Programmed electric stimulation following acute myocardial infarct. Significance of stimulation timing

To assess the influence of time on the inducibility by programmed electrical stimulation of ventricular arrhythmias after acute myocardial infarction, we studied 18 patients on the 5th and 24th day after infarction with a stimulation protocol employing a maximum of 3 right ventricular extrastimuli during sinus rhythm and at 3 paced cycle lengths. All patients were without documented sustained ventricular arrhythmias (sustained ventricular tachycardia or ventricular fibrillation) prior to the investigation. Sustained ventricular arrhythmias were induced in 2 patients on day 5, but in 9 on day 24 after infarction. This difference in incidence was statistically significant (p less than 0.05), as was the change in the distribution ratio of induced sustained ventricular arrhythmias from day 5 to day 24 (p less than 0.05). The types of arrhythmia induced on day 24 were sustained ventricular tachycardia with a mean cycle length of 207 ms in 6 cases (5 monomorphic, 1 polymorphic), and ventricular fibrillation in 3 cases. These 9 patients did not differ from the remaining 9 patients in maximal CPK, infarct site, number of stenosed coronary arteries, global left ventricular ejection fraction, and in the results of 24-hour Holter monitoring, but they had a significantly shorter right ventricular effective refractory period (223 +/- 10 ms versus 259 +/- 28 ms; p less than 0.05). During the follow-up period of 24 +/- 5 months no patient died, had syncopal attacks, or developed spontaneous episodes of sustained ventricular arrhythmia. The timing of programmed electrical stimulation with a maximum of 3 right ventricular extrastimuli strongly influences the inducibility of sustained ventricular arrhythmias after acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Efficacy and electrophysiologic effects of oral sotalol in patients with sustained ventricular tachycardia caused by coronary artery disease.

The efficacy of oral sotalol in preventing sustained ventricular tachycardia induction by invasive electrophysiological testing was assessed in 22 patients (60 +/- 9 years) with prior myocardial infarction. Programmed stimulation consisted of two basic drives followed by up to three extrastimuli at two right ventricular sites. At baseline, sustained monomorphic ventricular tachycardia was inducible in all patients. With sotalol (360 +/- 172 mg/day), it was no longer inducible in 10 patients; in 12 others, it remained inducible and its cycle length was only minimally prolonged (322 +/- 42 to 345 +/- 44 msec, p less than 0.05). Sotalol markedly prolonged sinus cycle length, uncorrected QT interval, and right ventricular effective and functional refractory periods, but had little effect on ventricular conduction time either in sinus rhythm or with right ventricular pacing. There was no significant difference in drug dose or in electrophysiologic effect of drug that related to efficacy, nor was there any correlation between drug-induced prolongation of ventricular tachycardia cycle length and its effects. Six patients received oral sotalol over the long term without spontaneous recurrence of ventricular tachycardia (follow-up: 23 +/- 18 months). These results demonstrate that sotalol is effective (45%) against sustained ventricular tachycardia induction at moderate doses and is well tolerated over a long term in the setting of remote myocardial infarction. However, its electrophysiologic effects as measured at invasive testing are not predictive of efficacy against ventricular tachycardia induction.     

Significance of timing programmed electrical stimulation after acute myocardial infarction

To assess the influence of time on the inducibility by programmed electrical stimulation of ventricular arrhythmias after acute myocardial infarction, 18 patients were studied on day 5 and day 24 after infarction with a stimulation protocol employing a maximum of three right ventricular extrastimuli during sinus rhythm and at three paced cycle lengths. All patients were without documented sustained ventricular arrhythmia (sustained ventricular tachycardia or ventricular fibrillation) before the investigation. Sustained ventricular arrhythmia was induced in two patients on day 5, but in nine on day 24 after infarction. This difference in incidence was statistically significant (p less than 0.05), as was the change in the distribution ratio of induced sustained ventricular arrhythmia from day 5 to day 24 (p less than 0.05). The types of arrhythmia induced on day 24 were sustained ventricular tachycardia with a mean cycle length of 207 ms in six cases (five monomorphic, one polymorphic), and ventricular fibrillation in three cases. These nine patients did not differ from the remaining nine patients in maximal serum creatine kinase, infarct site, number of stenosed coronary arteries, global left ventricular ejection fraction (47 +/- 7% versus 46 +/- 10%) and results of 24 hour ambulatory electrocardiographic (Holter) monitoring, but they had a significantly shorter right ventricular effective refractory period (223 +/- 10 ms versus 259 +/- 28 ms; p less than 0.05). During the follow-up period of 24 +/-5 months no patient died, had syncopal attacks or developed spontaneous episodes of sustained ventricular arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Late potentials on the signal-averaged electrocardiogram after canine myocardial infarction: correlation with induced ventricular arrhythmias during the healing phase

