A best evidence topic was written according to a structured protocol. Lack of evidence exists regarding the optimal timing for coronary artery bypass graft (CABG) surgery after non-ST myocardial infarction (NSTEMI). While some authors address the importance of the timing of surgery alone, others take into account the extent of myocardial damage. The question addressed was whether early or late CABG surgery improves hospital mortality and cardiovascular events after NSTEMI in stable patients. Using a designated search strategy, 459 articles were found, of which seven represented the best available evidence. All of these studies were level 3 (retrospective cohort studies). Studies could be divided into those which assessed CABG outcome based on preoperative cardiac troponin I (cTnI) level as a measure of the extent of myocardial damage and those which considered only the timing after myocardial infarction. Outcome measures included short-term survival, hospital mortality, length of hospital stay and major adverse cardiovascular events (MACEs). The biggest retrospective study analysing postoperative outcomes based on the timing of surgery after NSTEMI concluded that operative mortality is higher when surgery is performed within 6 h of the event. After 6 h, mortality is similar at any timepoint after 6h of NSTEMI. While other smaller studies agree that there are fewer postoperative complications when surgery is performed after 48 h of the event, no consensus is found regarding mortality between early (less than 48 h) and late CABG surgery. Taking into account preoperative cTnI values, CABG has a higher incidence of MACEs and hospital mortality in patients with cTnI >0.15 ng/ml. When surgery is performed within 24 h of symptoms, preoperative cTnI >0.72 ng/ml is associated with worse outcomes. In view of the methodological limitations and level of evidence of the studies included, it appears that surgery may be safely performed in NSTEMI patients at any time after the first 6 h of the event in patients with cTnI <0.15 ng/ml, whereas in those patients with higher values of cTnI, waiting for cTnI to reduce before considering surgery seems to be a wise option in order to decrease the incidence of MACEs and hospital mortality.
Background Bicuspid aortic valve patients have an increased risk of aortic dilatation. A deficit of nitric oxide synthase has been proposed as the causative factor. No correlation between flow-mediated dilation and aortic diameter has been performed in patients with bicuspid aortic valves and normal aortic diameters. Being a hereditary disease, we compared echocardiographic features and endothelial function in these patients and their first-degree relatives. Methods Comprehensive physical examinations, routine laboratory tests, transthoracic echocardiography, and measurements of endothelium-dependent and non-dependent flow-mediated vasodilatation were performed in 18 bicuspid aortic valve patients (14 type 1 and 4 type 2) and 19 of their first-degree relatives. Results The first-degree relatives were younger (36.7 ± 18.8 vs. 50.5 ± 13.9 years, p = 0.019) with higher ejection fractions (64.6% ± 1.7% vs. 58.4% ± 9.5%, p = 0.015). Aortic diameters indexed to body surface area were similar in both groups, the except the tubular aorta which was larger in bicuspid aortic valve patients (19.3 ± 2.7 vs. 17.4 ± 2.2 mm·m, p = 0.033). Flow-dependent vasodilation was similar in both groups. A significant inverse correlation was found between non-flow-dependent vasodilation and aortic root diameter in patients with bicuspid aortic valve ( R = -0.57, p = 0.05). Conclusions Bicuspid aortic valve patients without aortopathy have larger ascending aortic diameters than their first-degree relatives. Endothelial function is similar in both groups, and there is no correlation with ascending aorta diameter. Nonetheless, an inverse correlation exists between non-endothelial-dependent dilation and aortic root diameter in bicuspid aortic valve patients.
143 Background: To evaluate the incidence, severity and outcome of Trastuzumab-induced cardiotoxicity in HER2 positive Uruguayan breast cancer (BC) patients. Methods: Retrospective observational analysis of HER2 positive BC patients who were treated with Trastuzumab (TTZ) from January 2007 to December 2013 at two Uruguayan centers. Cardiac monitoring included physical examination and assessment of left ventricular ejection fraction (LVEF) by echocardiography that was evaluated before TTZ administration and every 12 weeks thereafter during the duration of therapy. Cardiovascular risk factors analyzed were: obesity (BMI ≥ 30 kg/m2), hypertension, diabetes, sedentary lifestyle and high cholesterol. Results: Sixty nine female patients were found in the databases of our institutions. Median age was 48 years (range: 27-73). Stage at diagnosis was as detailed: 19 % EI, 46 % EII, 29 % EIII and 4 % EIV. Eighty nine percent of patients received adjuvant TTZ , 4 % neoadjuvant TTZ and 7 % received it as a palliative therapy. Thirty patients (43, 5%) had at least one cardiovascular risk factors: 26% hypertension, 16% obesity, 9% sedentary lifestyle, and 4% high cholesterol. Median number of TTZ cycles was 15. Cycles were administered every 3 weeks at standard dose. Nineteen patients (27%) developed cardiotoxicity, of whom 12 had a transient suspension because of a reversible fall in LVEF, 2 had a irreversible reduction in LVEF, and 5 had a symptomatic heart failure. Eighty-nine percent of our patients (62 patients) completed treatment and the rest had a definitive suspension due to a irreversible reduction in LVEF or symptomatic heart failure. Most patients that developed cardiotoxicity (15 out of 19) had cardiovascular risk factors and also most of them (16 out of 19) had received anthracyclines before TTZ. Conclusions: Cardiotoxicity incidence was similar to the incidence reported in the literature and when it was present, in most cases was transient, asymptomatic, and reversible.
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