Surgical treatment of cardiac arrhythmias

This report describes 20 consecutive patients who underwent surgical procedures for treatment of cardiac arrhythmias.16 patients have been operated for WPW. syndrome, always using the epicardial approach, without extracorporeal circulation.Three patients underwent surgery for atrio-ventricular nodal reentrant tachycardia, using a discrete perinodal cryotreatment, during normothermic extracorporeal circulation.In one case we used cryoablation of the atrial myocardium below the coronary sinus to treat atrial flutter. This operation was performed under normothermic extracorporeal circulation. In our observations, there was no early or late death; postoperative complications developed in 1 patient (5%) due to pericarditis.Ablation of the AP was completely successful in all the cases (100%) operated for WPW as well as for AVNRT syndromes and atrial flutter.Abbreviations AV atrio-ventricular - AVNRT atrio-ventricular nodal reentrant tachycardia - MSEC millisecond - SD sudden death - VT ventricular tachycardia - WPW Wolff-Parkinson-White     

Value of Holter monitoring in assessing cardiac arrhythmias in symptomatic patients.

Holter electrocardiographic monitoring in 55 symptomatic patients with syncope, palpitations or dizziness uncovered significant arrhythmias in 30 patients (55 percent). By providing an observation period of at least 24 hours including a period of sleep, the procedure aided detection and diagnosis in both symptomatic and asymptomatic patients of transient arrhythmias or conduction abnormalities not documented by routine electrocardiograms. Bradyarrhythmias accounted for the majority of arrhythmias recorded in 21 or 30 symptomatic patients (70 percent); 15 had sinus bradycardia (35 to 55 beats/min) alone and 6 also had long episodes of sinus arrest of up to 5 seconds. Two had sinus bradycardia with periods of atrioventricular block with Wenckebach phenomenon. Five patients had a tachycardia-bradycardia syndrome; three had other episodic arrhythmias and one had pacemaker failure. In 15 (60 percent) of the 25 patients without arrhythmias, monitoring did not document the cause of symptoms. Holter monitoring is of considerable value in assessing the efficacy and adequacy of drug treatment, especially in patients with known heart disease, and in detecting pacemaker malfunction. However, very long periods of monitoring may be needed to make a diagnosis in those with only sporadic symptoms.     

Electrophysiology and pharmacology of cardiac arrhythmias. III. The causes and treatment of cardiac arrhythmias. Part B

Studies on the electrophysiologic mechanisms responsible for disturbances of cardiac rate, rhythm, and conduction, and studies on the actions and mechanisms of action of antiarrhythmic and other drugs, permit the development of an apparently reasonable approach to treatment of cardiac arrhythmias. Some of the rules derived from an appreciation of cardiac electrophysiology are generally applicable. Others appear to require further testing. There are many discrepancies between what can be predicted or expected and what happens; these discrepancies result from many factors. It is likely that cardiac disease in humans has effects on the electrical activity of cardiac cells which have not been reproduced in the laboratory. It is likely, also, that disease modifies the response of cardiac cells to drugs in ways that have not yet been discovered. Nevertheless, some progress has been made and further experiment and thought may provide both better understanding and new and better therapeutic agents.     

Nonpharmacologic treatment of life-threatening cardiac arrhythmias

Numerous nonpharmacologic modalities have been introduced for the management of patients with life-threatening arrhythmias. These include cardiac pacing, insertion of an automatic internal cardiac defibrillator (AICD), cardiac electrosurgery, and catheter ablative techniques. Each modality is effective; AICD shows particular promise because it has demonstrated remarkable efficacy in decreasing the incidence of sudden cardiac death in patients with malignant ventricular arrhythmias. Each modality also has its limitations or contraindications. Nonpharmacologic antiarrhythmic therapy represents an important advance against the serious public health problem of sudden cardiac death.     

Genomics and cardiac arrhythmias.

Sudden cardiac death in patients younger than 35 years of age is primarily due to genetic causes. Familial hypertrophic cardiomyopathy accounting for 30% to 40% is associated with structural heart disease while the Brugada syndrome and the long QT syndrome (LQTS) are associated with normal cardiac function. This is a review of the genetics of supraventricular and ventricular arrhythmias. Atrial fibrillation is mapped to nine chromosomal loci and four genes are identified. AMP-activated protein kinase is one gene responsible for Wolff-Parkinson-White syndrome. The LQTS and the Brugada syndromes are due to defects primarily in cardiac sodium and potassium ion channels. The role of single nucleotide polymorphisms in predisposing to arrhythmias in acquired disorders such as hypertrophy is discussed.