Improvement of myocardial performance (Tei) index closely reflects intrinsic improvement of cardiac function: assessment in revascularized hibernating myocardium.

BACKGROUND: Myocardial performance index (MPI), or Tei index, is an indicator of systolic and diastolic myocardial function. MPI increases in case of cardiac dysfunction; however, whether reversal of left ventricular dysfunction is also reflected by concomitant improvement (i.e., decrease) of MPI is unknown. METHODS: Fifty-two patients with chronic ischemic cardiomyopathy and viable myocardium by dobutamine stress echocardiography were studied by echocardiography before and more than 4 months after cardiac revascularization. Patients were in optimal medical therapy, which remained unchanged following revascularization. RESULTS: At baseline, ejection fraction (EF: 32 ± 6%) and wall motion score index (WMSI: 2.37 ± 0.32) were impaired, and MPI averaged 0.71 ± 0.19. Revascularization markedly improved EF (44 ± 10%, P < 0.0001) and WMSI (1.77 ± 0.44, P < 0.0001). MPI also improved (0.59 ± 0.26, P < 0.0001), and its decrease was significantly correlated with the improvement in EF (r =-0.68, P < 0.0001) and to the extent of viable myocardium (r =-0.45, P = 0.0007). Responders to revascularization (≥5% increase in EF at follow-up, n = 40% and 77%) achieved a significant improvement in MPI at follow-up in contrast with nonresponders (-23 ± 25% vs. 0.02 ± 0.18%, P = 0.001). Improvement in MPI was largely driven by a significant reduction in isovolumic contraction time (P < 0.001) with consequent prolongation of the ejection phase. CONCLUSION: In patients with chronic ischemic cardiomyopathy, MPI improves along with recovery of function, reflecting the intrinsic improvement of viable segments induced by revascularization.

Effect of revascularizing viable myocardium on left ventricular diastolic function in patients with ischaemic cardiomyopathy.

AIMS: In patients with ischaemic left ventricular (LV) dysfunction and viable myocardium, revascularization improves systolic function. Diastolic dysfunction is also present in such patients; however, whether revascularization improves diastolic function also is largely unknown. METHODS: Twenty-six patients with chronic ischaemic cardiomyopathy [ejection fraction (EF) 32 +/- 6%, wall motion score index (WMSI) 2.45 +/- 0.33] and viable myocardium (low-dose dobutamine echocardiography) were examined at baseline and > or =4 months after revascularization. Diastolic function was assessed by transmitral pulsed-wave Doppler and tissue Doppler imaging (TDI) at the mitral annulus. RESULTS: At baseline, 62% of patients showed non-restrictive filling (non-RF) pattern, and 38% restrictive filling (RF) pattern. After revascularization, along with improvement in systolic function (EF 43 +/- 10%, WMSI 1.78 +/- 0.47, P = 0.0002 for both), diastolic filling improved in most patients, with only three patients still exhibiting RF pattern (P = 0.016); furthermore, E' velocity increased (32 +/- 42%, P = 0.0028) and E/E' decreased (-19 +/- 31%, P = 0.0378) compared with baseline. Left ventricular filling pressure also decreased, from 17.5 +/- 6.8 to 13.1 +/- 6.5 mmHg (P = 0.005). Improvement of diastolic function by TDI was related to the extent of viability at baseline (P = 0.0098) and to LV reverse remodelling after revascularization (P = 0.0092). CONCLUSION: In patients with ischaemic cardiomyopathy, LV diastolic filling may largely improve after revascularization. Improvement of diastolic dysfunction is related to the amount of viable tissue and it may represent an additional advantage of revascularizing dyssinergic but viable myocardium.

RANKL Expression Is Increased in Circulating Mononuclear Cells of Patients with Calcific Aortic Stenosis.

We aimed to investigate whether the expression of the OPG/RANK/RANKL triad in peripheral blood mononuclear cells (PBMC) and circulating levels of markers of ectopic mineralization (OPG, FGF-23, PPi) are modified in patients with calcific aortic valve disease (CAVD). We found that patients affected by CAVD (n = 50) had significantly higher circulating levels of OPG as compared to control individuals (p = 0.003). No differences between the two groups were found in FGF-23 and PPi levels. RANKL expression was higher in the PBMC from CAVD patients (p = 0.018) and was directly correlated with the amount of valve calcification (p = 0.032). In vitro studies showed that treatment of valve interstitial cells (VIC) with RANKL plus phosphate was followed by increase in matrix mineralization (p = 0.001). In conclusion, RANKL expression is increased in PBMC of patients with CAVD, is directly correlated with the degree of valve calcification, and promotes pro-calcific differentiation of VIC.

Presence of extensive LV remodeling limits the benefits of CRT in patients with intraventricular dyssynchrony.

OBJECTIVES: The aim of this study was to evaluate whether, in patients with evidence of both electrical and mechanical left ventricular (LV) dyssynchrony, extensive LV dilation would affect response to cardiac resynchronization therapy (CRT). BACKGROUND: Cardiac resynchronization therapy is effective in heart failure patients with LV dysfunction and wide QRS complex. However, many patients still fail to respond. We hypothesized that presence of extensive LV dilation might prevent response to CRT, despite LV mechanical dyssynchrony. METHODS: We studied 78 heart failure patients (68 ± 9 years of age, 77% men) with both electrical (QRS width >120 ms) and mechanical intraventricular dyssynchrony (by tissue Doppler imaging and/or left lateral wall post-systolic contraction). Echocardiographic evaluation was performed at baseline and 6 to 8 months after CRT. As an indication of LV remodeling, end-diastolic volume index and end-systolic volume index (ESVI) and sphericity index were measured. Long-term (40 ± 23 months) clinical follow-up (events: cardiac death and hospital admission for heart failure) was also obtained. RESULTS: At follow-up after CRT, in the overall population, ejection fraction increased from 26 ± 6% to 35 ± 11% (p < 0.0001), whereas end-diastolic volume index (from 144 ± 43 ml/m(2) to 119 ± 55 ml/m(2)), ESVI (from 108 ± 37 ml/m(2) to 82 ± 49 ml/m(2), p < 0.0001 for both), and sphericity index (from 0.60 ± 0.22 to 0.53 ± 0.15, p = 0.0036) all significantly decreased. By multiple linear regression analysis, after controlling for confounding factors, change in LV ejection fraction at follow-up resulted independently and negatively associated with baseline ESVI (p = 0.001), with much lower improvement after implant in the highest tertile of baseline ESVI. During follow-up, 31 patients (39.7%) had a cardiac event. By Cox regression model, baseline ESVI was the most powerful predictor of events, with event-rate/year increasing with increasing tertiles of ESVI (6.3%, 10.1%, and 23.8%, respectively, p < 0.05). CONCLUSIONS: In this nonrandomized, open-label clinical study, despite intraventricular electrical and mechanical dyssynchrony, extensive LV remodeling at baseline negatively impacted CRT results in terms of LV function improvement and incidence of cardiac events at follow-up.

Advantages of deformation indices over systolic velocities in assessment of longitudinal systolic function in patients with heart failure and normal ejection fraction.

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.