Ambulatory heart rate and ST-segment depression during painful and silent myocardial ischemia in chronic stable angina pectoris

The relation between heart rate and ischemic ST-segment depression was studied in 70 patients with documented obstructive coronary artery disease (CAD) and reproducible effort angina. Symptom-limited treadmill exercise testing was performed before and after a 2-week placebo period and 24-hour FM ambulatory electrocardiographic monitoring at the end of the placebo period. The means (+/- standard deviation) of the basal and placebo values for exercise time, heart rate and maximal ST-segment depression were: 6.4 +/- 2.6 minutes vs 6.9 +/- 2.8 minutes (difference not significant [NS]), 125 +/- 17 beats/min vs 125 +/- 19 beats/min (NS) and 2.3 +/- 0.8 mm vs 2.1 +/- 0.8 (NS), respectively. Ambulatory monitoring revealed 205 episodes of significant ST-segment depression (J + 80 ms; 49 episodes with more than 1 mm, 83 with more than 2 mm, 39 with more than 3 mm and 34 with more than 4 mm). Of all episodes of ST-segment depression, 130 (64%) were asymptomatic. The episodes lasted for 3 to 110 minutes. The maximal 24-hour ambulatory heart rate and ST-segment depression during ischemic episodes were expressed as a percentage of those seen during exercise-induced ischemia. When all ambulatory ischemic episodes (both symptomatic and asymptomatic) were compared with exercise-induced ischemic changes in the individual patient, there was little difference in heart rate (91 +/- 15% vs 90 +/- 18%, NS) but there was a greater magnitude of ST-segment depression (122 +/- 57% vs 104 +/- 52%, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanisms of arrhythmias accompanying ST-segment depression on ambulatory monitoring in stable angina pectoris

To investigate the mechanisms of ischemic arrhythmias during daily life, 32 patients with stable angina pectoris and documented ischemic episodes were studied by 24-hour ambulatory electrocardiographic monitoring. The severity of arrhythmias observed at or before peak ST-segment depression (early arrhythmias) and arrhythmias presenting during or after resolution of the ST-segment changes (late arrhythmias) was graded according to a modified Lown classification. Eleven patients (34%) had ischemic arrhythmias and had a greater number of ischemic episodes (6.0 +/- 5.4 vs 2.3 +/- 1.5, p less than 0.001) than patients without ischemic arrhythmias. Ischemic episodes accompanied by arrhythmias had a greater ST-segment depression (2.8 +/- 1.6 mm vs 1.9 +/- 0.6 mm, p less than 0.001), and duration (18.2 +/- 14.8 minutes vs 5.7 +/- 2.6 minutes, p less than 0.001) than those without arrhythmias. Ventricular tachycardia was observed in 3 patients during the early phase of ischemia and in 2 during or after recovery. Early but not late ventricular tachycardias were preceded by prodromal ventricular ectopic activity. Late arrhythmias were more frequent and severe than early arrhythmias, with an increased incidence of R-on-T ectopic complexes. In patients with stable angina, potentially life-threatening arrhythmias are closely associated with severe repetitive episodes of ischemia, and different mechanisms produce early and late arrhythmias. Prevention or reduction of the severity of ischemic episodes occurring during daily life in patients with stable angina may be more effective than prophylactic antiarrhythmic therapy.     

Characterization of silent ischemia in patients with unstable angina: prognostic and therapeutic implications

