Prediction of long-term outcomes by signal-averaged electrocardiography in patients with unsustained ventricular tachycardia, coronary artery disease, and left ventricular dysfunction.

BACKGROUND: An abnormal signal-averaged ECG (SAECG) is a noninvasive marker of the substrate of sustained ventricular tachycardia after myocardial infarction. We assessed its prognostic ability in patients with asymptomatic unsustained ventricular tachycardia, coronary artery disease, and left ventricular dysfunction. METHODS AND RESULTS: A blinded core laboratory analyzed SAECG tracings from 1925 patients in a multicenter trial. Cox proportional hazards modeling was used to examine individual and joint relations between SAECG variables and arrhythmic death or cardiac arrest (primary end point), cardiac death, and total mortality. We also assessed the prognostic utility of SAECG at different levels of ejection fraction (EF). A filtered QRS duration >114 ms (abnormal SAECG) independently predicted the primary end point and cardiac death, independent of clinical variables, cardioverter-defibrillator implantation, and antiarrhythmic drug therapy. With an abnormal SAECG, the 5-year rates of the primary end point (28% versus 17%, P=0.0001), cardiac death (37% versus 25%, P=0.0001), and total mortality (43% versus 35%, P=0.0001) were significantly higher. The combination of EF <30% and abnormal SAECG identified a particularly high-risk subset that constituted 21% of the total population. Thirty-six percent and 44% of patients with this combination succumbed to arrhythmic and cardiac death, respectively. CONCLUSIONS: SAECG is a powerful predictor of poor outcomes in this population. The noninvasive combination of an abnormal SAECG and reduced EF may have utility in selecting high-risk patients for intervention.

Prediction of sustained ventricular tachycardia inducible by programmed stimulation in patients with coronary artery disease. Utility of clinical variables.

BACKGROUND: Cardiologists often use clinical variables to determine the need for electrophysiological studies to stratify patients for risk of sudden death. It is not clear whether this is rational in patients with coronary artery disease, left ventricular dysfunction, and nonsustained ventricular tachycardia. METHODS AND RESULTS: We analyzed the first 1721 patients enrolled in the Multicenter UnSustained Tachycardia Trial to determine whether clinical variables could predict which patients would have inducible sustained monomorphic ventricular tachycardia. The rate of inducibility of sustained ventricular tachycardia was significantly higher in patients with a history of myocardial infarction and in men compared with women. There was a progressively increased rate of inducibility with increasing numbers of diseased coronary arteries. There was a significantly lower rate of inducibility in patients with prior coronary artery bypass surgery and in patients who also had noncoronary cardiac disease. The rate of inducibility was higher in patients of white race, patients with recent (

Polymorphic ventricular tachycardia induced by programmed stimulation: response to procainamide.

OBJECTIVES: This study was designed to evaluate the effects of procainamide on polymorphic ventricular tachycardia induced by programmed stimulation and to correlate the responses with heart disease, left ventricular endocardial activation abnormalities and the signal-averaged electrocardiogram (ECG). BACKGROUND: Polymorphic ventricular tachycardia is induced frequently during electrophysiologic studies. In many patients this response is an artifact of programmed stimulation; in others, it appears to be clinically relevant. Previous observations have suggested that in some patients type IA antiarrhythmic agents can change the response to programmed stimulation from polymorphic to uniform ventricular tachycardia. METHODS: Programmed right ventricular stimulation was performed in the absence of antiarrhythmic drugs and after procainamide. Signal-averaged ECGs and left ventricular maps were performed during sinus rhythm in the absence of antiarrhythmic drugs. RESULTS: We evaluated 79 consecutive patients undergoing clinical electrophysiologic studies, in whom polymorphic ventricular tachycardia was the only arrhythmia induced in the absence of antiarrhythmic drugs. After procainamide administration, uniform monomorphic ventricular tachycardia was induced in 24 patients (Group 1), inducible polymorphic ventricular tachycardia persisted in 30 patients (Group 2) and no ventricular tachycardia could be induced in the remaining 25 patients (Group 3). Twenty-three (96%) of 24 patients developing uniform ventricular tachycardia after procainamide administration had coronary artery disease compared with 63% of Group 2 and 48% of Group 3 patients (p = 0.003). Left ventricular aneurysms were also found more frequently (46%) in the patients developing uniform ventricular tachycardia after procainamide than in either Group 2 or Group 3 (13% and 0%, respectively, p < 0.008). Abnormalities of the signal-averaged ECG typically seen in patients with spontaneous reentrant sustained ventricular tachycardia were significantly more frequent in patients who developed inducible uniform ventricular tachycardia after procainamide than in those who did not. Similarly, patients developing uniform ventricular tachycardia after procainamide had more extensive abnormalities of left ventricular endocardial activation revealed by catheter maps during sinus rhythm. CONCLUSIONS: The conversion of inducible polymorphic ventricular tachycardia to uniform ventricular tachycardia after procainamide administration occurs almost exclusively in patients with coronary disease, previous myocardial infarction and abnormal left ventricular function. This response may permit activation mapping of tachycardias, allowing the application of surgical or catheter ablation techniques that would otherwise not be possible in such patients.

