Pericardiectomy for constrictive pericarditis: a risk factor analysis for early and late failure.

Predictors of early and late failure of pericardiectomy for constrictive pericarditis (CP) have not been established. Early and late outcomes of a cumulative series of 81 (mean age 60 years; mean EuroSCORE II, 3.3%) consecutive patients from three European cardiac surgery centers were reviewed. Predictors of a combined endpoint comprising in-hospital death or major complications (including multiple transfusion) were identified with binary logistic regression. Non-parametric estimates of survival were obtained with the Kaplan-Meier method. Predictors of poor late outcomes were established using Cox proportional hazard regression. There were 4 (4.9%) in-hospital deaths. Preoperative central venous pressure > 15 mmHg (p = 0.005) and the use of cardiopulmonary bypass (p = 0.016) were independent predictors of complicated in-hospital course, which occurred in 29 (35.8%) patients. During follow-up (median, 5.4 years), preoperative renal impairment was a predictor of all-cause death (p = 0.0041), cardiac death (p = 0.0008), as well as hospital readmission due to congestive heart failure (p = 0.0037); while partial pericardiectomy predicted all-cause death (p = 0.028) and concomitant cardiac operation predicted cardiac death (p = 0.026), postoperative central venous pressure < 10 mmHg was associated with a low risk both of all-cause and cardiac death (p < 0.0001 for both). Ten-year adjusted survival free of all-cause death, cardiac death, and hospital readmission were 76.9%, 94.7%, and 90.6%, respectively. In high-risk patients with CP, performing pericardiectomy before severe constriction develops and avoiding cardiopulmonary bypass (when possible) could contribute to improving immediate outcomes post-surgery. Complete removal of cardiac constriction could enhance long-term outcomes.

Motoneuronal and muscle-selective removal of ALS-related misfolded proteins.

ALS (amyotrophic lateral sclerosis), a fatal motoneuron (motor neuron) disease, occurs in clinically indistinguishable sporadic (sALS) or familial (fALS) forms. Most fALS-related mutant proteins identified so far are prone to misfolding, and must be degraded in order to protect motoneurons from their toxicity. This process, mediated by molecular chaperones, requires proteasome or autophagic systems. Motoneurons are particularly sensitive to misfolded protein toxicity, but other cell types such as the muscle cells could also be affected. Muscle-restricted expression of the fALS protein mutSOD1 (mutant superoxide dismutase 1) induces muscle atrophy and motoneuron death. We found that several genes have an altered expression in muscles of transgenic ALS mice at different stages of disease. MyoD, myogenin, atrogin-1, TGFß1 (transforming growth factor ß1) and components of the cell response to proteotoxicity [HSPB8 (heat shock 22kDa protein 8), Bag3 (Bcl-2-associated athanogene 3) and p62] are all up-regulated by mutSOD1 in skeletal muscle. When we compared the potential mutSOD1 toxicity in motoneuron (NSC34) and muscle (C2C12) cells, we found that muscle ALS models possess much higher chymotryptic proteasome activity and autophagy power than motoneuron ALS models. As a result, mutSOD1 molecular behaviour was found to be very different. MutSOD1 clearance was found to be much higher in muscle than in motoneurons. MutSOD1 aggregated and impaired proteasomes only in motoneurons, which were particularly sensitive to superoxide-induced oxidative stress. Moreover, in muscle cells, mutSOD1 was found to be soluble even after proteasome inhibition. This effect could be associated with a higher mutSOD1 autophagic clearance. Therefore muscle cells seem to manage misfolded mutSOD1 more efficiently than motoneurons, thus mutSOD1 toxicity in muscle may not directly depend on aggregation.

Liberal bilateral internal thoracic artery use in people with diabetes neutralizes the negative impact of insulin-requiring status.

