Is delayed surgical revascularization in acute myocardial infarction useful or dangerous? New insights into an old problem.

OBJECTIVES: Haemodynamically stable patients admitted for coronary artery bypass grafting in acute myocardial infarction often undergo delayed surgery in order to avoid the risks of emergency surgery. However, initially stable patients undergoing delayed surgery may develop low cardiac output syndrome (LCOS) during the waiting period, which might be a major drawback of this strategy. We aim to define risk factors and clinical consequences of LCOS during the waiting period. METHODS: A total of 530 consecutive patients with acute myocardial infarction (33% non-ST-segment elevation myocardial infarction and 67% ST-segment-elevation myocardial infarction) underwent isolated coronary artery bypass grafting between 2008 and 2013. Outcomes after either immediate (<48 h after onset of symptoms) or delayed (>48 h after onset of symptoms) therapy were compared. Predictors of preoperative development of LCOS were identified using multivariate regression analysis. RESULTS: Of the 327 patients undergoing delayed therapy, 39 (12%) developed preoperative LCOS, resulting in increased mortality compared with patients who remained stable (21 vs 7.6%, P < 0.001). Immediate therapy resulted in similar mortality compared with delayed therapy (6.4 vs 7.6%; P = 0.68) and better 7-year survival (70 vs 55%; P < 0.001). Predictors of developing LCOS were reduced left ventricular function (odds ratio 4.4), renal impairment (odds ratio 3.0), acute pulmonary infection (odds ratio 3.4) and the extent of troponin elevation at admission (odds ratio 1.01 per increase by 1 µg/l). CONCLUSIONS: In patients with acute myocardial infarction undergoing delayed coronary artery bypass grafting, preoperative LCOS is a relevant and dangerous condition that can be avoided by operating immediately or by carefully selecting patients to be delayed according to the risk parameters identified preoperatively.

Impact of prophylactic administration of Levosimendan on short-term and long-term outcome in high-risk patients with severely reduced left-ventricular ejection fraction undergoing cardiac surgery - a retrospective analysis.

BACKGROUND: Patients with severely reduced left-ventricular ejection fraction carry a high risk of morbidity and mortality after cardiac surgery. Levosimendan can be used prophylactically in these patients having shown positive effects on short-term outcome. However, effects on long-term outcome and patient subgroups benefiting the most are unknown. We aim to address these topics with real-life data from our clinical practice. METHODS: Two hundred eigthy eight patients with preoperative LVEF ≤ 35% underwent cardiac surgery with cardiopulmonary bypass between 2009 and 2013. Thereof, 246 were included in the matched analysis. Eigthy two patients received 12.5mg Levosimendan starting at induction of anesthesia. Outcomes of patients undergoing coronary artery bypass grafting surgery (n = 103), isolated valve surgery/ascending aortic surgery (n = 45) and those undergoing combination procedures (n = 98) were analyzed separately. Additionally, multivariate regression analysis was conducted in order to identify predictors of short-term outcome parameters for different subgroups of patients. RESULTS: Thirty days mortality rates of 16% in the Levosimendan group and 21% in the control group (OR 0.7; 95%-CI 0.36-1.5; p = 0.37) were observed. Levosimendan showed a positive effect on postoperative renal function. A higher rate of new-onset atrial fibrillation (OR 4.0; 95%-CI 2.2-7-2; p < 0.0001) was observed in the Levosimendan group. Follow-up until three years postoperatively showed no differences in long-term survival between the groups. CONCLUSION: Prophylactic administration of Levosimendan did not affect overall short- and long-term outcomes. The value of prophylactic use of Levosimendan remains questionable and more data is needed to confirm subgroups that might benefit most.

Antiplatelet therapy early after bioprosthetic aortic valve replacement is unnecessary in patients without thromboembolic risk factors.

BACKGROUND: The use of antithrombotic therapy during the postoperative period after biological aortic valve replacement (AVR) in patients without thromboembolic risk factors remains controversial. Treatment with warfarin is recommended for the first 3 months after biological AVR. The use of antiplatelet therapy - mainly aspirin (ASA) - is suggested as an alternative treatment but its efficacy is still unsettled. Due to the increased risk of bleeding complications even no use of any antithrombotic or antiplatelet therapy was advocated. Given this ongoing dispute, the aim of this retrospective double-institutional study was to evaluate the necessity of antiplatelet treatment by ASA with no postoperative antiplatelet therapy in terms of survival, major bleedings and cerebral thromboembolism of patients undergoing biological AVR without thromboembolic risk factors. METHODS: From January 2001 to December 2003, 288 consecutive patients (72.8+/-7.5 years, 134 males) with sinus rhythm and no other thromboembolic risk factors underwent single biological AVR with porcine or bovine pericardial valves without concurrent coronary artery bypass graft surgery. By surgeons preference, 100 mg ASA was given to 132 patients, and 156 patients received no antiplatelet therapy. Patients were followed for cerebral ischemic events, major bleedings, need for repeat operation, NYHA class and survival at three time intervals postoperatively (30 days, 3 and 12 months). RESULTS: None of all patients died during the operation. Mortality within 30 days was 3.8% in the ASA and 3.9% in the no ASA group (p=0.777). There were no statistically significant differences for cerebral ischemia within 3 months after AVR (ASA 0.8% vs no ASA 1.3%: p=0.884) and 3 to 12 months after AVR (ASA 0.8% vs no ASA 0%; p=0.933). Major bleedings occurred in two ASA-treated patients and in one patient without antiplatelet therapy (p=0.884). The incidence of NYHA class III-IV after 3 months (1.5% vs 1.9%; p=0.850) and 12 months (9.0% vs 5.1%; p=0.278) were similar, as were the need for repeat operative AVR after 12 months (0.8% vs 0.6%; p=0.553). Survival rates at 12-month follow-up were 95.5% for ASA treatment and 94.9% for no ASA treatment (p=0.963). CONCLUSIONS: In patients without thromboembolic risk factors undergoing biological AVR administration of ASA confers no advantage compared to no antiplatelet therapy. Functional status, thromboembolic events and survival were not adversely affected by withholding any antiplatelet therapy. Guidelines need to be reviewed for the antithrombotic therapy of patients without risk factors undergoing bioprosthetic AVR.