What is the risk of sudden cardiac death in patients presenting with hemodynamically stable sustained ventricular tachycardia after myocardial infarction?

OBJECTIVES: This study sought to determine the long-term risk of sudden cardiac death in patients with hemodynamically stable sustained ventricular tachycardia complicating coronary artery disease. BACKGROUND: The prognosis and risk of sudden cardiac death in patients with a history of myocardial infarction and ventricular tachyarrhythmias have not been clearly defined. Prior studies are limited by a short follow-up period and by inclusion of patients with heterogeneous cardiac diseases and presenting arrhythmias. METHODS: A retrospective cohort analysis was performed on data from 124 patients, followed up for a mean of 36 +/- 30 months, who received electrophysiologically guided therapy for hemodynamically stable ventricular tachycardia after remote myocardial infarction. RESULTS: Seventy-eight patients were treated pharmacologically (medical group), and 46 patients underwent map-guided subendocardial resection (surgical group). Nine patients (7.3%) died suddenly, 5 (4.0%) died of noncardiac causes, 9 (7.3%) died of a perioperative complication, and 20 (23.4%) died of other cardiac causes. At 1, 2 and 3 years, sudden death occurred at cumulative rates of 2 +/- 1%, 3 +/- 2% and 7 +/- 3%, whereas total mortality was 20 +/- 4%, 28 +/- 4% and 32 +/- 5% (mean +/- SD). Sudden cardiac death (p = 0.047) and total mortality (p = 0.036) were higher in patients with multivessel disease and were similar for both treatment groups. CONCLUSIONS: Although the overall mortality in postinfarction patients presenting with hemodynamically stable ventricular tachycardia treated with electrophysiologically guided antiarrhythmic therapy is high, the risk of sudden death in these patients appears to be low (average 2.4%/year).

Sustained ventricular tachyarrhythmias during the early postinfarction period: electrophysiologic findings and prognosis for survival.

Forty patients with sustained tachycardia occurring 3 to 65 days after myocardial infarction underwent programmed ventricular stimulation within 3 months of the infarction. Patients were characterized clinically by a complicated initial 48 hours of hospitalization for their acute infarction (85% of study group). The development of bundle branch block in association with infarction occurred with an unusually high frequency (32%). Ventricular tachycardia similar in configuration to spontaneous arrhythmia was induced with programmed ventricular stimulation in 33 (83%) of the 40 patients. In 15 (45%) of these 33 patients, additional morphologically distinct ventricular tachycardia not seen clinically was initiated. The induction of ventricular tachycardia was not significantly related to the time after myocardial infarction at which spontaneous ventricular tachycardia was initially observed. Only 20 of the 40 patients are alive after a mean follow-up period of 20 +/- 15 months. Twelve of the 20 deaths were sudden cardiac deaths. Sixteen of the 33 patients with inducible ventricular tachycardia died; 8 of the 16 deaths were sudden. By comparison, four of the seven patients with no inducible ventricular tachycardia died (probability [p] = not significant), all suddenly. The mode of therapy did not influence subsequent survival. It appears that in patients with sustained ventricular tachycardia occurring more than 48 hours after a recent myocardial infarction, ventricular tachycardia similar to that clinically observed can usually be induced by programmed stimulation. In addition, multiple morphologically distinct ventricular tachycardias, some of which have not been previously observed, are frequently induced. Finally, the prognosis for survival is poor, regardless of inducibility or mode of therapy, and may in part be related to a changing arrhythmia substrate.

