Association of accelerated idioventricular rhythm and paroxysmal ventricular tachycardia in acute myocardial infarction

Ventricular Rhythms in Acute Myocardial Infarction

“…Some authors have claimed the rarity of such coexistence [17], while others have been impressed with the contrary [4], From the above it seems that rather convincing clinical evidence is being accumulated in the literature and probably in many intensive cardiac care units, indicating that there are many patients who develop, in the early phase of acute myocardial infarc tion, ventricular arrhythmias resembling the accelerated idioventricular type, but differing from it in course, duration and prognosis. The perti nent literature suggests that these variants may be produced either by a varying exit block from a rapid parasystolic focus [2,17,19], or by concealed or manifest re-entry created by slowed conduction within an area of enhanced phase 4 activity [4,20]. Similar mechanisms have been invoked to explain the appearance of random, nonparasystolic ventricular extrasystoles [19,24,25], It has been noted on the screening of routine electrocardiograms that such extrasystoles and even slow ventricular tachycardia with an irregular rate have been associated with cardiac disease and with other serious arrhythmias [23].…”

“…It is of interest to note that even those who attempted drug therapy in these patients pointed out the relative ineffectiveness of the various antiarrhythmic drugs in accelerated idioventricular rhythms [1]. More recently, however, there have been an increasing number of reports describing the coexistence of both slow and rapid ventricular rhythms with identical configuration in the same patient [4,10]. Some authors have claimed the rarity of such coexistence [17], while others have been impressed with the contrary [4], From the above it seems that rather convincing clinical evidence is being accumulated in the literature and probably in many intensive cardiac care units, indicating that there are many patients who develop, in the early phase of acute myocardial infarc tion, ventricular arrhythmias resembling the accelerated idioventricular type, but differing from it in course, duration and prognosis.…”

“…More recently, however, there have been an increasing number of reports describing the coexistence of both slow and rapid ventricular rhythms with identical configuration in the same patient [4,10]. Some authors have claimed the rarity of such coexistence [17], while others have been impressed with the contrary [4], From the above it seems that rather convincing clinical evidence is being accumulated in the literature and probably in many intensive cardiac care units, indicating that there are many patients who develop, in the early phase of acute myocardial infarc tion, ventricular arrhythmias resembling the accelerated idioventricular type, but differing from it in course, duration and prognosis. The perti nent literature suggests that these variants may be produced either by a varying exit block from a rapid parasystolic focus [2,17,19], or by concealed or manifest re-entry created by slowed conduction within an area of enhanced phase 4 activity [4,20].…”

“…However, the slow variant of ventricular tachycardia, the so-called ac celerated idioventricular rhythm, is considered to be a self limited, tran sient, benign type of dysrhythmia [15,18]. In more recent reports the presence of both the slow benign, and the rapid, hazardous ventricular rhythms, of the same configuration, have been observed in the same patient [4,10]. The present study was stimulated by the lack of accurate criteria to predict which of the patients with idioventricular rhythm are at risk for developing dangerous rapid ventricular arrhythmia, as well as relative unresponsiveness of idioventricular rhythm to conventional antiarrhythmic agents [ I ].…”

The Protean Manifestations of Blunt Cardiac Trauma in Children

“…Although an accelerated idioventricular rhythm is associated with myocardial injury and is observed in up to 46% of myocardial infarctions, 17 it is usually a benign arrhythmia in pediatric patients. 18 The mechanism of injury is thought to be caused by enhanced automaticity from injured Purkinje fibers.…”