficiency and LV myocardial power gradually reflect alterations in patients with AS and AS/AR, even when surrogate external myocardial efficiency, EF, mass and volume indices still remain compensated.
Highlights
In aortic valve disease (AVD) pressure-volume overload conditions trigger cardiac remodeling causing concentric or eccentric hypertrophy[1,2,3]
Significant disease-specific differences in geometrical and functional parameters were observed between groups (Table 2): Parameters of left ventricular hypertrophy including body surface area (BSA)-indexed myocardial volume, myocardial mass, left ventricular end systolic diameter (LVESD), myocardial wall thickness and mass-volume index were increased compared to controls
In the aortic stenosis (AS) group, there were no differences for end diastolic volume index (EDVI) and end systolic volume index (ESVI) compared to controls
Summary
In aortic valve disease (AVD) pressure-volume overload conditions trigger cardiac remodeling causing concentric or eccentric hypertrophy[1,2,3]. Increased energy requirements are known to result in adaptive changes in myocardial mass, left ventricle (LV) chamber size and interstitial fibrosis in order to maintain the pump function of the heart. In the resulting mechanisms of hypertrophy, the ventricle requires more energy for contraction and becomes less energetically efficient[15,16]. These changes are associated to stiffening of the heart and to decreased efficiency of the LV13,14. The aim was to assess surrogate markers for LV myocardial power and the resulting efficiency, using a non-invasive MRI technique without direct measurements of biochemical or cellular mechanisms of energy consumption. The objective was to apply this method in a cohort of patients with isolated aortic stenosis (AS) and combined aortic stenosis/regurgitation (AS/AR) in order to assess potential differences of these surrogate markers between groups
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