Signal-averaged electrocardiograms (ECGs) and programmed ventricular stimulation were serially performed in 12 dogs (3 weeks of age) after experimental anteroapical myocardial infarction. At electrophysiologic study, sustained ventricular tachyarrhythmia was induced in seven dogs on at least one occasion. Of a total of 39 electrophysiologic studies, sustained monomorphic ventricular tachycardia was induced in seven studies and ventricular fibrillation in eight studies. In the remaining studies, no ventricular arrhythmia could be induced with triple ventricular extrastimuli. There was considerable day to day variability in the response to programmed stimulation and the results of the signal-averaged ECG. The signal-averaged QRS complex was significantly longer in dogs with inducible ventricular tachycardia or fibrillation (61 +/- 5 versus 57 +/- 3 ms, p = 0.02), had a lower terminal QRS amplitude (24 +/- 20 versus 46 +/- 33 microV, p = 0.04) and a longer late potential duration (19 +/- 4 versus 15 +/- 3 ms, p = 0.003) compared with that in animals with no inducible ventricular arrhythmia. Late potentials were defined as a total QRS duration greater than 58 ms, a terminal QRS amplitude less than 20 microV and a late potential duration greater than 18 ms. Using this definition, late potentials were seen in two distinct phases--immediately after coronary ligation and then beyond the first 72 h after infarction. The appearance of late potentials coincided with a change in arrhythmia inducibility from no ventricular arrhythmia to initiation of sustained monomorphic ventricular tachycardia. There is a close relation between inducibility of ventricular tachycardia in experimental canine myocardial infarction and the appearance of late potentials on the surface ECG.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of transmural versus nontransmural myocardial infarction on inducibility of ventricular arrhythmias during sympathetic stimulation in dogs

Transmural myocardial infarction interrupts sympathetic nerves and denervates viable muscle distal to myocardial infarction. The effect of sympathetic stimulation on responses to programmed ventricular stimulation was studied in dogs without myocardial infarction (Group I: n = 5), with transmural anterior wall myocardial infarction (Group II: n = 6) and with nontransmural anterior wall myocardial infarction (Group III: n = 9). Ventricular effective refractory period during sympathetic stimulation decreased by 16 +/- 18, 1 +/- 2 and 12 +/- 8 ms (mean +/- SD) in viable muscle of the inferoapical left ventricle in Groups I, II and III, respectively, suggesting efferent sympathetic denervation by transmural myocardial infarction only. Sustained ventricular tachycardia or fibrillation was induced more easily during sympathetic stimulation in six of the six dogs with transmural infarction, but in only two of the nine dogs with nontransmural infarction (p less than 0.01). It is concluded that the partial sympathetic denervation produced by transmural myocardial infarction enhances the ease of induction of ventricular tachycardia and fibrillation during sympathetic stimulation. A similar mechanism may lead to increased risk for lethal arrhythmias during periods of high sympathetic tone in patients with transmural myocardial infarction.     

Programmed ventricular stimulation in patients with left ventricular dysfunction and ventricular tachycardia: effects of acute hemodynamic improvement due to nitroprusside

To assess the electrophysiologic effects of acute hemodynamic improvement in patients with left ventricular systolic dysfunction, 12 patients with a left ventricular ejection fraction less than 0.40 and a history of sustained monomorphic ventricular tachycardia were studied. All patients had underlying coronary artery disease. Patients underwent programmed cardiac stimulation in random order during a baseline period and with nitroprusside infusion. Mean pulmonary capillary wedge pressure decreased from 20 +/- 8 mm Hg at baseline study to 8 +/- 3 mm Hg during nitroprusside infusion (p less than 0.0001). Pulmonary artery, right atrial and systemic arterial pressures also decreased with nitroprusside (p less than 0.01). Cardiac output did not change. Left ventricular dimensions, determined by two-dimensional echocardiography, decreased significantly during nitroprusside infusion. The right ventricular effective refractory period, measured during ventricular drive trains at cycle lengths of 400 and 600 ms, were similar during baseline and nitroprusside periods (271 +/- 30 versus 274 +/- 31 ms at 600 ms, and 249 +/- 25 versus 246 +/- 18 ms at 400 ms). In 2 patients no ventricular arrhythmias were induced during either study period; in the other 10, ventricular tachyarrhythmias were induced during both periods. The mean number of extrastimuli required to induce a ventricular tachyarrhythmia was similar during the baseline period (1.8 +/- 0.6) and during nitroprusside infusion (1.9 +/- 0.7). As well, the mean cycle length of ventricular tachycardia induced was similar during the baseline period (347 +/- 61 ms) and during nitroprusside infusion (342 +/- 70 ms).(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrical and hemodynamic function produced by stimulation of atropine sensitive right ventricular nerves in humans