The occurrence of silent ischemia in various ischemic myocardial syndromes has attracted increasing attention. In unstable angina hemodynamic monitoring has suggested that the symptomatic and silent episodes of ischemia do not differ significantly. In two discrete studies we determined the characteristics and prognostic significance of silent ischemic episodes in unstable angina. In one study with 41 patients, there were 781 episodes of ischemia in Holter recordings: 392 (50%) with ST-segment depression, 242 (31%) with ST-elevation, 45 (6%) with ST-elevation and depression in different leads, 70 (9%) with pseudonormalization of T waves and 32 (4%) with T wave augmentation. Ventricular arrhythmias were associated with 18% of the episodes. The mean duration of ischemia was 14 minutes (range 30 seconds to almost twelve hours), the majority being less than five minutes. Only 154 (20%) of the 781 episodes of ischemia were associated with pain. Conversely, 77 episodes of chest pain were not associated with electrocardiographic changes. Analysis of the temporal sequence of heart rate during the development of ischemia (analysed in 415 episodes) showed that in only 43 (10%) the heart rate at the beginning of ischemia was significantly (exceeding 6 beats/minute) greater than that at five minutes (baseline) preceding the onset of ischemia. At the peak of ischemia, the mean heart rate increase was 10% and returned to baseline at the end of the ischemic episode. The data indicate that 80% of ischemic episodes in unstable angina are silent and over 90% are not triggered by increases in heart rate indicating that increased oxygen demand is an uncommon cause of ischemia in unstable angina.(ABSTRACT TRUNCATED AT 250 WORDS)     

Characteristics and clinical significance of silent myocardial ischemia in unstable angina

The frequency and duration of transient myocardial ischemia on Holter recordings, analyzed by the compact analog technique, were determined in 41 patients (all men, mean age 54) with unstable angina (33 with angiographic evidence). There were 781 episodes of ischemia: 392 (50%) with ST-segment depression, 242 (31%) with ST elevation, 45 (6%) with ST elevation and depression in different leads, 70 (9%) with pseudonormalization of T waves and 32 (4%) with T-wave augmentation. Ventricular arrhythmias were associated with 18% of the episodes. The mean duration of ischemic episodes was 14 minutes (range 30 seconds to almost 12 hours); most were less than 5 minutes. Only 154 (20%) of the 781 episodes of ischemia were associated with pain. Conversely, 77 episodes of chest pain were not associated with electrocardiographic changes. Analysis of the temporal sequence of heart rate during the development of ischemia (analyzed in 415 episodes) showed that in only 43 (10%) the heart rate at the beginning of ischemia was significantly (greater than 6 beats/min) higher than that at 5 minutes (baseline) before the onset of ischemia. At the peak of the ischemic abnormality, the mean heart rate increase was 10% and returned to baseline at the end of the ischemic episode. The data indicate that 80% of ischemic episodes in unstable angina are silent and over 90% are not triggered by increases in heart rate; apparently increased oxygen demand is an uncommon cause of ischemia in unstable angina. Although most of the episodes were short-lived, some were extremely protracted without the development of myocardial infarction. The findings are of therapeutic significance.     

Long-duration electrocardiographic recording in 33 patients with obstructive cardiomyopathy

A prospective study of arrhythmias was performed in 33 patients with hypertrophic cardiomyopathy with obstruction by Holter monitoring. The aim of the study was to assess the incidence of "occult" arrhythmias in this condition and to establish a "profile" of high risk patients from clinical, echocardiographic and haemodynamic data. The Holter monitoring demonstrated asymptomatic arrhythmias in 31 of the 33 patients (94%). A supraventricular arrhythmia was detected in 15 cases (45%), including 7 episodes of supraventricular tachycardia (21%). Ventricular arrhythmias were observed in 28 patients (85%), including 5 episodes of ventricular tachycardia (15%). Some patients presented several types of arrhythmia. A number of patients with arrhythmia including short bursts of ventricular tachycardia were asymptomatic during Holter monitoring; conversely, other patients complained of dizziness or syncope but had no arrhythmias. A retrospective study of clinical, echocardiographic and haemodynamic data showed no difference between patients with and patients without arrhythmias. Medium-dose betablocker therapy (propranolol, 110 mg/day) did not seem to protect patients with hypertrophic cardiomyopathy with obstruction from arrhythmias. We conclude that Holter monitoring should form part of the routine evaluation of patients with cardiomyopathy with obstruction, and that potentially dangerous arrhythmias should be treated by anti-arrhythmic agents other than betablockers. This attitude could reduce the incidence of syncope and eventually decrease the risk of sudden death in this condition.     

