BackgroundAtrial fibrillation (AF) remains the most common complication after cardiac surgery. The present study aim was to derive an effective bedside tool to predict postoperative AF and its related complications.Methods and ResultsData of 17 262 patients undergoing adult cardiac surgery were retrieved at 3 European university hospitals. A risk score for postoperative AF (POAF score) was derived and validated. In the overall series, 4561 patients (26.4%) developed postoperative AF. In the derivation cohort age, chronic obstructive pulmonary disease, emergency operation, preoperative intra‐aortic balloon pump, left ventricular ejection fraction <30%, estimated glomerular filtration rate <15 mL/min per m2 or dialysis, and any heart valve surgery were independent AF predictors. POAF score was calculated by summing weighting points for each independent AF predictor. According to the prediction model, the incidences of postoperative AF in the derivation cohort were 0, 11.1%; 1, 20.1%; 2, 28.7%; and ≥3, 40.9% (P<0.001), and in the validation cohort they were 0, 13.2%; 1, 19.5%; 2, 29.9%; and ≥3, 42.5% (P<0.001). Patients with a POAF score ≥3, compared with those without arrhythmia, revealed an increased risk of hospital mortality (5.5% versus 3.2%, P=0.001), death after the first postoperative day (5.1% versus 2.6%, P<0.001), cerebrovascular accident (7.8% versus 4.2%, P<0.001), acute kidney injury (15.1% versus 7.1%, P<0.001), renal replacement therapy (3.8% versus 1.4%, P<0.001), and length of hospital stay (mean 13.2 versus 10.2 days, P<0.001).ConclusionsThe POAF score is a simple, accurate bedside tool to predict postoperative AF and its related or accompanying complications.

SUMMARY. To determine the compensatory reserve capacity of the ventricular myocardium following infarction, the left coronary artery in rats was ligated, and the animals were killed 40 days later. Infarcts affecting an average 23% of the left ventricle were characterized by a 27% hypertrophic growth of the remaining myocardium that produced a complete replacement of the necrotic tissue. In contrast, infarcts with an average 50% loss of mass resulted in 83% expansion of the spared myocardium that was inadequate for a complete restoration of ventricular tissue. Myocyte hypertrophy was 26% and 78% in small and large infarcts, respectively. Cellular hypertrophy in both cases involved significant increases in myocyte transverse area and myocyte length. After large infarcts, there was an 18% reduction in capillary surface and a 16% increase in the diffusion distance. Corresponding values for small infarcts were -10% and 9%. These alterations combined with the deficient reconstitution of myocardial mass following large infarcts resulted in 25%, 29%, and 30% deficits in the absolute amounts of capillary lumen, surface, and length per ventricle respectively. Even with small infarcts, a deficit was seen in capillary luminal surface (-16%), and length (-19%). In conclusion, we have demonstrated that cardiac hypertrophy following myocardial infarction is consistent with cellular shape changes characteristic of a combination of concentric and eccentric hypertrophic growth. However, cardiac muscle cells appear to be unable to compensate for the loss of mass induced by a 50% infarct. The inadequate adaptation of the capillary vasculature in the infarcted hearts suggests that the injured ventricle is more vulnerable to additional ischemic episodes. (Circ Res 58: 26-37, 1986)

