940-73 Predictive Value for Major Arrhythmic Events of Ventricular Arrhythmias Detected in the Subacute Phase of a Fibrinolysed Myocardial Infarction. An Analysis of the GISSI-2 Data Base

The relationship between ventricular arrhythmias (VA) in the subacute phase of a myocardial infarction and subsequent major arrhythmic events (MAE) was mainly defined in the prefibrinolytic era, We examined the large population of patients enrolled in the GISSI-2 study in order to evaluate the significance and predictive power for MAE (sustained ventricular tachycardia -SVT-and sudden death -SD-) of VA detected by Holter monitoring during the subacute phase of a fibrinolysed acute myocardial infarction (AMI). Of the 12,381 pts. enrolled in the GISSI-2 study, an Holter monitoring was available in 8,676 and a six month follow-up was completed in 7,713. During the follow-up 84 pts. died suddenly and 26 experienced one or more SVT. The relationship between VA and MAE was evaluated by odds ratio (OR) and their 95% confidence intervals. OR for MAE was 4.5 (2.7–7.5) if the Holter showed > 10 ventricular ectopic beats per hour; 2.3 (1.5–3.7) if couplets were present; 3.3 (1.5–7.0) if nonsustained ventricular tachycardias (NSVT) were noticed; 3.0 12.0–4.5) if any complex VA was detected. A multivariate analysis (Cox modell including the major prognostic determinants confirmed the independent prognostic value of VA in the Holter recording except for NSVT. Any arrhythmic parameter had a very low positive predictive power (from 2.4 to 3.0%). In conclusion, our data show that VA still have, in the fibrinolytic era, a prognostic significance for MAE, but the predictive power is very low and is therefore mandatory to add other variables to identify the pts. more at risk

Arrhythmias Originating in the Atria

Atrial flutter, atrial tachycardias, and atrial fibrillation are the main sustained atrial tachycardias. Reentry, increased automaticity, and triggered activity are atrial arrhythmia's main mechanisms. Atrial flutter is the clinical and theoretical model of reentry. Its classification is based on the atrial chamber involved and the arrhythmia's anatomic path. Ablative procedures for atrial fibrillation have created several new reentrant tachycardias. Electrocardiography (ECG) identifies the site of origin of focal atrial tachycardias and the mechanism of these arrhythmias. ECG is fundamental in the diagnosis of atrial fibrillation and often allows understanding of its mechanism of origin and maintenance

The QRS Complex. Normal Activation of the Ventricles

The ventricular conduction system starts below the His bundle, where it bifurcates into the right and left bundle branches that taper out to the subendocardial Purkinje network, which activates the ventricular myocardium. This system is responsible for the synchronized and almost simultaneous activation of both ventricles. On the surface ECG, the ventricular conduction system lies in the terminal portion of the PR interval, whereas the QRS complex is comprised of the electrical currents originating from ventricular depolarization. This article reviews the main electroanatomical features of the ventricular conduction system and the effects of its delay on the QRS

General Approach to a Wide QRS Complex

Wide QRS complex is present when the normal activation pattern is modified by various mechanisms and clinical conditions. Correct interpretation is crucial for appropriate decision making. When approaching an electrocardiogram (ECG) with wide complex tachycardia, one must differentiate between ventricular tachycardia and supraventricular tachycardia conducted with aberrancy. ECG criteria are used and algorithms developed to aid in differential diagnosis. They are based on finding ECG signs of ventriculoatrial dissociation and QRS morphologies inconsistent with classic bundle branch block. The conditions able to modify structurally the normal activation of the heart may alter spontaneous ventricular activation during supraventricular tachycardia, creating differential diagnosis problems

Advanced Concepts of Atrioventricular Nodal Electrophysiology: Observations on the Mechanisms of Atrioventricular Nodal Reciprocating Tachycardias

Atrioventricular node reentrant tachycardia (AVNRT) is a supraventricular arrhythmia easily diagnosed by 12-lead electrocardiogram. What is far more challenging, is the understanding of the reentrant circuit in its typical and atypical presentations. The function of the atrioventricular node is still incomplete and this knowledge gap is reflected in the reconstruction of the pathways used by AVNRT in its multiform presentations. This article illustrates the heterogeneous electrocardiographic manifestations of AVNRT. We reconstruct the reentrant circuits involved using more recent understanding of the anatomic and electrophysiologic characteristics of the atrioventricular node

Intraventricular Delay and Blocks

From the atrioventricular node, electrical activation is propagated to both ventricles by a system of specialized conducting fibers, His Purkinje System (HPS), guaranteeing a fast, synchronous depolarization of both ventricles. From the predivisional common stem, a right and left branch separate, subdividing further in a fairly predictable fashion. Synchronous ventricular activation results in a QRS with specific characteristics and duration of less than 110 milliseconds. Block or delay in any part of the HPS changes the electrocardiographic (ECG) morphology. This article discusses the use and limitations of standard ECG in detecting abnormal ventricular propagation in specific areas of the HPS