Episodes Of ST Segment Elevation Research Articles

КЛИНИЧЕСКИЙ СЛУЧАЙ ВАЗОСПАСТИЧЕСКОЙ СТЕНОКАРДИИ У ПАЦИЕНТА С ГАСТРОЭЗОФАГЕАЛЬНОЙ РЕФЛЮКСНОЙ БОЛЕЗНЬЮ

Introduction. The combination of CAD and GERD is a common clinical situation. In recent years, more and more information has appeared indicating that the coexistence of both diseases is not accidental. Clinical example. A 51-year-old man was admitted to the KGBUZ "AKKD" by transfer from the Central District Hospital with complaints of burning, pressing pains behind the sternum without a clear connection with physical activity, more often in the early morning hours, lasting up to 5 minutes, stopped by sitting, drinking cold water. Upon admission, the state of the average degree. BMI 23.9 kg/m2. Temperature 36.6 0С. NPV 16 per min. SpO2 - 96%. Heart rate 55 beats. in min. AD = 110/60 mm. rt. Art. Vesicular breathing in the lungs, no wheezing. The heart sounds are clear, the rhythm is correct. There are no edema. The abdomen is soft and painless. ECG at admission: sinus rhythm with a heart rate of 55 per minute. Negative T wave II, III, aVF, V7-V9. From the anamnesis: he had not previously controlled blood pressure, he did not take regular medications. Long history of smoking. During the year, he began to notice rare episodes of burning behind the sternum lasting up to 10 minutes without a clear connection with physical activity. He was examined at the place of residence, EGD was performed, where a hernia of the esophageal opening of the diaphragm, chronic atrophic gastritis were diagnosed. During the week before hospitalization, the condition worsened in the form of a decrease in exercise tolerance, an increase in burning sensation, pressing pain behind the sternum. On May 11, 23, due to a long-term pain syndrome behind the sternum, he called an ambulance, was hospitalized at the Central District Hospital, and then transferred to the AKKD. Upon admission to the AKKD, emergency coronary angiography was performed, where subocclusion of the circumflex artery (OA) was diagnosed, stenting of the OA with a drug-eluting stent. Echocardiography revealed hypokinesis along the lateral wall, the ejection fraction of the left ventricle was 59%. Laboratory: troponin I at admission and in dynamics within the reference values; dyslipidemia. After PCI in the department, daily recurrences of burning in the epigastrium and behind the sternum more often at night. Repeated EGD - reflux gastritis with metaplasia, cardiac insufficiency. HMECG recorded episodes of ST segment elevation in II, III, aVF, V5-V6, duration up to 70 minutes; frequent polymorphic ventricular extrasystole. Taking into account recurrent pains, the results of HMECG, a control coronary angiography was performed - the coronary arteries were without pathology, the OA stent was passable. Treatment was corrected, antianginal therapy was increased with beta-blockers, dihydropyridine calcium antagonists and long-acting nitrates, as well as therapy with proton pump inhibitors. During therapy, the condition improved, anginal pain did not recur. According to HMECG in dynamics - no ischemic changes. Discharged from the hospital in a satisfactory condition with recommendations. Conclusion. To date, a number of pathophysiological mechanisms have been established, both causing the pathogenetic relationship between IHD and GERD, and contributing to their mutual aggravation. The basis of the occurrence of associated angina pectoris is the esophagocardial reflex, caused by irritation of the esophagus and the development of coronary spasm as a result. In patients with variant angina pectoris, a time relationship was found between periods of esophageal spasm and episodes of ECG-registered ischemia. At the same time, it was found that with impaired esophageal motility in patients with coronary artery disease, a vicious circle may form: esophagospasm provokes myocardial ischemia, which, in turn, contributes to new episodes of esophageal spasm.

