Impact of physical deconditioning on ventricular tachyarrhythmias in trained athletes.

OBJECTIVES: The purpose of this research was to evaluate the impact of athletic training and, in particular, physical deconditioning, on frequent and/or complex ventricular tachyarrhythmias assessed by 24-h ambulatory (Holter) electrocardiogram (ECG). BACKGROUND: Sudden deaths in athletes are usually mediated by ventricular tachyarrhythmias. METHODS: Twenty-four hour ambulatory ECGs were recorded at peak training and after a deconditioning period of 19 +/- 6 weeks (range, 12 to 24 weeks) in a population of 70 trained athletes selected on the basis of frequent and/or complex ventricular tachyarrhythmias (i.e., > or =2,000 premature ventricular depolarization [PVD] and/or > or =1 burst of non-sustained ventricular tachycardia [NSVT]/24 h). RESULTS: A significant decrease in the frequency and complexity of ventricular arrhythmias was evident after deconditioning: PVDs/24 h: 10,611 +/- 10,078 to 2,165 +/- 4,877 (80% reduction; p < 0.001) and NSVT/24 h: 6 +/- 22 to 0.5 +/- 2, (90% reduction; p = 0.04). In 50 of the 70 athletes (71%), ventricular arrhythmias decreased substantially after detraining (to <500 PVDs/24 h and no NSVT). Most of these athletes with reduced arrhythmias did not have structural cardiovascular abnormalities (37 of 50; 74%). Over the 8 +/- 4-year follow-up period, each of the 70 athletes survived without cardiac symptoms. CONCLUSIONS: Frequent and/or complex ventricular tachyarrhythmias in trained athletes (with and without cardiovascular abnormalities) are sensitive to brief periods of deconditioning. In athletes with heart disease, the resolution of such arrhythmias with detraining may represent a mechanism by which risk for sudden death is reduced. Conversely, in athletes without cardiovascular abnormalities, reduction in frequency of ventricular tachyarrhythmias and the absence of cardiac events in the follow-up support the benign clinical nature of these rhythm disturbances as another expression of athlete's heart.     

T-wave alternans phase following ventricular extrasystoles predicts arrhythmia-free survival

OBJECTIVE: The purpose of this study was to assess the value of T-wave alternans (TWA) following ventricular extrasystoles in predicting arrhythmia-free survival. BACKGROUND: Stratifying risk for sudden death in patients with coronary disease and moderate left ventricular (LV) dysfunction remains a challenge. We hypothesized that, in such patients, a discontinuity in beat-to-beat T-wave alternation (TWA phase reversal) following single ventricular extrasystoles reflects transiently exaggerated repolarization dispersion, and predicts spontaneous ventricular arrhythmias. METHODS: We studied 59 patients with ischemic LV dysfunction (mean LV ejection fraction 38.7 +/- 5.3%) and nonsustained ventricular tachycardia undergoing programmed stimulation. TWA was computed spectrally from the ECG during ventricular pacing, and TWA phase reversal was reflected by a discontinuity in T-wave oscillation after single ventricular extrasystoles. RESULTS: Patients induced into ventricular arrhythmias (n = 36) had greater TWA magnitude (V(alt): 6.60 +/- 6.46 microV vs 2.61 +/- 1.97 microV; P = .001) and more frequent TWA phase reversal (62.1% vs 44.4%; P = .02) than those who were not (n = 23). During a mean follow-up of 36 +/- 12 months, positive TWA (V(alt) > or =1.9 microV) and TWA phase reversal both (P < .05) predicted events (all-cause mortality, ventricular tachycardia, ventricular fibrillation). Univariate predictors of arrhythmia-free survival were TWA phase reversal (P < .005), positive TWA (P < .05), age (P = .008), and LV mass index (P = .043). On multivariate analysis, only TWA phase reversal and age predicted events; if TWA phase was excluded, only positive TWA and age predicted events. CONCLUSION: Phase reversal in TWA following ventricular extrasystoles predicts spontaneous ventricular arrhythmias and all-cause mortality in patients with moderate ischemic LV dysfunction and was a better predictor than positive TWA or programmed ventricular stimulation.     

