Aims To define the hitherto unknown aetiology/mechanism distributions of mitral regurgitation (MR) in the community and the linked clinical characteristics/outcomes. Methods and results We identified all isolated, moderate/severe MR diagnosed in our community (Olmsted County, MN, USA) between 2000 and 2010 and classified MR aetiology/mechanisms. Eligible patients (n = 727) were 73 ± 18 years, 51% females, with ejection fraction (EF) 49 ± 17%. MR was functional (FMR) in 65%, organic (OMR) in 32% and 2% mixed. Functional MR was linked to left ventricular remodelling (FMR-v) 38% and isolated atrial dilatation (FMR-a) 27%. At diagnosis FMR-v vs. FMR-a, vs. OMR displayed profound differences (all P < 0.0001) in age (73 ± 14, 80 ± 10, 68 ± 21years), male-sex (59, 33, 51%), atrial-fibrillation (28, 54, 13%), EF (33 ± 14, 57 ± 11, 61 ± 10%), and regurgitant-volume (38 ± 13, 37 ± 11, 51 ± 24 mL/beat). Dominant MR mechanism was Type I (normal valve-movement) 38%, Type II (excessive valve-movement) 25%, Type IIIa (diastolic movement-restriction) 3%, and Type IIIb (systolic movement-restriction) 34%. Outcomes were mediocre with excess-mortality vs. general-population in FMR-v [risk ratio 3.45 (2.98–3.99), P < 0.0001] but also FMR-a [risk ratio 1.88 (1.52–2.25), P < 0.0001] and OMR [risk ratio 1.83 (1.50–2.22), P < 0.0001]. Heart failure was frequent, particularly in FMR-v (5-year 83 ± 3% vs. 59 ± 4% FMR-a, 40 ± 3% OMR, P < 0.0001). Mitral surgery during patients’ lifetime was performed in 4% of FMR-v, 3% of FMR-a, and 37% of OMR. Conclusion Moderate/severe isolated MR in the community displays considerable aetiology/mechanism heterogeneity. Functional MR dominates, mostly FMR-v but FMR-a is frequent and degenerative MR dominates OMR. Outcomes are mediocre with excess-mortality particularly with FMR-v but FMR-a, despite normal EF incurs notable excess-mortality and frequent heart failure. Pervasive undertreatment warrants clinical trials of therapies tailored to specific MR cause/mechanisms.
Intrathoracic anastomotic leak after esophagectomy is associated with significant morbidity and mortality. Contained leaks often can be managed nonoperatively. When surgical management is required, esophagogastric continuity can often be maintained in the majority of patients. Long-term functional results are satisfactory and similar in both the reoperative and nonoperative groups. However, a noncontained leak adversely affected long-term survival.
(1) Comparable PGs were found among the TAVs in different models; (2) pinwheeling indices were found to be different between both TAVs; (3) turbulence patterns among both TAVs translated according to RSS were different. Rigid aortic models yield more conservative estimates of turbulence; (4) both TAVs exhibit peak maximal RSS that exceeds platelet activation 100 Pa threshold limit.
Objective Valve in valve (ViV) procedures using transcatheter aortic valves (TAV) are increasingly performed to treat degenerated bioprosthetic surgical aortic valves (SAV) due to being less invasive than redo aortic valve replacement. The objective of this study is to quantify the changes in aortic sinus blood flow dynamics before and after ViV to gain insight into mechanisms for clinical and sub-clinical thrombosis of leaflets. Methods A detailed description of the sinus hemodynamics for ViV implantation was performed in-vitro. A Medtronic Hancock II porcine bioprosthesis was modeled as SAV and a Medtronic CoreValve and Edwards Sapien were used as the TAVs. High-resolution particle image velocimetry (PIV) was employed to compare the flow patterns from these two valves within both the left coronary and non-coronary sinuses in vitro. Results Velocity and vorticity within the surgical valve sinuses reached peak values of 0.7 m/s and 1000 s−1, with a 70% decrease in peak fluid shear stress near the aortic side of the leaflet in the non-coronary sinus. With the introduction of TAV, peak velocity and vorticity were reduced to around 0.4 m/s and 550 s−1 and 0.58 m/s and 653 s−1 without coronary flow and 0.60 m/s and 631 s−1 and 0.81 m/s and 669 s−1 with coronary flow for CoreValve and Sapien ViV respectively. Also, peak shear stress was around 38% higher along the aortic side of the coronary vs non-coronary TAV leaflet. Conclusions Decreased flow and shear stress in ViV indicates higher risk of leaflet thrombosis secondary to flow stasis in the non-coronary sinus.
Purpose The impact of postoperative complications on long‐term survival is not well characterized. We sought to study the prevalence of postoperative complications after cardiac surgery and their impact on long‐term survival. Methods Operative survivors (n = 26,221) who underwent coronary artery bypass grafting (CABG) (n = 13,054, 49.8%), valve surgery (n = 8667, 33.1%) or combined CABG and valve surgery (n = 4500, 17.2%) from 1993 to 2019 were included in the study. Records were reviewed for postoperative complications and long‐term survival. Propensity‐match analysis was performed between patients who did and did not have a postoperative complication. The associations between postoperative complications and survival were assessed using a Cox‐proportional model. Results Complications occurred in 17,463 (66.6%) of 26,221 operative survivors. A total of 17 postoperative complications were analyzed. Postoperative blood product use was the commonest (n = 12,397, 47.3%), followed by atrial fibrillation (n = 8399, 32.0%), prolonged ventilation (n = 2336, 8.9%), renal failure (n = 870, 3.3%), reoperation for bleeding (n = 859, 3.3%) and pacemaker/ICD insertion (n = 795, 3.0%). Stroke (hazard ratio [HR]: 1.55; 95% confidence interval [CI]: 1.36–1.77), renal failure (HR: 1.45; 95% CI: 1.33–1.58) and pneumonia (HR: 1.23; 95% CI: 1.11–1.36) had the strongest impact on long‐term survival. Long‐term survival decreased as the number of postoperative complications increased. Conclusions Postoperative complications after cardiac surgery significantly impact outcomes that extend beyond the postoperative period. Stroke, renal failure, and pneumonia are particularly associated with poor long‐term survival.
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