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(1) we claim a "sensitivity" for this combined protocol of 61%; and (2) our results indicate that patients with syncope of unknown origin must be tilted nearest as possible to the last syncope to increase the positive responses of HUT test.

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To determine whether ventricular short-term enlargement following acute myocardial infarction is related to increased left filling pressures and whether early treatment with captopril alters this process we studied 68 patients with a first acute myocardial infarction. Forty patients with a pulmonary capillary pressure equal or above 17 mmHg were randomized to treatment with conventional therapy plus captopril (n 20) or placebo (n 20), in a double blind fashion. The remaining 28 patients (non-dysfunction group) were treated conventionally. During the first 72 h, afterload showed a prompt decrease in the captopril group as compared to placebo. Changes from baseline to 14 days in end-diastolic and end-systolic left ventricular volume indexes determined by radionuclide ventriculography were: non-dysfunction, 85.6 (+/- 21) vs 88 (+/- 20) and 44 (+/- 17) vs 44 (+/- 17) ml.m-2; captopril (n 20), 96.6 (+/- 18) vs 99 (+/- 19) and 66 (+/- 22) vs 65 (+/- 22) ml.m-2; placebo (n 20), 96 (+/- 25) vs 113 (+/- 19) (P < 0.001) and 63 (+/- 18) vs 74 (+/- 22) ml.m-2 (P < 0.01). This study indicates that short-term ventricular enlargement is related to the degree of ventricular dysfunction and that captopril may improve this process.

The CARTAGOMAX study assessed the safety and efficacy of bivalirudin during real-world cardiac intervention. This was a single-center prospective study. Patients with acute coronary syndrome undergoing percutaneous coronary intervention were anticoagulated with bivalirudin alone or unfractionated heparin plus a glycoprotein IIb/IIIa inhibitor. Propensity score matching was performed to control for baseline imbalances and yielded 1168 patients. There was lower incidence of the composite outcome of death from any cause or major bleeding at 30 days (P = 0.005), 6 months (P = 0.005), and 12 months (P = 0.001) of follow-up in the bivalirudin group, compared with the heparin plus glycoprotein inhibitor group. The administration of bivalirudin was associated with lower rate of all-cause mortality at 1 year of follow-up (P = 0.009). The incidence of major bleeding was lower in the bivalirudin group at 1, 6, and 12 months of follow-up (P = 0.002, P = 0.013 and P = 0.017, respectively). The incidence of stroke and reinfarction were similar between groups during follow-up. The rate of stent thrombosis were slightly higher in the bivalirudin group, without reaching statistical significance at 1 and 12 months of follow-up (P = 0.06, P = 0.04, P = 0.07 at 1, 6, and 12 months, respectively). The CARTAGOMAX study found that the use of bivalirudin during percutaneous coronary intervention was associated with lower incidence of the composite outcome of death from any cause or major bleeding during follow-up. The use of bivalirudin was associated with similar rates of stroke, reinfarction, and stent thrombosis compared with heparin plus glycoprotein inhibitor. Bivalirudin proved to be a safe and effective anticoagulant during percutaneous coronary intervention.