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PubMed2000

[Activity of transmembrane calcium transport and levels of endothelin-1 in patients with variant angina].

Recent studies showed that coronary artery spasm may be due to disturbances of secretory and excretory endothelial activity in atherosclerotic coronary artery. However, this theory does not explain the reasons of coronary artery spasm when endothelium is not damaged. There must be other patomechanisms of coronary artery spasm. The aim of our study was examination of calcium efflux through the lymphocytic cell membrane and determination of endothelin-1 plasma levels in patients with variant angina in order to define the participation of these factors in pathogenesis of coronary artery spasm. The survey was made in 76 patients with ischaemic heart disease. All patients were divided into 2 groups. The first group consisted of 48 patients with variant angina (d.b.s.), the other consisted of 28 patients with stable angina (d.b.w.). The control group (g.k.) was composed of 25 healthy people. Patients were administered 100 ml of trometamol (TRIS, pH = 10.5) intravenously for 5 minutes. After stopping the infusion the examined patient was breathing deeply for 5 minutes at a rate of 40/min. The endothelin-1 (ET-1) plasma levels and transmembrane calcium transport in lymphocytes were determined before and just after the hyperventilation test, as well as 10 minutes after the test. ET-1 plasma concentrations were estimated with a radioimmunologic assay. The method of estimation of transmembrane calcium transport was elaborated in Laboratory of Department of Cardiology of Medical University of Wrocław. We showed that ET-1 plasma levels and transmembrane calcium transport in patients with d.b.s. before the test were normal. There was an increase in transmembrane calcium efflux in patients with d.b.s. during coronary artery spasm that had been caused by ET-1. ET-1 plasma levels were still high 10 min. after the coronary artery spasm. Disturbances of transmembrane calcium transport and increased endothelin-1 plasma level may be the primary factors responsible for coronary artery spasm.

Adult↗
PubMed1996

[The relation between coronary vasospasm and coronary obstructive lesions in patients with variant angina].

A series of 38 patients with variant angina in whom coronary arteriography was performed was reviewed to investigate the relation between coronary vasospasm and coronary obstructive lesions. 10 of the 38 (26.3%) patients had completely normal coronary arteriograms; 4 (10.5%) had insignificant coronary artery disease (< 50% stenosis); 24 (63.2%) had significant (> or = 50% stenosis) coronary artery disease, including single vessel disease in 12 cases, multiple vessel disease in 11 cases and left main trunk disease in one case. The results of this study showed that the incidence of coronary vasospasm increased with the severity of coronary stenosis and was highest at 75%-90% stenosis of the ischemia-related artery in those patients with significant coronary disease. In this study of 38 patients, coronary vasospasm involved the left anterior descending artery (LAD) in 25 patients (65.8%), right coronary artery (RCA) in 10 (26.3%) and left circumflex artery (LCX) in 2 (5.3%), but in patients with in significant stenosis (< 50%), LAD was involved in 50.0%, RCA in 42.9% and LCX in 7.1%. These results indicate that coronary vasospasm occurs frequently in patients with severe stenosis of the LAD.

Adult↗
PubMed1979

[Clinical and angiographic study and pathogenic mechanism of Prinzmetal's angina. Apropos of 31 cases].

31 patients presenting with Prinzmetal variant angina were divided into three groups according to their angiographic appearances. Group I comprised 9 patients with normal or coronary arteries with lesions less than 50% narrowing. Group II comprised 12 patients with single vessel disease. Group III comprised the other 10 patients with significant lesions on two or all three principal arteries. No clinical or electrocardiographical differences were found between the groups as to age, sex or the clinicapresentation of the chest pain. Most patients with normal or nearly normal coronary arteries had normal electrol cardiogrammes between attacjs (8 out of 9) and electrical changes mainly over the inferior wall (8 out of 9). Exercise electrocardiography reproduced ST elevation in 4 of the 9 patients but, in contrast to the patients in the other two groups, never ST depression. However, these features are not specific for patients in Group I as they were observed in 4 patients in the other two groups. Spontaneous or induced coronary spasm were observed in 27 patients, confirming its role as the mechanism of Prinzmetal angina, whatever the anatomical appearance of the coronary tree.

Adult↗
PubMed1994

Comparison of the distribution of myocardial blood flow between exercise-induced and hyperventilation-induced attacks of coronary spasm: a study with thallium-201 myocardial scintigraphy.