In mammalian ventricles including humans, it is recognized that parasympathetic ganglia innervate the heart. Little is known about the location and function of right ventricular parasympathetic nerves in humans. We hypothesized that in humans: (1) there are parasympathetic ganglia that supply the right ventricle that can be stimulated via an endocardial catheter and (2) stimulation of these fibers will alter the electrical and hemodynamic function of the right ventricle. Parasympathetic nerve stimulation was performed via an endocardial catheter placed along several sites of the right ventricle, superior vena cava, and right internal jugular area in humans. The spatial extent of parasympathetic innervation was mapped in 1-cm zones across the right ventricle. Cardiac output, heart rate, and atrioventricular conduction were monitored to provide independent assessment of parasympathetic innervation. In all 22 patients, ventricular refractoriness shortened from 12 ± 3 to 3 ± 1 ms during parasympathetic nerve stimulation, and the greatest shortening of refractoriness was observed at the base of the right ventricle (p = 0.01). No significant shortening in ventricular refractoriness occurred in areas beyond 2 cm from the right ventricular base. These results were compared by using T table test. The parasympathetic nerve stimulation protocol decreased cardiac output, reaffirming the principle effect of parasympathetic ganglia. Atropine was administered in seven patients. All effects from nerve stimulation were abolished after atropine administration. These results were also compared by using T table test. These data provide the first demonstration of the electrical and hemodynamic function by stimulation of atropine sensitive nerves of the human right ventricle. Greater understanding of parasympathetic innervation may lead to novel therapies for arrhythmias.     

Usefulness of QRS prolongation in predicting risk of inducible monomorphic ventricular tachycardia in patients referred for electrophysiologic studies

QRS prolongation on surface electrocardiography has been identified as a marker for increased cardiac mortality. A potential mechanism for increased mortality is ventricular tachycardia (VT). This study aimed to evaluate the relation between bundle branch block and sustained monomorphic VT inducibility in patients referred for electrophysiologic studies. We analyzed a cohort of 777 patients (age 63 +/- 18 years, 67% men, left ventricular [LV] ejection fraction [EF] 45% +/- 16, prior myocardial infarction 41%) referred for electrophysiologic studies between 1994 and 2001 who underwent programmed stimulation for VT. Forty-five percent of patients were referred for syncope or a history of VT and/or ventricular fibrillation. Thirty-one percent of patients had prolonged QRS duration (> or =120 ms). Patients with prolonged QRS duration were older, had lower LVEFs, and were more likely to have a history of myocardial infarction. Prolonged QRS was a significant predictor of sustained monomorphic VT inducibility (p <0.0001). On multivariate analysis correcting for age, sex, LVEF, history of myocardial infarction, medications, and QRS conduction delay proved to be independently associated with sustained monomorphic VT inducibility (relative risk 3.290, 95% confidence interval 2.185 to 4.953 for prolonged vs normal QRS duration). Thus, a prolonged QRS duration on surface electrocardiography is a strong, independent predictor of inducible sustained monomorphic VT. Conduction delay may be an important risk factor, providing a substrate for the development of reentrant monomorphic VT, and furthermore suggests a potential mechanism for the increased mortality observed in patients with prolonged QRS.     