Phasic aortocoronary bypass graft blood velocity during ventricular arrhythmias in man.

With use of the Doppler ultrasonic flowmeter catheter, phasic aortocoronary bypass graft blood velocity was measured in 16 conscious subjects during ventricular arrhythmias. Ventricular extrasystoles reduced peak systolic and diastolic graft blood velocities by 20 to 80 percent, generally in relation to their respective coupling intervals. When extrasystoles appeared in closely coupled salvos diastolic bypass blood velocity virtually ceased. Nineteen episodes of ventricular tachycardia produced an average 50 percent decrease in peak graft blood velocity (control mean +/- 1 standard deviation blood velocity 28 +/- 11 cm/sec; value during ventricular tachycardia 14 +/- 8 cm/sec, P less than 0.001). An "overshoot" of peak blood velocity was observed after ventricular extrasystoles and tachycardia. All such changes in aortocoronary bypass blood velocity related to tachyarrhythmia were more prominent during the systolic fraction of flow. It is concluded that (1) ventricular arrhythmias adversely influence aortocoronary bypass graft function, and (2) this finding supports an aggressive approach to the treatment of these arrhythmias in subjects with bypass grafts.     

Effect of oxprenolol on ventricular arrhythmias: the European Infarction Study experience

In 736 patients, 24 hour electrocardiographic recordings were performed 14 to 36 days after acute myocardial infarction before the start of randomized treatment with 320 mg of slow release oxprenolol (n = 358) or placebo (n = 378). Follow-up 24 hour electrocardiographic recordings were obtained 5 to 12 days (median 10) and 3, 6 and 12 months after the first administration of the study medication. Oxprenolol-treated patients had a significantly lower daytime heart rate as compared with the placebo group, whereas no difference was found at night. At baseline, 22.1% of the patients allocated to oxprenolol treatment and 29.6% of the placebo group had more than 30 ventricular extrasystoles in 1 hour at least once during 24 hour monitoring; multiform ventricular extrasystoles were present in 58.4 and 62.7%, ventricular couplets in 29.6 and 33.9% and ventricular tachycardia (3 or more consecutive ventricular extrasystoles) in 21.5 and 20.9% of the oxprenolol-treated and placebo-treated patients, respectively. During the 1 year follow-up period, the prevalence of these arrhythmias did not change significantly in either treatment group. There was a trend toward a reduction in the daytime frequency of ventricular couplets in the oxprenolol group. After 3 and 6 months, only multiform ventricular extrasystoles were significantly less frequent in the oxprenolol group than in the placebo group (47.4 and 42.7% versus 59.7 and 57.9%, respectively). Twelve months after the acute event, however, multiform ventricular extrasystole frequency was the same in both groups of patients (52.1 versus 51.0%, respectively). Thus, oxprenolol had a weak suppressant effect on ventricular tachyarrhythmias in survivors of myocardial infarction.     

Effects of acute and prolonged administration of propafenone on internal defibrillation in the pig.

Some antiarrhythmic sodium channel blocking drugs have been found to increase the energy necessary for internal defibrillation. Propafenone is a new drug that has been shown to be efficacious in the therapy of supraventricular and ventricular arrhythmias, and is of potential use in patients with defibrillators. The effects of short-term and prolonged propafenone administration on the internal defibrillation threshold (DFT) were determined in 43 pigs randomized to one of four groups: saline infusion (n = 10); propafenone infusion (n = 10); placebo administration for 8 days (n = 10); or propafenone administration for 8 days (n = 13). Two mesh electrodes were sutured on the right lateral and left lateral epicardial surface and current was delivered from the right electrode to the left electrode. Triplicate DFTs were obtained before and at 40 and 80 minutes after infusion of drug or placebo. In pigs receiving long-term administration, after baseline DFTs were obtained the electrodes were removed and the chest was closed. Following 8 days of drug or placebo administration, DFTs were redetermined. No changes were observed in the short- or long-term control groups. DFTs were lower after propafenone administration: either short-term infusion (20 +/- 6.2 joules at baseline; 15.6 +/- 5 joules at 40 minutes, p less than 0.05; 10.2 +/- 6 joules at 80 minutes, p less than 0.001) or long-term administration (17.8 +/- 2.6 joules at baseline versus 12 +/- 3.2 joules on drug, p less than 0.002). Decreased ventricular cycle lengths were found with acute administration of propafenone. Three pigs died during long-term administration of propafenone.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dietary fish oil protects against stretch-induced vulnerability to atrial fibrillation in a rabbit model

