Rate-Control or Rhythm-Contol: Where do we stand?

Atrial fibrillation is the most common sustained rhythm disturbance and its prevalence is increasing worldwide due to the progressive aging of the population. Current guidelines clearly depict the gold standard management of acute symptomatic atrial fibrillation but the best-long term approach for first or recurrent atrial fibrillation is still debated with regard to quality of life, risk of new hospitalizations, and possible disabling complications, such as thromboembolic stroke, major bleeds and death. Some authors propose that regaining sinus rhythm in all cases, thus re-establishing a physiologic cardiac function not requiring a prolonged antithrombotic therapy, avoids the threat of intracranial or extracranial haemorrhages due to Vitamin K antagonists or aspirin. On the contrary, advocates of a rate control approach with an accurate antithrombotic prophylaxis propose that such a strategy may avoid the risk of cardiovascular and non cardiovascular side effects related to antiarrhythmic drugs. This review aims to explore the state of our knowledge in order to summarize evidences and issues that need to be furthermore clarified

Rate-Control or Rhythm-Control: Where do we stand?

Atrial fibrillation is the most common sustained rhythm disturbance and its prevalence is increasing worldwide due to the progressive aging of the population. Current guidelines clearly depict the gold standard management of acute symptomatic atrial fibrillation but the best-long term approach for first or recurrent atrial fibrillation is still debated with regard to quality of life, risk of new hospitalizations, and possible disabling complications, such as thromboembolic stroke, major bleeds and death. Some authors propose that regaining sinus rhythm in all cases, thus re-establishing a physiologic cardiac function not requiring a prolonged antithrombotic therapy, avoids the threat of intracranial or extracranial haemorrhages due to Vitamin K antagonists or aspirin. On the contrary, advocates of a rate control approach with an accurate antithrombotic prophylaxis propose that such a strategy may avoid the risk of cardiovascular and non cardiovascular side effects related to antiarrhythmic drugs. This review aims to explore the state of our knowledge in order to summarize evidences and issues that need to be furthermore clarified

Results of biventricular endomyocardial biopsy in survivors of cardiac arrest with apparently normal hearts.

Seventeen young patients (10 males and 7 females, aged 14 to 38 years, mean 26.4) without overt organic heart disease, who had been resuscitated from sudden cardiac arrest and referred to our institution during the period 1984 to 1993 for diagnostic evaluation and electrophysiologic study-guided antiarrhythmic therapy, were studied. Patients underwent noninvasive (electrocardiography, echocardiography [2-dimensional and Doppler], and magnetic resonance imaging) and invasive (left ventricular [LV], right ventricular [RV], and coronary angiography, ergonovine testing, electrophysiologic study, and biventricular endomyocardial biopsy) cardiac studies. Six to 8 biopsy fragments per patient were processed for histology and electron microscopy and read by a pathologist blinded to clinical data. Antiarrhythmic drug testing included amiodarone, propafenone, and metoprolol. A cardioverter-defibrillator was implanted in patients with persistently inducible sustained ventricular tachycardia or ventricular fibrillation. Sequential cardiac biopsy specimens were obtained in patients with active myocarditis undergoing immunosuppressive treatment. Periodic 3-month follow-ups included echocardiography and Holter monitoring. Two groups of patients were distinguished by invasive and noninvasive examinations: group I consisted of 9 patients with entirely normal parameters; group II consisted of 8 patients with structural, nonspecific cardiac abnormalities. In this latter group, mild to moderate dilatation and hypokinesia of the left ventricle were documented in 4 patients, concentric LV hypertrophy was seen in three patients, and RV dysfunction was noted in 1 patient. Histologic examination was abnormal in in all patients and revealed specific lesions in 65% of them; LV biopsy specimens allowed a diagnosis in 3 of 7 myocarditic patients with normal RV histology.(ABSTRACT TRUNCATED AT 250 WORDS

Effect of bunaphtine on right atrial repolarisation in man.

Using a bipolar suction electrode technique, right atrial monophasic action potentials were recorded in 11 patients with recurrent attacks of paroxysmal atrial tachyarrhythmia. The right atrial monophasic action potential total duration, measured at 90 per cent level of repolarisation, in sinus rhythm, ranged between 217 and 394 ms. N(2-diethylamine-ethyl)N(n-buthyl)-naphtamide (Bunaphtine) was administered by an intracardiac catheter at an average dosage of 1-78 mg/kg body weight in order to evaluate its effect on atrial repolarisation. Monophasic action potential recordings were performed during drug administration and thereafter every minute for an average observation period of 12-2 minutes. The drug induced a significant lengthening of atrial repolarisation (mean 18.4%) strongly correlated with a significant reduction of relative repolarisation rate of phase 3 (RRR ph3). The effect was more obvious in patients with short repolarisation and was not correlated with significant variations in heart rate. When basic cycle length was maintained constant by atrial pacing an increase in total duration of right atrial monophasic action potential was seen. Administration of the drug was followed by an appreciable reduction of inhomogeneity of repolarisation as measured from different sites in the atrium. In 2 patients conversion from atrial fibrillation to sinus rhythm occurred during drug infusion with a progressive lengthening of right atrial monophasic action potential; this suggests that the antiarrhythmic properties of Bunaphtine are related to its direct effect on repolarisation. Thus, as far as atrial tissue is concerned Bunaphtine can be considered a Class 3 antiarrhythmic drug according to the classification of Vaughan-Williams