Combination antiarrhythmic therapy for management of malignant ventricular arrhythmia

The efficacy of combination drug therapy in the suppression of ambient ventricular arrhythmia was retrospectively evaluated in a study of 49 patients discharged from the hospital taking 2 membrane-active antiarrhythmic agents. Thirty-one patients (63%) had ischemic heart disease, 15 had miscellaneous cardiac disorders and 3 were free of ostensible heart disease. Therapy in all patients had previously been unsuccessful with an average of 3.7 single membrane-active drugs. Antiarrhythmic agents were discontinued for at least 48 hours to determine baseline arrhythmia levels by Holter monitoring and maximal exercise treadmill testing. Ventricular premature beats were evaluated according to the grading system of Lown and Wolf. Data on ventricular ectopic activity were obtained during Holter monitoring and exercise testing for both a control ("drug-free") period and for a period of combination therapy. During the control period, ventricular tachycardia was recorded during 23% of monitored hours, and the level was nearly twofold greater during stress testing. After institution of combined therapy, the percent of monitored hours of arrhythmia were reduced during Holter monitoring, with a greater reduction in couplets and ventricular tachycardia than in single ventricular premature beats. Ventricular tachycardia was more difficult to provoke by exercise testing in patients taking combination therapy than in control subjects. These data indicate that combination therapy can significantly reduce the density of ventricular ectopic activity in patients refractory to monotherapy. During an average follow-up of 26 months, 23 patients (47%) were able to receive decreased drug dosages, affording diminished adverse effects and improved tolerance to long-term use.     

Incidence of ventricular arrhythmias during transient myocardial ischemia in patients with stable coronary artery disease

To determine the incidence of ventricular arrhythmias related to episodes of transient myocardial ischemia during ambulatory electrocardiographic (ECG) monitoring, 97 patients with stable angina pectoris, angiographically proved coronary artery disease and an abnormal exercise test were studied. A total of 573 episodes with ST segment depression were documented: in 118 episodes (21%) the patients were symptomatic and in 455 (79%) they remained asymptomatic. Ventricular arrhythmias (greater than 5 premature ventricular beats/min, bigeminy, couplets or salvos of premature ventricular beats) occurred during 27 (5%) ischemic episodes in a subset of 10 patients (10%) (group A). The other 87 patients (90%) (group B) showed exclusively ischemic episodes without ventricular arrhythmias. Comparison of patients in group A and group B showed no differences in hemodynamic, angiographic, exercise testing and ambulatory ECG monitoring data. Ischemic episodes with and without ventricular arrhythmias showed a similar duration and amplitude of ST segment depression and a comparable heart rate at the onset of ischemia. Both types of ischemic episodes, with and without arrhythmias, occurred predominantly during the morning hours between 6:00 AM and noon, and both types remained asymptomatic to within similar percentages. The data demonstrate that ventricular arrhythmias are related to transient myocardial ischemia in only a few patients with stable angina pectoris; these arrhythmias are related neither to the degree of ischemia during ambulatory ECG monitoring nor to the occurrence of anginal symptoms.     

比较远程心电监测与心电图、动态心电图在心律失常及心肌缺血中的诊断价值

目的探讨远程心电监测诊断心律失常、心肌缺血的临床价值。方法采用远程心电监测检查78例明确诊断为心脏病或存在心脏不适的患者,所有患者同时行常规12导联心电图检查,其中42例患者行24h动态心电图检查。比较远程心电监测与常规心电图及24h动态心电图在心律失常及缺血性ST-T改变检出率方面的差异。结果 78例患者中,远程心电监测及常规心电图分别检出62例、46例心律失常患者(P<0.05),同时分别检出14例、6例患者心电图存在缺血性ST-T改变(P<0.05);在完善24h动态心电图检查的42例患者中,远程心电监测与24h动态心电图分别检出34例、30例心律失常患者(P>0.05),同时分别检出10例、7例心电图有缺血性ST-T改变的患者(P>0.05)。结论远程监测无论在心律失常还是缺血性ST-T改变的检出率均高于常规心电图组;远程监测对心律失常及缺血性ST-T改变的检出率与24h动态心电图无显著差异。     