Usefulness of electrophysiologic study to determine the clinical tolerance of arrhythmia recurrences during amiodarone therapy.

The relation of clinical and electrophysiologic variables to outcome was evaluated in 121 patients treated with amiodarone for sustained ventricular tachyarrhythmias. Electrophysiologic study was performed in all patients a mean of 14 days after beginning amiodarone therapy. Forty-six patients who were given oral amiodarone therapy experienced arrhythmia recurrence. Multivariate analysis was performed using 16 clinical and electrophysiologic variables to determine which factors were associated with 1) arrhythmia recurrence and 2) a poorly tolerated arrhythmia recurrence (that is, cardiac arrest or sudden cardiac death) during oral amiodarone therapy. No variable predicted arrhythmia recurrence. Five variables correlated significantly with a poorly tolerated arrhythmia recurrence. Hemodynamic stability of the arrhythmia induced on electrophysiologic testing during amiodarone therapy had the best predictive value (p less than 0.001). Younger age, lower ejection fraction, a poorly tolerated rhythm at clinical presentation and absence of left ventricular aneurysm were also associated with a poorly tolerated arrhythmia recurrence. Only 3 of 57 patients who had a well tolerated arrhythmia induced on electrophysiologic testing during amiodarone therapy had recurrence of a poorly tolerated arrhythmia versus 19 of 47 who had hemodynamically unstable arrhythmias induced during amiodarone therapy (p less than 0.001). Thus, electrophysiologic testing during amiodarone therapy appears useful in identifying patients who are prone to have catastrophic arrhythmia recurrences and could allow for the institution of additional or alternative modes of therapy.

Differences in inducibility and prognosis of in-hospital versus out-of-hospital identified nonsustained ventricular tachycardia in patients with coronary artery disease: clinical and trial design implications.

OBJECTIVES: The goal of this study was to describe the influence of the clinical setting (in-hospital vs. out-of-hospital) in which nonsustained ventricular tachycardia (NSVT) is discovered on the rate of inducibility of sustained ventricular tachycardia (VT), arrhythmic events and survival in patients with coronary artery disease (CAD) and left ventricular (LV) dysfunction. BACKGROUND: In-hospital presentation of sustained VT is independently associated with lower long-term overall survival. The impact of the clinical setting in which NSVT is documented is unknown. METHODS: In the Multicenter Unsustained Tachycardia Trial (MUSTT), designed to assess the benefit of randomized antiarrhythmic therapy guided by electrophysiologic testing in patients with asymptomatic NSVT, CAD and LV dysfunction, eligible patients were enrolled irrespective of the setting in which the index arrhythmia was discovered. In this retrospective analysis, we compared the rate of VT inducibility and outcome of MUSTT-enrolled patients with in-hospital versus out-of-hospital presentation of NSVT. RESULTS: Monomorphic sustained VT was induced in 35% and 28% of the patients whose index NSVT occurred in-hospital and out-of-hospital, respectively (adjusted p = 0.006). Cardiac arrest or death due to arrhythmia at two- and five-year follow-ups were 14% and 28% for untreated patients with in-hospital-identified NSVT and 11% and 21% for the out-of-hospital group (adjusted p = 0.10). Overall mortality rates at two- and five-year follow-ups were 24% and 48% for inpatients and 18% and 38% for outpatients (adjusted p = 0.018). In patients randomized to antiarrhythmic therapy, there was no significant interaction between patient status (in-hospital vs. out-of-hospital) and treatment impact on the rates of total mortality (p = 0.98) and arrhythmic events (p = 0.08). CONCLUSIONS: In patients with CAD and impaired LV function, asymptomatic NSVT identified in-hospital, compared with that identified out-of-hospital, is associated with a higher rate of induction of sustained VT and overall mortality. Therefore, in similar patients, the clinical setting in which NSVT is discovered should be taken into account when formulating patient risk, treatment and clinical trial design.

