Diastolic bulging of the interventricular septum (IVS) toward the left ventricle was observed by real-time cross-sectional echocardiography in three patients with primary pulmonary hypertension and one patient with secondary pulmonary hypertension after closure of an atrial septal defect. M-mode echocardiography showed a characteristic abnormal pattern of septal motion in diastole and in systole. In two patients, we attempted to correlate M-mode motion to the interventricular pressure gradient. During diastole, the interventricular pressure gradient between the left and right ventricles was negative and the pressure gradient curve was very similar to the M-mode echogram of the IVS. Banding studies in which acute right ventricular hypertension was produced in dogs showed similar shape changes, suggesting that the diastolic shape and motion of the septum are determined by the interventricular pressure gradient between the ventricles. Diastolic bulging of the IVS toward the left ventricle in our patients results from negative interventricular pressure gradient between the left and right ventricles during diastole.

To clarify the determinants of pulmonary valve (PV) motion in pulmonary hypertension, we examined the correlations among PV echo patterns, the pulmonary artery (PA) flow curve just above the PA orifice and the pulmonary artery-right ventricle (PA-RV) pressure gradient. By constricting the PA, we could produce a variety of PV echo patterns, including midsystolic semiclosure in open-chest dogs. Throughout the experiments, the PV echo pattern and PA flow curve were similar in pattern and timing. When the PV echo showed midsystolic semiclosure with reopening. The PA flow curve showed a transient decrease followed by a transient increase during midsystole. The PA-RV pressure gradient became transiently positive (PA pressure greater than RV pressure) and then negative in midsystole only when the PV echo showed midsystolic semiclosure with reopening. In conclusion, PV motion during systole may be instantaneously determined by PA flow change and the PA-RV pressure gradient during the cardiac cycle in experimental pulmonary hypertension.

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Background: Atrial cardiomyopathy is known as an underlying pathophysiological factor in the majority of AF patients. Left atrial low-voltage areas (LVAs) are reported to coincide with fibrosis, and to likely represent atrial cardiomyopathy. This study aimed to delineate differences in the long-term prognosis of patients stratified by the size of LVAs. Methods: This observational study included 1,488 consecutive patients undergoing initial ablation for AF. LVAs were defined as regions with a bipolar peak-to-peak voltage of < 0.50 mV. The total study population was divided into 3 groups stratified by LVA size: patients with no LVAs (n=1136), those with small (< 20 cm2, n=250) LVAs, and those with extensive (≥ 20 cm2, n=102) LVAs. Composite endpoints of death, heart failure, and stroke were followed for up to 5 years. Results: Composite endpoints developed in 105 (7.1%) of 1488 patients, and AF recurrence occurred in 410 (27.6%). Composite endpoints developed more frequently in the order of patients with extensive LVAs (19.1%), small LVAs (10.8%), and no LVAs (5.1%; p for trend<0.0001). Multivariable analysis revealed that LVA presence was independently associated with higher incidence of composite endpoints, irrespective of AF recurrence (modified hazard ratio=1.73, 95% confidence interval=1.13-2.64, p=0.011) Conclusions: LVA presence and its extent were both associated with poor long-term composite endpoints of death, heart failure, and stroke, irrespective of AF recurrence or other confounders. Underlying atrial cardiomyopathy appears to define a poor prognosis after AF ablation.

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