Transdermal nitroglycerin patches for silent myocardial ischemia during antianginal treatment

Because silent ischemia is not associated with an increase in heart rate and, being asymptomatic, its treatment requires constant therapeutic plasma levels of the drug used, a transdermal nitroglycerin patch (Deponit) was selected for treatment of this condition. Eight patients with documented silent ischemia were studied. All patients also had angina on effort treated with calcium antagonists (n = 8) and beta blockers (n = 6). They were evaluated by 24-hour ambulatory electrocardiographic monitoring. The transdermal nitroglycerin patch, 20 to 30 mg/24 hours, reduced the number of silent ischemic episodes from 9.25 +/- 5.52 to 2.4 +/- 2.0 episodes per 24 hours (p less than 0.001). The maximal ST-segment depression was reduced from 3.1 +/- 0.7 to 0.9 +/- 0.7 mm (p less than 0.001). Ventricular premature beats were significantly reduced, by 50%. Symptomatic ischemic episodes were completely suppressed. Thus, transdermal nitroglycerin, in moderate doses, is effective in suppressing silent ischemia in patients with angina pectoris who have silent ischemic episodes despite treatment with other antianginal agents.     

Characterization and therapy of ventricular arrhythmias due to transient myocardial ischemic attacks in variant angina

Forty-two patients with variant angina were studied by ambulatory ECG monitoring to determine the incidence and the characteristics of ventricular arrhythmias during ischemic attacks. Twenty-six patients had no ventricular arrhythmias in 633 ischemic attacks; 16 patients had ventricular arrhythmias in 116/586 ischemic attacks. The number of ischemic attacks per day and the magnitude of ST elevation were significantly (p less than 0.05) greater in patients with ventricular arrhythmias. Ventricular arrhythmias appeared at the onset or at the peak of ST elevation (first phase) in 17 ischemic attacks, during the resolution of ST elevation (second phase) in 43 attacks, during both the phases in 9 attacks. ST alternans appeared during 6 ischemic attacks with arrhythmias. Two episodes of ventricular fibrillation and 22 runs of ventricular tachycardia occurred during the first phase, 17 episodes of ventricular tachycardia were recorded during the second phase. Ventricular tachycardia of the second phase compared with ventricular tachycardias of the first phase were significantly (p less than 0.01) slower, uniform and initiated by a late premature beat. Incidence of arrhythmias of the second phase was strictly correlated with the duration of ischemic attacks. Nine patients who showed ventricular arrhythmias during the second phase of ischemic attacks were enrolled in a cross-over study to assess the antiarrhythmic effects of nifedipine (120 mg/day) and verapamil (480 mg/day). During treatment with nifedipine, the frequency of ischemic attacks declined by 85%, while the frequency of attacks with arrhythmias declined by 97% (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of spironolactone on ventricular arrhythmias in congestive heart failure secondary to idiopathic dilated or to ischemic cardiomyopathy