Ephedrine-Induced Coronary Artery Vasospasm in a Patient with Prior Cocaine Use

Ephedrine-Induced Coronary Artery Vasospasm in a Patient with Prior Cocaine Use

Autonomic changes associated with spontaneous coronary spasm in patients with variant angina

This study sought to investigate whether changes in nervous autonomic tone may have a role in the mechanisms triggering spontaneous coronary spasm in variant angina. Previous studies have suggested that both sympathetic and vagal activation may act as a trigger of epicardial artery spasm in patients with variant angina, but the actual role of autonomic changes in spontaneous coronary spasm remains unknown. We analyzed the changes in heart rate variability associated with episodes of ST segment elevation detected on Holter monitoring in 23 patients with variant angina (18 men, 5 women; mean [+/-SD] age 59 +/- 12 years). For study purposes, episodes of transmural ischemia lasting > or = 3 min and without any ST segment changes in the previous 40 min were selected for analysis. Heart rate variability indexes were calculated at 2-min intervals, at 30,15,5 and 1 min before ST elevation and at peak ST segment elevation. Ninety-three of 239 total ischemic episodes (39%) fulfilled the inclusion criteria. The results showed that 1) high frequency (HF) (0.04 to 0.15 Hz), a heart rate variability index specific for vagal activity, decreased in the 2 min preceding ST segment elevation (p < 0.001) and returned to basal levels at peak ST segment elevation; 2) heart rate and low frequency (0.04 to 0.15 Hz), which are partially correlated with sympathetic activity, showed a significant increase at peak ST segment elevation (p < 0.001 for both); 3) the pattern of the HF reduction before ST segment elevation was consistently confirmed in several subgroups of ischemic episodes, including those of patients with or without coronary stenoses, those of patients with anterior or inferior ST segment elevation, those occurring during daily or nightly hours and silent episodes. There were no significant variations in heart rate variability in control periods selected from Holter tapes of patients and before ST segment elevation induced by balloon inflation in 20 patients undergoing coronary angioplasty. Our data show that changes in autonomic tone are likely to contribute to trigger or predispose to epicardial spasm. In particular, although not excluding an active role for adrenergic mechanisms, our data suggest that a vagal withdrawal may often be a component of the mechanisms leading to spontaneous coronary vasospasm.

Preconditioning by transient myocardial ischemia confers protection against ischemia-induced ventricular arrhythmias in variant angina.

In experimental models, ischemic preconditioning of the heart protects against ischemic damage and ventricular arrhythmias during subsequent coronary occlusion. In this study, we investigated whether protection against ischemic suffering and ischemia-induced arrhythmias may occur after spontaneous transmural ischemia in humans. We performed 24-hour Holter monitoring in 10 patients with variant angina who developed complex ventricular arrhythmias (CVAs, more than five premature ventricular beats per minute or repetitive ventricular arrhythmias) during episodes of ST-segment elevation. A total of 150 episodes of ST-segment elevation were detected on Holter monitoring, 21 (14%) of which showed CVAs. Episodes separated from the previous one by a time interval of < or = 30 minutes or by a time interval of > 30 minutes did not differ in either magnitude or duration of ST-segment elevation, but CVAs occurred more frequently in the second group (3% versus 29%, P < .0001). The time interval from the preceding ischemic episode was longer for the episodes with compared with those without CVAs (197 +/- 275 versus 57 +/- 87 minutes, P < .001), but these two groups of episodes also had similar severities and durations of ST-segment elevation. Finally, when we analyzed 13 clusters of two to six ischemic episodes, CVAs were found much more frequently in the first (92%) than in the last (23%, P = .009) episode of the clusters, while ST-segment elevations were similar (2.1 +/- 1.6 versus 2.2 +/- 1.1 mm) and ischemia durations shorter in the first than in the last episode (3.9 +/- 3.6 versus 6.1 +/- 1.7 minutes, P = .03). Our data indicate that preconditioning by transient ischemia induces a significant protection against ischemia-induced CVAs in patients with variant angina. This beneficial effect was not related to a reduction in either severity or duration of ischemia, suggesting that arrhythmic protection was a direct consequence of preconditioning rather than an epiphenomenon of ischemic protection.

