Preoperative 6-minute walk test adds prognostic information to Euroscore in patients undergoing aortic valve replacement.

AIMS: The authors investigated the additive prognostic value of the 6-minute walk test (6MWT) to Euroscore in patients with severe aortic stenosis undergoing aortic valve replacement (AVR) METHODS AND RESULTS: 208 patients with severe AS underwent the 6MWT before AVR, as part of a randomised trial (ASSERT) comparing stented and stentless aortic valves. Clinical follow-up was available for 200 patients up to 12 months. The rate of death, myocardial infarction (MI) or stroke (time to first event) was 13% (n = 14) in patients walking <300 metres compared to 4% (n = 4) in those who walked > or =300 metres (p = 0.017). When rate of death, MI or stroke by Euroscore risk was stratified by 6-minute walking distance, the 6MWT added prognostic information. In a Cox regression analysis 6MWT distance was the only variable retained as an independent predictor of the composite outcome of death, MI or stroke at 12 months (HR 0.28 95% CI 0.09 to 0.85, p = 0.025). CONCLUSIONS: The 6MWT is safe and feasible to carry out in patients with severe aortic stenosis before AVR, and provides potentially important functional and prognostic information to clinical assessment and the Euroscore risk score.

Infarto cerebral como forma de presentación de un síndrome takotsubo / Cerebral infarct as a clinical presentation of takotsubo syndrome

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C-reactive protein and the stress tests for the risk stratification of patients recovering from unstable angina pectoris.

We assessed the 90-day prognostic value of stress tests and C-reactive protein (CRP) after medical stabilization of unstable angina. We included 139 consecutive patients with unstable angina who were free of complications or did not undergo revascularization during hospitalization. Blinded CRP assays and a stress test (95 exercise electrocardiograms, 44 dobutamine echocardiograms) were performed within the first week after discharge. Of 139 participants, 44 (31.6%) had an ischemic stress test response. CRP was elevated (> 1.5 mg/dl) in 40 patients (28.7%). CRP >1.5 mg/dl was more frequently observed among patients who experienced death or myocardial infarction at 90 days (88.2% vs 20.5%, p <0.0001). Compared with the stress tests, CRP showed greater sensitivity (88% vs 47%) and specificity (81% vs 70%) for increased risk, and higher positive (37.5% vs 18.2%) and negative (98% vs 90%) predictive values. The area under the receiver operating curve of the relation with the 90-day outcome increased from 0.58 +/- 0.07 to 0.83 +/- 0.05 when the CRP data were added to the stress tests results (p <0.001). Elevation of CRP differentiated stress tests negative patients with increased risk of major events during follow-up. In patients who respond to medical treatment for unstable angina, CRP elevation may be a better parameter than the stress test in identifying the presence of persistent plaque instability.

Independent prognostic value of elevated C-reactive protein in unstable angina.

BACKGROUND: There is growing evidence of the prognostic importance of C-reactive protein (CRP) in unstable angina. However, the independent value of CRP relative to other conventional markers at different stages of treatment has not been established. Therefore, we assessed the in-hospital and 90-day prognostic values of serum CRP in unstable angina. We also compared the relation of CRP at admission and discharge with 90-day outcome. METHODS AND RESULTS: One hundred ninety-four consecutive patients were included in a derivation (n = 105) and a validation set (n = 89). Serum CRP was measured at admission, at 48 hours, and at hospital discharge. A cutoff point of 1.5 mg/dL for CRP provided optimum sensitivity and specificity for adverse outcome, based on the receiver operator curves. No association was found between CRP on admission and in-hospital outcome. CRP at admission, adjusted for age, ECG findings on admission, silent ischemia, left ventricular wall motion score, and high-risk clinical presentation, was related to the combined end point of refractory angina, myocardial infarction, or death at 90 days (hazard ratio [HR] 1.9, 95% CI 1.2 to 8.3, P = 0.002). CRP at hospital discharge was the strongest independent marker of an adverse outcome (HR 3.16, 95% CI 2.0 to 5.2, P = 0.0001). These results were confirmed in the validation set (CRP at discharge: HR 3. 3, 95% CI 2.0 to 7.69, P = 0.0001). CONCLUSIONS: In unstable angina, CRP is a strong independent marker of increased 90-day risk. Compared with CRP at admission, CRP at discharge is better related to later outcome and could be of great utility for risk stratification.

A multicenter, randomized study of argatroban versus heparin as adjunct to tissue plasminogen activator (TPA) in acute myocardial infarction: myocardial infarction with novastan and TPA (MINT) study.

OBJECTIVES: This study examined the effect of a small-molecule, direct thrombin inhibitor, argatroban, on reperfusion induced by tissue plasminogen activator (TPA) in patients with acute myocardial infarction (AMI). BACKGROUND: Thrombin plays a crucial role in thrombosis and thrombolysis. In vitro and in vivo studies have shown that argatroban has advantages over heparin for the inhibition of clot-bound thrombin and for the enhancement of thrombolysis with TPA. METHODS: One hundred and twenty-five patients with AMI within 6 h were randomized to heparin, low-dose argatroban or high-dose argatroban in addition to TPA. The primary end point was the rate of thrombolysis in myocardial infarction (TIMI) grade 3 flow at 90 min. RESULTS: TIMI grade 3 flow was achieved in 42.1% of heparin, 56.8% of low-dose argatroban (p = 0.20 vs. heparin) and 58.7% of high-dose argatroban patients (p = 0.13 vs. heparin). In patients presenting after 3 h, TIMI grade 3 flow was significantly more frequent in high-dose argatroban versus heparin patients: 57.1% versus 20.0% (p = 0.03 vs. heparin). Major bleeding was observed in 10.0% of heparin, and in 2.6% and 4.3% of low-dose and high-dose argatroban patients, respectively. The composite of death, recurrent myocardial infarction, cardiogenic shock or congestive heart failure, revascularization and recurrent ischemia at 30 days occurred in 37.5% of heparin, 32.0% of low-dose argatroban and 25.5% of high-dose argatroban patients (p = 0.23). CONCLUSIONS: Argatroban, as compared with heparin, appears to enhance reperfusion with TPA in patients with AMI, particularly in those patients with delayed presentation. The incidences of major bleeding and adverse clinical outcome were lower in the patients receiving argatroban.

