Fate of patients with prehospital resuscitation for ST-elevation myocardial infarction and a high rate of early reperfusion therapy (results from the PREMIR [Prehospital Myocardial Infarction Registry]).

Patients with acute ST-segment elevation myocardial infarction (STEMI) needing prehospital cardiopulmonary resuscitation (CPR) have a very high adverse-event rate. However, little is known about the fate of these patients and predictors of mortality in the era of early reperfusion therapy. From March 2003 through December 2004, 2,317 patients with prehospital diagnosed STEMI were enrolled in the Prehospital Myocardial Infarction Registry. One hundred ninety patients (8.2%) underwent prehospital CPR and were included in our analysis. Overall 90% of patients were treated with early reperfusion therapy, 56.3% received prehospital thrombolysis and 1/2 of these patients received early percutaneous coronary intervention after thrombolysis, 28.4% of patients were treated with primary percutaneous coronary intervention, and 5.3% received in-hospital thrombolysis. Total mortality was 40.0%. The highest mortality was seen in patients with asystole (63%) or pulseless electric activity (64%). Independent predictors of mortality were need for endotracheal intubation and older age, whereas ventricular fibrillation as initial heart rhythm was associated with survival. In conclusion, in this large registry with prehospital diagnosed STEMI, incidence of prehospital CPR was about 8%. Even with a very high rate of early reperfusion therapy, in-hospital mortality was high. Especially in elderly patients with asystole as initial heart rhythm and with need for endotracheal intubation, prognosis is poor despite aggressive reperfusion therapy.

Reperfusion rate and inhospital mortality of patients with ST segment elevation myocardial infarction diagnosed already in the prehospital phase: results of the German Prehospital Myocardial Infarction Registry (PREMIR).

AIMS: We sought to evaluate the in-hospital fate of patients with ST segment elevation myocardial infarction (STEMI) diagnosed already in the prehospital phase by physican equipped ambulances. METHODS: A total of 2326 consecutive STEMI patients were included in PREMIR. For this analysis 218 patients with prehospital cardiopulmonary resuscitation were excluded. RESULTS: The median time between symptom onset and 12-lead ECG was 85 min. The median time intervals between the diagnostic 12-lead ECG and prehospital fibrinolysis were 10 min, until inhospital fibrinolysis 52 min and until primar PCI 86min, respectively. Reperfusion therapy with prehospital fibrinolysis (24%), inhospital fibrinolysis (13%) or primary PCI (45%) was performed in 82% of the patients. Inhospital mortality was 6.0% in patients with prehospital fibrinolysis (n = 504), 5.8% in patients with inhospital fibrinolysis (n = 278), 4.5% in patients with primary percutaneous coronary intervention (n = 962) and 16.2% in patients without early reperfusion therapy (n = 377), respectively. In the multivariate propensity score analysis comparing prehospital fibrinolysis and primary PCI we observed no significant difference in the odds for in-hospital mortality (odds ratio: 1.57, 95% CI: 0.94-2.63). The final discharge diagnosis was STEMI in 90% of the patients, in patients with prehospital fibrinolysis 95%. CONCLUSIONS: In patients with STEMI already diagnosed in the prehospital phase the ischemic time is short, accuracy of the diagnosis is high and reperfusion therapy is performed in over 82%. Inhospital mortality was not different between prehospital fibrinolysis and primary PCI.

Intestinal ischaemia during cardiac arrest and resuscitation: comparative analysis of extracellular metabolites by microdialysis.

Intestinal ischaemia is a major complication of shock syndromes causing translocation of bacteria and endotoxins and multiple organ failure in intensive care patients. The present study was designed to use microdialysis as a tool to monitor intestinal ischaemia after cardiac arrest and resuscitation in pigs. For this purpose, microdialysis probes were implanted in pig jejunal wall, peritoneum, skeletal muscle and brain, and interstitial fluid was obtained during circulatory arrest (induced by ventricular fibrillation) and after return of spontaneous circulation (ROSC). Cardiac arrest for 4 min caused a prolonged (60 min) reduction of blood flow in jejunal wall, muscle and brain as determined by the ethanol technique. This was accompanied by cellular damage in heart muscle and brain as indicated by increased levels of troponin-I and protein S-100, respectively. Plasma levels of glucose, lactate and choline were increased at 15-60 min following cardiac arrest. In contrast, cardiac arrest induced a rapid but variable decrease of interstitial glucose levels in all monitored organs; this decrease was followed by an increase over baseline during reperfusion. In the intestine, lactate, glutamate and choline levels were increased during ischaemia and reperfusion for 60-120 min; intestinal and peritoneal samples yielded parallel changes of lactate levels. Brain and muscle samples showed similar changes as in intestinum and peritoneum except for glutamate, which was increased in brain but not in muscle. We conclude that intestinal ischaemia occurs as a consequence of cardiac arrest and resuscitation and can be monitored by in vivo microdialysis. Comparative analysis by multi-site microdialysis reveals that the intestine is equally or even more sensitive to ischaemia than brain or muscle.

Hypertonic-hyperoncotic solutions reduce the release of cardiac troponin I and s-100 after successful cardiopulmonary resuscitation in pigs.

UNLABELLED: In some patients, cardiopulmonary resuscitation (CPR) can revive spontaneous circulation (ROSC). However, neurological outcome often remains poor. Hypertonic-hyperoncotic solutions (HHS) have been shown to improve microvascular conductivity after regional and global ischemia. We investigated the effect of infusion of HHS in a porcine CPR model. Cardiac arrest was induced by ventricular fibrillation. Advanced cardiac life support was begun after 4 min of nonintervention and 1 min of basic life support. Upon ROSC, the animals randomly received 125 mL of either normal saline (placebo, n = 8) or 7.2% NaCl and 10% hydroxyethyl starch 200,000/0.5 (HHS, n = 7). Myocardial and cerebral damage were assessed by serum concentrations of cardiac troponin I and astroglial protein S-100, respectively, up to 240 min after ROSC. In all animals, the levels of cardiac troponin I and S-100 increased after ROSC (P < 0.01). This increase was significantly blunted in animals that received HHS instead of placebo. The use of HHS in the setting of CPR may provide a new option in reducing cell damage in postischemic myocardial and cerebral tissues. IMPLICATIONS: Infusion of hypertonic-hyperoncotic solutions (HHS) after successful cardiopulmonary resuscitation in pigs significantly reduced the release of cardiac troponin I and cerebral protein S-100, which are sensitive and specific markers of cell damage. Treatment with HHS may provide a new option to improve the outcome of cardiopulmonary resuscitation.

Improvement in stroke quality management by an educational programme.

Time after symptom onset in ischaemic stroke has to be as short as possible to increase success of treatment. We prospectively analysed latencies from symptom onset until the start of therapy and the rate of thrombolysis in 196 patients with suspected stroke sequentially admitted to the hospital before (6 weeks prior, n = 83) and after (n = 113) initiating an educational stroke programme (EP). A total of 345 dispatchers, paramedics, and emergency staff were trained, each person for at least 2 h. The mean pre-hospital time interval from symptom onset until admission was significantly decreased by nearly 2 h (p < 0.05). Thrombolytic therapy frequencies increased from 2 to 10.5% (p < 0.01) because the overall mean time interval from admission to the start of therapy significantly decreased (p < 0.01) by 69 min after the EP, with increasing numbers of patients suitable for acute stroke therapies within a 0- to 3-hour treatment window.