Exercise and hyperventilation tests are often used as the provocative tests for coronary artery spasm. To examine the distribution of myocardial blood flow during exercise-induced and hyperventilation-induced attacks of coronary spasm, thallium-201 myocardial scintigraphy was performed in 47 patients with variant angina. The extent and severity scores and severity index (severity score/extent score) of scintigraphic perfusion defect were calculated. In 32 patients, anginal attack associated with ST elevation on the electrocardiogram was induced by exercise; in 23 patients, the attack was induced by hyperventilation. In patients with either anterior or inferior wall ischemia, both the extent and severity scores and severity index in the scintigram were significantly greater in exercise-induced anginal attack than those in hyperventilation-induced attack. In patients with simultaneous anterior and inferior wall ischemia, they tended to be greater in exercise-induced attack. In eight patients in whom anginal attack was induced by both exercise and hyperventilation, these scores and index were significantly greater in exercise-induced attack than those in hyperventilation-induced attack. These data suggest that myocardial ischemia during exercise-induced attack is enhanced as compared with that during hyperventilation-induced attack. Thallium-201 scintigraphy combined with exercise testing seems to be more sensitive for detecting myocardial ischemia induced by coronary spasm.

Aged↗
PubMed1992

Long-term study of recurrent vasospastic angina using coronary angiograms during ergonovine provocation tests.

Chronologic changes of coronary spasm were examined by repeated ergonovine provocation tests during angiography. A total of 322 patients who had variant angina without severe atherosclerosis demonstrated a positive response to the first test. Ninety of these patients had recurrent variant anginal symptoms after an angina-free period of 38 +/- 12 months (mean +/- SD). Of these 90 patients, 76 (84%) had symptoms or electrocardiographic (ECG) findings similar to those of the first test. The initial 9 of these 76 patients underwent a second provocation test and showed coronary responses analogous to those on the first test. Of the 90 patients, 14 (16%) had different symptoms or ECG findings from those elicited at the first episode. All 14 patients again had a positive response to a second ergonovine test and the following angiographic changes were observed in the three major vessels between the two tests. Of the 21 vessels that had spasm on the first test, eight vessels (19%) did not have spasm on the second test. Of the 21 vessels that did not demonstrate spasm on the first test, 10 (24%) demonstrated spasm on the second test. In the present study it is concluded that the majority of patients with recurrent angina seemed to have consistency in the location of coronary spasm, while in some patients the fluctuation of coronary spasm was confirmed by two ergonovine provocation tests.

Adult↗
PubMed1992

Ergonovine maleate testing during cardiac catheterization: a 10-year perspective in 3,447 patients without significant coronary artery disease or Prinzmetal's variant angina.

The utility of ergonovine testing for coronary artery spasm was assessed in 3,447 patients with angiographically insignificant (less than 50% diameter stenosis) or no coronary artery disease. No patients clinically had Prinzmetal's variant angina. Overall, 4% had a positive ergonovine test result, defined by spasm causing greater than or equal to 75% focal stenosis. Complications related to ergonovine use occurred in 11 patients (0.03%). In a training sample of 1,136 patients (studied between 1980 and 1984), two independent predictors of spasm were found by using multivariate analysis: the amount of visible coronary artery disease on the coronary angiogram (p less than 0.0001) and a smoking history (p = 0.001). A model to predict spasm based on these variables was validated in a test group of 2,311 patients who received ergonovine from 1985 to 1989. This model allowed the identification of a subset of 400 patients in the validation sample who had a 10% positive test rate compared with a 2% positive test rate in the remaining patients. These results should permit clinicians who use provocative testing in the catheterization laboratory to reserve testing for the subset of this group of patients most likely to have abnormal findings.

Angina Pectoris, Variant↗
PubMed1982

Short- and long-term responses to diltiazem in patients with variant angina.

