Pacing-induced myocardial ischemia does not affect the endothelial release of coagulant and fibrinolytic factors into the coronary circulation.

The present study addresses the potential effects of pacing-induced myocardial ischemia on the secretion of coagulant and fibrinolytic factors within the coronary circulation. In 6 patients undergoing programmed ventricular stimulation with repeated induction of clinical ventricular tachycardia, the coronary release of tissue-type plasminogen activator (t-PA) antigen, plasminogen activator inhibitor (PAI) capacity, von Willebrand factor antigen (WF:Ag), and prostacyclin (6-keto-PGF 1a) was measured. Blood samples were collected simultaneously from the ascending aorta and the coronary sinus at baseline and immediately after the induction of ventricular tachycardia. The occurrence of pacing-induced myocardial ischemia was established by myocardial net lactate production. Myocardial ischemia was induced in every patient by repeated pacing trials. Pacing-induced ischemia did not affect the coronary release of any of the above factors. Consequently, there was no alteration of transcardiac gradients of thrombin-antithrombin complexes and D-dimer. The present results indicate that pacing-induced myocardial ischemia does not affect the release of coagulant and fibrinolytic endothelial factors or prostacyclin into the coronary circulation.     

Sustained ventricular arrhythmias: differences between survivors of cardiac arrest and patients with recurrent sustained ventricular tachycardia

Clinical, angiographic, echocardiographic and electrophysiologic data were examined in 101 patients with a history of sustained ventricular arrhythmia not associated with acute myocardial infarction. These patients included 66 survivors of out of hospital cardiac arrest and 35 patients presenting with hemodynamically well tolerated sustained ventricular tachycardia. On univariate analysis, patients in the cardiac arrest group had a lower incidence of previous myocardial infarction and left ventricular aneurysm and a higher ejection fraction compared with the ventricular tachycardia group. During electrophysiologic testing, the arrhythmia induced in the patients in the cardiac arrest group was fast and polymorphic and frequently degenerated into ventricular fibrillation. In contrast, in the ventricular tachycardia group, a slower, monomorphic and hemodynamically well tolerated ventricular tachycardia was commonly induced. On multivariate analysis, a polymorphic pattern of the induced ventricular arrhythmia was the only independent variable that distinguished the survivors of cardiac arrest from those presenting with sustained ventricular tachycardia. These results suggest that 1) the survivors of cardiac arrest and patients presenting with sustained well tolerated ventricular tachycardia are clinically distinct groups; and 2) the polymorphic tachycardia induced during programmed electrical stimulation in the survivors of cardiac arrest may indicate an unstable tachycardia mechanism. This may explain why these patients present with ventricular fibrillation and cardiac arrest, whereas others present with hemodynamically stable ventricular tachycardia.     

Effect of programmed ventricular stimulation on myocardial lactate extraction in patients with and without coronary artery disease

The arterial-coronary sinus lactate difference was measured in 17 patients after each step of a programmed ventricular stimulation protocol consisting of single, double, and triple extrastimuli, first at a basic drive cycle length of 600 msec, then at 400 msec, with an inter-train interval of 4 seconds. Four patients had no structural heart disease, four had an idiopathic dilated cardiomyopathy, and nine had coronary artery disease with a significant stenosis in at least one branch of the left coronary artery. Net myocardial lactate production during programmed ventricular stimulation was observed in three patients with coronary artery disease, but not in any patient without coronary artery disease. Among the patients who had coronary artery disease, net myocardial lactate production generally occurred in the patients who had more severe coronary artery disease. Exercise-induced ischemia, as demonstrated by a stress thallium-201 test, did not correlate with myocardial lactate production during programmed ventricular stimulation. Programmed ventricular stimulation, with a stimulation protocol typically used in many electrophysiology laboratories, is capable of inducing myocardial ischemia in at least some patients who have coronary artery disease. This finding suggests that myocardial ischemia may potentially influence the results of programmed ventricular stimulation in some patients with coronary artery disease.     

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.     