Clinical observation of spontaneous anginal attacks and multivessel spasm in variant angina pectoris with normal coronary arteries: Evaluation by 24-hour 12-lead electrocardiography with computer analysis

Using a new, computerized 24-h 12-lead electrocardiographic (ECG) recording and analysis system (the EAGLE system), we sought to evaluate the clinical manifestations of ischemic episodes in patients with variant angina and normal coronary arteries. Although the prognosis of variant angina without significant organic stenosis is generally good, the incidence of multivessel spasm, a major prognostic factor, is surprisingly high in provocation tests. A total of 122 patients with suspected variant or unstable angina underwent 24-h examination with the EAGLE system and two-channel Holter monitoring. Thirty patients in this group were diagnosed as having variant angina with normal or nearly normal coronary arteries. Twenty-two (73%) of these 30 patients developed anginal attacks with ST segment elevation during monitoring and were enrolled in the study. The 22 patients had a total of 138 episodes of transient ST segment elevation and 13 episodes of ST segment depression. No arrhythmias were observed during ST segment depression, but 26 episodes of ST segment elevation (19%) were associated with arrhythmias: 7 with premature ventricular contractions, 3 with ventricular bigeminy, 3 with complete atrioventricular (AV) block, 1 with complete AV block and couplets of premature ventricular contractions and 12 with marked sinus bradycardia (< 45 beats/min). Ten (45%) of the 22 patients had multivessel spasm. We observed three different patterns of multivessel spasm: 1) spasm at a different site on different occasions (migratory spasm); 2) spasm that sequentially affected two different sites; 3) simultaneous spasm at more than one site. The duration of ST segment elevation was much longer in patients with sequential and simultaneous spasm than in those with single-vessel spasm, and arrhythmias were more frequent during these two types of multivessel spasm. Although the prognosis of multivessel spasm is believed to be poor, this may not necessarily be so. Anginal attacks due to sequential and simultaneous multivessel spasm seem to be more dangerous than those involving single-vessel spasm or migratory multivessel spasm.

Characteristics and prognostic importance of ST-segment elevation on Holter monitoring early after acute myocardial infarction

The correlation between episodes of ST-segment elevation on Holter monitoring, clinical characteristics, left ventricular function, exercise testing, and long-term prognosis was determined in 123 consecutive patients 55 ± 8 years old (mean ± SD) with a first acute myocardial infarction (AMI). During 36 hours of Holter recording 11 ± 5 days after AMI, 11 patients (9%) had 91 episodes of ST-segment elevation (group 1), whereas 112 patients had no such episodes (group 2). Most episodes of ST-segment elevation occurred in leads with pathologic Q waves or small, indistinct R waves. Large, anterior Q-wave AMIs were more prevalent in group 1 than in group 2, and in-hospital heart failure also occurred more frequently in group 1 patients (82% vs 23%; p < 0.0005). Regional and global left ventricular function was reduced in group 1 compared with group 2: ejection fraction 33 ± 11% vs 50 ± 11% (p = 0.0001). All episodes of ST-segment elevation were asymptomatic and did not correlate with different indicators of myocardial ischemia. Indeed, exercise-induced ST-segment depression was more prevalent in group 2 than in group 1: 57 vs 18% (p < 0.035). Over a mean of 5 years (range 4 to 6) of follow-up, an association between episodes of ST-segment elevation on Holter monitoring and (1) cardiac death (Kaplan-Meier analysis; p < 0.005), and (2) cardiac death and nonfatal reinfarction (Kaplan-Meier analysis; p < 0.025) was found. If, however, the symptomatic need for coronary revascularization was included as an end point, no association between episodes of ST-segment elevation and long-term outcome could be demonstrated (Kaplan-Meier analysis; p = NS).

Efficacy of slow-release nifedipine on ischemic attacks in patients with variant angina

We examined the effects of slow-release nifedipine on ischemic attacks in eight patients with variant angina. The study period was divided into four parts: placebo I period; nifedipine I period, when 20-mg slow-release nifedipine was given once a day at 10:00 p.m.; placebo II period; and nifedipine II period, when 20-mg slow-release nifedipine was given twice a day at 10:00 p.m. and 6:00 a.m. Each period consisted of 4 days, and 48-hour Holter monitoring was done at the end of each period. There was a significant decrease in the number of the episodes per 48 hours during the nifedipine I and nifedipine II periods as compared with the placebo I period (2.4 +/- 2.2 vs. 25.7 +/- 12.3, p less than 0.01; and 0.1 +/- 0.1 vs. 25.7 +/- 12.3, p less than 0.01, respectively). The total duration of episodes of ST-segment elevation per 48 hours decreased significantly during the nifedipine I period and the nifedipine II period as compared with the placebo I period (2.4 +/- 2.2 vs. 87.6 +/- 30.2 minutes, p less than 0.01; and 0.3 +/- 0.3 vs. 87.6 +/- 30.2 minutes, p less than 0.01, respectively). The total duration of the episodes also decreased significantly during the nifedipine II period as compared with the placebo II period (0.3 +/- 0.3 vs. 31.6 +/- 20.1 minutes, p less than 0.05). We concluded that 20-mg slow-release nifedipine given once a day at 10:00 p.m., or twice a day at 10:00 p.m. and 6:00 a.m., is highly effective in suppressing ischemic episodes in patients with variant angina.