Analysis of the resetting phenomenon in sustained uniform ventricular tachycardia: incidence and relation to termination.

UNLABELLED: Although the phenomenon of resetting has been studied in several experimental and clinical rhythms, it has not been systematically analyzed in ventricular tachycardia. To define the incidence and determinants of resetting as well as its relation to ventricular tachycardia termination, the response to programmed stimulation was prospectively studied during 78 electrically induced episodes of sustained, uniform ventricular tachycardia (mean cycle length 365 +/- 59 ms) in 53 patients. Single and double ventricular extrastimuli were introduced during 78 and 39 episodes of ventricular tachycardia, respectively. Rapid ventricular pacing was performed during 27 episodes. Resetting occurred in response to single ventricular extrastimuli in 43 (55%) of 78 ventricular tachycardias, to double extrastimuli in 31 (79%) of 39 ventricular tachycardias and to rapid pacing in 23 (85%) of 27 ventricular tachycardias. No ventricular tachycardia characteristic distinguished those tachycardias that were reset from those not reset. Termination of ventricular tachycardia occurred in 7 (9%) of 78 episodes with single ventricular extrastimuli, 14 (36%) of 39 episodes with double ventricular extrastimuli and 13 (48%) of 27 episodes with rapid pacing. Termination was less frequent than resetting with both single (9 versus 55%) and double (36 versus 79%) extrastimuli, as well as rapid pacing (48 versus 85%). Resetting preceded termination in 7 of 7 ventricular tachycardias terminated with single ventricular extrastimuli, 12 of 14 terminated with double ventricular extrastimuli and 9 of 13 terminated by rapid pacing. Ventricular tachycardias that were terminated could not be differentiated from those that were reset without termination. IN CONCLUSION: Resetting with programmed extrastimuli is common in hemodynamically stable sustained ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular endocardial activation during right ventricular pacing: effect of underlying heart disease.

Endocardial catheter mapping of the left ventricle was performed in 40 patients during right ventricular pacing to determine the effect of underlying myocardial infarction on endocardial activation. Group I comprised 18 patients without infarction, Group II 12 patients with inferior infarction and Group III 10 patients with anteroseptal infarction. Thirty-nine of the 40 patients had only a single left ventricular breakthrough site located on the midseptum in 33 cases, apical septum in 4 cases and basal septum in 2 cases. The earliest left ventricular local activation time during right ventricular pacing was earlier in Group III (40 +/- 11 ms) than in Group I (55 +/- 17 ms) and Group II (60 +/- 15 ms) (p less than 0.01). Total endocardial activation time was significantly longer in Group III (118 +/- 30 ms) than in Group I (76 +/- 14 ms) and Group II (72 +/- 20 ms) (p less than 0.001). The latest left ventricular site of activation during right ventricular pacing was the inferoposterior base in 14 (77%) of the 18 Group I patients, and 10 (83%) of the 12 Group II patients. The latest site of activation in Group III patients was variable. It is concluded that: left ventricular endocardial activation patterns and conduction times are influenced by the site of previous infarction. Longer total endocardial activation in Group III suggests that specialized conducting tissue in the septal and anterior walls may play an important role in left ventricular activation during right ventricular pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Cycle length-dependent effects on normal and abnormal intraventricular electrograms: effect of procainamide.