INTRODUCTION: Dietary fish oil is thought to reduce sudden cardiac death by suppressing ventricular arrhythmias but little is known about its impact on atrial arrhythmias. We examined the effect of dietary fish oil on the rabbit model of stretch-induced vulnerability to atrial fibrillation (AF). METHODS AND RESULTS: Six-week-old rabbits were fed standard rabbit pellets supplemented with 5% tuna fish oil (n = 6) or supplemented with 5% sunflower oil (n = 6) for 12 weeks. Six rabbits raised on the standard diet were used as controls. In Langendorff-perfused hearts intraatrial pressures were increased in a stepwise manner and rapid burst pacing applied to induce AF at increasing intraatrial pressures until AF was sustained (>1 minute). Atrial refractory periods were recorded at each pressure. Increased atrial pressure resulted in a reduction in atrial refractory period and a propensity for induction of sustained AF. Higher pressures were needed to induce and sustain AF in the fish oil group compared with the sunflower oil and control groups. The stretch-induced drop in refractory period was also less marked in the fish oil group. Red blood cell, atrial, and ventricular omega-3 fatty acid levels were significantly higher in the fish oil group. The ratio of atrial n-6/n-3 polyunsaturated fatty acids was 13 +/- 0.9 with sunflower oil and 1.5 +/- 0.01 with fish oil (P < 0.001). CONCLUSIONS: Incorporation of dietary omega-3 fatty acids into atrial tissue reduces stretch-induced susceptibility to AF.     

Ventricular arrhythmias during ergonovine-induced episodes of variant angina

Of 95 consecutive patients with active variant angina who underwent ergonovine testing in the coronary care unit while off treatment, 24 (25%) developed serious ventricular arrhythmias: ventricular tachycardia in eight, bigeminy in seven, pairs in five, and frequent ventricular extrasystoles in four. Ergonovine-induced arrhythmias were observed more often in patients with anterior than inferior ST segment elevation (p less than 0.05). ST segment elevation was significantly higher (10.3 +/- 8.1 vs 3.1 +/- 2.1 mm) in patients who developed arrhythmias. All ventricular arrhythmias began within 3 minutes after the onset of ST segment elevation. The intravenous administration of nitroglycerin eliminated arrhythmias in 22 of 24 cases; in only two patients did ventricular arrhythmias develop after the administration of nitroglycerin. Serious ventricular arrhythmias were found during spontaneous variant angina attacks in 14 of 24 patients with ergonovine-induced arrhythmias compared to 16 of 71 patients without ergonovine-induced arrhythmias (p less than 0.001). We conclude that arrhythmias during ergonovine testing are most often caused by ischemia and not reperfusion. Patients with arrhythmias during ergonovine-induced attacks are more likely to have arrhythmias during spontaneous attacks.     

Effects of mexiletine, propafenone and flecainide on signal-averaged electrocardiogram.