Clinical features and prognosis of patients with out of hospital cardiac arrest and a normal electrophysiologic study

Nineteen patients survived a cardiac arrest not associated with an acute myocardial infarction, and had a normal electrophysiologic study with no inducible ventricular tachycardia despite programmed stimulation with one to three extrastimuli at two or more ventricular sites. Among 14 patients who had obstructive coronary artery disease, cardiac arrest occurred during exertion or an episode of angina pectoris in 11; 24 hour ambulatory electrocardiographic recordings demonstrated infrequent or no premature ventricular complexes in 10 and an ischemic response occurred during stage I or II (Bruce protocol) in 6 of 9 patients who underwent exercise testing. Treatment of these patients consisted of myocardial revascularization (eight patients) or antianginal medications (six patients). Only three patients were also treated with an antiarrhythmic drug. Over a follow-up period of 26 +/- 15 months (mean +/- standard deviation), only one patient died suddenly. Two patients who had coronary artery spasm were treated with coronary vasodilator medications and had no recurrence of cardiac arrest over 7 and 36 months of follow-up, respectively. Three patients who had cardiomyopathy or no identifiable structural heart disease were treated with nadolol or amiodarone and had no recurrence of cardiac arrest over 3 to 27 months of follow-up. Among patients who survive a cardiac arrest and have a normal electrophysiologic study, those with obstructive coronary artery disease or coronary artery spasm generally have an excellent prognosis with treatment directed primarily at the underlying heart disease. The clinical features of these patients suggest that cardiac arrest was related to ischemia rather than a primary arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Surgical coronary revascularization in survivors of prehospital cardiac arrest: its effect on inducible ventricular arrhythmias and long-term survival

In a selected subgroup of 50 survivors of cardiac arrest, the impact of surgical myocardial revascularization on inducible arrhythmias, arrhythmia recurrence and long-term survival was examined. The effects of several clinical, angiographic and electrophysiologic variables on arrhythmia recurrence and survival were also analyzed. All patients had a prehospital cardiac arrest and severe operable coronary artery disease and underwent myocardial revascularization. Preoperative electrophysiologic study was performed in 41 patients; 33 (80%) had inducible ventricular arrhythmias. Of 42 patients studied off antiarrhythmic drugs postoperatively, 19 (45%) had inducible ventricular arrhythmias. Thirty patients with inducible arrhythmias preoperatively underwent postoperative testing off antiarrhythmic drugs; arrhythmia induction was suppressed in 14 (47%). By multivariate analysis, the induction of ventricular fibrillation at the preoperative electrophysiologic study was the only significant predictor of induced ventricular arrhythmia suppression by coronary surgery (p less than 0.001). Inducible ventricular fibrillation was not present postoperatively in any of the 11 patients who manifested this arrhythmia preoperatively. In contrast, inducible ventricular tachycardia persisted in 80% of patients in whom preoperative testing induced this arrhythmia. Patients were followed up for 39 +/- 29 months. There were four arrhythmia recurrences; one was fatal. There were three nonsudden cardiac deaths and three noncardiac deaths. By life-table analysis, 5 year survival, cardiac survival and arrhythmia-free survival rates were 88%, 98%, and 88%, respectively. Depressed left ventricular ejection fraction and advanced age were predictive of death (p = 0.015 and 0.026, respectively) and cardiac death (p = 0.037 and 0.05, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Efficacy of combination therapy with mexiletine and a type IA agent for inducible ventricular tachyarrhythmias secondary to coronary artery disease

The efficacy of combination therapy using a type IA agent (quinidine or procainamide) and a type IB agent (mexiletine) in suppressing inducible sustained ventricular tachyarrhythmias was studied in 23 patients undergoing serial drug testing with programmed stimulation. All patients had coronary artery disease (CAD) with previous myocardial infarction and abnormal left ventricular function (mean ejection fraction 35%). Fifty-five percent of the patients presented with syncope or cardiac arrest. In 19 patients therapy had failed during empiric trials of 1 to 3 antiarrhythmic agents. All 23 patients had inducible sustained ventricular tachyarrhythmias (18 had uniform morphology sustained ventricular tachycardia (VT) and 5 had ventricular fibrillation [VF]) during control electrophysiologic study, and therapy had failed with a type IA agent and mexiletine alone. The combination therapy of mexiletine and the type IA agent prevented induction of any ventricular tachyarrhythmias in 8 of 23 patients. In 15 patients, the combination significantly prolonged the tachycardia cycle length and reduced the symptoms associated with the induced arrhythmia. Patients more likely to respond to the combination had shorter cycle lengths and polymorphic configuration of the control-induced arrhythmia. The increased efficacy of the combination therapy could not be attributed to higher plasma drug levels for the combination, as there was no significant difference in plasma levels for each drug when given alone or in combination. Thus, the increased efficacy most likely reflects a synergistic electropharmacologic effect of the 2 agents.(ABSTRACT TRUNCATED AT 250 WORDS)     

