Journal of the American Society of Echocardiography最新文献

Background: Aortic regurgitation (AR) is a prevalent valve disease with a long latent period before symptoms appear. Recent data has suggested the role of novel markers of myocardial overload in assessing onset of decompensation.

Methods: The aim of this study was to evaluate the role of unsupervised cluster analyses in identifying different clinical clusters, including clinical status, and a large number of echocardiographic variables including left ventricular volumes, and their associations with mortality. Patients with moderate to severe or greater chronic AR identified using echocardiography at the Mayo Clinic in Rochester, Minnesota, were retrospectively analyzed. The primary outcome was all-cause mortality censored at aortic valve surgery. Uniform manifold approximation and projection with the k-means algorithm was used to cluster patients using clinical and echocardiographic variables at the time of presentation. Missing data were imputed using the multiple imputation by chained equations method. A supervised approach trained on the training set was used to find cluster membership in a hold-out validation set. Log-rank tests were used to assess differences in mortality rates among the clusters in both the training and validation sets.

Results: Three distinct clusters were identified among 1,100 patients (log-rank P for survival < .001). Cluster 1 (n = 337), which included younger males with severe AR but fewer symptoms, showed the best survival at 75.6% (95% CI, 69.5%-82.3%). Cluster 2 (n = 235), including older patients and more females with elevated filling pressures, showed intermediate survival of 64.2% (95% CI, 56.8%-72.5%). Cluster 3 (n = 253), characterized by severe symptomatic AR, demonstrated the lowest survival of 45.3% (95% CI, 34.4%-59.8%) at 5 years. Similar clusters were identified in the internal validation cohort.

Conclusions: Distinct clusters with variable echocardiographic features and mortality differences exist within patients with chronic moderate to severe or greater AR. Recognizing these clusters can refine individual risk stratification and clinical decision-making after verification in future prospective studies.

Background: Fontan circulatory failure with impaired systolic function is well documented; however, its mechanisms are not fully understood. The aim of this study was to explore myocardial functional reserve in adolescent patients with Fontan circulation in response to exercise or acute preload increase.

Methods: The study included 32 patients (median age, 16.7 years; range, 15.4-17.9 years; 12 female patients) with Fontan circulation. Echocardiographic imaging was performed during exercise using a recumbent cycle ergometer and during heart catheterization with a rapid infusion of 0.9% saline infusion at 5 mL/kg body weight. Myocardial peak longitudinal strain (LS) was measured in a four-chamber view during specific time intervals before, during, and after exercise (LS_stress) and volume load (LS_cath). During catheterization, central venous pressure and ventricular end-diastolic pressure were simultaneously recorded. A control group of 16 healthy individuals participated in the exercise test.

Results: Mean LS_stress was less negative for patients than for control subjects (P ≤ .001 at all stages); however, it significantly improved from -18.4 ± 5.5% at baseline to -22.0 ± 6.5% (P = .004) at maximal loading. LS_stress at maximal loading did not correlate with changes in heart rate. During catheterization, mean LS_cath was -19.6 ± 6.0% at baseline and did not improve significantly at 1.00 to 2.00 minutes and at 4.00 to 6.00 minutes after saline infusion. In more than half of the patients, LS_cath worsened or improved by less than -2% after saline infusion. Worsening of LS_cath correlated with central venous pressure and ventricular end-diastolic pressure in all conditions (P ≤ .017). There was no difference in LS_stress or LS_cath between the morphologic right ventricle and the morphologic left ventricle.

Conclusions: Patients with Fontan circulation demonstrate systolic myocardial functional reserve that can be recruited with exercise stress but not with an acute increase in preload.

Background: Although the correction of the proximal isovelocity surface area (PISA) method has been shown to improve the accuracy of assessing the severity of secondary tricuspid regurgitation (STR), its clinical impact remains to be investigated. The aim of this study was to compare the association of the quantitative parameters of STR severity obtained from the corrected and conventional PISA methods with outcomes.

Methods: Both conventional and corrected effective regurgitant orifice area (EROA) (EROA vs corrected EROA [EROAc]), regurgitant volume (RegVol) (RegVol vs corrected RegVol [RegVolc]), and regurgitant fraction (RegFr) (RegFr vs corrected RegFr [RegFrc]) were measured in 519 consecutive patients (mean age, 75 ± 12 years; 44% men; 74% with ventricular STR) with moderate and severe STR. The end point was a composite of heart failure hospitalization and death.

Results: EROAc, RegVolc, and RegFrc were significantly larger than EROA, RegVol, and RegFr (P < .001 for all). After a mean follow-up period of 19 ± 15 months, 210 patients reached the end point. Using time-dependent receiver operating characteristic curves, the parameters obtained from the corrected PISA method were more closely associated with outcomes at 2 years than those obtained with the conventional PISA method: EROAc vs EROA (P < .001), RegVolc vs RegVol (P = .001), and RegFrc vs RegFr (P < .001) for ventricular STR. Conversely, no significant differences were detected for atrial STR. After multivariable adjustment, both uncorrected and corrected EROA, RegVol, and RegFr were independently associated with the end point. Using the new five-grade severity scheme, patients reclassified using the corrected PISA method had a significantly higher rate of events compared with those not reclassified among those with ventricular STR (P = .0086). Conversely, this relationship was not statistically significant in patients with atrial STR (P = .061).

Conclusions: Correcting the PISA method provides larger quantitative parameters of STR severity that are more closely associated with outcomes in patients with ventricular STR.