AIMS: Bilateral internal thoracic artery (BITA) grafts are underused in insulin-dependent diabetic patients because of increased risk of postoperative complications. The impact of the insulin-requiring status on outcomes after routine BITA grafting was investigated in this retrospective study. METHODS: Skeletonized BITA grafts were used in 3228 (71.6%) of 4508 consecutive patients having multivessel coronary disease who underwent isolated coronary bypass surgery at the authors' institution from January 1999 to August 2015. Among these BITA patients, diabetes mellitus and the insulin-requiring status were present in 972 (30.1%) and 237 (7.3%) cases, respectively. After the one-to-one propensity score-matching, 215 pairs of insulin-dependent/noninsulin-dependent people with diabetes were compared as the postoperative outcomes. The operative risk was calculated for each patient according to the logistic European System for Cardiac Operative Risk Evaluation (logistic EuroSCORE). RESULTS: As expected, insulin-dependent people with diabetes had higher risk profiles than noninsulin-dependent people with diabetes (median logistic EuroSCORE, 4.1 vs. 3.5%, P = 0.086). However, there were no differences in in-hospital mortality both in unmatched and propensity score-matched series (2.5 vs. 2%, P = 0.65 and 2.8 vs. 1.9%, P = 0.52, respectively). In propensity score-matched pairs, only prolonged invasive ventilation (P = 0.0039) and deep sternal wound infection (P = 0.071) were more frequent in insulin-dependent people with diabetes. No differences were found as the late outcomes. CONCLUSION: In diabetic patients, the insulin-requiring status is by itself a risk factor neither for in-hospital death nor for poor late outcomes after routine BITA grafting. Only the risk of prolonged invasive ventilation and deep sternal wound infection are increased early after surgery.

[A quality improvement program in cardiac surgery. Four-year experience from the Ospedali Riuniti of Trieste]. / Un programma di miglioramento della qualità in cardiochirurgia. Quattro anni di esperienza agli Ospedali Riuniti di Trieste.

BACKGROUND: Dissatisfaction with clinical outcomes prompted an intervention to assess and improve processes and outcomes in a cardiac surgery unit. METHODS: Starting on September 1st, 1998, 1836 consecutive patients requiring a heart operation in our unit were prospectively enrolled by recording a series of anamnestic, clinical and procedural descriptors in a dedicated database. Expected mortality rates were estimated by means of nine different stratification models, one of which also allowed the prediction of excess intensive care unit and total hospital length of stay. Communication within the team has been re-engineered during the time frame studied. Some procedures have been modified and some others newly introduced according to a problem-oriented approach. RESULTS: One hundred and twenty-one patients died before discharge or within 30 days of the operation. The overall observed mortality rate (6.6%) was not significantly different from the predicted estimates (relative risk-RR 0.9, 95% confidence interval-CI 0.7-1.2 compared with EuroSCORE and RR 1.2, 95% CI 0.9-1.6 compared with the "Provincial Adult Cardiac Care Network" model). Two out of seven "dedicated" coronary surgery models predicted a mortality rate significantly lower than observed. Both rates of intensive care and total postoperative length of stay exceeding predefined thresholds turned out to be significantly higher than the predicted estimates: 14.3 vs 10.1% for intensive care (RR 1.4, 95% CI 1.2-1.7) and 13.6 vs 10.6% for total postoperative stay (RR 1.3, 95% CI 1.1-1.5). During the study period the yearly raw mortality rate gradually decreased, for the series as a whole, from 9.5% during the year 1999 to 4.1% during the year 2002, and for the coronary surgery sample from 6.5 to 2.1%, with no significant differences from the expected estimates over the 3 most recent years. A similar trend was noted for both intensive care unit and total hospital length of stay. CONCLUSIONS: Implementing an internal continuous quality improvement program effectively assisted in improving surgical outcomes by motivating people involved, drawing attention to procedures to be re-engineered and by providing the proper benchmarks for assessing the results.

A life-threatening manifestation of tachycardia-induced cardiomyopathy.

A 74-year-old man was referred to hospital for sustained dyspnea. The patient was normotensive (110/70 mmHg) with clinical evidence of congestive heart failure. ECG showed atrial flutter (145 bpm). Transthoracic echocardiography demonstrated a mildly dilated left ventricle with severe systolic dysfunction and a big irregular mobile mass, a mildly dilated right ventricle with moderate systolic dysfunction and a large mass protruding into the cavity. The patient was treated surgically for high embolic and sudden death risk after coronarography, which showed a single stenosis (70%) of the left anterior descending coronary. Myocardial biopsy demonstrated interstitial and endocardial fibrosis, no inflammatory pattern. After 6 months of follow-up echocardiography was normal.