Clinical predictors of in-hospital prognosis in unstable angina: ECLA 3. The ECLA Collaborative Group.

OBJECTIVES: Because of recent changes in the treatment of unstable angina, we wanted to reassess the short-term prognostic value of clinical and echocardiographic variables. METHODS: This was an observational, prospective study that included 1038 nonselected consecutive patients admitted to coronary care units for unstable angina. RESULTS: Baseline characteristics were age 60.18 +/- 16 years, history of prior myocardial infarction in 336 patients (32%), and a history of previous angina in 817 patients (78.7%). Angina during the 48 hours before admission was observed in 1004 patients (96.7%) and ST-segment changes on admission electrocardiogram occurred in 385 patients (37%). In-hospital treatment consisted of nitrates in 81.4% of patients, aspirin in 88.6%, beta-blockers in 71%, intravenous heparin in 34.5%, subcutaneous heparin in 23%, and angioplasty or coronary artery bypass grafting in 25.1%. After admission, angina occurred in 443 patients (40.8%), refractory angina in 223 patients (21.5%), and death or myocardial infarction in 84 patients (8.1%). At admission, the independent predictors of myocardial infarction or death identified by multivariate logistic regression analysis were ST-segment depression (odds ratio [OR] 2.13, 95% confidence interval [CI] 1.23 to 3.68, P =.006), prior angina (OR 2.23, 95% CI 0.98 to 5.05, P =.05), number of episodes of angina within the previous 48 hours (OR 1.63, 95% CI 0.98 to 2.70, P =.05), and history of smoking (OR 0.69, 95% CI 0.56 to 0.85, P =.004). Age greater than 65 years (OR 1.49, 95% CI1.09 to 2.03, P = 0.03) was significantly related to in-hospital death. The area under the receiver operating characteristic curve for application of this model was 0.59. Sensitivity was 80% with a specificity of only 33%. Refractory angina after admission showed a strong relation with an adverse short-term outcome. CONCLUSIONS: With current therapy, clinical and electrocardiographic variables provide useful information about the short-term outcome of unstable angina. However, this model has low specificity to identify high-risk patients. Future studies about the incremental value of the new serum markers such as troponin T and C-reactive protein to assist in identification of high-risk patients are necessary.

Early treatment with low-dose enalapril after acute myocardial infarction: an equilibrium radionuclide angiographic study. Enalapril despues del Infarto (EDI) Trial Investigators.

BACKGROUND: To further elucidate the mechanisms involved in the treatment of acute myocardial infarction (AMI) with angiotensin-converting enzyme inhibitors, we compared the effects on left ventricular volumes of early (< 48 hours) versus late (45 days) administration of a fixed low dose of enalapril (10 mg) in patients with AMI. We also analyzed the changes of left ventricular volumes after withdrawal of the study drug. Reduced dilation of the left ventricle is one of the beneficial effects of angiotensin-converting enzyme inhibition after AMI. However, the nature of this effect is not completely understood. METHODS AND RESULTS: We included 89 patients within 48 hours after onset of a first AMI and radionuclide left ventricular ejection fraction less than 45%. The study was double-blind and compared enalapril and placebo with a crossover design. All patients were randomly assigned to a sequence A (enalapril, 45 days; placebo, 45 days) or B (placebo, 45 days; enalapril, 45 days). The end point was the change of left ventricular volume at 45 and 90 days. Thrombolysis was administered to 26 patients (70%) in group A and 25 (75%) in group B. All pretreatment clinical variables were similar in both groups. Median and 95% confidence intervals (CIs) of left ventricular diastolic volumes were 46.8 ml/m2 (39 to 61 ml/m2) and 46.6 ml/m2 (39 to 60 ml/m2) for groups A and B, respectively. Baseline end systolic volumes were 28.5 ml/m2 (20 to 36 ml/m2) and 28.9 ml/m2 (23 to 28 ml/m2) in the same groups. Placebo treatment during the initial 45 days was associated with an increase of left ventricular diastolic volume of 8.75 ml/m2 (95% CI, 3.25 to 17.1 ml/m2; p < 0.01) and end-systolic volume of 4.20 ml/m2 (95% CI, 0.00 to 10.1 ml/m2; p < 0.05). No significant changes during other phases of the study were observed. At 45 days left ventricular diastolic volume was 11.1 ml/m2 (95% CI, 0.5 to 2.2 ml/m2), greater in placebo-treated patients compared with patients receiving enalapril. CONCLUSIONS: In patients with a first Q wave AMI and left ventricular ejection fraction less than 45%, treatment with enalapril can prevent left ventricular dilation. This protective effect involves at least partially a structural modification of the left ventricle. Hence, maximal benefit can be obtained only with early initiation of treatment.