The ST segment of the ambulatory electrocardiogram in a normal population.

The behaviour of the ST segment in everyday life was studied by ambulatory electrocardiography in 111 normal volunteers. Fifteen were excluded because of abnormal exercise responses (10 subjects) and significant postural ST segment shifts (five subjects). This left 62 men and 34 women, mean (SD) age 40.5 (12.6) years (range 20-67 years). Ambulatory monitoring of leads CM5 and CC5 for 24 hours was followed by a maximal treadmill exercise test. The tapes of the ambulatory monitoring were analysed by a computer aided system. The computer printed trend plots of the ST segment (measured both at the J point and at J + 60 ms) to detect episodes of ST segment elevation and depression, which were confirmed by visual analysis of real time printouts. Twelve subjects showed "ischaemic" ST segment depression and nine subjects showed ST segment elevation. Eight people with ambulatory ST segment changes were studied during exercise by radionuclide ventriculography and thallium-201 imaging scans. Although seven of the eight thallium studies were normal, radionuclide ventriculography showed functional impairment in five cases. Seven of the 10 subjects with abnormal exercise tests were similarly investigated and their results followed the same pattern, with normal thallium images in six and functional impairment in four. Ambulatory electrocardiography was repeated in 20 people after a median of 20 days. The ST segment changes were reproducible. ST segment changes of an apparently ischaemic nature occur even in a carefully defined normal population but they do not necessarily represent latent clinically significant coronary artery disease. This indicates that ST segment changes seen in patients with known obstructive coronary artery disease should be interpreted with caution.

The haemodynamic response to myocardial ischaemia in ambulant patients with variant angina.

The haemodynamic response to myocardial ischaemia in patients with variant angina during ambulatory activity is unknown. Ambulatory pulmonary artery pressure monitoring with a transducer tipped catheter and simultaneous frequency modulated electrocardiograms was used to assess changes in left ventricular function in five male patients (mean age 51.8 years) during variant angina; four patients had coronary artery stenosis and one had normal coronary arteries. Two hundred and seventy hours of ambulatory recordings were analysed. Twenty episodes (12 painful, 8 silent) of ST segment change greater than 1 mm occurred. Episodes tended to occur more frequently in the early morning hours. Six episodes of painful ST elevation were associated with a rise in pulmonary artery diastolic pressure. In the remaining episodes ST segment elevation was of shorter duration and there was no rise in pulmonary artery diastolic pressure. Pain was usually a late feature. Silent ST segment elevation occurred at rest and pulmonary artery diastolic pressure increased in all but one episode. Silent exertional ST segment depression was associated with a greater increase in pulmonary artery diastolic pressure than that seen during ST segment elevation. ST segment depression preceded or followed ST segment elevation in two episodes. The onset of ST segment elevation nearly always preceded the onset of a rise in pulmonary artery diastolic pressure. Ergometrine maleate provocation produced a rise in pulmonary artery diastolic pressure in three patients. In one there was no response to 1000 micrograms but spontaneous episodes of ST segment elevation were recorded during ambulatory monitoring. Treadmill exercise resulted in both ST segment elevation and depression with a similar haemodynamic response during both types of electrocardiographic change. When there is important coronary artery disease in two or more vessels ST segment changes may occur in different territories during treadmill exercise and during spontaneous episodes. Ambulatory pulmonary artery diastolic pressure monitoring is a useful technique for the investigation of variant angina.