The effects of mexiletine, propafenone and flecainide on the parameters of signal-averaged electrocardiogram in 40 subjects with symptomatic and repetitive ventricular arrhythmias were studied. Mexiletine (n = 16) suppressed ventricular arrhythmias in 10 patients and did not produce any significant changes in filtered QRS duration (fQRS), root mean square voltage of the final 40 ms of filtered QRS (RMS40) or low amplitude terminal component duration (LAS40). Acute (n = 8, 450 mg) and chronic (n = 16, 600-1200 mg.day-1) administration of propafenone determined a significant increase in fQRS (from 123 +/- 2.2 to 139 +/- 3 ms) and a reduction in RMS40 (from 54 +/- 8.8 to 34 +/- 6.7 microV); as a consequence the incidence of ventricular late potentials rose from 43 to 62%. The observed effects were independent of anti-arrhythmic efficacy, which was 86% for this drug. Acute (n = 8, 200 mg) and chronic (n = 13, 200-300 mg.day-1) administration of flecainide was associated with a marked prolongation in fQRS (from 123 +/- 2.8 to 138 +/- 4.1 ms) and a reduction in RMS40 (from 69 +/- 11.5 to 47 +/- 11 microV); thus determining an increase in the incidence of ventricular late potentials from 29 to 48%. Changes in signal-averaged electrocardiogram were not related to drug efficacy, which was 81%. These data indicate that 1c anti-arrhythmic drugs consistently modified the parameters of signal-averaged electrocardiogram; the observed changes might reflect an inhomogeneous slowing of intramyocardial impulse propagation.     

Effect of low oral doses of disopyramide and amiodarone on ventricular and atrial arrhythmias of chagasic patients with advanced myocardial damage

Low-dose (7 mg/kg per day) disopyramide administration to arrhythmic chagasic patients decreased the frequency of ventricular extrasystoles in 4 of 17 patients (24%) and suppressed most complex ventricular arrhythmias in 12 of 15 patients (80%). This assessment was made from 72-h continuous Holter monitoring recorded during the course of this double blind, placebo-controlled randomized crossover study. Seven patients (41%) complained of anticholinergic side effects, but no contractile or conduction system depression was seen. Amiodarone (200 mg) given on a single blind, placebo-controlled basis to 9 of these patients reduced the frequency of ventricular extrasystoles in 6 of 9 patients (67%) and suppressed complex ventricular ectopy in 6 of 7 patients (85%). One patient was unable to tolerate this drug (11%). Both drugs seemed less effective in controlling supraventricular arrhythmias, although disopyramide eliminated paroxysms of supraventricular tachycardia in 9 of 13 (69%) and amiodarone in all 6 patients with this arrhythmia. Amiodarone appears to be a better antiarrhythmic drug for chagasic patients, due to its greater effectiveness and lower incidence of side effects.     

Anti-arrhythmic effect of amiodarone in the 24 hours following a single oral loading dose. Clinical and pharmacological study

This study demonstrated the rapid antiarrhythmic effects of oral amiodarone (Am). A single 30 mg/kg dose was given to 67 patients, 18 with supraventricular arrhythmias (atrial extrasystoles: 11 cases, reciprocating tachycardia: 4 cases, intraatrial reentrant tachycardia: 2 cases, paroxysmal atrial fibrillation, AF: 1 case). Eighteen patients had permanent AF. Thirty-one patients had ventricular arrhythmias (ventricular extrasystoles, VES, isolated or in salvos: 22 cases, and ventricular tachycardia, VT: 19 cases). The effect on atrial extrasystoles was significant 4 to 13 hours after AM and maximal (-98% +/- 3.6%) at 7.7 +/- 1 hours. They recurred in 3 cases at the 18th hour. No significant effects were observed on the other supraventricular tachycardias. The effect on the atrioventricular node (AVN) assessed by the ventricular response to permanent AF, was significant after the 3rd hour and maximal ( = 38 +/- 6 bpm) at the 7th hour. The reduction in the frequency of VES was significant from the 5th to the 19th hour of treatment. Control of VT was obtained in 5 cases between the 3rd and 8th hours. The treatment was well tolerated as no side effects were reported. The plasma concentration (PC) of amiodarone (54 patients) and of N-desethylamiodarone (NDA) (36 patients) were measured; the maximal values were 2.53 +/- 1.5 mg/l for Am and 0.22 +/- 0.1 mg/l for NDA. A 60% decrease in the number of VES was observed with PC of Am of 1.90 +/- 0.3 mg/l and a 20% reduction in the ventricular response to AF at PC of Am of 1.50 +/- 0.33 mg/l.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prevalence, therapeutic modification and prognostic significance of ventricular arrhythmias in the mitral valve prolapse syndrome