Electrophysiologic effects of diprafenone in supraventricular and ventricular tachycardia

The electrophysiologic effects of diprafenone were evaluated in 31 patients (9 X AV nodal reentrant tachycardia, 9 X Wolff-Parkinson-White syndrome, 4 X paroxysmal atrial fibrillation, 10 X recurrent ventricular tachycardia). Electrophysiologic studies were performed before and after intravenous infusion of 1.5 mg/kg body weight diprafenone in a period of 10 minutes. Diprafenone prolonged the mean RR interval during sinus rhythm from 690 +/- 109 ms to 789 +/- 93 ms and the maximal sinus node recovery time from 1081 +/- 216 ms to 1300 +/- 398 ms (p less than 0.001). The effective refractory period of the right atrium increased from 195 +/- 22 ms to 210 +/- 28 ms (p less than 0.01) and of the right ventricle from 220 +/- 20 ms to 235 +/- 20 ms (p less than 0.001). Diprafenone produced a prolongation of the antegrade effective refractory period of the AV node from 260 +/- 35 ms to 294 +/- 39 ms (p less than 0.01) and of the retrograde effective refractory period from 265 +/- 76 ms to 400 +/- 130 ms (p less than 0.001). The effective refractory periods of the Kent bundle increased: antegrade from 299 +/- 45 ms to 413 +/- 133 ms, retrograde from 252 +/- 33 ms to 286 +/- 169 ms (p less than 0.05). Suppression of inducibility was observed in 12 of 17 patients with supraventricular reentrant tachycardia, in 5 of 8 patients with atrial fibrillation and in 7 of 10 patients with recurrent ventricular tachycardia. The rate of supraventricular tachycardias decreased under the influence of the substance.(ABSTRACT TRUNCATED AT 250 WORDS)     

Efficacy of propafenone in preventing ventricular tachycardia: inverse correlation with rate-related prolongation of conduction time

The efficacy of propafenone in preventing induction of ventricular tachycardia was evaluated in 25 consecutive patients (mean age 62 +/- 8 years) with remote myocardial infarction who underwent programmed electrical stimulation for ventricular arrhythmia using up to three extra-stimuli after basic drive at the right ventricular apex. In nine patients (Group A), propafenone prevented induction of sustained ventricular tachycardia (noninducible in four, nonsustained [less than 30 s] in five). In the other 16 patients (Group B), sustained ventricular tachycardia was still inducible; in 11 of the 16, the tachycardia configuration was unchanged but the cycle length was significantly longer (431 +/- 99 versus 284 +/- 44 ms, p less than 0.001). Propafenone did not significantly affect either sinus cycle length or AH and HV intervals. However, it prolonged QRS duration during sinus rhythm equally in both groups of patients. With ventricular pacing, propafenone also prolonged right ventricular effective and functional refractory periods and surface QRS duration. There was greater lengthening of the paced surface QRS duration when drug therapy was ineffective (for example, +35 +/- 12 ms in Group A versus +69 +/- 23 ms in Group B at a basic drive of 400 ms, p less than 0.01). Drug-induced prolongation of a paced QRS complex greater than 40 ms had a 94% positive predictive value for drug failure to prevent induction of ventricular tachycardia. Drug-induced percent prolongation of ventricular tachycardia cycle length in Group B did not correlate well with percent QRS prolongation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiological changes of angiotensin-converting enzyme inhibition after myocardial infarction

To investigate whether prevention of remodeling would translate into a more stable electrophysiological profile, the investigators randomized 56 patients to treatment with angiotensin-converting enzyme (ACE) inhibition or placebo for 3 months after myocardial infarction. Programmed electrical stimulation revealed no significant differences in inducibility of monomorphic sustained ventricular tachycardia (VT), whereas ventricular fibrillation (VF) tended to be lower in the ACE-inhibitor group. Effective refractory periods were consistently longer, and dispersion of refractoriness was significantly shorter in the ACE-inhibitor group. The investigators conclude that in this small patient group ACE inhibition may mildly add to a more stable electrophysiological profile.     

Clinical predictors of arrhythmia inducibility in survivors of cardiac arrest: importance of gender and prior myocardial infarction

Clinical characteristics that correlate with arrhythmia inducibility were determined in 150 consecutive survivors of cardiac arrest. All underwent electrophysiologic study with a uniform protocol when they were not receiving antiarrhythmic drugs. A ventricular tachyarrhythmia (sustained monomorphic ventricular tachycardia, ventricular fibrillation or nonsustained ventricular tachycardia) was induced in 113 patients (75%). The strongest correlates of inducing a tachyarrhythmia were male gender (p less than 0.0001) and a history of prior myocardial infarction (p less than 0.0001). Induction of sustained monomorphic tachycardia alone was also strongly related to gender and prior infarction; in particular, none of 26 women without prior infarction had induction of sustained monomorphic ventricular tachycardia. Among patients with induced sustained tachyarrhythmias, those with induced monomorphic ventricular tachycardia were distinguished from those with induced ventricular fibrillation in they were more likely to have coronary artery disease (p = 0.0001), healed myocardial infarction (p = 0.0002), left ventricular aneurysm (p = 0.0007) and ventricular tachycardia documented at the time of cardiac arrest (p = 0.02). Other variables showing significant correlations with arrhythmia inducibility were ejection fraction, documentation of ventricular tachycardia at the time of cardiac arrest and presence of an intraventricular conduction delay. However, stepwise logistic regression identified male gender and healed myocardial infarction as the only independent predictors of arrhythmia inducibility. On the basis of these two variables alone, arrhythmia inducibility or noninducibility could be correctly predicted in 89% of the patients in this series.     