Usefulness of programmed stimulation in idiopathic dilated cardiomyopathy

The response to programmed electrical stimulation and the clinical outcome was determined in 47 patients with nonischemic dilated cardiomyopathy (DC). Thirteen patients (group 1) presented with sustained uniform ventricular tachycardia (VT), 14 (group 2) presented with cardiac arrest and 20 (group 3) presented with nonsustained VT. The mean ejection fraction of the study population was 28 +/- 9%. The response to programmed stimulation was related to arrhythmia presentation. In all patients in group 1 sustained, uniform VT was induced, compared with 1 patient in group 2 and 2 patients in group 3 (p less than 0.001). There were 14 sudden cardiac deaths and 1 cardiac arrest during a mean follow-up of 18 +/- 14 months. The only 4 patients who presented with sustained VT or a cardiac arrest in whom sustained arrhythmia induction was suppressed with antiarrhythmic therapy remain alive. Nine of the 23 patients (4 in group 2 and 5 in group 3) in whom no sustained ventricular arrhythmia was induced died suddenly, with 5 of the 9 receiving empiric antiarrhythmic therapy. Three other patients, who had a slower and hemodynamically tolerated VT at the time of arrhythmia induction, died suddenly. Thus, in patients with nonischemic DC, uniform, sustained VT is always and almost solely initiated in patients who present with this arrhythmia; although few patients presenting with sustained VT or cardiac arrest have inducibility of the arrhythmias suppressed with therapy, if it is suppressed the patient appears to have a good prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

The nature of ventricular arrhythmias during ergonovine-induced vasospastic angina pectoris

The peak incidence of ventricular fibrillation in acute myocardial infarction usually occurs during the first hours after the onset. Electrophysiological changes immediately after the onset have been studied in animal models, but are still incompletely understood in humans. For clarification of the characteristic features of ventricular arrhythmias during acute myocardial ischemia, ventricular arrhythmias were studied in 81 patients with vasospastic angina pectoris induced by ergonovine. Ventricular arrhythmias occurred in 45 of these patients, including ventricular tachycardia in 15, and ventricular fibrillation requiring repeated DC defibrillation in two patients. Most ventricular extrasystoles occurred before the ST segment reached maximum elevation, while reperfusion arrhythmias were less common. In many patients the coupling intervals varied, and the configuration was multiform. It is concluded that ventricular arrhythmias occurring during ergonovine-induced coronary spasm show different characteristics from those occurring during chronic ischemia. As the arrhythmias in this study seem, in some ways, to resemble arrhythmias occurring at the onset of myocardial infarction, the results might provide useful information on ventricular arrhythmias in myocardial ischemia in humans.     

Nonventricular arrhythmias as precursors of ventricular fibrillation in patients with out-of-hospital cardiac arrest

Ventricular tachycardia (VT) and ventricular fibrillation (VF) are the most common arrhythmias documented at the time of resuscitation in survivors of out-of-hospital cardiac arrest unassociated with an acute myocardial infarction. However, 20% and 40% of these patients will not manifest inducible ventricular arrhythmias during subsequent electrophysiologic studies. The optimal management of these patients has been controversial. In a consecutive series of 100 survivors of out-of-hospital cardiac arrest with documented VF, six were identified by either clinical or electrophysiologic data as having a nonventricular arrhythmia as the immediate precursor of VF. Two of these patients had rapid, hypotensive supraventricular arrhythmias induced with programmed cardiac stimulation. In four patients, bradyarrhythmias (sinus arrest two; atrioventricular block two) preceded and caused the episode of VF. Therapy directed at these nonventricular arrhythmias prevented recurrence of cardiac arrest in all patients. In survivors of out-of-hospital cardiac arrest, nonventricular arrhythmias represent a treatable potential etiology that may be overlooked during the patient's evaluation.     