BackgroundBleeding after cardiac surgery requiring surgical reexploration and blood component transfusion is associated with increased morbidity and mortality. Although prothrombin complex concentrate (PCC) has been used satisfactorily in bleeding disorders, studies on its efficacy and safety after cardiopulmonary bypass are limited.MethodsBetween January 2005 and December 2013, 3454 consecutive cardiac surgery patients were included in an observational study aimed at investigating the efficacy and safety of PCC as first-line coagulopathy treatment as a replacement for fresh frozen plasma (FFP). Starting in January 2012, PCC was introduced as solely first-line treatment for bleeding following cardiac surgery.ResultsAfter one-to-one propensity score–matched analysis, 225 pairs of patients receiving PCC (median dose 1500 IU) and FFP (median dose 2 U) were included. The use of PCC was associated with significantly decreased 24-h post-operative blood loss (836 ± 1226 vs. 935 ± 583 ml, p < 0.0001). Propensity score–adjusted multivariate analysis showed that PCC was associated with significantly lower risk of red blood cell (RBC) transfusions (odds ratio [OR] 0.50; 95 % confidence interval [CI] 0.31–0.80), decreased amount of RBC units (β unstandardised coefficient −1.42, 95 % CI −2.06 to −0.77) and decreased risk of transfusion of more than 2 RBC units (OR 0.53, 95 % CI 0.38–0.73). Patients receiving PCC had an increased risk of post-operative acute kidney injury (AKI) (OR 1.44, 95 % CI 1.02–2.05) and renal replacement therapy (OR 3.35, 95 % CI 1.13–9.90). Hospital mortality was unaffected by PCC (OR 1.51, 95 % CI 0.84–2.72).ConclusionsIn the cardiac surgery setting, the use of PCC compared with FFP was associated with decreased post-operative blood loss and RBC transfusion requirements. However, PCC administration may be associated with a higher risk of post-operative AKI.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-015-1172-6) contains supplementary material, which is available to authorized users.

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Acute fulminant myocarditis (AFM) may represent a life-threatening event, characterized by rapidly progressive cardiac compromise that ultimately leads to refractory cardiogenic shock or cardiac arrest. Venoarterial extracorporeal membrane oxygenation (VA-ECMO) provides effective cardiocirculatory support in this circumstance, but few clinical series are available about early and long-term results. Data from a multicenter study group are reported which analyzed subjects affected by AFM and treated with VA-ECMO during a 5-year period

Mitral valve replacement is a suitable option for patients with chronic ischemic mitral regurgitation and impaired left ventricular function. It provides better results in terms of freedom from reoperation with comparable valve-related complication rates.

Left ventricular free-wall rupture is one of the most fatal complications after acute myocardial infarction. Surgical treatment of post-infarction left ventricular free-wall rupture has evolved over time. Direct closure of the ventricular wall defect (linear closure) and resection of the infarcted myocardium (infarctectomy), with subsequent closure of the created defect with a prosthetic patch, represented the original techniques. Recently, less aggressive approaches, either with the use of surgical glues or the application of collagen sponge patches on the infarct area to cover the tear and achieve haemostasis, have been proposed. Despite such modifications in the therapeutic strategy and surgical treatment, however, postoperative in-hospital mortality may be as high as 35%. In extremely high-risk or inoperable patients, a non-surgical approach has been reported.

In our morphometric study of the effects of exercise on the heart, male Wistar-Kyoto rats at 5 weeks of age were subjected daily to a moderate treadmill running program that lasted for 7 weeks. The heart responded to physical conditioning by different magnitudes of tissue growth of the right (22%) and left (7%) ventricular myocardium, the latter change not statistically significant. The increase in right ventricular volume was associated with a 25% enlargement of ventricular area, a 26% average lengthening of the myocytes, and no change in sarcomere length and in ventricular midwall thickness. Exercise produced significant alterations in the quantitative parameters of the microvasculature of the right ventricle, but no appreciable changes in the left ventricle. Right ventricular hypertrophy was characterized by an absolute 44% growth of the endothelial luminal surface brought about through a 16% increase in capillary numerical density, and a 41% augmentation of the total length of the capillary network. Maximum diffusion distance from the capillary wall to the mitochondria of myocytes decreased 10% as a result of capillary proliferation and the lack of lateral expansion of myocyte cross-sectional area. Evaluation of the subcellular constituents of myocytes showed no change in the mitochondria:myofibrils volume ratio, indicating a growth of these components proportional to each other and to the growth of the myocyte population as a whole. It was concluded that, as a result of running exercise, right ventricular growth is analogous to eccentric hypertrophy in which the structural adaptations of the capillary bed can be expected to improve the diffusion and transport of oxygen within the tissue.