Epidemiologic studies have shown an important increase in the high mortality of patients with congestive heart failure (CHF) despite optimal medical management. Ventricular arrhythmia was recognized as the most common cause of death in this population. Electrolyte imbalance, myocardial fibrosis, left ventricular dysfunction, and inappropriate neurohumoral activation are presumed responsible for sudden cardiac death. In this study, we focused on the deleterious effects of the overproduction of aldosterone that occurs in patients with CHF. Secondary hyperaldersteronism can be part of several factors thought to be responsible for sudden cardiac death. We randomized 35 patients (32 men, aged 48 +/- 9 years) with systolic dysfunction (ejection fraction 33 +/- 5%) and New York Heart Association class III CHF secondary to dilated or ischemic cardiomyopathy into 2 groups. The treatment group received spironolactone, an aldosterone receptor antagonist, along with standard medical management using furosemide, angiotensin-converting enzyme inhibitors, and digoxin. The control group received only the standard medical treatment. Holter monitoring was used to assess the severity of ventricular arrhythmia. After 20 weeks, patients who received spironolactone had a reduced hourly frequency of ventricular premature complexes (VPCs) (65 +/- 18 VPCs/hour at week 0 and 17 +/- 9 VPCs/hour at week 16) and episodes of nonsustained ventricular tachycardia (VT) (3.0 +/- 0.8 episodes of VT/24-hour period at week 0, and 0.6 +/- 0.3 VT/24-hour period at week 16). During monitored treadmill exercise, a significant improvement in ventricular arrhythmia was found in the group receiving spironolactone (39 +/- 10 VPCs at week 0, and 6 +/- 2 VPCs at week 16). These findings suggest that aldosterone may contribute to the incidence of ventricular arrhythmia in patients with CHF, and spironolactone helps reduce this complication.     

Predictive value of presyncope in patients monitored for assessment of syncope

BACKGROUND: The purpose of this study was to assess the diagnostic value of recording the cardiac rhythm during presyncope in patients undergoing monitoring for undiagnosed syncope. METHODS AND RESULTS: Eighty-five patients (age, 59 +/- 18 years; 44 men, 41 women) with recurrent unexplained syncope underwent prolonged monitoring with an implantable loop recorder. Patients were examined for syncope, which was either recurrent or associated with at least 2 presyncopal episodes. Patients had a mean of 5.1 +/- 5.5 syncopal episodes in the previous 12 months, and 70% of patients had symptoms for >2 years. Sixty-two (73%) patients had recurrent symptoms during a 12-month follow-up period. Of 150 recurrent events captured by the implantable loop recorder, there were 38 (25%) episodes of syncope and 112 (75%) episodes of presyncope. Syncope alone recurred in 12 patients, presyncope in 25, and both in 16. An arrhythmia was present in 64% of syncopal events (bradycardia in 16, tachycardia in 2) versus 25% for presyncopal events (bradycardia in 7, tachycardia in 3, P =.001). An arrhythmia was detected in 9 (56%) of the 16 patients with both syncope and presyncope, which was present in all recorded episodes of syncope compared with 6 of 9 presyncopal episodes. Patient-related failure to freeze the device after symptoms occurred in 21 (36%) of 59 syncopal events compared with 15 (12%) of 127 presyncopal events (P =.0001). CONCLUSIONS: Syncope is more likely to be associated with an arrhythmia than is presyncope in patients undergoing extended monitoring. Presyncope is a nonspecific end point that is frequently associated with sinus rhythm. Patients undergoing extended monitoring for syncope should continue to be monitored after an episode of presyncope unless an arrhythmia is detected.     