Electrophysiologic and hemodynamic studies in patients resuscitated from cardiac arrest

Fifty-two patients resuscitated from cardiac arrest underwent electrophysiologic studies. The earliest documented arrhythmia at the time of initial or recurrent (18 patients) cardiac arrest was ventricular fibrillation (30 patients) or ventricular tachycardia (20 patients); in 2 patients no arrhythmia was documented before defibrillation. Programmed ventricular stimulation revealed inducible arrhythmias in 33 patients (63 percent). Of the 30 patients with ventricular fibrillation as the initial arrhythmia, 13 had inducible arrhythmias—ventricular fibrillation (4 patients), sustained ventricular tachycardia (6 patients) and nonsustained ventricular tachycardia (3 patients). In the 20 patients with ventricular tachycardia as the initial arrhythmia, sustained ventricular tachycardia was initiated in 17 patients and torsade de pointes in 1. Patients with inducible arrhythmias had longer mean A-H and H-V intervals than those without inducible arrhythmias (91.1 versus 76.6 ms and 62.5 versus 50.3 ms, respectively). Prolonged H-V intervals (17 of 33) and intraventricular conduction defects (18 of 33) were more common in patients with than in those without inducible arrhythmias (4 of 19 and 7 of 19, respectively). Mean cardiac index was lower (2.4 versus 3.9 liters/min per m²), left ventricular end-diastolic pressure higher (17.0 versus 9.4 mm Hg), and ejection fraction lower (36.1 versus 57.2 percent) in the group with inducible arrhythmias than in those in whom no arrhythmia could be induced. These data suggest that (1) ventricular tachycardia often precipitates cardiac arrest; and (2) electrophysiologic testing may provide data on which to base therapy in patients resuscitated from cardiac arrest.     

Effect of isoproterenol on induction of ventricular tachyarrhythmias in the normal and infarcted canine heart

The influence of isoproterenol on induction of ventricular arrhythmias was evaluated in 10 normal dogs and 17 dogs with experimentally induced myocardial infarction. Programmed stimulation (using up to 6 extrastimuli) was performed before and then during infusion of isoproterenol (2 micrograms/minute followed by 4 micrograms/minute). Isoproterenol facilitated induction of sustained monomorphic ventricular tachycardia (cycle length 163 +/- 26 msec) in 5 of the 10 animals with no inducible baseline arrhythmia (P less than 0.05). Isoproterenol did not affect cycle length or the number of extrastimuli required in animals with baseline ventricular tachycardia (cycle length 158 +/- 15 msec before versus 163 +/- 17 msec during isoproterenol, P = 0.3; extrastimuli 3.8 +/- 0.6 before versus 3.8 +/- 0.4 during isoproterenol infusion, P = 0.3). Isoproterenol did not significantly facilitate induction of ventricular fibrillation in either normal dogs or those studied after production of myocardial infarction. We conclude that infusion of isoproterenol increases the incidence of inducible ventricular tachycardia in the infarcted heart, but does not facilitate the induction of ventricular fibrillation in infarcted or normal hearts, despite the use of an aggressive protocol for programmed stimulation. Isoproterenol is, therefore, a safe and useful adjunct to programmed stimulation in this setting.     

Hemodynamic and electrophysiologic evaluation of patients with hypertrophic cardiomyopathy surviving cardiac arrest

Hemodynamic and electrophysiologic studies were performed in 30 survivors of sudden cardiac arrest with hypertrophic cardiomyopathy (HC) to determine responsible factors. Electrophysiologic abnormalities alone were present in 27 patients (90%): sinus node dysfunction in 14 (47%), delayed atrio-ventricular nodal conduction in 1 (3%), abnormal His-Purkinje conduction in 7 (23%), an inducible atrial tachycardia in 7 (23%), and inducible sustained ventricular arrhythmia in 21 (70%). Sustained ventricular arrhythmia was polymorphic ventricular tachycardia (VT) in 18 patients (86%), monomorphic VT in 2 patients (7%) and ventricular fibrillation in 1 patient (3%). In 1 patient the arrhythmia recorded during an episode of cardiac arrest and induced at electrophysiologic study was polymorphic VT. VT was induced with less than or equal to 2 extra-stimuli in only 1 patient (3%) but with less than or equal to 3 extra-stimuli in 20 patients (97%). Potential causes of sudden cardiac arrest were found in all patients and were multiple in 13 patients (43%). These were (1) ventricular electrical instability in 21 patients (70%), (2) severe left ventricular outflow tract obstruction in 8 patients (27%), (3) bradycardia in 5 patients (17%), (4) myocardial ischemia associated with hypotension in 5 patients (17%), and (5) atrial tachycardia resulting in hypotension in 4 patients (13%). Of the 21 patients with inducible sustained ventricular arrhythmia, 17 received an implantable defibrillator device and 4 were treated with antiarrhythmic drugs. Seven patients underwent left ventricular septal myectomy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Significance of ST segment depression during paroxysmal supraventricular tachycardia