The effect of procainamide (mean concentration 9.1 +/- 2.0 micrograms/ml) on cycle length-dependent changes in electrographic characteristics was determined in 10 patients with prior myocardial infarction. Intracardiac bipolar electrograms were recorded from an abnormal left ventricular site in the distribution of prior (greater than 6 month) myocardial infarction and from a normal right ventricular site. Pacing was performed for 15 beats from the right ventricular apex at cycle lengths of 600 (or 500), 400 and 300 ms. In the control state, the QRS width, the normal electrogram and in 9 of the 10 patients the abnormal electrogram did not change with decreasing cycle lengths. After procainamide the mean QRS width increased from 203 +/- 32 to 240 +/- 50 ms (+18%, p less than 0.01) at a paced cycle length of 600 (or 500) ms, from 198 +/- 34 to 245 +/- 59 ms (+24%, p less than 0.01) at a paced cycle length of 400 ms and from 197 +/- 36 to 258 +/- 67 ms (+31%, p less than 0.01) at a paced cycle length of 300 ms.(ABSTRACT TRUNCATED AT 250 WORDS)

Limited role of intravenous propafenone hydrochloride in the treatment of sustained ventricular tachycardia: electrophysiologic effects and results of programmed ventricular stimulation.

The electrophysiologic effects and response to programmed ventricular stimulation of intravenous propafenone, an experimental antiarrhythmic agent, were studied in a group of 14 patients with both clinical and induced sustained ventricular tachycardia. Twelve of the 14 patients had not responded to conventional antiarrhythmic drug therapy. Propafenone had no significant effect on sinus cycle length (836 +/- 170 ms before and 750 +/- 124 ms after propafenone), P wave duration (108 +/- 24 ms before and 106 +/- 23 ms after propafenone) or PR interval (181 +/- 45 ms before and 194 +/- 53 ms after propafenone). QRS duration and ventricular effective refractory periods increased significantly (109 +/- 20 to 130 +/- 21 ms and 235 +/- 24 to 256 +/- 19 ms, respectively). Ventricular tachycardia remained inducible or occurred spontaneously in 13 of 14 patients after propafenone administration. Neither mode of initiation nor mode of termination of ventricular tachycardia was predictably altered. Additional forms of ventricular tachycardia were seen in six patients. Cycle length of ventricular tachycardia was 303 +/- 73 ms before and 346 +/- 143 ms after propafenone (p = NS). In conclusion, intravenous propafenone does not significantly affect sinus rate, intraatrial conduction or atrioventricular conduction. Ventricular refractoriness and intraventricular conduction are prolonged. The mode of initiation, mode of termination and ventricular tachycardia cycle length are not predictably altered, but ventricular tachycardia occasionally occurs spontaneously after propafenone. Intravenous propafenone rarely prevents induction of ventricular tachycardia in patients with sustained ventricular tachycardia refractory to conventional antiarrhythmic agents.

Comparative electrophysiologic effects of intravenous and oral procainamide in patients with sustained ventricular arrhythmias.

Thirty-three patients with sustained ventricular arrhythmias underwent electrophysiologic testing after intravenous and again after oral procainamide administration. Two groups were identified: group 1 included 15 patients with concordant serum procainamide concentrations with less than a 3 micrograms/ml difference after intravenous (mean 8.6 +/- 2.7) and oral (mean 8.8 +/- 2.7) procainamide administration, with mean N-acetylprocainamide concentrations of 1.0 +/- 0.6 and 6.2 +/- 2.8 micrograms/ml, respectively. Group 2 included 18 patients with discordant serum procainamide concentrations after intravenous (mean 9.5 +/- 5.9 micrograms/ml) and oral (mean 14.1 +/- 5.2 micrograms/ml) procainamide, with mean N-acetylprocainamide concentrations of 0.9 +/- 0.5 and 10.7 +/- 5.7 micrograms/ml, respectively. In group 1, response to programmed stimulation was the same after intravenous and oral procainamide administration, with no inducible ventricular arrhythmia in 5 of 15 patients. In group 2, 3 of 18 patients had no inducible arrhythmia after intravenous compared with 7 of 18 patients after oral procainamide administration. There was a different response to programmed stimulation after oral compared with intravenous procainamide in 6 of 18 patients in group 2 but in none of 15 patients in group 1 (p = 0.02). The effective procainamide concentration was greater than the ineffective concentration in five of the six patients with a discordant response, and the effective route of administration was oral in five of the six patients. The change in ventricular refractoriness in group 1 was similar after intravenous (28 +/- 23 ms) and oral (29 +/- 19 ms) procainamide, whereas in group 2, refractoriness was increased more after oral (33 +/- 21 ms) than intravenous (20 +/- 17 ms) procainamide administration and paralleled the difference in procainamide concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Antiarrhythmic drug therapy in the Multicenter UnSustained Tachycardia Trial (MUSTT): drug testing and as-treated analysis.

