Background-The purpose of this study was to determine whether implementation of recent guidelines improves in-hospital mortality from acute ST-elevation myocardial infarction (STEMI) in a metropolitan area. Methods and Results-We organized a network that consisted of the Viennese Ambulance Systems, which is responsible for diagnosis and triage of patients with acute STEMI, and 5 high-volume interventional cardiology departments to expand the performance of primary percutaneous catheter intervention (PPCI) and to use the fastest available reperfusion strategy in STEMI of short duration (2 to 3 hours from onset of symptoms), either PPCI or thrombolytic therapy (TT; prehospital or in-hospital), respectively. Implementation of guidelines resulted in increased numbers of patients receiving 1 of the 2 reperfusion strategies (from 66% to 86.6%). Accordingly, the proportion of patients not receiving reperfusion therapy dropped from 34% to 13.4%, respectively. PPCI usage increased from 16% to almost 60%, whereas the use of TT decreased from 50.5% to 26.7% in the participating centers. As a consequence, in-hospital mortality decreased from 16% before establishment of the network to 9.5%, including patients not receiving reperfusion therapy. Whereas PPCI and TT demonstrated comparable in-hospital mortality rates when initiated within 2 to 3 hours from onset of symptoms, PPCI was more effective in acute STEMI of Ͼ3 but Ͻ12 hours' duration. Conclusions-Implementation of recent guidelines for the treatment of acute STEMI by the organization of a cooperating network within a large metropolitan area was associated with a significant improvement in clinical outcomes.
We measured fibrinogen levels as well as the fibrinolytic parameters tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) in plasma samples obtained at basal conditions and after stimulating the fibrinolytic system by venous occlusion (VO). Samples were taken from patients with primary pulmonary hypertension (PPH), with secondary thromboembolic pulmonary hypertension (SPHTH), with secondary pulmonary hypertension due to congenital heart disease with Eisenmenger's reaction (SPHCD), and from healthy control individuals (CON). Fibrinogen levels were not significantly different between the groups with PPH and SPHTH or between SPHCD and CON. The latter groups, however, exhibited significantly lower fibrinogen plasma levels compared with PPH or SPHTH (p < 0.01). Basal plasma levels of t-PA antigen, t-PA activity, and PAI-1 activity, respectively, did not differ significantly between the study groups. After VO, mean t-PA activity levels increased to a higher extent in control subjects compared with patients with PPH, or SPHTH, or SPHCD, with significant differences only between CON and SPHTH or CON and PPH (p < 0.03). Patients with PPH and SPHTH exhibit both increased fibrinogen plasma levels and a diminished fibrinolytic response compared with healthy subjects. Moreover, the fibrinogen plasma levels in patients with SPHCD are in normal range, and the fibrinolytic response is similar to CON compared with PPH and SPHTH, thus indicating the existence of a comparable prothrombotic situation in patients with PPH and SPHTH.
Of 2608 consecutive patients with acute myocardial infarction, 24 developed subacute free wall rupture (= 0.92%; 95% C.I. = 0.6-1.4). Clinical manifestations varied widely (shock on admission; 25% of cases; severe arrhythmias followed by shock: 17%; shock during hospital stay: 42%; symptoms suggestive of infarct extension without shock: 17%). The electrocardiograms were confusing rather than revealing: 56% of patients showed new ST segment elevations of 0.2 to 1 mV in the infarct-related leads, while autopsy or creatinine phosphokinase evidence of infarct extension was missing. In the first 21 cases, therefore, no definitive diagnosis was made before autopsy. Using 197 infarct patients in cardiogenic shock or with infarct extension during the acute stage, i.e. a patient group with comparable clinical manifestations, as control group, a logistic regression model was generated in which the variables age, lateral wall involvement and history of hypertension were used for estimating the probability of subacute rupture. In fact, probability may rise to more than 40% in major subgroups. As death occurred after a median interval of 8 h (45 min-6.5 weeks) following the onset of rupture symptoms, echocardiography must be performed urgently in all cases presenting symptoms of shock or infarct extension. Pretest probability which can be roughly estimated from our model as well as sensitivity and specificity of individual echocardiographic or clinical parameters are indispensable for correct therapeutic decisions. The routine application of this algorithm in our department contributed to a timely diagnosis in the last three consecutive cases of whom one patient survived.
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