82 patients clinically and echocardiographically identified as having mitral valve prolapse were examined with regard to the incidence of ventricular arrhythmias and their therapeutic and prognostic implications. 73 patients (89%) had ventricular extrasystoles in the 24 hour ambulatory ECG, 33 (40%) of them with an average of more than 30/h. Severe forms like multiform or paired ventricular extrasystoles and nonsustained ventricular tachycardias have been registered in 28 (34%), 26 (32%) and 9 patients (11%) respectively. There is a correlation between the incidence of the arrhythmias and time of registration which corresponds to a natural logarithm. A prolongation of the time of registration to more than 24 hours therefore implies no essential benefit. The incidence and the number of ventricular arrhythmias demonstrated a significant decrease during sleep. The incidence of ventricular pairs and/or ventricular tachycardias was 13% during the night (0-6 h) in comparison with at least 22% during the three daytime periods (6-12 h, 12-18 h and 18-24 h). There was no correlation between the incidence or severity of ventricular arrhythmias and the patients' ages of left ventricular performance.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of antihypertensive therapies by noninvasive techniques

We compared the antihypertensive effects of the beta-blocker atenolol and the converting enzyme inhibitor lisinopril during 12 weeks of treatment in patients with mild to moderate essential hypertension. Atenolol (n = 10) significantly decreased conventionally measured blood pressure from 144/103 to 135/93 mm Hg and lisinopril (n = 9) from 150/104 to 130/92 mm Hg. Based on data derived from automated 24-h ambulatory blood pressure monitoring, atenolol decreased the average whole-day systolic pressure by 18 +/- 6 mm Hg (p less than 0.02) and the diastolic pressure by 11 +/- 2 mm Hg (p less than 0.01). Lisinopril produced decreases of 27 +/- 5 mm Hg (p less than 0.01) and 13 +/- 2 mm Hg (p less than 0.001). Examination of the 24-h blood pressure patterns showed that the efficacies of the two drugs were similar. Each appeared to be effective throughout the whole-day monitoring period, although only lisinopril significantly decreased blood pressure during the final four-h period (4 AM to 8 AM) preceding the next day's dose. Neither drug produced significant echocardiographic changes in left ventricular wall thickness or muscle mass during the short-term treatment. Lisinopril and atenolol effectively decrease blood pressure during a 24-h period. Moreover, we found that automated whole-day blood pressure monitoring is a useful tool for comparing the efficacy and duration of action of differing antihypertensive agents.     

Ontogeny of pulsatile secretion of gonadotropin-releasing hormone in the bull calf during infantile and pubertal development

During the infantile period of development in the bull calf (birth to 6 weeks of age), there is a virtual absence of episodic secretion of LH. Transition from infancy to the prepubertal period (6-10 weeks of age) is characterized by the onset of episodic LH release. This study was conducted to characterize the ontogeny of episodic GnRH release during these developmental periods. During the primary experiment, calves at 2, 5, 8, and 12 weeks of age (n = 4/age) were surgically fitted with cannulae for the collection of mixed hypophyseal portal and cavernous sinus blood. Hypophyseal portal and cavernous sinus and jugular blood samples were collected over a 9- to 12-h period at 10 min intervals. No pulses of LH were observed in calves at 2 or 5 weeks of age. At 8 and 12 weeks of age, pulsatile LH release became evident with a mean of 1.0 +/- 0.3 and 2.20 +/- 0.7 pulses/10 h, respectively. Unlike LH secretion, calves at both 2 and 5 weeks of age released GnRH in a pulsatile manner (3.5 +/- 0.2 and 5.0 +/- 0.6 pulses/10 h, respectively). The frequency of pulsatile GnRH release increased from 7.9 +/- 0.4 pulses/10 h at 8 weeks of age to 8.9 +/- 0.7 pulses/10 h at 12 weeks of age. These findings demonstrate the presence of pulsatile secretion of GnRH during the infantile period of development. Furthermore, the postnatal ontogeny of pulsatile LH release in this species is associated with an increase in the frequency of pulsatile GnRH secretion.     