During paroxysmal supraventricular tachycardia, patients frequently experience chest pain and marked ST segment depression suggesting acute myocardial ischemia. The purpose of this study was to assess whether ST depression during supraventricular tachycardia is caused by myocardial ischemia as reflected by net myocardial lactate production. Twenty-five patients (14 men, 11 women) who had a history of paroxysmal supraventricular tachycardia and a mean age (+/- SD) of 38 +/- 14 years underwent electrophysiologic testing. Twenty-four of these patients had no evidence of coronary disease, whereas one patient had undergone previous coronary bypass surgery. Nineteen patients had orthodromic and six patients had atrioventricular node reentrant tachycardias. A 12 lead electrocardiogram and simultaneous femoral artery and coronary sinus blood samples for lactate determinations were obtained at baseline and at 5 and 10 min of supraventricular tachycardia. Mean baseline heart rate of 83 +/- 12 beats/min increased to 180 +/- 25 beats/min during supraventricular tachycardia. All patients had 1 to 8 mm of ST segment depression in 1 to 9 of the 12 leads. Chest pain occurred in 64% of patients during supraventricular tachycardia. Baseline myocardial lactate extraction was 28 +/- 13% with no significant change at 5 or 10 min of tachycardia. In contrast, in a comparison group of seven patients with known coronary artery disease, atrial pacing at 168 +/- 26 beats/min in five patients resulted in greater than or equal to 1 mm ST depression in 2 to 7 of the 12 leads and a change in lactate extraction from a baseline of 29 +/- 13% to -27 +/- 20% (p less than 0.05) indicating net myocardial lactate production.(ABSTRACT TRUNCATED AT 250 WORDS)     

Induction of ventricular fibrillation versus monomorphic ventricular tachycardia during programmed stimulation. Role of premature beat conduction delay.

BACKGROUND. Premature stimuli can cause ventricular fibrillation (VF) during electrophysiological testing. The electrophysiological correlations associated with the onset of VF were evaluated in 40 patients who had this rhythm induced during programmed ventricular stimulation. These parameters were compared with those observed in 51 patients who had inducible sustained monomorphic ventricular tachycardia (VT) and 45 patients who had no inducible sustained ventricular tachyarrhythmias. METHODS AND RESULTS. Shortest premature coupling intervals for S2, S3, and S4 at induction of tachycardia or before achieving refractoriness, corresponding conduction latencies (defined as the time from the premature stimulus to the upstroke of the depolarization wave front recorded 35 mm away from the stimulation site), and ventricular activation times (defined as the time from the premature stimulus to the end of the depolarization wave) were compared. The mean coupling intervals were longest in the inducible VT patients: 300 +/- 30, 254 +/- 57, and 228 +/- 32 msec for S2, S3, and S4, respectively. In the inducible VF group, the coupling intervals were 260 +/- 37, 208 +/- 20, and 213 +/- 30 msec. In the group with no inducible VT or VF, these coupling intervals were 251 +/- 24 (p less than 0.01 versus inducible VT group), 209 +/- 27 (p less than 0.001 versus inducible VT group), and 194 +/- 21 msec (p less than 0.05 versus inducible VT and VF groups). The coupling interval of the last premature extrastimulus was above 200 msec in 70% of the patients in whom VF was induced. The largest increases in latency and activation times were recorded in patients in whom VF was induced. The cumulative increase in latency, defined as increased conduction time from baseline, summed for all the premature stimuli was also the greatest at initiation of VF. In contrast, the smallest increases in these parameters were noted in the patients with no inducible VT or VF. Measurements of total activation time yielded similar results as those recorded for latencies. The most important parameters distinguishing the VT patient population from the other two groups were the low ejection fractions and the longer coupling intervals at which VT was induced, whereas in the VF group, the most important discriminating factor was cumulative activation time. Sixty-three percent of the inducible VF patients presented with abnormal hearts (myocardial infarction or cardiomyopathy), whereas 88% of the inducible VT patients had abnormal hearts. In contrast, only 25% of the patients in whom no arrhythmia was induced presented with abnormal hearts. Mean ejection fraction was 32 +/- 15% for the inducible VT group, 45 +/- 13%* for the inducible VF group, and 51 +/- 17%* for patients with no inducible VT/VF (*p less than 0.001 versus VT). CONCLUSIONS. The results suggest that 1) initiation of ventricular tachycardia during programmed ventricular stimulation occurs with minimal conduction latency; 2) because of the large overlap in coupling intervals where VF or VT were induced, a single coupling interval cannot be recommended to adequately separate these groups; and 3) induction of VF was preceded by increased latency and prolongation of the local activation time. These parameters should not be allowed to prolong if VF is to be avoided during programmed stimulation. In addition, 4) the initiation of VF during electrophysiological studies is often associated with the presence of structural heart disease; such structural disease may promote conduction latency and the development of VF.     

