Abstract: BACKGROUND AND OBJECTIVE: Evidence is growing regarding the prognostic value of markers of inflammation in unstable angina/non-ST segment elevation myocardial infarction (UA/NSTEMI). However, the independent value of these variables has not been systematically investigated in prospective studies. The main objective of the SIESTA study is to assess the relative prognostic roles of C-reactive protein, fibrinogen, neopterin, interleukins 6, 8, 10 and 18, tumor necrosis factor, e-selectin, endothelin 1, tissue factor, VCAM-1, ICAM-1, pregnancy-associated plasma protein-A, B-type natriuretic peptide, leukocytes, troponin I or T and serum creatine kinase-MB (CKMB) in UA/NSTEMI patients. PATIENTS AND METHOD: SIESTA is a prospective, multicenter trial involving patients with chest pain suggestive of acute coronary syndrome (ACS) within 48 hours of enrolment and at least one of the following: abnormal troponin levels, electrocardiographic signs of ischaemia or previously documented vascular disease. Clinical outcome data and serial biochemical determinations will be assessed during hospital admission and at 30, 180 and 365 days of follow-up. The TIMI (Thrombolysis In Myocardial Infarction) and PEPA (Proyecto de Estudio del Pronóstico de la Angina) risk scores will be also validated. Study variables will include death due to any cause, cardiac death, non-fatal myocardial infarction, unstable angina requiring re-admission, emergency revascularization and a composite of death, myocardial infarction and need for emergency hospitalization or myocardial revascularization. Each of these conditions will be treated as secondary end-points when assessed individually.This study will provide valuable prospective information about the prognostic value of inflammatory markers in real life ACS patients of Mediterranean origin.
Abstract: INTRODUCTION: The prognostic value of enzyme peaks, the sum of the ST segment and reperfusion arrythmias during myocardial infarction remains unclear. AIM: The aim of this study was to relate the early enzymatic peaks, the sum of the ST segment and reperfusion arrythmias after thrombolytic therapy with postinfarction angina, Killip class and mortality during the acute phase of myocardial infarction. PATIENTS AND METHODS: Of 187 patients receiving fibrinolytic therapy, 169 were consecutively and prospectively included in the study. The following myocardial enzymes were determined: CK, MB, TGO, LDH. Electrocardiograms were performed prior to and 2, 6, 12 and 24 hours after the administration of the fibrinolytic drug. RESULTS: The mean age of the patients was 60.12 +/- 11.3 years, with 138 (81.7%) being males. Myocardial infarction was anterior in 74 (43.7%) and inferior in 95 cases (56.3%). Reperfusion arrythmias were observed in 65 cases (38.5%). One hundred thirty-one (77.5%) were Killip class I, 12 (7.1%) presented postinfarction angina, and 8 (4.7%) died. A peak was observed in MB at 6 hours in cases of anterior myocardial infarction and the sum of the ST segment decreased less than 50% in the first 2 hours. No statistically significant correlation was observed between the enzymatic peaks, the reperfusion arrythmias, Killip class, postinfarction angina or early mortality. The greater the ST segment sum, the greater the severity according to the Killip class. On multivariate analysis no model was found to be related to postinfarction angina. However, age was related to mortality and sex and age were associated with heart failure. CONCLUSIONS: In our population, the variables studied were not found to be useful to determine the prognosis during the early phase of acute myocardial infarction.
Abstract: We present a case of a sixty-nine-year-old male admitted to the hospital because of an acute respiratory failure that needed intubation and mechanical ventilation. Shortly after several attempts of right and left (the last one successful) subclavian vein cannulation (the last one successful) he developed a bilateral tension pneumothorax with important hemodynamic repercussion, a critical hypoxia and an ST elevation in inferior leads. Other more typical electrocardiographic changes could be observed: decrease in QRS amplitude and diminishing of precordial R voltage. After removing the air of the right pleural space, all the electrocardiographic signs disappeared returning to normal without electric or enzymatic assay of myocardial necrosis.
Abstract: The hemodynamic effects of a new drug: molsidomine (M) were evaluated in 9 patients with congestive myocardiopathy. To that end, with a 4-channel Swan-Ganz catheter and cardiac output computer, the following hemodynamic parameters were measured in the control condition (CC) and 5, 15 and 30 minutes after sublingual administration of 4 mg of M: heart rate (HR), systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP), cardiac index (CI), stroke volume index (SVI), systemic vascular resistance (SVR), pulmonary vascular resistance (PVR) and the stroke work index (SWI). Comparing the data in CC and at the end of the study, we found a decrease of 80 +/- 5 to 76 +/- 5 b/m (p less than 0.01) in HR, of 91 +/- 4 to 84 +/- 4 mmHg (p less than 0.01) in MAP and of 3087 +/- 151 to 2758 +/- 131 d/c/s-5 in SVR (p less than 0.02); a drop in PWP of 27 +/- 3 to 20 +/- 3 mmHg (p less than 0.001) and in PVR of 1367 +/- 293 to 1115 +/- 256 d/c/s-5 (p less than 0.001); an increase in SVI of 31 +/- 3 to 34 +/- 2 ml/b/m2 (p less than 0.05) and non-significant changes in CI of 2380 +/- 96 to 2459 +/- 82 ml/m2 (p less than 0.03) and in the SWI of 34 +/- 4 to 37 +/- 4 gm/m2 (p less than 0.1). We conclude that in patients with severe heart failure, the fundamental effects of M appears to be vasodilation in both pulmonary and systemic circulations demonstrated by a fall in PWP, PVR, MAP and SVR together with a mild increase in SVI without significant changes in CI and SWI.