Prostaglandin modulation of early afterdepolarizations and ventricular tachyarrhythmias induced by cesium chloride combined with efferent cardiac sympathetic stimulation in dogs

Prostaglandins inhibit efferent cardiac sympathetic nerve effects by acting at presynaptic sites and may act to suppress some arrhythmias. In the present study, the effects of intravenous administration of prostacyclin (PGI2) and prostaglandin E2 (PGE2) on early afterdepolarizations and ventricular tachycardia induced by cesium chloride (0.5 mmol/liter per kg body weight intravenously) combined with stimulation of bilateral ansae subclaviae in anesthetized dogs were examined. The right atrium was paced at a constant cycle length of 600 ms. A left ventricular endocardial monophasic action potential catheter was used to detect early afterdepolarizations. Prostacyclin (0.2 microgram/kg per min) reduced the amplitude of the early afterdepolarizations (39.2 +/- 8.4% of the monophasic action potential amplitude during control study to 28.7 +/- 5.5%, n = 10; p less than 0.001) as well as the prevalence of ventricular tachycardia (11 of 14 dogs during control study to 5 of 14 dogs; p = 0.031). Prostaglandin E2 (0.2 to 0.6 microgram/kg per min) did not significantly reduce the early afterdepolarization amplitude (34.7 +/- 8.9% to 25.1 +/- 10.7%, n = 8; p = 0.085) or the prevalence of ventricular tachycardia (8 of 10 versus 6 of 10 dogs; p = 0.50). Alpha- and beta-adrenoceptor blockade with combined intravenous administration of propranolol (0.5 mg/kg) and phentolamine (0.3 mg/kg) decreased the amplitude of the early afterdepolarizations induced by cesium chloride and bilateral ansae subclaviae stimulation from 38.6 +/- 11.2% to 18.8 +/- 3.3% (n = 6; p = 0.005). Additional administration of PGI2 further reduced the early afterdepolarization amplitude from 18.8 +/- 3.3% to 9.8 +/- 4.8% (n = 6; p = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Combination of theophylline and salbutamol for arrhythmias in severe COPD

We conducted a single-bind placebo controlled study using 24-hour continuous ambulatory electrocardiographic recordings. The arrhythmogenic potential of the combination of salbutamol and theophylline was investigated in 25 ambulatory subjects with severe chronic airflow obstruction (mean age 65 +/- 8 SD, mean FEV1 31 percent +/- 13 SD predicted). Asymptomatic arrhythmias were very prevalent in the study population: 76 percent of the patients had runs of supraventricular tachycardia while 24 percent had runs of ventricular tachycardia. Individual arrhythmia frequency showed greater between-test variability than previously described in non-COPD subjects. The mode of administration of salbutamol may have affected arrhythmia frequency in that subjects using aerosol nebulizers had more ventricular extrasystoles than those using metered dose inhalers. Although the addition of theophylline to salbutamol significantly increased heart rate and supraventricular extrasystoles, there was no statistically significant increase in ventricular arrhythmias.     