Narrow QRS ventricular tachycardia from the posterior mitral annulus without involvement of the His-Purkinje system in a patient with prior inferior myocardial infarction

A 54-year-old man with prior inferior myocardial infarction suffered from monomorphic ventricular tachycardia (VT) with narrow QRS complex of 120 ms. During VT, a fragmented prepotential preceding QRS onset by 30 ms at the right ventricular posterior septum and a late diastolic potential preceding QRS onset by 70 ms at the infarcted posterior mitral annulus were recorded. Radiofrequency energy delivered to the late diastolic potential at the posterior mitral annulus eliminated VT. During sinus rhythm, the late diastolic potential shifted to the end of QRS complex and no Purkinje potentials were observed. Synchronized excitation of both ventricles from the posterior infarcted mitral annulus in this patient may make the QRS width during VT narrow, without involvement of the His-Purkinje system.     

Effects of intravenous amiodarone on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia induction.

AIMS: Intravenous amiodarone has recently emerged as an important drug for the acute treatment of ventricular tachyarrhythmias. However, electrophysiological actions and the efficacy of the drug in the suppression of ventricular tachycardia inducibility have not yet been fully established. The present study was designed to address these issues. METHODS AND RESULTS: The study group consisted of 18 patients (all males, mean age 75 +/- 14 years), who underwent electrophysiological study due to a history of sustained ventricular tachyarrhythmia or syncope with non-sustained ventricular tachycardia detected on ambulatory ECG monitoring. The effects of 5 mg.kg(-1) or 10 mg.kg(-1) of intravenous amiodarone on (1) ventricular refractoriness (QTc interval, right ventricular effective refractory period and monophasic action potential duration), (2) intraventricular conduction (paced-QRS and signal-averaged QRS duration), and (3) ventricular tachycardia inducibility, were examined. The drug had no significant effect on ventricular refractoriness. However, a relatively small but significant slowing of intraventricular conduction was seen (paced-QRS duration: 182 +/- 27 ms vs 191 +/- 28 ms, P<0.0007; 183 +/- 32 ms vs 195 +/- 33 ms, P<0.0007; and 177 +/- 21 ms vs 192 +/- 24 ms, P<0.003, at the cycle lengths of 600, 500 and 400 ms, respectively). This effect was more evident during extrasystolic beats than during stable pacing (for example, at the cycle length of 600 ms, the magnitude of amiodarone-induced lengthening of QRS duration was 23.9 +/- 17.6 ms vs 9.7 +/- 7.2 ms, P<0.009, respectively). Intravenous amiodarone did not prevent induction of sustained ventricular tachycardia in any of five patients inducible at baseline. Of six patients with non-sustained ventricular tachycardia, five had sustained ventricular tachycardia or fibrillation induced after amiodarone infusion. CONCLUSION: Intravenous amiodarone does not prolong ventricular refractoriness, slows intraventricular conduction and may facilitate inducibility of sustained ventricular arrhythmias.     

Influence of right ventricular site of stimulation and infarct location on the inducibility of ventricular tachycardia in patients with coronary artery disease

No prior studies have evaluated the relationship between the site of right ventricular stimulation, the site of prior infarction, and the inducibility of ventricular tachycardia (VT). This study was performed to determine if the location of pathologic Q waves influences the inducibility of VT at various right ventricular sites in patients with coronary artery disease (CAD) and a history of myocardial infarction (MI). In 30 patients with a history of sustained, monomorphic VT, CAD, prior MI, and pathologic Q waves, programmed ventricular stimulation was performed at the right ventricular apex, septum, and outflow tract, in random order. There was electrocardiographic evidence of an MI that was inferior in 11 patients, anterior in 10 patients, and both inferior and anterior in 9 patients. Sustained, monomorphic VT was induced in 27 of 30 patients (90%). There were no significant differences among the three sites in the rate of inducibility of VT. The rate of inducible VT at each of the three right ventricular sites was not affected by the location of prior infarction. In conclusion, among patients with sustained, monomorphic VT, CAD, and a history of MI, the incidence of inducible sustained, monomorphic VT is not influenced by the location of prior infarction, regardless of whether programmed ventricular stimulation is performed at the right ventricular apex, septum, or outflow tract.     