Comparison of verapamil and propranolol therapy for angina pectoris at rest: A randomized, multiple-crossover, controlled trial in the coronary care unit

The effects of oral verapamil (V), 400 mg/day, oral propranolol (P), 300 mg/day, and placebo were compared in 10 patients admitted to the coronary care unit because of frequent attacks of angina at rest. Testing was done according to a randomized, double-blind, multiple-crossover, placebo-controlled trial, consisting of 8 consecutive 48-hour treatment periods with V or P or placebo. Three patients had variant angina, 5 had episodes of both ST-segment elevation and depression and 2 had only ST-segment depression. One patient had no critical coronary stenoses, 1 had 1-vessel disease, 7 had 2-vessel disease and 1 had 3-vessel disease. Electrocardiographic monitoring and tape recording were continued during the 16 days of the trial. A total of 1,602 episodes of transient diagnostic ST shift were recorded during the trial (1,309 episodes of ST-segment elevation, 293 of ST-segment depression); 43% were painless. Mean blood levels of V and P at the end of the active phases were 161 ± 89 and 120 ± 45 ng/ml, respectively. In the group as a whole, the average number of diagnostic ischemic ST-segment shifts per 24 hours was significantly reduced relative to corresponding placebo periods during V (2.6 ± 2.4 vs 11.9 ± 8.6; p < 0.01) but not during P treatment (11.9 ± 8.6 vs 12.0 ± 7.3). Similar statistically significant reductions were observed in the number of anginal attacks and nitroglycerin tablets consumed. Considering individual patients, V reduced ischemic episodes during both active phases in all patients, whereas P was effective only in 1. In particular, P was not effective in 3 patients with severe limitation of exercise tolerance, but did not increase consistently the number or duration of episodes in the 3 patients with variant angina.

Transient myocardial ischemia with minimal electrocardiographic changes: An echocardiographic study in patients with Prinzmetal's angina

In patients with Prinzmetal's angina, episodes of transient T wave abnormalities (T abn) are often documented in addition to the typical episodes of ST segment elevation (ST↑). As the interpretation of these minor ECG changes is still uncertain, we investigated if transient T abn are associated with reversible ventricular asynergies, similar to episodes with ST↑. For this purpose an ECG lead and a two-dimensional echocardiographic projection, which showed clear-cut changes during previous episodes of ST↑, were simultaneously monitored in five patients with Prinzmetal's angina for a total of 13 hours and 20 minutes. In all patients, the 30 episodes of ST↑ recorded were all accompanied by reversible ventricular asynergiss. Furthermore, in four of these patients, 14 episodes of T abn (peaking, flattening, or the appearance of a diphasic T wave) were recorded. All T abn were associated with reversible asynergies, as detected by three independent observers. The mechanical impairment occurred in the same ventricular wall both during ST↑ and during T abn. During T abn the degree of mechanical impairment appeared less severe (hypokinesia in 12 and akinesia in two episodes) than during ST↑ (hypokinesia in one, akinesia in 25, and dyskinesia in four episodes) ( p < 0.001). The duration of asynergies was less during T abn (107 ± 76 seconds) than during ST↑ (169 ± 83 seconds) ( p < 0.05). Chest pain was reported in 5 of 14 episodes of T abn (36%) and in 20 of 30 (66%) episodes of ST↑ ( p < 0.05). An incomplete coronary spasm in one patient and an increase in left ventricular filling pressure in another were documented during T abn. In conclusion, in patients with Prinzmetal's angina, minor T abn are accompanied by reversible ventricular asynergies, sugcesting the ischemic nature of the phenomenon.

Ischaemia related ventricular arrhythmias in patients with variant angina pectoris.