Cardiac arrhythmias and left ventricular hypertrophy in dipper and nondipper patients with essential hypertension

To evaluate the behavior of cardiac arrhythmias in dipper and nondipper hypertensive patients, 48-h ambulatory blood pressure monitoring, 24-h Holter electrocardiogram recording and echocardiographic studies were performed in 56 untreated outpatients with essential hypertension. These patients were divided into 2 groups according to the presence (dipper, n=33) or absence (nondipper, n=23) of reduction of both systolic and diastolic blood pressure during nighttime by an average of more than 10% of daytime blood pressure. Mean 48-h systolic and diastolic blood pressures did not differ between the 2 groups. Nondipper patients had a significantly larger left atrial dimension (31.9+/-3.8 vs 35.6+/-3.7 mm; p<0.01), left ventricular mass index (114+/-26 vs 136+/-36 g/m2; p<0.05), as well as a larger number of total supraventricular (16+/-19 vs 89+/-197 beats; p<0.05) and ventricular ectopic beats (7+/-14 vs 47+/-96 beats; p<0.05) during daytime as compared with dippers. In conclusion, nondipper hypertensive patients are likely to experience supraventricular and ventricular arrhythmias more frequently than dippers. A blunted nocturnal blood pressure fall may be involved in the appearance of cardiac arrhythmias in patients with essential hypertension.     

Ventricular arrhythmias in aortic valve disease before and after aortic valve replacement.

In order to evaluate the effect of aortic valve replacement on the incidence of ventricular arrhythmias in patients with aortic valve disease, 24-hour ambulatory electrocardiographic recordings were obtained before surgery in 96 patients without coronary artery disease (aortic stenosis n = 50, combined aortic stenosis and regurgitation n = 19 and aortic regurgitation n = 27). Following aortic valve replacement, repeat recordings were obtained after 13 +/- 4 days and 18 +/- 7 months. Ventricular arrhythmias were in all cases classified according to Lown and were compared with clinical, echocardiographic and hemodynamic data. Preoperatively, ventricular premature beats were observed in 85 patients (89%) and were frequent (greater than 30 ventricular premature beats/hour) in 20 (21%). Multiformity was found in 27 (28%), couplets in 18 (19%) and ventricular tachycardia in 11 (11.5%). The occurrence of ventricular arrhythmias was not related to the type or severity of valve lesions. Patients with severe ventricular arrhythmias (Lown class 3 or 4: 37%) had a greater thickness of their interventricular septum 13.9 +/- 2.5 mm, vs 11.7 +/- 2.6 (p less than 0.05); a higher LV mass 176 +/- 34 g/m2, vs 134 +/- 39 (p less than 0.05) and a lower left ventricular ejection fraction 47 +/- 12%, vs 57 +/- 11, (p less than 0.01). Two weeks postoperatively, the incidence and severity of ventricular arrhythmias had increased: ventricular premature beats were noted in 92% and were severe in 50%. No correlation was found between ventricular arrhythmias and preoperative or operative data. Eighteen months after surgery, ventricular premature beats were still observed in 81% of patients but remained frequent in 7% only. Severe ventricular arrhythmias were noted in 27%. Patients with severe ventricular arrhythmias had at the time of this late recording a lower radionuclide left ventricular ejection fraction 57 +/- 14%, vs 73 +/- 9 (p less than 0.02) and a higher enddiastolic diameter 63 +/- 15 mm, vs 48 +/- 7, (p less than 0.01). This study indicates that ventricular arrhythmias are common in patients with aortic valve disease. The severity of arrhythmias is influenced by the LV consequences of valve lesion both pre- and late postoperatively. The frequency and severity of ventricular arrhythmias increase early after surgery and do not correlate with preoperative or operative data.     

Effect of transmural versus nontransmural myocardial infarction on inducibility of ventricular arrhythmias during sympathetic stimulation in dogs