Short- and long-term effects of diltiazem on angina frequency were studied in 12 patients with variant angina (pain at rest with S-T elevation). Each patient first entered a double-blind short-term trial. Either diltiazem, in two dosage schedules (120 and 240 mg/day), or placebo was administered in a randomized double-blind program over 10 weeks. Significant decreases in frequency of angina were observed when diltiazem treatment periods were compared with placebo periods. Six patients were asymptomatic, one had 50 percent or greater decrease, and two had a smaller decrease in angina frequency. Two patients showed no important improvement during short-term diltiazem therapy. One patient experienced ventricular fibrillation in the placebo period and was advanced to treatment with open label diltiazem before responses could be ascertained in the double-blind trial. All other patients were then advanced to open label diltiazem therapy and followed up for an average of 16 months (range 8 to 23). Responses during the short-term trial accurately predicted responses during long-term therapy. Of the six patients who were asymptomatic during short-term therapy, five remained asymptomatic and one had rare episodes of angina. One other patient continued to have a good response (50 percent or greater decrease in angina frequency) and two other patients had a partial response. The two patients who did not respond during short-term therapy did not respond during long-term therapy.

Adult↗
PubMed1996

Comparison of clinical and laboratory findings between patients with diffuse three-vessel coronary artery spasm and other types of coronary artery spasm.

Our purpose was to compare patients with diffuse three-vessel coronary artery spasm and other types of coronary artery spasm without significant organic stenosis, and to elucidate clinical characteristics and risk factors. Patients were divided into two groups: group I consisted of 26 patients showing other types of coronary artery spasm; group II consisted of 5 patients with diffuse three-vessel coronary artery spasm. The mean age of patients in groups I and II was 52 and 50 years, respectively. The incidence of variant angina was higher in men than in women. The incidence of smoking was high in each group, but not significantly different. Exercise tests showed no significant differences between groups. All mean values of laboratory data, including lipoprotein (a) and low-density lipoprotein cholesterol in the two groups, were within normal ranges. There was no significant difference between groups. The incidence of spontaneous spam was much higher in patients with diffuse three-vessel coronary artery spasm (P < 0.01). Electrocardiographic (ECG) findings before the spasm were almost normal. All 5 patients with diffuse three-vessel coronary artery spasm demonstrated no important ST segment changes with episodes of angina during a coronary angiography on 12-lead ECG, compared to patients with other types of coronary artery spasm (P < 0.01). First, we conclude, diffuse three-vessel coronary artery spasm mostly occurs spontaneously. Second, we emphasize that diffuse three-vessel coronary artery spasm must be considered when 12-lead ECG shows no important ST segment changes with episodes of angina. Third, it is not easy to distinguish diffuse three-vessel coronary artery spasm from other types of coronary artery spasm on the basis of history, laboratory data, or electrocardiographic findings, including exercise tests.

Angina Pectoris, Variant↗
PubMed1989

[Various clinical and vasomotor coronary responses to calcium block in mixed angina and Prinzmetal's angina, expression of various physiopathologic mechanisms].

Impedance to flow due to coronary spasm is currently interpreted as the mechanism of Prinzmetal angina. Flow impedance, probably of vasomotor origin, superimposed on severe coronary stenosis is also viewed as the trigger for the spontaneous component of mixed angina. The major question that we attempted to answer in this study was whether mixed angina may be considered a variant of the Prinzmetal form, or a particular manifestation of the classic effort form. For these purposes we investigated the acute vasomotor response to calcium channel blockade (nifedipine 10 mg sl) of both significant (greater than 50%) stenotic lesions and of normal coronary vessels in 22 patients with mixed angina and in 14 patients with Prinzmetal angina, and correlated it with the clinical response to treatment (nifedipine 20 mg qid). Calcium channel blockade, in fact, is considered as a specific remedy in the presence of an altered coronary vasomotility. The clinical response was evaluated through ambulatory Holter monitorings of 48 hour duration, while on placebo, nifedipine and placebo again. In mixed angina an angiographic evaluation showed that the residual lumen diameter of significant lesions was unchanged in 2, enhanced in 11 and reduced in 9 patients after sl nifedipine; lumen variations from base line ranged from +1.5 to -1.3 mm. Acute stenosis widening or narrowing correlated closely with the efficacy or not of the treatment. In the Prinzmetal group the vast majority of the lesions had compliant portions which invariably responded with dilatation (the residual coronary lumen increased by an average of 69% of base line); 100% of patients in this group responded favourably to treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Long-term prognosis of patients with variant angina.

