Ventricular asynchrony: A shift to the right?

Excerpt

Evaluation of ventricular function has been a focus of nuclear medicine since 1971, when Zaret et al demonstrated that abnormalities of left ventricular (LV) wall motion and ejection fraction (EF) could be determined by injection of Tc-99m human serum albumen and acquiring images at end-diastole and end-systole.1 Multi-gated equilibrium radionuclide ventriculography (RNV) and first-pass imaging further refined characterization of LV asynergy and performance.2,3 Clinical trials soon showed that noninvasively determined LVEF was a strong predictor of survival in a broad range of heart diseases.4,5 Further work demonstrated that synchronicity of LV contraction could be derived from RNV by Fourier analysis of pixel by pixel labeled RBC time-activity curves, assigning a phase to each pixel (percent of the R-R interval from 0°-360°) to identify time of maximum contraction.6 Synchronicity has important effects on LV performance: patients with inter- or intra-ventricular asynchrony have lower LVEF relative to normal control subjects.7 Mechanisms for reduced ventricular performance resulting from dyssynchrony remain unclear, but Sweeney et al suggested early-contracting segments stretch and deform later-contracting ones, and vice versa, expending energy in the process, resulting in lower rate of pressure rise, lower developed pressure, prolonged ejection, and reduced EF.8 The most ubiquitous methods to measure asynchrony are by tissue doppler echocardiographic techniques, which use low frequency signals to measure myocardial wall deformation, and calculate strain, strain rate, delay in contraction of opposing LV walls (four basal LV segments on 4-chamber view), and dispersion of time to peak systolic contraction.9 …