Miyuki Annoura

Cholesterol paradox in patients with paroxysmal atrial fibrillation.

Hypercholesterolemia is a major risk factor for coronary heart disease (CHD), but the associations among lipids, lipoproteins and paroxysmal atrial fibrillation (PAF) have not yet been reported. The associations among lipids, lipoproteins and PAF were examined in a case-control study, in which cases and controls were defined as those with/without definite ECG-detectable PAF, respectively. CHD patients were excluded from the study. The mean values of serum total cholesterol (TC), triglyceride (TG) and high density lipoprotein-cholesterol (HDL-C), after adjusting for age and gender, in patients with PAF were lower than those in patients without PAF (175 ± 4 mg/dl vs. 190 ± 3 mg/dl, 104 ± 7 mg/dl vs. 123 ± 6 mg/dl, 46.0 ± 1.7 mg/dl vs. 51.8 ± 1.4 mg/dl, respectively), as assessed by an analysis of covariance. After controlling for age and gender, TC, TG and HDL-C (all in quartiles) were inversely and linearly (p < 0.05) associated with the percentage of patients with PAF, as assessed by a multiple logistic regression analysis. The associations between TC or TG and PAF varied with the HDL-C level: significant when HDL-C was low (p < 0.05), but not when HDL-C was high. The odds ratio (relative risk of PAF) for patients with both low TC or TG and low HDL-C was 4.08 (95% CI: 1.81–9.57) times or 9.40 (3.25–32.0) times higher (p < 0.01) than that for patients with high TC or TG and high HDL-C, respectively. In conclusion, low serum levels of TC and TG were found in PAF patients, while reduced HDL-C may cause PAF. Hypolipoproteinemia including low HDL-C may affect atrial vulnerability and cause atrial fibrillation.

Effects of an Angiotensin II Antagonist on Reperfusion Arrhythmias in Dogs

Losartan, an angiotensin II receptor antagonist with no bradykinin potentiating property, provides the opportunity to study the consequences of blocking angiotensin II. The objective of this study was to evaluate the antiarrhythmic responses of reperfusion arrhythmia to hsartan in dogs. The effects of losartan on ventricular tachyarrhythmias induced during occlusion and reperfusion of the left anterior descending coronary artery were investigated in 30 dogs. The animals were randomized to receive either losartan (n = 15) or saline (n = 15). The VF inducing threshold was measured before occlusion and after reperfusion. Losartan (50 μg/kg per min) or saline was intravenously administered 5 minutes before occlusion and continued throughout the entire study period. The incidence of ventricular tachyarrhythmias during reperfusion was lower in the losartan group than in the control group (4/15 vs 6/15). There was no significant change in VF inducing threshold between the period before occlusion and during reperfusion in the losartan group (10.9 ± 5.7 vs 11.1 ± 5.7mA, P = NS), whereas there was a significant decrease in the control group (15.5 ± 4.4 vs 7.7 ± 3.9 mA, P < 0.01). Blockade of the angiotensin II receptor has beneficial effects on reperfusion arrhythmias.

Wavelength index: a predictor of the response to disopyramide in paroxysmal lone atrial fibrillation.

We investigated whether the new parameter wavelength index could predict the response to chronic disopyramide therapy in patients with paroxysmal atrial fibrillation (AF). Twenty-seven patients with AF underwent electrophysiologic studies and the wavelength index was determined before and after intravenous administration of disopyramide. Then all patients were treated with oral disopyramide for 6 months. In 17 patients, AF was eliminated (group A), while it persisted in another 10 patients (group B). The ratio of the wavelength index before and after intravenous disopyramide was higher in group A than in group B. Thus, the wavelength index proved useful for predicting the response of AF to disopyramide.

Mechanism of Antiarrhythmic Effects of Class Ic Drugs in Paroxysmal Atrial Fibrillation in Man

While class Ic antiarrhythmic drugs are effective in treating patients with atrial fibrillation, their mechanism of action is poorly understood. We performed electrophysiological studies before and after their administration to 22 patients with paroxysmal atrial fibrillation. Atrial refractoriness, maximal interatrial conduction delay and the wavelength index were measured at two basic cycle lengths (600 or 400 ms). Both drugs studied increased atrial refractoriness and wavelength index. Flecainide reduced the maximal interatrial conduction delay, but pilsicainide did not. Each drug increased the wavelength index in a tachycardia-dependent manner. Class Ic drugs may reduce atrial vulnerability by increasing the wavelength of the reentrant circuit during periods of rapid heart rate.

Electrophysiological Properties in Paroxysmal Atrial Fibrillation Complicated with the Wolff-Parkinson-White Syndrome: Comparison with Paroxysmal Atrial Fibrillation Alone

Electrophysiological studies were performed in 26 patients with atrial fibrillation (AF). Thirteen patients had the Wolff-Parkinson-White (WPW) syndrome (group A), and another 13 patients did not have the WPW syndrome (group B). The right atrium effective refractory period was significantly shorter in group A than in group B. The wavelength index which was defined as the ratio of the refractory period to the conduction delay was significantly lower in group A than in group B. Accordingly, patients in group A had a greater tendency to produce atrial reentry than those in group B.

Use of monophasic action potentials to evaluate postpacing T wave changes.

We examined the relationship between postpacing T wave changes and monophasic action potentials recorded from the ventricle in dogs. MAPs were recorded from the right and left ventricle before and after cessation of pacing. The duration of the MAP was calculated as the time in milliseconds from the upstroke to 90% repolarization (MAPD90). T waves in limb leads were flat or had a biphasic pattern, eventually becoming negative after pacing. The Q-T interval of the escape beat after pacing was prolonged compared with the control. After right ventricular pacing, the average duration of MAPD90 in the right ventricle, but not in the left ventricle, was prolonged. (right MAPD: control 275 +/- 10 ms; after pacing: 311 +/- 17 ms, p < 0.05; left MAPD: control: 266 +/- 23 ms, after pacing: 284 +/- 26 ms, NS). After left ventricular pacing, the average duration of MAPD90 in the left ventricle, but not in the right ventricle, was prolonged (right MAPD: control: 247 +/- 75 ms, after pacing: 287 +/- 39 ms, NS; left MAPD: control: 257 +/- 23 ms, after pacing: 303 +/- 25 ms, p < 0.05). Furthermore, the average duration of MAPD90 at the pacing site became progressively prolonged over time. These results suggest that myocardial cells retain the memory of abnormal repolarization associated with pacing.