In patients with AF, the LA stiffness index is related to left ventricular diastolic dysfunction, LA dilatation, and collagen synthesis and may predict AF recurrences after PVI.

Background— Fatal arrhythmia is commonly observed in cardiac sarcoidosis, but clinical effects of a systematic treatment approach are still uncertain. This study sought to describe both clinical and electrophysiological characteristics and outcomes of systematic treatment approach to ventricular tachycardia (VT) associated with cardiac sarcoidosis. Methods and Results— We enrolled 37 consecutive patients (11 men; age, 56±11 years) with a diagnosis of sustained VT associated with cardiac sarcoidosis. Clinical effects of a systematic treatment approach including medical therapy (both steroid and antiarrhythmic agents), in association with radiofrequency catheter ablation, were evaluated. All patients received antiarrhythmic agents, and 34 received steroid therapy. During a 39-month follow-up, 23 (62%) patients were free from any VT episodes with medical therapy. Multivariable Cox regression analyses revealed that the absence of gallium-67 myocardial uptake was an independent predictor for VT recurrence (hazard ratio, 7.51; 95% confidence interval, 1.65–34.26; P <0.01). Fourteen patients who experienced VT recurrences even while on drug therapy underwent radiofrequency catheter ablation. Electrophysiological study revealed that the mechanisms of VTs could be classified into 2 subgroups: Purkinje-related or scar-related VT. The QRS duration of VT was narrower in Purkinje-related than in scar-related VTs (157±23 versus 183±22 ms; P <0.05). After a 33-month follow-up subsequent to the radiofrequency catheter ablation, 6 of 14 patients experienced VT recurrence. The number of VTs sustained during electrophysiological study was higher in the patients with VT recurrence than in those without (3.7±1.4 versus 1.9±0.8; P <0.01). Conclusions— A systematic treatment approach to cardiac sarcoidosis with VT successfully suppressed VT recurrences in the majority of patients studied.

Left ventricular (LV) systolic wall strain is a new candidate for prognostic indicator of hypertensive heart failure. It remains unclear how underlying transmural structural remodeling corresponds to LV wall systolic deformation as hypertensive hypertrophy progresses. We fed 68 Dahl salt-sensitive rats a high-salt (hypertensive group) or low-salt diet (control group) from 6 weeks old. At 10, 14, and 18 weeks, pressure-volume relation, transmural distribution of LV fibrosis, and myocyte hypertrophy were evaluated. LV global longitudinal and circumferential strain was measured with speckle tracking echocardiography. Emax was preserved throughout the study period, whereas τ and end-diastolic pressure-volume relation progressively deteriorated from 14 weeks (diastolic dysfunction stage). Lung weight increased significantly at 18 weeks (decompensated stage). Histological percentage area fibrosis and collagen type I/III, myocyte hypertrophy, and α-myosin heavy chain isoform increased in the subendocardial layer at 14 weeks and progressed into the midlayer at 18 weeks. Longitudinal strain progressively deteriorated in the hypertensive group versus control group at 14 weeks (hypertensive group: -17±3%, control: -27±4%; P<0.001), and circumferential strain decreased at 18 weeks (hypertensive group: -17±2%, control: -27±3%; P=0.002). After adjustment for systolic wall stress, subendocardial percentage area fibrosis was selected as the independent determinant of longitudinal strain. This study showed that LV wall strain alternations were accompanied by fibrosis and myocyte hypertrophy from subendocardium to epicardium, and longitudinal strain related significantly to subendocardial layer fibrosis. Longitudinal strain could be a surrogate of subendocardial fibrotic changes and may be useful for risk stratification of hypertensive heart failure.

The presence of SVPCs in 12-lead electrocardiograms was a strong predictor of AF development, and associated with increased risk of CVD in general population.