Apical hypertrophic cardiomyopathy presenting with sustained monomorphic ventricular tachycardia and electrocardiographic changes simulating coronary artery disease and left ventricular aneurysm

A 52-year-old male presented with sustained monomorphic ventricular tachycardia as the initial manifestation of apical hypertrophic cardiomyopathy. The electrocardiogram during normal sinus rhythm showed a pattern of an old anterior wall myocardial infarction with aneurysm formation. Cardiac catheterization documented angiographically normal coronary arteries. Apical hypertrophic cardiomyopathy was documented at cardiac catheterization and by echocardiogram and Doppler studies. Monomorphic ventricular tachycardia was reproducibly initiated and terminated during electrophysiological studies and antiarrhythmic drugs failed to control the tachycardia. At the time of implantation of a cardioverter defibrillator, left ventricular apical biopsy revealed pathologic findings characteristic of hypertrophic cardiomyopathy.     

Trans-esophageal stimulation of the heart: electrophysiological properties of the heart of healthy subjects IV

The aim of the study to compare left atrial and ventricular electrophysiological properties determined by transesophageal stimulation with those of right atrium and ventricle measured by other authors using transvenous cardiac stimulation. 45 healthy persons (13 females and 32 males) with average age 37 years underwent the study. Transesophageal pacemaker SP-5 made by TEMED and an universal diagnostic electrode for atrial as well as ventricular stimulation were used to obtain ++noise-free recordings. ECG was recorded by 6-channel Mingograph 61 (Simens-Elema) with a paper speed - 100 mm/s. Left atrial effective refractory period (ERP LA), left ventricular effective refractory period (ERP LV), ERP of a-v conduction system measured from atrium and ventricle (ERP AVCS A, ERP AVCS R) were determined basing on generally acceptable criteria. Parameters were measured during sinus rhythm as well as atrial and ventricular stimulation with a pacing cycle length of 700 and 500 ms. There were also determined maximal antero- and retrograde 1:1 conduction via a-v node and a-v conduction time in both directions during atrial and ventricular pacing with a cycle length of 600 ms. No retrograde a-v conduction was stated in 33% of patients. Shortening of left atrial and ventricular effective refractory periods was respective to shortening of pacing cycle length from 700 to 500 ms: ERPLA-256-245-235 ms, for ERPLV-278-248-241 ms for ERP AVCS A-301, 405, 360 ms and for ERP AVCS R during sinus rhythm-312 ms. Maximal anterograde 1:1 a-v conduction was 162/min and retrograde one 156/min.(ABSTRACT TRUNCATED AT 250 WORDS)     

Inducible polymorphic ventricular tachycardia and ventricular fibrillation in a subgroup of patients with hypertrophic cardiomyopathy at high risk for sudden death

This investigation was undertaken to elucidate the underlying electrophysiologic substrate in hypertrophic cardiomyopathy and to identify possible predictors of sudden death in this patient population. Programmed stimulation was performed in 18 patients aged 14 to 64 years (mean 36) believed to be at high risk for sudden death on the basis of prior cardiac arrest or syncope, nonsustained ventricular tachycardia on Holter ambulatory electrocardiographic (ECG) monitoring or a family history of frequent sudden death. Polymorphic ventricular tachycardia that deteriorated to ventricular fibrillation was reproducibly induced in 8 (44%) of the 18 patients (Group A). This rhythm was induced in all three patients with a history of cardiac arrest. No sustained monomorphic ventricular tachycardia was induced. Group B comprised the 10 patients in whom a sustained arrhythmia could not be reproducibly initiated. The electrophysiologic substrate was distinctly different in patients with, than in those without, inducible sustained arrhythmia. The refractory period was shorter at the right ventricular outflow tract (232 +/- 22 ms) compared with the apex (264 +/- 12 ms) in Group A (p less than 0.005) whereas there was no difference in Group B (271 +/- 25 ms versus 271 +/- 13 ms). The local ventricular electrogram of most patients in both groups was prolonged and markedly multiphasic. However, 5 of the 8 Group A patients exhibited a double electrogram (V-V') with premature stimulation compared with 1 of the 10 patients in Group B (p less than 0.02). A positive R wave in lead aVR of the scalar ECG and poor R wave progression in the precordial leads were more common in Group A than in Group B (p less than 0.001 and p less than 0.001, respectively). The reason for the distinctly different electrophysiologic substrate and the high prevalence of inducible polymorphic arrhythmia is unclear. It may relate to the underlying myocardial architecture in these patients, characterized by myocardial cellular disarray and fibrosis.     