The role of silent ischemia, the arrhythmic substrate and the short-long sequence in the genesis of sudden cardiac death

To study the role of silent ischemia and the arrhythmic substrate in the genesis of sudden cardiac death, 67 patients were studied (mean age 62 +/- 12 years). Of these, 14 patients (Group 1) had an in-hospital episode of ventricular tachycardia or fibrillation while wearing a 24 h Holter ambulatory electrocardiographic (ECG) monitor, 33 (Group II) had a documented episode of sustained ventricular tachycardia or fibrillation, or both, and 20 (Group III) had angina pectoris but no ventricular tachycardia or fibrillation. Eight Group I survivors underwent programmed electrical stimulation or ECG signal averaging, or both. All Group II patients underwent 24 h Holter monitoring and ECG signal averaging to detect late potentials before programmed electrical stimulation. Group III patients underwent both 24 h Holter recording and coronary angiography. The 24 h ECG tapes were analyzed for ST segment changes, prematurity index and characteristics of ventricular premature depolarizations. Any ST depression greater than or equal to 1 mm for greater than 30 s was considered to be a reflection of silent ischemia, and the induction of ventricular tachycardia or fibrillation by programmed electrical stimulation or the presence of late potentials, or both, was considered to be a reflection of the arrhythmia substrate. Silent ischemia preceded ventricular tachycardia in only 2 (14%) of the 14 Group I patients. The prematurity index was less than 1 in only 18% of ventricular tachycardia episodes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Amelioration of the effects of ischemic cardiac arrest by the intracoronary administration of cardioplegic solutions.

Interruption of coronary flow during cardiac surgical procedures provides a bloodless flaccid heart and allows precise and rapid correction of complex cardiac defects. However, myocardial damage occurs in direct proportion to the duration of the ischemia. As the induction of cardioplegia simulataneous with the initiation of cardiac ischemia helps to preserve cardiac energy reserves and thus myocardial integrity, the identification of a consistently reliable cardioplegic technique is desirable. Isolated perfused working rat hearts were made ischemic for one hour by aortic cross-clamping and were compared with hearts rendered cardioplegic at the onset of ischemia by the intracoronary administration of 5 ml of a hypothermic solution: 1) Krebs-Henseleit buffer, 2) Ringer's lactate, 3) tetrodotoxin, 4) potassium chloride, or 5) potassium citrate. Cardiac output, heart rate, aortic pressure and coronary flow were determined pre and post-ischemia. When compared to time-matched controls and hearts arrested with potassium or tetrodotoxin, the ischemia and ischemia-Ringer's lactate groups showed significant post cross-clamp depression of all measured parameters. Intracoronary Ringer's lactate, although often used as an adjunct to ischemic arrest, was not of significant value. In contrast, hearts arrested with tetrodotoxin, potassium chloride or potassium citrate showed no significant post-ischemic functional or histologic deficit. Perfusion with hypothermic Krebs-Henseleit buffer protected the myocardium better than did Ringer's lactate but less well than the tetrodotoxin or isotonic high potassium solutions. The induction of hypothermic metabolic arrest of the heart by briefly perfusing the coronary arteries via the aortic root with isotonic buffered solutions results in markedly improved myocardial tolerance to one hour of ischemia and avoids the problems of low cardiac output and ventricular irritability previously reported with hypertonic potassium citrate arrest.     

