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Objectives: Acute pulmonary embolism can be a life-threatening condition with a high mortality. The treatment choice is a matter of debate. The early and late outcomes of patients treated with surgical pulmonary embolectomy for acute pulmonary embolism in a single center were analyzed., Methods: All consecutive patients operated on for pulmonary embolism between January 2002 and March 2017 were reviewed. Patient demographics and pre- and postoperative clinical data were retrieved from our patient registry, and risk factors for in-hospital and long-term mortality were identified., Results: In total, 175 patients (mean age 59±3 years, 50% male) were operated on for acute pulmonary embolism. In-hospital mortality was 19% (34/175). No differences were found when comparing surgery utilizing a beating heart or cardioplegic arrest. Risk factors for in-hospital mortality were age >70 years [odds ratio (OR) 4.8, confidence interval (CI) 1.7-13.1, p=0.002], body surface area <2 m 2 (OR 4.7, CI 1.6-13.7, p=0.004), preoperative resuscitation (OR 14.1, CI 4.9-40.8, p<0.001), and the absence of deep vein thrombosis (OR 9.6, CI 2.5-37.6, p<0.001). Follow-up was 100% complete with a 10-year survival rate of 66.4% in 141/175 patients surviving to discharge. Once discharged from hospital, none of the risk factors identified for in-hospital mortality were relevant for long-term survival except the absence of deep vein thrombosis (OR 3.2, CI 1.2-8.2, p=0.019). The presence of malignancy was a relevant risk factor for long-term mortality (OR 4.3, CI 1.8-10.3, p=0.001)., Conclusion: Surgical pulmonary embolectomy as a therapy for acute pulmonary embolism demonstrates excellent short- and long-term results in patients with an otherwise life-threatening disease, especially in younger patients with a body surface area >2 m 2 and pulmonary embolism caused by deep vein thrombosis. Pulmonary embolectomy should therefore not be reserved as a treatment of last resort for clinically desperate circumstances., (©2018 Dohle K., et al., published by De Gruyter, Berlin/Boston.)

Background: This study analyzes the myocardial force-generating capacity in infective endocarditis (IE) using an experimental model of isolated human atrial myocardium. In vivo , it is difficult to decide whether or not alterations in myocardial contractile behavior are due to secondary effects associated with infection such as an altered heart rate, alterations of preload and afterload resulting from valvular defects, and altered humoral processes. Our in vitro model using isolated human myocardium, in contrast, guarantees exactly defined experimental conditions with respect to preload, afterload, and contraction frequency, thus not only preventing confounding by in vivo determinants of contractility but also excluding effects of other factors associated with sepsis, hemodynamics, humoral influences, temperature, and medical treatment., Methods: We analyzed right atrial trabeculae (diameter 0.3-0.5 mm, initial length 5 mm) from 32 patients undergoing aortic and/or mitral valve replacement for acute valve incompetence caused by IE and 65 controls receiving aortic and/or mitral valve replacement for nonendocarditic valve incompetence. Isometric force amplitudes and passive resting force values measured at optimal length in the two groups were compared using Student's t-test., Results: There were no significant differences between the groups in terms of the passive resting force. The isometric force amplitude in the endocarditis group, however, was significantly lower than in the nonendocarditis group (p=0.001). In the endocarditis group, the calculated active force, defined as the isometric force amplitude minus the resting force, was significantly lower (p<0.0001) and the resting force/active force ratio was significantly higher (p<0.0001). Using linear regression to describe the function between resting force and active force, we identified a significant difference in slope (p<0.0001), with lower values found in the endocarditis group., Conclusion: Our data suggest that the force-generating capacity of atrial myocardium is significantly reduced in patients with IE. In these patients, an elevated resting force is required to achieve a given force amplitude. It remains unclear, however, whether this is due to calcium desensitization of the contractile apparatus, presence of myocardial edema, fibrotic remodeling, disruption of contractile units, or other mechanisms., (©2017 Buschmann K., et al., published by De Gruyter, Berlin/Boston.)