The long-term prognosis of variant angina and the factors influencing it were assessed in 217 consecutive patients hospitalized in our coronary care unit and followed for a mean of 65 months (range 2 to 123). Cardiac death occurred in 30 patients and an additional 54 experienced a nonfatal myocardial infarction. Survival at 1 and 5 years was 95% and 89%, respectively; survival without infarction was 83% and 69%. Coronary disease and the degree of disease activity were strong predictors of survival by Cox analysis. Survival at 1 year was 99%, and that at 5 years was 95% and 94%, respectively, for patients with one-vessel disease (n = 81) and for those without stenoses of 70% or greater (n = 87). Survival at 1 and 5 years was only 87% and 77% for those with multivessel disease (n = 40). The Cox analysis selected left ventricular function, initial treatment, extent score, duration of angina at rest, and disease activity as multivariate predictors of survival without infarction. Coronary disease was a strong predictor (p less than .0001) of survival without infarction by univariate analysis. Treatment with nifedipine, diltiazem, or verapamil improved survival without infarction compared with other medical treatment (p = .002). Myocardial infarction occurred most commonly soon after diagnosis in patients with a short history of angina at rest. Late coronary events were almost never preceded by resting angina.

Adult↗
PubMed1983

Non-pharmacological provocation of coronary vasospasm. Experience with prolonged hyperventilation in the coronary care unit.

Results are reported of prolonged hyperventilation as a provocation test in a consecutive series of six patients with a clinical diagnosis of Prinzmetal's variant angina (PVA) and a control series of eight patients. All the patients with PVA responded to the hyperventilation test (HVT) with significant ST deviation (five with elevation, one with depression) and typical anginal pain. None of the eight patients in the control series were positive responders. Sustained attacks of serious arrhythmias were recorded in one patient with PVA. Sensitivity to HVT showed circadian variations; the tests were positive only in the early morning at the time of the reported spontaneous attacks. Beta blockade changed a negative HVT response to a positive one in one case. Treatment with calcium channel blockers suppressed the positive response in all patients. After cessation of long-term treatment with calcium channel blockers, HVT suggested spontaneous remission in spasm tendency in three out of four patients with PVA from a previous series of 12 patients. It is concluded that HVT as a non-pharmacological provocation test may prove an effective and comparatively safe procedure with potential for controlling the efficacy of drug treatment and confirming spontaneous remission of vasospastic disease. Optimal facilities for resuscitation should be at hand during the test due to risk of provoking life-threatening arrhythmias.

Adult↗
PubMed1984

Concomitant calcium antagonist plus isosorbide dinitrate therapy for markedly active variant angina.

The present study was performed to assess the efficacy of concomitant calcium antagonist/isosorbide dinitrate therapy in patients with frequent episodes of variant angina and to compare such combination therapy with isosorbide dinitrate alone. We enrolled nine such patients (six men and three women, aged 47 +/- 9 [mean +/- standard deviation] years) in a long-term comparison of (1) oral isosorbide dinitrate (117 +/- 63 mg per day) alone, (2) verapamil (453 +/- 75 mg per day) + isosorbide dinitrate (given in the same dose as stated above), and (3) nifedipine (71 +/- 14 mg per day) + isosorbide dinitrate (also given in the same dose as stated), each administered for 2 months. During isosorbide dinitrate therapy, these nine patients averaged 23.7 +/- 37.3 chest pains per week, consumed 24.4 +/- 47.4 sublingual nitroglycerin tablets per week, and demonstrated 46.5 +/- 43.2 episodes per week of transient ST segment deviations on calibrated two-channel Holter monitoring. During therapy with verapamil/isosorbide dinitrate and nifedipine/isosorbide dinitrate, the frequency of angina and ST segment deviations was dramatically reduced (verapamil/isosorbide dinitrate, 3.9 +/- 3.6 chest pains per week and 3.5 +/- 2.6 ST segment deviations per week, p less than 0.05; nifedipine/isosorbide dinitrate, 3.1 +/- 4.0 chest pains per week and 5.5 +/- 6.6 ST segment deviations per week, p less than 0.05). In all respects, verapamil/isosorbide dinitrate and nifedipine/isosorbide dinitrate were similar to one another.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Transient appearance of collaterals during vasospastic occlusion in patients without obstructive coronary atherosclerosis.