Transmural myocardial infarction interrupts sympathetic nerves and denervates viable muscle distal to myocardial infarction. The effect of sympathetic stimulation on responses to programmed ventricular stimulation was studied in dogs without myocardial infarction (Group I: n = 5), with transmural anterior wall myocardial infarction (Group II: n = 6) and with nontransmural anterior wall myocardial infarction (Group III: n = 9). Ventricular effective refractory period during sympathetic stimulation decreased by 16 +/- 18, 1 +/- 2 and 12 +/- 8 ms (mean +/- SD) in viable muscle of the inferoapical left ventricle in Groups I, II and III, respectively, suggesting efferent sympathetic denervation by transmural myocardial infarction only. Sustained ventricular tachycardia or fibrillation was induced more easily during sympathetic stimulation in six of the six dogs with transmural infarction, but in only two of the nine dogs with nontransmural infarction (p less than 0.01). It is concluded that the partial sympathetic denervation produced by transmural myocardial infarction enhances the ease of induction of ventricular tachycardia and fibrillation during sympathetic stimulation. A similar mechanism may lead to increased risk for lethal arrhythmias during periods of high sympathetic tone in patients with transmural myocardial infarction.     

Electrophysiologic effects of thrombolytic therapy in patients with a transmural anterior myocardial infarction complicated by left ventricular aneurysm formation

To assess the effects of early thrombolytic therapy on the incidence of clinical and induced ventricular arrhythmias in high risk postmyocardial infarction patients, 32 patients with a transmural anterior myocardial infarction complicated by left ventricular aneurysm formation were prospectively evaluated. Sixteen patients (Group A) received routine care because of contraindication to thrombolytic therapy or other factors and 16 (Group B) received either tissue plasminogen activator or streptokinase within 6 h of the onset of chest pain. The two groups were similar in left ventricular ejection fraction (mean +/- SD, 28 +/- 9% [Group A] versus 30 +/- 8% [Group B]) and occurrence of spontaneous nonsustained ventricular tachycardia, new bundle branch block and congestive heart failure. Group B patients had higher peak creatine kinase MB levels (446 +/- 336 versus 205 +/- 120 IU; p = 0.017) and earlier time to peak creatine kinase values (13.4 +/- 6.6 versus 19.1 +/- 6.1 h; p = 0.006). Twenty patients who had no clinical sustained ventricular arrhythmias underwent electrophysiologic study 13 +/- 6 days after infarction. Ventricular tachycardia was induced during the study in 7 (88%) of 8 Group A patients, but in only 1 (8%) of 12 Group B patients given thrombolytic therapy (p = 0.0008). During a mean follow-up period of 11 +/- 8 months, eight Group A patients (50%) died suddenly or were resuscitated from sustained ventricular tachycardia; all Group B patients are alive and have had no clinical arrhythmic events (p = 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)     

非酒精性脂肪性肝病大鼠血浆前列环素与血栓素的变化及其与肝脏损伤的关系

目的 探讨非酒精性脂肪性肝病(NAFLD)大鼠血浆前列环素(PG12)和血栓索(TX)A2的动念变化及其与肝组织学改变之间的关系。 方法 48只模型组SD大鼠给予高脂肪高胆固醇饮食饲养,分批于第8、12、16、24周处死,24只正常饮食大鼠作对照。放射免疫法检测血浆PGI 2和TXA 2的稳定代谢产物6酮-前列环素1α(PGF1 α)和TXB2含量,光镜观察肝组织切片病理学改变。 结果 模型组大鼠8周呈现单纯性脂肪肝,12～24周从脂肪性肝炎进展至脂肪性肝纤维化。模型组大鼠血浆TXB 2在造模第8、24周分别为(52.4±3.15)ng/L和(117.7±7.47)ng/L,对照组为(41.1±1.45)ng/L,t值为9.12和31.34,P<0.01和P<0.001。 血浆PGF1 α水平在造模8、24周分别为(31.1±1.6)ng/L和(3.4±2.4)ng/L,对照组为(36.5±1.7)ng/L,t值为6.27和34.62,P<0.01和,P<0.001。模型组大鼠血浆TXB2和PGF1 α水平分别与其肝组织损伤程度呈显著正相关(r=0.537,P<0.001)及负相关(r=-0.452,P<0.01)。 结论 持续24周的高脂饮食可以成功复制大鼠NAFLD模型,模型大鼠血浆TXA 2与PGI 2平衡失调,可能参与NAFLD的发病。