芬太尼后处理联合缺血后适应对兔心肌缺血再灌注损伤心肌坏死标志物的影响

目的 观察芬太尼后处理联合缺血后适应对兔心肌缺血再灌注损伤心肌坏死标志物及心肌梗死面积的变化,探讨其对心肌缺血再灌注损伤的保护作用.方法 32只日本大耳白兔,采用结扎左冠状动脉前降支30 min、复灌120 min建立心肌缺血再灌注损伤模型.按“随机数字表法”随机分为4组,每组8只：假手术组,动脉下仅穿线不结扎;缺血再灌注组,直接恢复再灌注;缺血后适应组,缺血后适应后恢复再灌注;芬太尼后处理＋缺血后适应组,缺血28 min给予芬太尼5μg· kg-1后处理,30 min予以缺血后适应.测定各组心肌坏死标志物（心肌肌钙蛋白Ⅰ浓度与肌酸激酶同工酶蛋白活力浓度）、计算心肌梗死面积及观察室性心律失常发生率.结果 芬太尼后处理＋缺血后适应组较缺血后适应组、缺血再灌注组外周血心肌肌钙蛋白Ⅰ浓度、肌酸激酶同工酶酶蛋白活力浓度降低,心肌梗死面积减小,差异均有统计学意义（P＜0.05）.缺血后适应组较缺血再灌注组外周血心肌肌钙蛋白Ⅰ浓度、肌酸激酶同工酶酶蛋白活力浓度降低,心肌梗死面积减小,差异均有统计学意义（P＜0.05）.芬太尼后处理＋缺血后适应组、缺血后适应组较缺血再灌注组室性心律失常发生率降低[0 vs.50％（4/4）,P＜0.05;12.5％（1/7）vs.50％（4/4）,P＜0.05],差异均有统计学意义（P＜0.05）.结论 芬太尼后处理联合心肌缺血后适应显著降低兔心肌缺血再灌注心肌肌钙蛋白Ⅰ浓度、肌酸激酶同工酶酶蛋白活力浓度,减少心肌梗死面积,降低室性心律失常发生率,可减轻心肌缺血再灌注损伤.     

Usefulness of carvedilol in unstable angina pectoris

The safety and efficacy of adding oral carvedilol (25 mg twice daily) to standardized treatment of unstable angina was assessed in a multicenter, randomized, double-blind, placebo- controlled trial on 116 patients with acute unstable angina. Patients were monitored in an intensive care unit and underwent 48-hour Holter monitoring to assess transient ischemia. Carvedilol as adjunctive therapy resulted in a significant reduction of median heart rate (65 vs 75 beats/min, p <0.05), mean systolic blood pressure (133 vs 130 mm Hg, p <0.05), and mean rate-pressure product (8,337 vs 10,042, p <0.05). Carvedilol reduced the ischemic burden during 48 hours of treatment by 75% (49 vs 204 minutes), including a 36% reduction of patients with ischemic episodes (p <0.05), a 66% reduction of the mean number of ischemic episodes (8 vs 24, p <0.05), and a 76% reduction in the mean duration of ischemic episodes (50 vs 205 minutes, p <0.05). Side effects occurred in 8 of 59 patients (13.6%) in the carvedilol group and in 5 of 54 patients (8.8%) given placebo. Although not significant, the early onset of maximal blood pressure reduction and the delayed effect on heart rate were closely correlated to drug-induced hypotension and bradycardia in the carvedilol group. Thus, carvedilol as an adjunctive to standardized treatment effectively reduces heart rate and blood pressure, and thus the ischemic burden in patients with unstable angina pectoris, but requires close monitoring of patients at risk for bradycardia or hypotension.     

Day-to-day variability of myocardial ischemic episodes in coronary artery disease

Twenty patients with chronic stable angina pectoris, proved coronary artery disease, positive treadmill stress test response, and at least 2 episodes of ischemia per day underwent 72 hours of Holter monitoring during daily activities. During this period they had 389 ischemic episodes: 104 (27%) symptomatic and 285 (73%) silent. Marked variability was observed between patients in the number of ischemic episodes (range 2 to 15 per day, mean 6.5), duration of ischemia (range 6 to 419 minutes/day, mean 76.5), maximal ST depression (range 1 to 6 mm, mean 3.4) and heart rate at the beginning of ST depression (range 75 to 105 beat/min, mean 91). The day-to-day variability in individual patients between the different days in the number of ischemic episodes was 36%, in duration 51%, and in maximal degree of ST depression 31%. Only 9% variability was noted in heart rate at the beginning of ST depression. Similar day-to-day variability in individual patients was noted in the symptomatic and silent episodes. For clinical purposes of evaluation of ischemia during daily activities, 1 day of monitoring appears to be sufficient because within the first day, 78% of the maximal number of ischemic episodes, 64% of their duration, and 84% of the maximal degree of ST depression were detected. However, for evaluation of anti-ischemic drugs at least 2 monitoring days are required.     

