QT interval dispersion in ventricular beats: a noninvasive marker of susceptibility to sustained ventricular arrhythmias.

Increased QT dispersion (QTd) calculated from sinus beats has been shown to identify patients prone to sustained VT. However, predictive accuracy of this parameter is limited. Electrophysiological properties of the myocardium may be altered by a premature ventricular beats, which is a well-established trigger for sustained VT. Therefore, the author hypothesised that QTd in spontaneous or paced ventricular beats may improve identification of patients with inducible sustained VT. In 28 consecutive patients (men, mean age 61 +/- 13 years) who underwent programmed ventricular stimulation, the values of QTd calculated in sinus and ventricular beats were compared between inducible and noninducible patients. The mean QTd values obtained using three different methods differed significantly, QTd in paced ventricular beats being the highest, QTd in spontaneous ventricular beats was intermediate, and QTd in sinus beats was the lowest (83.9 +/- 30 vs 63.0 +/- 29 ms vs 53.9 +/- 27 ms, P < 0.0001 and P < 0.004, respectively). In 13 (46%) patients sustained VT was induced. QTd values were significantly higher in inducible than noninducible patients (QTd sinus beats: 67.5 +/- 31 vs 42.1 +/- 11 ms, P = 0.02; QTd spontaneous ventricular beats: 79.3 +/- 35 vs 46.7 +/- 13 ms, P = 0.008, and QTd-paced ventricular beats: 104.8 +/- 32 vs 65.9 +/- 9 ms, P = 0.0009). The receiver operator characteristic curves showed that at a sensitivity level of 100%, the highest specificity for identification of inducible patients had QTd measured in paced ventricular beats (87%) followed by QTd in spontaneous ventricular beats (45%), and QTd in sinus beats (40%). In conclusion, (1) QTd in ventricular beats is greater than in sinus beats, and (2) QTd calculated from paced ventricular beats identifies patients with inducible sustained VT better than QTd measured during sinus rhythm.

Susceptibility to neuromediated syncope after acute myocardial infarction.

BACKGROUND: Syncope after acute myocardial infarction (AMI) is a common clinical problem. It may be hypothesised that remodelling and neurohormonal changes following AMI may predispose to neuromediated syncope. DESIGN: To address this issue we prospectively evaluated the incidence of positive results of head-up tilt-table testing in 40 patients following AMI and 40 age and sex matched controls without a history of syncope. The mechanisms of tilt-induced changes in autonomic tone were assessed using spectral analysis of heart rate variability. The patients were followed-up for one year. RESULTS: Positive results of tilt-test occurred in 4 (10%) controls and 13 (33%) AMI patients (P = 0.01). No significant differences in sympathovagal interaction (assessed by a low frequency/high frequency ratio) were detected between the groups before tilting (2. 9 +/- 1.9 vs. 3.1 +/- 2.2; NS). However, dynamic changes of this parameter differed significantly during the first 5 symptomless minutes of the active phase of tilt-test. The ratio increased in the majority of controls (87%) and decreased in the majority of patients (62%) (P < 0.0001). During one year follow-up, syncope or presyncope occurred in 10 (25%) AMI patients but did not occur in any control subject (P < 0.001). The sensitivity, specificity and predictive accuracy of an early tilt-test after AMI for the prediction of syncope or presyncope was 70%, 80% and 78%, respectively. CONCLUSION: Patients after AMI are prone to neuromediated reactions. Sympathetic withdrawal seems to be the most likely mechanism of syncope. The role of tilt testing for identification of patients susceptible to syncope or presyncope after AMI needs further investigation.

Low-dose glucose-insulin-potassium is ineffective in acute myocardial infarction: results of a randomized multicenter Pol-GIK trial.

We aimed to assess the clinical efficacy of glucose-insulin-potassium (GIK) in acute myocardial infarction. Experimental data provided evidence of the beneficial effects of GIK on ischemic myocardium. The clinical trials, mostly uncontrolled and conducted mainly before the thrombolytic era, were inconclusive due to the small number of patients and discrepancies in protocols. In order to evaluate the efficacy of this intervention, we have performed a prospective multicenter randomized study. The study consisted of 954 patients with acute myocardial infarction (MI) randomized within 24 hours from the onset of symptoms to low-dose GIK (n = 494), which consisted of 1000 mL 10% dextrose, 32-20 U insulin, and 80 mEq K-, or to the control group (n = 460), which was given 1000 mL 0.89% sodium chloride, by intravenous 24-hour infusion at a rate of 42 mL/h. Cardiac mortality and the occurrence of cardiac events at 35 days did not differ between GIK and control-allocated patients (32 (6.5%) vs. 21 (4.6%), respectively; OR 1.45, 95% CI 0.79-2.68, P = 0.20; and 214 (43.3%) vs. 192 (41.7%), OR 1.07, 95% CI 0.82-1.38, P = 0.62). Total mortality at 35 days was significantly higher in the GIK than in the control group (44 (8.9%) vs. 22 (4.8%), respectively, OR 1.95, 95% CI 1.12-3.47, P = 0.01). The excess of non-cardiac deaths in the GIK group may have occurred by chance. Low-dose GIK treatment does not improve the survival and clinical course in acute MI.