Coronary angiography of both right and left coronary arteries, using the Sones technique, was performed during the attack of total spastic obstruction in 11 patients with clinically documented history of variant angina. None of the patients had more than 70% stenosis of organic atherosclerosis in any coronary artery and none had a history of myocardial infarction. Total spastic obstruction occurred spontaneously in 3 of 11 patients, and was provoked by ergonovine maleate in eight patients. Six patients had total spastic obstruction in the left anterior descending coronary artery, four patients had total obstruction in the right coronary artery, and one patient had total obstruction in the left anterior descending and right coronary arteries. In 7 of 11 patients, the coronary artery distal to the total spastic obstruction received collaterals from the nonspastic artery. The collaterals disappeared promptly when the spastic coronary artery was patent. These patients had ST segment elevation in the ECG during the attacks. In the remaining four patients, the spastic artery did not receive any collaterals from the nonspastic artery, associated with ST segment elevation during the attacks. These findings suggest that the brief, repetitive total occlusion of the coronary artery may stimulate the enlargement of collaterals. These collaterals may not always function to prevent the ischemia of the myocardium on the ECG.

Adult↗
PubMed1983

Coronary arterial spasm in ischemic heart disease and its pathogenesis. A review.

Coronary arterial spasm plays an important role iun the production not only of variant angina but, also, of resting angina other than variant angina, of some exertional angina, and of some acute myocardial infarction. Coronary arterial spasm is most likely to occur at rest, particularly from midnight to early morning, and is usually not provoked by exercise in the daytime. This is related to the fact that the tone of coronary artery is increased from midnight to early morning, whereas it is decreased in the daytime after physical activities. Coronary arterial spasm can be induced by exercise, cold pressor test, hyperventilation, Valsalva maneuver, and the administration of pharmacological agents such as sympathomimetic agents (epinephrine, norepinephrine, etc.), beta-blocking agents (propranolol, etc.), parasympathomimetic agents (methacholine, pilocarpine, etc.), ergot alkaloids (ergonovine, ergotamine, etc.), alcohol, and others, particularly in the morning when spontaneous coronary arterial spasm is most likely to occur. Diltiazem and nifedipine, calcium-blocking agents, prevent coronary arterial spasm induced by these procedures in almost all patients. Phentolamine, an alpha-blocking agent, also suppresses coronary arterial spasm induced by these procedures in 81% of the patients. On the other hand, propranolol, a beta-blocking agent, is not only ineffective in suppressing coronary arterial spasm in 82% of the patients, but aggravates coronary arterial spasm in 41% of the patients. The acute attack of coronary arterial spasm can be promptly relieved by the administration of nitroglycerin.

Angina Pectoris, Variant↗
PubMed1989

[Induction of coronary arterial spasm by intracoronary administration of acetylcholine in patients with vasospastic angina].

To examine whether intracoronary injections of acetylcholine induce coronary artery spasm in patients with vasospastic angina, incremental doses (20, 30 and 50 micrograms) were injected directly into the coronary arteries in 12 patients with variant angina (Group A: rest angina with electrocardiographic ST-segment elevation during attacks), 19 with vasospastic angina (Group B: rest angina and/or effort angina with variable threshold in the treadmill exercise stress test), 11 with organic coronary artery stenosis but without angina (Group C), and 14 without coronary artery disease (Group D). A temporary cardiac pacemaker was positioned in the right ventricle. Coronary artery spasm was defined as severe vasoconstriction (greater than or equal to 90% of reduction in the luminal diameter) with chest pain and/or ischemic changes in the electrocardiogram. Intracoronary injection of acetylcholine induced spasm of at least one coronary artery in all 12 patients (100%) of Group A, in 18 (95%) of Group B, in two (18%) of Group C, and in two (14%) of Group D. Thus, the sensitivity of this method for inducing coronary spasm was 100% in group A, 95% in Group B, and 97% in Group A plus Group B. The specificity for inducing spasm was 86% in Group D, and 84% in Group C and Group D. When acetylcholine was injected separately into the left and right coronary arteries, spasm of both the coronary arteries was observed in two (40%) of Group A, in five (33%) of Group B, and none (0%) of Group C and Group D. Acetylcholine (20 micrograms) induced coronary spasm in 10 (83%) of Group A and only in nine (47%) of Group B.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1982

Effects of intravenous prostacyclin in variant angina.