Effects of coronary artery bypass surgery and angioplasty on the total ischemic burden: a study of exercise testing and ambulatory ST segment monitoring.

To assess the effects of standard therapeutic interventions on the total ischemic burden, 86 patients with stable angina underwent 48 hours of ambulatory ST segment monitoring and treadmill exercise testing before and at a mean of 10 weeks after coronary artery bypass surgery (CABG) (group 1, N = 46) or percutaneous transluminal coronary angioplasty (PTCA) (group 2, N = 40). There were 72 male and 14 female patients with a mean age of 56.4 years. All patients had documented coronary artery disease (24, single-vessel; 28, two-vessel; 34, three-vessel disease). Both groups were characteristically similar apart from more severe coronary artery disease (p less than 0.001) and more previous myocardial infarctions (p less than 0.05) in group 1. Groups with CABG and PTCA had significant prolongation of exercise time after intervention (group 1: 7.6 to 9.8 minutes, p less than 0.0001; group 2: 8.1 to 10.0 minutes, p less than 0.001), and both interventions led to a significant reduction in ischemic responses (group 1: 33 to 4, p less than 0.001; group 2: 20 to 13, p less than 0.05) to exercise. During a total of 7643 hours of ST segment monitoring, 253 episodes of ischemia were recorded in 3768 hours before and 44 ischemic episodes in 3875 hours after intervention (group 1, 113 episodes in 24 patients and 21 episodes in 10 patients; group 2, 140 episodes in 13 patients and 23 episodes in six patients). Both interventions reduced the mean frequency of ischemia per 24 hours (group 1: 1.24 to 0.22 episodes per 24 hours; p less than 0.01; group 2: 1.9 to 0.3 episodes per 24 hours; p less than 0.05). Almost 28% (N = 24) of resting electrocardiographic findings were altered as a result of intervention.(ABSTRACT TRUNCATED AT 250 WORDS)     

Characteristics of silent myocardial ischemia during out-of-hospital activities in asymptomatic angiographically documented coronary artery disease

Ambulatory electrocardiographic monitoring is useful in documenting characteristics of both painful and silent myocardial ischemia occurring during out-of-hospital activities in patients with angina and coronary artery disease (CAD), but few data are available concerning silent myocardial ischemia during ambulatory electrocardiographic monitoring in asymptomatic patients with CAD. Accordingly, 480 hours of ambulatory electrocardiographic monitoring were recorded in 10 asymptomatic patients with CAD not receiving cardiac drugs (48 hours/patient). All 10 patients had silent myocardial ischemia on treadmill exercise testing, with initial ST-segment depression at 2 to 6 minutes in 7 patients and more than 6 minutes in 3 patients. During ambulatory electrocardiographic monitoring, 64 episodes of silent myocardial ischemia (1 mm of ST-segment depression for at least 1 minute) were recorded, ranging from 1 to 17 episodes/patient/48 hours. Of the 64 silent myocardial ischemic episodes, 30 (47%) occurred between 6 am and noon. Duration of silent myocardial ischemia was 798 minutes (range 1 to 80). ST-segment depression ranged from 1 to 4.5 mm. Heart rate at onset of the episodes on ambulatory electrocardiographic monitoring ranged from 65 to 150 beats/min (mean 98), which was significantly less than that during treadmill exercise testing in the same patients (mean 120). At cardiac catheterization, 7 patients had 2- or 3-vessel CAD and 3 had 1-vessel CAD. Thus, silent myocardial ischemia is common during daily life in asymptomatic CAD patients with positive treadmill exercise tests.     

