Abstract
BackgroundIntuitively, cardiac dyssynchrony is the inevitable result of myocardial injury. We hypothezised that radial dyssynchrony reflects left ventricular remodeling, myocardial scarring, QRS duration and impaired LV function and that, accordingly, it is detectable in all patients with heart failure.Methods225 patients with heart failure, grouped according to QRS duration of <120 ms (A, n = 75), between 120-149 ms (B, n = 75) or ≥150 ms (C, n = 75), and 50 healthy controls underwent assessment of radial dyssynchrony using the cardiovascular magnetic resonance tissue synchronization index (CMR-TSI = SD of time to peak inward endocardial motion in up to 60 myocardial segments).ResultsCompared to 50 healthy controls (21.8 ± 6.3 ms [mean ± SD]), CMR-TSI was higher in A (74.8 ± 34.6 ms), B (92.4 ± 39.5 ms) and C (104.6 ± 45.6 ms) (all p < 0.0001). Adopting a cut-off CMR-TSI of 34.4 ms (21.8 plus 2xSD for controls) for the definition of dyssynchrony, it was present in 91% in A, 95% in B and 99% in C. Amongst patients in NYHA class III or IV, with a LVEF<35% and a QRS>120 ms, 99% had dyssynchrony. Amongst those with a QRS<120 ms, 91% had dyssynchrony. Across the study sample, CMR-TSI was related positively to left ventricular volumes (p < 0.0001) and inversely to LVEF (CMR-TSI = 178.3 e (-0.033 LVEF) ms, p < 0.0001).ConclusionRadial dyssynchrony is almost universal in patients with heart failure. This vies against the notion that a lack of response to CRT is related to a lack of dyssynchrony.
Highlights
Central to the paradigm underpinning cardiac resynchronization therapy (CRT) is the concept that cardiac dyssynchrony contributes to the clinical syndrome of heart failure and that its correction translates to a clinical benefit
In an attempt to identify patients who were most likely to have left ventricular (LV) dyssynchrony, the CArdiac REsynchronization in Heart Failure (CARE-HF) study [1] adopted inclusion criteria of an LVEF ≤ 35% and a QRS ≥ 120 ms. It has since been recognized, that cardiac dyssynchrony is present in patients with higher LVEFs [2,3] and in those with a QRS ≤ 120 ms. [4,5,6,7,8,9,10] cardiac dyssynchrony appears to be common in virtually all forms of heart failure, [11] where it behaves as a continuous variable, rather than as a dichotomous entity pivoting on the arbitrary cut-offs of an LVEF ≤ 35% and QRS ≥ 120 ms. [11,12]
We have previously shown that a measure of radial dyssynchrony, derived from cardiovascular magnetic resonance (CMR) tissue synchronization imaging, is a powerful predictor of mortality and morbidity after CRT in patients with a QRS ≥ 120 ms
Summary
Central to the paradigm underpinning cardiac resynchronization therapy (CRT) is the concept that cardiac dyssynchrony contributes to the clinical syndrome of heart failure and that its correction translates to a clinical benefit. In an attempt to identify patients who were most likely to have left ventricular (LV) dyssynchrony, the CArdiac REsynchronization in Heart Failure (CARE-HF) study [1] adopted inclusion criteria of an LVEF ≤ 35% and a QRS ≥ 120 ms. [9] We hypothesized that intraventricular dyssynchrony is a reflection of left ventricular remodeling, myocardial scarring and impaired LV function and that, it should be detectable in all patients with heart failure. We hypothezised that radial dyssynchrony reflects left ventricular remodeling, myocardial scarring, QRS duration and impaired LV function and that, it is detectable in all patients with heart failure
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