OBJECTIVES: Using data from the Multicenter UnSustained Tachycardia Trial (MUSTT), we examined the factors used to select antiarrhythmic drug therapy and their impact on outcomes. BACKGROUND: The MUSTT examined the use of programmed ventricular stimulation (PVS) to guide antiarrhythmic therapy in patients with coronary arteriosclerosis, left ventricular dysfunction and asymptomatic, unsustained ventricular tachycardia (VT). Trial outcomes may reflect factors used to select antiarrhythmic drug therapy. METHODS: We compared subgroups of patients with inducible sustained VT randomized to PVS-guided antiarrhythmic therapy (n = 351), in particular those receiving PVS-guided antiarrhythmic drug therapy (n = 142) versus no antiarrhythmic therapy (controls, n = 353). RESULTS: "Effective" antiarrhythmic drug therapy (i.e., the term "effective" was used to denote therapy that resulted in noninducible VT or hemodynamically stable induced VT) was found for 142 of the 351 patients (43%), most often at the first or second PVS session (125/142, 88%). Mortality among the 142 patients did not differ from that among control patients. Of these 142 patients, the PVS end point was noninducibility in 91 patients and stable VT in 51 patients. Mortality did not differ between these two groups either, but arrhythmia was numerically more frequent in the PVS-induced stable VT group. Mortality was greatest in the few patients receiving propafenone (unadjusted p = 0.07, adjusted p = 0.14 vs. controls), but mortality with all agents did not differ from that of controls, even after adjustment. CONCLUSIONS: Even when presenting the results as favorably as possible, we found no benefit with PVS-guided drug therapy in patients with clinical unsustained VT who had inducible sustained VT. These findings are unaltered by using different end points for PVS or considering the response to individual drugs.

Bradycardic syncope in 2 patients who recently began gatifloxacin treatment.

Gatifloxacin is a synthetic broad-spectrum 8-methoxyfluoroquinolone approved by the United States Food and Drug Administration in December 1999. Few side effects of this new antibiotic have been reported, and there are no previous case reports of bradyarrhythmias. We report 2 cases of syncope due to bradycardia in patients who recently began treatment with gatifloxacin.

Nosocomial respiratory tract infection and colonization with Acinetobacter calcoaceticus. Epidemiologic characteristics.

Nosocomial respiratory tract infection with Acinetobacter calcoaceticus occurs frequently in many hospitals. An outbreak of respiratory tract infections in an intensive care unit provided an opportunity to study clinical and epidemiologic characteristics of such infections. Retrospective studies demonstrated that A. calcoaceticus in sputum was significantly associated with endotracheal intubation (p = 0.03) and continuous positive pressure ventilation (p less than 0.02). After control measures had interrupted the outbreak, a prospective microbiologic investigation demonstrated that one third of the hospital personnel had transient hand colonization with multiple strains of A. calcoaceticus. Pharyngeal, vaginal and rectal carriage was rare. A pulmonary therapist with chronic dermatitis had persistent hand colonization with the epidemic strain, and he contaminated respiratory therapy equipment. Cross contamination of respiratory therapy equipment occurred while in use, but no other inanimate reservoir was demonstrated. Although previous studies have implied that the inanimate hospital environment has unique reservoirs of A. calcoaceticus, these reservoirs were not implicated in this outbreak. Human skin must be considered an important reservoir of A. calcoaceticus.

Cycle-length response of ventricular tachycardia associated with coronary artery disease to procainamide and amiodarone.