Intravenous amiodarone is safe and seems to be effective in termination of paroxysmal supraventricular tachyarrhythmias.

BACKGROUND: Paroxysmal atrial fibrillation (PAF) and paroxysmal supraventricular tachycardia (PSVT) leading to hemodynamic compromise are among the most common reasons for admission to the coronary care unit (CCU) and need prompt and efficient therapy. Direct current cardioversion is the therapy of choice, but if found contraindicated or unavailable some antiarrhythmic agents are usually given to restore sinus rhythm. Many of these drugs have obvious limitations, especially in patients with acute myocardial infarction and/or heart failure. HYPOTHESIS: The aim of the present study was to assess the safety and efficacy of intravenous amiodarone in the acute termination of PAF or PSVT refractory to other antiarrhythmic agents in a large group of patients consecutively admitted to our CCU. METHODS: In the present study, we evaluated the safety and efficacy of amiodarone given intravenously in 142 consecutive patients with PAF or PSVT lasting < 24 h. In 37% of patients no evidence of underlying heart disease which may have caused arrhythmias were defined. A median of two other antiarrhythmic agents given prior to the first amiodarone injection had been ineffective. RESULTS: Sinus rhythm was restored in 91 patients (64%) (65% in the PAF group and 61% in the PSVT group). The mean time to rhythm conversion was 5.5 +/- 6.1 h for patients with PAF and 1.2 +/- 1.2 h for patients with PSVT. The mean dose of amiodarone administered up to conversion was 340 +/- 220 mg for PAF and 220 +/- 105 mg for PSVT. Except for transient first-degree atrioventricular block in two patients, no adverse effects possibly related to amiodarone were observed (including proarrhythmia and incidence or aggravation of heart failure symptoms). CONCLUSION: Amiodarone given intravenously for acute termination of supraventricular tachyarrhythmias is completely safe and seems effective. The results of this study, which is the largest ever made, indicate a need of randomized, controlled trials for the ultimate assessment of the efficacy of amiodarone in this clinical setting.

The incidence of asymptomatic paroxysmal atrial fibrillation in patients treated with propranolol or propafenone.

Anti-arrhythmic therapy for paroxysmal atrial fibrillation leads to complete symptomatic relief in a number of patients. The elimination of symptoms may be associated either with a complete elimination of arrhythmia or with a conversion of symptomatic atrial fibrillation into asymptomatic episodes of arrhythmia. The aim of the study was to evaluate the occurrence of asymptomatic paroxysmal atrial fibrillation in 52 patients treated with propafenone (35 drug trials) or propranolol (34 drug trials) by means of ambulatory ECG Holter monitoring. Propafenone was clinically effective (complete relief of symptoms) in 26 (74%) patients. However, in 7 cases (27%) asymptomatic episodes of arrhythmia were still recorded when awake. In patients treated with propranolol clinical symptoms were absent in 18 (53%). However, in 4 (22%) patients attacks of paroxysmal atrial fibrillation were present. The mechanism of drug-induced conversion of symptomatic episodes of atrial fibrillation into asymptomatic spells of arrhythmia was a marked shortening in duration of episodes in 7 patients (from 2215 +/- 3843 s to 16 +/- 10 s, N.S.) or by a significant slowing of ventricular response during atrial fibrillation in 4 patients (from 125 +/- 27 to 84 +/- 8 beats/min, P = 0.05). In conclusion, in a significant proportion of patients with symptomatic paroxysmal atrial fibrillation asymptomatic episodes of arrhythmia may occur while on anti-arrhythmic drug therapy. Some of these patients, particularly those with other risk factors for stroke such as advanced age or the presence of organic heart disease, may require anti-coagulant therapy or change in anti-arrhythmic treatment, and can be selected on the basis of ambulatory ECG monitoring.