Myocardial ischemia in patients awaiting coronary artery bypass grafting

The results of ambulatory ECG monitoring are described in a group of patients that have not previously been characterized. Fifty men who were initially seen for elective CABG surgery underwent 48 hours of continuous ambulatory ECG monitoring. ST segment deviation from baseline, trended every 15 seconds, was quantified for duration, maximum ST segment change, area under the ST segment-time curve (AUC), and average ST segment change for the episode (AUC/duration). Ischemic episodes, 87% of which were silent, occurred in 42% of the patients. Symptomatic episodes had greater maximum ST segment change than silent episodes (-2.4 vs -1.9 mm; p less than 0.05) but were shorter in duration (11 vs 18 minutes; p less than 0.05). Episodes that were unrelated to heart rate, that is, episodes with less than 20% increase in heart rate over the baseline rate at the onset of ischemia, made up 75% of all ischemic events and occurred in 90% of patients (19 of 21). Heart rate-related and unrelated ischemic episodes did not differ in duration, maximum ST segment change, AUC, or average ST segment change. It was concluded that: (1) as with patients with unstable angina, patients with severe coronary artery disease continue to have frequent episodes of silent myocardial ischemia despite intensive medical therapy; (2) painful episodes have greater maximum ST segment change but are shorter than silent ones; (3) most ischemic episodes (75%) occur without an initial increase in heart rate; and (4) heart rate-related and unrelated episodes are quantitatively similar.     

The Nifedipine-Total Ischemia Awareness Program: a national survey of painful and painless myocardial ischemia including results of antiischemic therapy

The Nifedipine-Total Ischemia Awareness Program was designed to evaluate the prevalence, prognostic implications and effect of therapy on painful and painless myocardial ischemic episodes in a nationwide study of patients with angina pectoris. Three hundred forty-eight patients with at least 2 anginal attacks/week while taking antianginal medications were enrolled at 53 participating centers between September 1, 1986 and March 31, 1988; 312 of the 348 patients formed the study group, while 36 patients formed the control group. At least 1 episode of ST-segment depression during two 48-hour periods of Holter monitoring was present in 136 of the 312 patients in the study group. In these 136 patients, there was a total of 372 episodes of ST-segment depression, of which only 69 (18%) were painful; 85% of the 136 patients had either painless episodes only or both painless and painful episodes. Despite apparently adequate antianginal therapy, 48 patients had greater than or equal to 3 episodes of ST-segment depression/48 hours of ambulatory electrocardiographic monitoring, and 38 patients greater than 60 minutes of ST-segment depression. After nifedipine was administered, there was a 23% reduction in the mean number of episodes of ST-segment depression (2.7 +/- 0.3 to 2.1 +/- 0.2, p less than 0.01). The most pronounced effects were found in the 48 patients with greater than or equal to 3 episodes of ST-segment depression and the 38 patients with greater than or equal to 60 minutes of total ischemic time.(ABSTRACT TRUNCATED AT 250 WORDS)     

Computer-detected ventricular tachycardia in the coronary care unit: prognosis in patients with and without acute myocardial infarction

Survival (for up to 6 years) in coronary care unit (CCU) patients with ventricular tachycardia (VT) was studied with the aid of an automated arrhythmia monitoring system. Ventricular tachycardia was defined as four or more consecutive ventricular beats with a rate above 120 per min. During an 18-month period. VT was observed in 102 individuals (13%) out of 800 patients without acute myocardial infarction (AMI). The 102 patients were compared with age- and sex-matched patients with AMI and VT and a group with AMI but without VT. Hospital mortality was 27% in patients with AMI and VT, 23% in patients with AMI without VT, and 16% in non-AMI patients with VT (NS). First year mortality after discharge was 20% in the non-AMI group compared to 12% in the AMI groups (NS). The 1-6 years survival curves also did not differ significantly between the groups with a yearly mortality of between 5 and 6%. Acute myocardial infarction patients with rapid VT (greater than 150 min-1) or long VT (more than 10 beats) had a higher hospital mortality, otherwise the number or type of VT episodes did not relate to short- or long-term prognosis in the studied groups. Ventricular tachycardia in the CCU did not seem to be an indicator of poor long-term prognosis. It is concluded that long-term prognosis in patients with VT in the CCU was little influenced by a current diagnosis of AMI.