We undertook this study to determine if the cycle-length response of ventricular tachycardia (VT) to procainamide and amiodarone is similar in the individual patient. We enrolled 40 patients with uniform, monomorphic VT at a baseline, drug-free electrophysiologic study, after procainamide infusion and during oral amiodarone therapy. We found a significant correlation (p less than 0.01) between VT cycle-lengths on the 2 agents as well as the percent change in cycle length from baseline. Only 60% of the patients exhibited VT rates within 10% between the 2 agents. Importantly, less than 20% of patients had further slowing of the VT rate (greater than 10% slowing) during amiodarone therapy as compared to procainamide. Thus, although the cycle-length response of VT to procainamide correlates with the cycle-length response to amiodarone, 40% of patients have a disparate response (greater than 10% difference in cycle length) to the 2 agents; additional slowing of VT rates in response to amiodarone beyond that seen with procainamide is unlikely. These results have important implications regarding the institution of amiodarone therapy and the need for repeat electrophysiologic testing during amiodarone therapy.

Prognosis following sustained ventricular tachycardia occurring early after myocardial infarction.

Eighty-seven patients with sustained ventricular tachycardia (VT) between 3 and 90 days after acute myocardial infarction (AMI) were evaluated to define factors associated with a high risk of arrhythmia recurrence or death. Most patients had poor left ventricular function (mean ejection fraction 29 +/- 12%), multivessel coronary artery disease (71%) and inducible sustained VT with programmed stimulation (87%). During a mean follow-up of 26 months, 36 patients (41%) died and 21 patients had arrhythmia recurrence (with 19 sudden deaths). Factors independently associated with mortality included: (1) treatment before 1981 (p less than 0.01); (2) anterior AMI (p less than 0.05); (3) short time from AMI to first episode of VT (p less than 0.06); and (4) multivessel coronary artery disease (p less than 0.07). Factors independently associated with arrhythmia recurrence were: (1) medical treatment (as opposed to surgical) (p less than 0.01); (2) greater than or equal to 3 episodes of spontaneous VT (p = 0.01); (3) multivessel coronary disease (p less than 0.05); and (4) anterior AMI (p less than 0.07). Medically and surgically treated patients did not differ significantly in overall survival (49 vs 61%, respectively), although short-term (6 month) surgical survival improved from 31% during the first half of the study to 96% in the latter half (p less than 0.01). For patients with sustained VT early after AMI the risk of death and arrhythmia recurrence can be assessed based on clinical and angiographic characteristics; in addition, surgical treatment is associated with a lower incidence of arrhythmia recurrence than medical treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Endocardial mapping during sinus rhythm in patients with coronary artery disease and nonsustained ventricular tachycardia.

Programmed stimulation in patients with nonsustained ventricular tachycardia (VT) and coronary artery disease (CAD) induces sustained VT in 30 to 50% of patients. The presence of inducible, sustained VT identifies patients at high risk for sudden death. This study sought to determine whether patients with nonsustained VT who have inducible, sustained VT would have differences of left ventricular endocardial activation and conduction compared with those of patients without inducible, sustained VT. Thirty-six patients with CAD referred for evaluation of nonsustained VT underwent programmed ventricular stimulation and catheter mapping of left ventricular endocardial activation. Using previously validated methods, electrograms were classified as normal, abnormal or fractionated based on measurement of local electrogram duration and amplitude. Programmed stimulation induced sustained, uniform VT in 16 of 36 patients (44%). Patients with inducible, sustained, uniform VT had significantly more sites with abnormal (48%) and fractionated (5.5%) electrograms than did those without inducible VT (35% abnormal and 0.4% fractionated; p = 0.05 and 0.01, respectively). Patients with inducible VT had a mean of 15% of mapped sites displaying late electrograms versus only 3% in those without inducible VT (p < 0.01). The duration of the longest local electrogram in patients with inducible, sustained, uniform VT was 128 ms compared with 100 ms in those without inducible VT (p < 0.001). Thus, patients with CAD presenting with nonsustained VT who have inducible, sustained, uniform VT have significantly greater degrees of local conduction slowing and delayed activation than do those without inducible, sustained, uniform VT. These observations support reentry as the mechanism of the induced arrhythmias in these patients.

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)