Among patients with unstable angina or myocardial infarction without ST-segment elevation, prasugrel did not significantly reduce the frequency of the primary end point, as compared with clopidogrel, and similar risks of bleeding were observed. (Funded by Eli Lilly and Daiichi Sankyo; TRILOGY ACS ClinicalTrials.gov number, NCT00699998.).
1. The effect of intravenous boluses of verapamil (0.15 mg/kg), flecainide (2 mg/kg), amiodarone (5 mg/kg), and sotalol (1.5 mg/kg) on mean arterial pressure, heart rate (HR), cardiac output (CO), total peripheral resistance (TPR), and peak rate of change of left ventricular pressure (LV dP/dt) were assessed in the conscious rabbit. 2. All four drugs had negative inotropic effects: verapamil reduced peak LV dP/dt by 19 +/- 4% (mean +/- s.e.m.; P < 0.01), flecainide by 27 +/- 9% (P < 0.001), amiodarone by 11 +/- 2% (P < 0.01) and sotalol by 13 +/- 3% (P < 0.01). 3. The drugs had different effects on CO as a result of differences in their actions on peripheral blood vessels: verapamil and amiodarone produced, respectively, a 12 +/- 4% (P < 0.03) and 16 +/- 6% (P < 0.01) increase in CO associated with a substantial vasodilatory effect (TPR reduced 15 +/- 7% [P < 0.05] and 20 +/- 5% [P < 0.01], respectively). Flecainide caused only a small (6 +/- 1%; P < 0.01) increase in CO and sotalol had no effect on either CO or TPR. 4. Bolus intravenous injections of verapamil, flecainide and amiodarone produced an increase in HR, while sotalol reduced HR by 10 +/- 2% (P < 0.01). The increase in HR and cardiac output seen with verapamil, flecainide and amiodarone was in part secondary to reflex increase in sympathetic tone and these changes were abolished after total cardiac autonomic blockade. 5. The modest reduction in cardiac performance associated with sotalol was abolished by cardiac autonomic blockade, suggesting that the predominant effect of sotalol on contractility was mediated through its beta-adrenoceptor blocking effect.
The utility of transesophageal electrocardiography using a bipolar 'pill electrode' was assessed in 17 consecutive patients with tachycardia presenting to our casualty department. Standard 12-lead electrocardiography showed regular narrow QRS tachycardia in 12 patients, and five patients had wide QRS tachycardia. Esophageal atrial electrogram recordings were obtained in 14 patients (82%), and these were helpful in determining the mechanism of tachycardia in 11 patients (78%). Of these 11, seven patients fulfilled criteria for atrioventricular junctional (AVJ) tachycardia based on measurement of the minimum interval between the onset of ventricular depolarisation and earliest atrial (esophageal) activity. One of these patients had presented with a wide QRS tachycardia. The other four patients were diagnosed as having ventricular tachycardia (VT) following diagnosis of AV dissociation. Atrial overdrive pacing, via the pill electrode, successfully reverted four of the nine patients (44%) with narrow QRS tachycardia but no patient with VT. Esophageal recording during tachycardia is a simple, relatively non-invasive technique which is helpful in suggesting the mechanism of tachycardia both in patients with narrow and wide QRS tachycardia, and may have a therapeutic role in patients with AVJ tachycardia.
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