Alteration of left ventricular performance by left bundle branch block simulated with atrioventricular sequential pacing.

The effects of atrioventricular (AV) sequential pacing-induced left bundle branch block (LBBB) on left ventricular (LV) performance were evaluated during cardiac catheterization in 9 randomly selected patients being investigated for chest pain. All patients were in normal sinus rhythm with a normal P-R interval and QRS duration. LV performance was assessed by both hemodynamic and angiographic measurements. The maximal rate of LV pressure increase (dP/dt), rate of maximal LV pressure decrease (-dP/dt), LV end-diastolic pressure (LVEDP), end-diastolic volume (LVEDV), end-systolic volume (LVESV), stroke volume and percent ejection (EF) were measured during right atrial and AV sequential pacing at a constant pacing rate. The average pacing rate was 97 +/- 3 beats/min (mean +/- standard error of the mean). In each patient, both dP/dt and -dP/dt decreased significantly (p less than 0.001) during AV sequential pacing compared with atrial pacing at the same rate, from 1,541 +/- 68 to 1,319 +/- 56 mm Hg/s for dP/dt and from 1,506 +/- 86 to 1,276 +/- 92 for -dP/dt. LVEDP did not change significantly when atrial (17 +/- 3 mm Hg) and AV sequential pacing (16 +/- 2 mm Hg) were compared. Mean LVEDV did not change during atrial (135 +/- 13 ml) or AV sequential pacing (137 +/- 14 ml). In contrast, the LVESV during AV sequential pacing was higher by 15 ml (23%) (from 48 +/- 10 to 63 +/- 12 ml) (p less than 0.001); as a result, the stroke volume was lower by 13 ml (15%) and the EF decreased by 10%, from 66 to 56% (-15%).(ABSTRACT TRUNCATED AT 250 WORDS)

Asynchronous ventricular pacing: a rare cause of ventricular tachycardia.

Asynchronous cardiac pacing may induce ventricular tachycardia and fibrillation, particularly in patients with ischemic heart disease and possibly other types of myocardial abnormalities. All patients with implanted asynchronous pacemakers, and those whose demand pacemakers operate in asynchronous mode for any reason, are to be considered at risk from this complication. In patients with serious myocardial abnormalities consistent demand pacing should be assured, even if it requires early pacemaker replacement. Anti-arrhythmic agents may prove useful for temporary suppression of pacemaker-induced arrhythmias.

ECG manifestations of myocardial ischemia.

Exercise ECG is widely used for the diagnosis of ischemic heart disease. The most common ECG sign of myocardial ischemia is flat or down-sloping ST-segment depression of 1.0 mm or greater. This report draws attention to other much less common, but possibly equally important, ECG manifestations of myocardial ischemia. Serial ECGs obtained during the treadmill stress test of a 40-year-old man with angiographically proven coronary artery disease exhibited virtually all known ECG signs of ischemia, namely, ST-segment depression, ST-segment elevation and alternans, intraventricular conduction abnormalities, and U-wave inversion.

Pseudodysrhythmias in ambulatory ECG monitoring.

Artifacts mimicking a variety of dysrhythmias occur relatively frequently in ambulatory ECG (Holter) monitoring records. Proper interpretation is imperative if serious therapeutic errors are to be avoided. Two-channel recording systems may facilitate recognition of some, but not all, of these artifacts. Pseudodysrhythmias may mimic paroxysmal supraventricular tachycardia and atrial fibrillation, atrial dissociation, extrasystoles, and sinus pauses. There are several causes of pseudodysrhythmias. Failure to recognize these patterns may result in serious errors in patient management.

Pseudo atrioventricular block.

Pseudo first- and second-degree atrioventricular (AV) block can occur due to depressive effects of concealed junctional discharges on AV conduction of sinus impulses. Pseudo AV block is not indicative of a primary impairment of AV conduction and is reversible by interventions that suppress ectopy.

Cellular electrophysiological marker of irreversible ischemic myocardial injury.

Glass microelectrode studies on posterior papillary muscle (PPM) slice preparations from 20 pentobarbital-anesthetized dogs (15 subjected to prior circumflex coronary artery ligation, 5 to sham ligation) have resulted in the definition of an electrophysiological marker of irreversible ischemic injury, namely, findings of areas composed of cells unable to generate a significant resting potential (less than -25) mV), designated "electrically inactive areas." Electrically inactive areas were essentially confined to PPM from dogs with circumflex coronary ligation; the incidence and distribution of the areas was related to duration of ischemia. Correlative phase- and light-microscopic studies demonstrated close correspondence between such areas and morphological evidence of irreversible ischemic injury. Analysis of frequency and distribution of electrically inactive areas permits quantitative assessment of the extent and spatial distribution of irreversible injury. This method has been used to quantitate injury in PPM from dogs that had been subjected to ligation for varying time periods. The potential utility of this method for evaluation of interventions designed to protect against ischemic injury and to assess electrical properties of surviving cells is considered.

Lenegre's disease in youth.

The case of a 22-year-old white male without known heart disease who presented with activity related lightheadedness at age 19 and dizziness and fatigue at age 21 is described. Standard electrocardiograms (ECG's) revealed intermittent complete trifascicular block. Rapid progression of symptoms over the succeeding eight months resulted in increasing incapacity. Holter monitoring demonstrated that symptoms were related to development of second and higher degrees of A-V block. Normal A-H interval and markedly prolonged H-Q interval on His bundle electrograms indicated that block was infranodal and localized to bundle branch system. Conduction problems aside, clinical and laboratory evaluation, including echocardiograms and cardiac catheterization, were unremarkable. Progression of bilateral bundle branch disease in a young patient without other demonstrable heart lesions and a negative family background conforms with criteria for Lenegre's disease. To our knowledge, this represents the youngest reported patient with this entity. Possible electrophysiologic basis of block and of exercise induced improvement in A-V conduction also are considered.