Comparison of the results of programmed ventricular stimulation from the right ventricular apex and outflow tract: a randomized, prospective study

Objective: The aim of this prospective study was to analysethe yield of programmed ventricular stimulation at the rightventricular apex compared with the outflow tract. Methods: A stepwise randomized cross-over protocol of programmedventricular stimulation with alternating stimulation at bothsites was used in 66 patients who were studied because of sustainedventricular tachycardia (n = 30), ventricular fibrillation (n= 7), or non-sustained ventricular tachycardia and/or syncope(n = 29). Results: There were no significant differences between the resultsof stimulation from either right ventricular site with regardto the presence or absence of structural heart disease, spontaneousarrhythmia, ejection fraction or effective refractory periods.Overall, monomorphic ventricular tachycardia was inducible in33 patients (50%); in 25 patients (75.8%), this arrhythmia wasinduced from both sites. However, in only 17 of these 25 patients(68%) did the induced monomorphic ventricular tachycardias havethe same morphologies and similar (± 50 ms) cycle lengths.Ventricular fibrillation was inducible in 11 patients (17%),mostly by three extrastimuli (n=8; 73%). Conclusions: (1) stimulation from at least two right ventricularsites is desirable because of their independent contributionto the induction of ventricular tachyarrythmias, (2) the non-inducibilityor inducibility at one ventricular site does not predict theeffect at another stimulation site, (3) the effective refractoryperiod at the right ventricular apex and outflow tract do notdiffer, (4) the inducibility of multiple ventricular tachycardiamorphologies emphasizes the importance of documenting the causeof spontaneous arrhythmias with multiple electrocardiographicleads to ensure the correct interpretation of arrhythmias inducedby programmed stimulation, (5) clinical or haemodynamic featurescannot predict whether one or more stimulation sites will berequired for induction of ventricular tachycardia. These resultsare important for the diagnostic evaluation and assessment ofpharmacological or non-pharmacological interventions.     

Long-term reproducibility and significance of provokable ventricular arrhythmias after myocardial infarction

The long-term reproducibility and significance of inducible ventricular arrhythmias were assessed in 21 survivors of a myocardial infarction. Programmed ventricular stimulation performed a mean of 12 +/- 2 days (range 8 to 18) after infarction provoked ventricular fibrillation in 2 patients, sustained monomorphic ventricular tachycardia in 8 and nonsustained ventricular tachycardia in 11. Patients were restudied using the same protocol a mean of 8 +/- 2 months (range 4 to 11) after infarction. All patients underwent programmed ventricular stimulation studies in the absence of antiarrhythmic drug treatment. Ventricular tachyarrhythmias could be reinitiated in 16 patients (76%): ventricular fibrillation in 2, sustained ventricular tachycardia in 5 (monomorphic in 4) and nonsustained ventricular tachycardia in 9. A preponderance of inferior infarction was observed among patients with reinducible tachycardias (9 of 16 patients versus 0 of 5 with noninducible tachycardias) (p less than 0.05). No significant difference existed between patients with and without reinducible arrhythmias with respect to severity of coronary artery disease, degree of left ventricular dysfunction, occurrence of ventricular fibrillation in the acute phase of infarction and ventricular arrhythmias detected by 24 hour ambulatory electrocardiographic (Holter) monitoring. There was no significant difference between patients with and without a positive late study in stimulation thresholds, ventricular refractory periods, time interval between initial and repeat testing and use of beta-adrenergic blocking agents. During a mean follow-up period of 17 months (range 10 to 23) one patient with inducible sustained monomorphic ventricular tachycardia at both studies died suddenly. The remaining patients have survived follow-up without experiencing an arrhythmic event.(ABSTRACT TRUNCATED AT 250 WORDS)