Cardiology
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Comparative Study
Risk stratification of in-hospital mortality in patients hospitalized for chronic congestive heart failure secondary to non-ischemic cardiomyopathy.
The study population consisted of 234 consecutive patients hospitalized for acute exacerbation of congestive heart failure secondary to non-ischemic cardiomyopathy. Of the 234 patients, there were 55 in-hospital deaths. Their medical records were deliberatively reviewed and the association of 38 clinical, hemodynamic and biochemical variables with in-hospital mortality was evaluated by multiple stepwise logistic regression analysis. ⋯ In stratified analyses, the rates of in-hospital mortality rose rapidly as the number of risk factors increased: 0 risk factors, 2.5%; 1 risk factor, 5.1%; 2 risk factors, 36.4%; 3 risk factors, 75%, and no less than 4 risk factors, 100%. In conclusion, our study identified 6 variables that correlated with in-hospital death in patients with heart failure secondary to non-ischemic cardiomyopathy. The identification of these variables may allow more accurate risk stratification of individuals at risk of in-hospital mortality in this clinical setting.
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Sudden cardiac arrest survivors have a high risk of suffering from recurrent arrhythmic events. Recent studies have shown that these patients have a significantly decreased mortality rate, if they are supplied with an implantable cardioverter/defibrillator (ICD). The aim of this study was to evaluate the long-term prognosis of patients with electrophysiologically guided antiarrhythmic drug therapy in comparison to patients with ICD. 204 consecutive survivors of sudden cardiac arrest were enrolled in this study. ⋯ A reduction of the mortality risk was observed in the ICD group by up to 61% (all-cause mortality), 52% (cardiac mortality) and 97.2% (arrhythmogenic mortality). In arrhythmic event survivors with ICD, arrhythmic and overall mortality rates are significantly lower compared to patients with an EPS-guided drug therapy. In the secondary prevention of sudden cardiac death, ICD should be the first choice of antiarrhythmic therapy.
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Octogenarians are the fastest growing segment of the population and little is known about the results of cardiopulmonary resuscitation (CPR) after in-hospital cardiac arrest in this population. ⋯ In comparison with other life-saving strategies, CPR in octogenarians is effective. The favorable cost-effectiveness ratio is highly dependent on the patients' preference for quality rather than quantity of life, as expressed by the utility assumptions.
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To assess the short-term reliability of temporary epicardial pacing wires in patients after open heart surgery and to determine the influence of preoperative factors on the performance of these wires. ⋯ Although both atrial and ventricular temporary epicardial leads are reliable for short-term use, their function deteriorates on a daily basis. Perioperative factors are generally not helpful in predicting the performance of temporary epicardial pacing wires.
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Cellular mechanisms of adenosine include a direct effect on the activation of the adenosine-sensitive potassium current (I(K,Ado)) and an indirect effect on antagonism of catecholamine-stimulated adenylate cyclase activity. However, previous studies evaluating the influence of catecholamine activity on the electrophysiologic effects of adenosine have yielded conflicting results. We tested the hypotheses that if adenosine exerts its atrioventricular (AV) nodal blocking effects directly by activating the I(K,Ado) potassium current, rather than indirectly by reversing the catecholamine effects, then pretreatment with beta-adrenergic blockade would not potentiate the effects of adenosine in terminating AV nodal-dependent supraventricular tachycardia (SVT). ⋯ Intravenous esmolol infusion (up to 100 mg total dose) usually fails to terminate AV nodal-dependent SVT. In the esmolol-resistant tachycardia, esmolol pretreatment does not produce a positive synergistic effect on the efficacy of adenosine-induced termination of SVT. Therefore, in this tachycardia adenosine may exert its effects on AV nodal conduction directly by activation of the I(K,Ado) potassium current, rather than by antagonizing the beta-adrenergic system.