A lack in prostacyclin (PGI2) production due to atherosclerosis may play a role in the pathophysiology of some of the clinical manifestations of ischemic heart disease and in particular, of coronary vasospasm. We therefore evaluated the effects of i.v. PGI2 in nine patients with variant angina and six normal volunteers. In normal subjects, PGI2 (2.5, 5, 10 and 20 micrograms/kg/min) had significant antiplatelet effects, caused a dose-dependent decrease in both systolic and diastolic arterial pressure and a decrease in pulmonary resistance. Heart rate increased in a dose-dependent manner, but no consistent effects on myocardial contractility (evaluated by ultrasound) were observed. Side effects were negligible and readily reversible. Although producing obvious antiplatelet and vasodilatory effects, PGI2 did not affect the number, severity and duration of spontaneous ischemic episodes due to coronary vasospasm in five patients and ergonovine-induced spasm in three. However, the number of ischemic episodes was consistently reduced in one patient during four consecutive periods of PGI2 infusion alternated with placebo. a severe, prolonged ischemic episode with ST elevation and pain was consistently observed in this patient every time PGI2 was discontinued. In the appropriate environment, PGI2 can be administered safely to patients with ischemic heart disease. Occasionally, PGI2 may result in a complete disappearance of ischemic episodes due to coronary vasospasm, but usually it is ineffective. These conflicting results could be related to different etiologies of coronary spasm.

Adult↗
PubMed1993

Efficacy of amlodipine besilate therapy for variant angina: evaluation by 24-hour Holter monitoring.

The efficacy of amlodipine, a calcium antagonist, was investigated in 12 patients with variant angina. Amlodipine was administered at a dose of 5 mg once daily, and efficacy was assessed from the frequency of anginal attacks, the frequency of ST elevation or depression, and the extent of ST segment changes [ST segment elevation or depression (mm) x duration (seconds)] on the Holter ECG before and after treatment. The frequency of ST elevation during the observation period was 1.67 +/- 0.33 times/day (symptomatic attacks: 1.17 +/- 0.21/day; asymptomatic attacks: 0.50 +/- 0.19/day), and this significantly decreased to zero per day (both symptomatic and asymptomatic attacks) after treatment (p < 0.05). The extent of ST segment elevation during the observation period was 507.5 +/- 156.6 mm.sec/day (symptomatic: 382.5 +/- 102.9 mm.sec/day; asymptomatic: 125.0 +/- 62.0 mm.sec/day), and such changes were completely suppressed (both symptomatic and asymptomatic) by treatment (p < 0.05). The frequency of ST depression was 2.08 +/- 0.42 times/day (symptomatic: 0.25 +/- 0.13/day; asymptomatic: 1.83 +/- 0.37/day) during the observation period, while it was 1.50 +/- 0.36 times/day (symptomatic: 0.25 +/- 0.13/day; asymptomatic: 1.25 +/- 0.30/day) after treatment. Although anginal attacks remained unchanged, asymptomatic attacks tended to decrease (p = 0.07).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Ventricular ectopic activity with spontaneous variant angina: frequency and relation to transient ST segment deviation.

This study was performed (1) to assess the frequency of ventricular ectopic activity (ventricular bigeminy, couplets, or ventricular tachycardia) during spontaneous variant angina; (2) to assess the relation between ventricular ectopy and the severity and duration of ischemia; and (3) to evaluate the precise temporal relation between episodes of ischemia and ventricular ectopy. Fifteen ambulatory patients with variant angina (12 men, 3 women, aged 50 +/- 8 [mean +/- SD] years) had Holter monitoring for 24 hours/week for 10 months (total, 10,238 hours of monitoring), from which the following were measured during each episode of ST deviation (elevation or depression): duration of ST deviation (minutes), maximal ST deviation (millivolts), presence of ventricular ectopic activity, and timing of ventricular ectopy in relation to ST deviation. Of 645 episodes of ST deviation, 79 (12.2%) had associated ectopy, almost all of which occurred in three patients. The 79 episodes of ST deviation with ectopy lasted 4.6 +/- 3.3 minutes and averaged 0.16 +/- 0.12 mV, whereas the 566 episodes of ST deviation without ectopy lasted 4.7 +/- 6.1 minutes and averaged 0.17 +/- 0.11 mV (NS in comparison to the 79 episodes with ectopy). Of 489 episodes of ST elevation, 72 (14.7%) were accompanied by ventricular ectopy; of 156 episodes of ST depression, only seven (4.5%) had ectopy (chi 2 = 11.531, p less than 0.001). Of the 79 episodes of ventricular ectopy, almost all appeared during a period of increasing or maximal ST deviation, whereas only two appeared as ST deviation was resolving.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