Background—: Left ventricular (LV) mechanical discoordination, often referred to as dyssynchrony, is often observed in patients with heart failure regardless of QRS duration. We hypothesized that different myocardial substrates for LV mechanical discoordination exist from (1) electromechanical activation delay, (2) regional differences in contractility, or (3) regional scar and that we could differentiate electromechanical substrates responsive to cardiac resynchronization therapy (CRT) from unresponsive non–electrical substrates. Methods and Results—: First, we used computer simulations to characterize mechanical discoordination patterns arising from electromechanical and non–electrical substrates and accordingly devise the novel systolic stretch index (SSI), as the sum of posterolateral systolic prestretch and septal systolic rebound stretch. Second, 191 patients with heart failure (QRS duration ≥120 ms; LV ejection fraction ≤35%) had baseline SSI quantified by automated echocardiographic radial strain analysis. Patients with SSI≥9.7% had significantly less heart failure hospitalizations or deaths 2 years after CRT (hazard ratio, 0.32; 95% confidence interval, 0.19–0.53; P <0.001) and less deaths, transplants, or LV assist devices (hazard ratio, 0.28; 95% confidence interval, 0.15–0.55; P <0.001). Furthermore, in a subgroup of 113 patients with intermediate electrocardiographic criteria (QRS duration of 120–149 ms or non–left bundle branch block), SSI≥9.7% was independently associated with significantly less heart failure hospitalizations or deaths (hazard ratio, 0.41; 95% confidence interval, 0.23–0.79; P =0.004) and less deaths, transplants, or LV assist devices (hazard ratio, 0.27; 95% confidence interval, 0.12–0.60; P =0.001). Conclusions—: Computer simulations differentiated patterns of LV mechanical discoordination caused by electromechanical substrates responsive to CRT from those related to regional hypocontractility or scar unresponsive to CRT. The novel SSI identified patients who benefited more favorably from CRT, including those with intermediate electrocardiographic criteria, where CRT response is less certain by ECG alone.

Aims: The objective of the current study is to investigate the risk of heart failure (HF) after implantation of a pacemaker (PM) with a right ventricular pacing (RVP) lead in comparison to a matched cohort without a PM and factors associated with this risk. Methods and results: All patients without a known history of HF who had a PM implanted with an RVP lead between 2000 and 2014 (n = 27 704) were identified using Danish nationwide registries. An age- and gender-matched control cohort (matched 1:5, n = 138 520) without PM and HF was identified to compare the risk. Outcome was the cumulative incidence of HF including fatal HF within the first 2 years of PM implantation, with all-cause mortality and myocardial infarction (MI) as competing risks. Due to violation of proportional hazards, the follow-up period was divided into three time-intervals: 180 days–2 years. The cumulative incidence of HF including fatal HF was observed in 2937 (10.6%) PM patients. Risks for the three time-intervals were 180 days (HR 1.11, 95% CI 1.04–1.17). Among patients with a PM device, factors associated with increased risk of HF were male sex (HR 1.33, 95% CI 1.24–1.43), presence of chronic kidney disease (CKD) (HR 1.64, 95% CI 1.29–2.09), and prior MI (1.77, 95% 1.50–2.09). Conclusions: Pacemaker with an RVP lead is strongly associated with risk of HF specifically within the first 6 months. Patients with antecedent history of MI and CKD had substantially increased risk.

Background—: Adverse right ventricular (RV) remodeling has significant prognostic and therapeutic implications to patients with pulmonary hypertension (PH). However, differentiating RV adaption from adverse remodeling associated with poor outcomes is difficult. We hypothesized that novel 3-dimensional (3D) wall motion tracking echocardiography can differentiate morphological features of RV adaption from adverse remodeling heralding an unfavorable short-term prognosis in patients with PH. Methods and Results—: We studied 112 subjects: 92 patients with PH and 20 normal controls with 3D wall motion tracking for RV end-systolic volume index (ESVi), RV ejection fraction (EF), and RV global area strain. Patients with PH also had invasive hemodynamic measurements. Pressure–volume relations classified patients with PH into 3 groups, such as RV adapted, RV adapted–remodeled, and RV adverse–remodeled. The predefined combined end point was PH-related hospitalization, death, or lung surgery (lung transplantation or pulmonary endarterectomy) during 6 months. The 92 patients with PH had significantly larger RV volumes, lower RVEF and global area strain than normal controls as expected. Patients with PH classified as RV adapted (ESVi, ≤ 72 mL/m ² ) had a more favorable clinical outcome than those classified as RV adapted–remodeled (ESVi, 73–113 mL/m ² ) or RV adverse–remodeled (ESVi, ≥ 114 mL/m ² ): hazard ratio, 0.15; 95% confidence intervals, 0.07 to 0.39; P <0.0001. RV adverse–remodeled patients (ESVi, ≥ 114 mL/m ² ) had worse short-term outcome than the RV adapted–remodeled patients: hazard ratio, 2.2; 95% confidence interval, 0.91 to 5.39; P =0.04. Conclusions—: Quantitative 3D echocardiography in patients with PH demonstrated morphological subsets of RV adaption and remodeling associated with clinical outcomes.

Left atrial (LA) strain imaging, which measures the deformation of the LA using speckle-tracing echocardiography (STE), has emerged recently as an exciting tool to help provide diagnostic and prognostic information for patients with a broad range of cardiovascular (CV) pathologies. Perhaps due to the LA’s relatively thin-walled architecture compared with the more muscular structure of the left ventricle (LV), functional changes in the left atrium often precede changes in the LV, making LA strain (LAS) an earlier marker for underlying pathology than many conventional echocardiographic parameters. LAS imaging is typically divided into three phases according to the stage of the cardiac cycle: reservoir strain, which is characterized by LA filling during systole; conduit strain, which describes LA deformation during passive LV filling; and booster strain, which provides information on the LA atrium during LA systole in late ventricular diastole. While additional large-population studies are still needed to further solidify the role of LAS in routine clinical practice, this review will discuss the current evidence of its use in different pathologies and explore the possibilities of its applications in the future.