Myocardial ischemia and induction of sustained ventricular tachyarrhythmias: evaluation using dobutamine stress echocardiography-electrophysiologic testing

INTRODUCTION: This study examined the relationship between dobutamine facilitation of ventricular tachyarrhythmia (VT) inducibility with programmed electrical stimulation (PES) and dobutamine stress-induced myocardial ischemia. METHODS AND RESULTS: Twenty patients with prior myocardial infarction and cardiac arrest or sustained VT but no sustained VT induced at baseline electrophysiologic testing underwent repeat PES during dobutamine infusion. Ischemia (new or worsened wall-motion abnormality) was documented by echocardiography performed in conjunction with PES. Eight patients were receiving Class I or III antiarrhythmic drugs and seven beta-blockers. Dobutamine facilitated induction of sustained VT in 16 patients (80%) and provoked ischemia in 13 patients (65%). Induction of VT was associated with ischemia in 9 patients (56%). VTs associated with ischemia were induced at higher dobutamine doses (26 +/- 11 vs 11 +/- 10 microg/kg per min, P = 0.02) than were VTs without ischemia (n = 7). Among 13 patients with provoked ischemia, 9 (69%) had VTs induced and 4 remained noninducible. The onset of ischemia occurred at the same dose as induction of VT in 5 patients and at a lower dose in 4 patients. Monomorphic VT (318 +/- 59 ms) was induced in 13 patients, of whom 8 (62%) had ischemia. The ECG morphology of VT suggested an origin in a myocardial segment that demonstrated initial viability at low doses then ischemic dysfunction at higher doses preceding VT induction in 7 (88%) of 8 patients. CONCLUSION: Dobutamine enhances inducibility of sustained VTs during PES. The temporal and anatomic association of dobutamine-induced ischemia and VT suggests that at high dobutamine doses, ischemia may contribute to ventricular arrhythmia inducibility in some patients.     

Prevalence of supraventricular tachycardia and tachyarrhythmias in resuscitated cardiac arrest

Supraventricular arrhythmias are considered to be benign when the ventricular rate is slowed and treated by anticoagulants. The aim of this study was to determine the possible influence of these arrhythmias in resuscitated cardiac arrest. Between 1980 and 2002, 151 patients were admitted after a cardiac arrest. Supraventricular arrhythrmias were identified as a possible cause of the cardiac arrest in 21 patients. They underwent echocardiography, exercise stress test, Holter ECG monitoring , coronary angiography and electrophysiological investigation. After these investigations, three patients had a malignant form of the Wolff-Parkinson-White syndrome, two were asymptomatic and, in the third patient, ventricular fibrillation was induced by treatment with diltiazem. In 8 patients, a rapid supraventricular arrhythmia was considered to be the cause of cardiac arrest by cardiogenic shock; 2 patients had hypertrophic cardiomyopathy, 5 had severe dilated cardiomyopathy which regressed in one patient. In ten patients, cardiac arrest due to ventricular tachycardia or fibrillation was provoked by a rapid (> 220 beats/min) supraventricular arrhythmia; two patients had no apparent underlying cardiac pathology. In the others, myocardial ischaemia or acute cardiac failure were considered to be the cause of the cardiac arrest. The authors conclude that rapid supraventricular arrhythmias may cause cardiac arrest either by cardiogenic shock or degenerescence to ventricular tachycardia or fibrillation. Usually, this event occurs in patients with severe cardiac disease but it may occur in subjects without cardiac disease or by an arrhythmia-induced cardiomyopathy.     

Complex ventricular extrasystole. Value of technics of programmed electric stimulation

The incidence and significance of ventricular arrhythmia induced by programmed electrical stimulation in subjects with complex ventricular ectopy were studied in 46 consecutive subjects: 34 with heart disease, 12 with an apparently normal heart. The procedure consisted of delivering on one spontaneous and 2 imposed rhythms one, two, then three extrastimuli. Significant arrhythmia with more than 6 ventricular complexes was induced in 17 patients (37%), including 6 (13%) with sustained ventricular tachycardia and 11 with unsustained ventricular tachycardia. Induction of ventricular arrhythmia was observed in 12 of the 14 patients with a history of myocardial infarction. At the end of a mean follow-up period of 12 +/- 4 months, there were 2 sudden deaths, and 3 patients had clinically sustained ventricular tachycardia. Clinical ventricular tachycardia occurred in the group of 17 patients inducible during programmed electrical stimulation. The patients who died suddenly belonged to the group of 29 patients without induced ventricular arrhythmia. This study shows a high proportion of significant stimulation-induced arrhythmia in patients who had suffered from myocardial infarction more than 3 months previously and who had complex ventricular ectopy. Owing to the good condition of this group of patients after a mean follow-up of 12 months, we were unable to determine the influence of stimulation-induced arrhythmia on mortality. However, it must be noted that spontaneous sustained tachycardia occurred in the group of patients with significant induced ventricular arrhythmia.