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Aims: Tissue Doppler imaging (TDI) systolic velocities have been used to detect impaired systolic function in patients with heart failure and normal ejection fraction (HFnEF). However, many patients do not show alterations by this technique, and furthermore, myocardial systolic velocities can be affected by tethering, translation, and loading conditions. Thus, uncertainties remain about the detection of abnormal systolic function in HFnEF patients. The aim of this study was, therefore, to compare systolic velocities vs. TDI-derived deformation indices for detection of possible abnormalities of systolic function in HFnEF patients, taking into account loading conditions. Methods and Results: We studied 40 patients with systolic heart failure (SHF: EF ≤ 40%), 47 HFnEF patients, and 50 controls (C). Systolic velocities of the mitral annulus (pulsed-wave TDI) were measured at four sites and averaged; concomitantly, peak negative TDI-derived strain and strain rate of the four walls were measured in apical, four-, and two-chamber views. Ejection fraction was 65 ± 6% in C, 62 ± 7% in HFnEF, and 29 ± 7% in SHF (P< 0.001 vs. both). In HFnEF patients, systolic velocities and peak negative global longitudinal strain rate and strain were higher than in SHF (P< 0.0001 for all), but lower than in C (P< 0.0001 for all). After controlling for age, left ventricular mass index, end-diastolic volume index, and circumferential end-systolic stress, differences between groups remained significant for deformation indices but not for TDI velocities. By velocity/strain-stress relationship analysis, peak global longitudinal strain was more sensitive than peak systolic motion in detecting systolic dysfunction in HFnEF patients (64 vs. 40%, P< 0.05). Conclusion: In patients with HFnEF, TDI-derived deformation indices may more accurately detect abnormal systolic function than myocardial velocities. [ABSTRACT FROM AUTHOR]

Increased dispersion of the QT interval has been observed during pacing or exercise stress testing in patients with coronary artery disease (CAD). It has not been established whether this phenomenon is a consequence of ischemia. Therefore, we sought to evaluate whether dipyridamole-induced myocardial ischemia, as directly detected by echocardiographic monitoring of regional contractile function, would affect QT dispersion. Twenty-four patients with nonsignificant and 34 patients with significant CAD but no previous myocardial infarction underwent dipyridamole stress echocardiography while not taking medications. QT dispersion was measured on a 12-lead electrocardiogram at baseline and at various times after dipyridamole infusion. Dipyridamole infusion did not influence QT dispersion in patients without CAD. QT dispersion was similarly unaffected in patients with CAD in whom dipyridamole did not induce wall motion abnormalities. In contrast, in patients with positive dipyridamole stress test findings, QT dispersion increased from 60 +/- 17 ms at baseline to 94 +/- 25 ms during peak infusion (p <0.0001), with a time course mirroring that of development of contractile abnormalities. QT dispersion returned to 63 +/- 25 ms upon relief of ischemia by administration of aminophylline. The increase in QT dispersion was significantly related to the extent of contractile dysfunction induced by dipyridamole. Although ST-segment depression occurred in only 40% of patients with positive dipyridamole stress test findings, 88% of such patients had an increase in QT dispersion. Analysis of the receiver-operating characteristic curve showed that a QT dispersion increase of > or =20 ms identified positive findings for dipyridamole stress echocardiography with 68% sensitivity and 91% specificity. Thus, QT dispersion is acutely affected by myocardial ischemia induced by the administration of dipyridamole. Measurement of QT dispersion may improve detection of stress-induced ischemia on surface electrocardiograms. [ABSTRACT FROM AUTHOR]

An abstract of the article "Reversibility of Restrictive Filling During Low-Dose Dobutamine Echocardiography Predicts Reverse LV Remodeling After Revascularization in Ischemic Cardiomyopathy," by E. Carluccio and colleagues is presented.