Twenty-three patients with variant angina were studied by Holter monitoring both to assess the incidence of serious ventricular arrhythmias (a risk factor of sudden death in variant angina), during ischaemic episodes and to examine the time-relation of the arrhythmias to ST changes. Serious ventricular arrhythmias were observed in 12/23 patients (52%). In the 23 patients, a total of 491 episodes of ST segment elevation were recorded during 954 h of Holter monitoring; serious ventricular arrhythmias were found in only 46 ischaemic episodes (9.4%). Six out of 12 patients showed serious ventricular arrhythmias at the onset of ischaemic episodes or during maximal ST elevation (phase 1), one patient during return or immediately after return of ST to baseline (phase 2) and five patients during both phases. Thirty-three out of 46 ischaemic episodes (76%) showed serious ventricular arrhythmias during phase 1, eight (17%) during phase 2, and five (11%) during both phases. Serious ventricular arrhythmias were neither related to previous myocardial infarction nor to the presence of serious ventricular arrhythmias during inter-crisis periods, whereas a good relationship with severity of ischaemic episodes, as assessed by the magnitude and duration of ST elevation, was found. A modest relationship with anterior ST elevation was also found. (1) serious ventricular arrhythmias occur in a high percentage of variant angina patients, but in only a small proportion of ischaemic episodes; (2) serious ventricular arrhythmias are related to the severity of ischaemia and occur predominantly at the onset of ischaemic episodes and/or during maximal ST elevation; in only a few cases do they occur during resolution of ischaemic episodes.

Ergonovine-induced myocardial ischemia: no role for serotonergic receptors?

Because ergonovine appears to produce coronary contractions by a serotonergic (5-HT) mechanism, we attempted to prevent ergonovine-induced ischemia in patients with vasospastic angina by pretreatment with ketanserin, a new selective 5-HT blocker. We studied seven patients with consistently positive results of ergonovine testing (ST segment elevation in three and ST segment depression in four). Ergonovine testing was performed before and after a bolus of 10 mg of ketanserin (all patients) and infusion of 2 to 4 mg/hr for 8 hr (six patients). To assess 5-HT blockade during ketanserin infusion, the constrictor response of hand veins to 5-HT was tested before and after ketanserin. Despite evidence of 5-HT blockade in hand veins, ergonovine-induced ischemia was not prevented by ketanserin in any patient, and there was no significant change in the dose of ergonovine required to provoke ischemia. In one patient, four spontaneous episodes of ST segment elevation occurred during infusion of ketanserin. The plasma concentrations of ketanserin at the time of ergonovine testing ranged from 61 to 127 ng/ml (mean 102) and were well above those that completely inhibit canine coronary 5-HT contractions in vitro. Although human coronary arteries may differ in their responsiveness to 5-HT or ketanserin, these data suggest that ischemia from ergonovine-induced coronary vasospasm is not mediated by 5-HT receptors.

Clinical characteristics and prognosis of patients with postinfarction angina caused by coronary artery spasm.

Clinical features and the course of 15 patients with postinfarction angina caused by coronary artery spasm are described. Episodes of postinfarction angina in the patients recurred at rest in the early recovery phase and were accompanied by transient ST-segment elevation. The area where ST-segment elevations were demonstrated on a 12-lead ECG always included the leads with newly developed abnormal Q waves. Pain resolved spontaneously or after sublingual nitroglycerin in several minutes. Holter ECGs during a 24-h period demonstrated frequent episodes of ST-segment elevation that were not always associated with chest pain. Treatment with calcium antagonist and/or nitrates effectively suppressed angina, and only one patient developed reinfarction. The patient's subjective symptoms were abolished by diltiazem and isosorbide dinitrate. A Holter ECG of the patient revealed silent ST-segment elevations before and after the reinfarction and an increase of the drugs completely suppressed the recurrence of silent ischemic ECG changes. Coronary arteriograms were obtained from 8 patients, which demonstrated more than 75% segmental stenosis on one coronary artery in 5 patients and no significant obstruction in the remaining 3. All patients performed a treadmill exercise stress test before discharge and most demonstrated excellent tolerance. All patients experienced no form of chest pain for an average of 25 months follow-up under medication. We conclude that among patients with postinfarction angina, those cases caused by coronary artery spasm have a relatively good prognosis.

Ambulatory electrocardiographic ST segment changes in healthy volunteers.

Twenty four hour ambulatory monitoring was performed on 120 healthy volunteers using a frequency modulated recorder: 50 men and 50 women below 40 years and 20 men between 40 and 60 years were studied. Twenty eight subjects had episodes of ST segment elevation (range 1-3 mm), which occurred almost invariably at night with a slow heart rate 62.4 +/- 10.4 beats/min). ST segment elevation occurred most often in men, and was not found in subjects over the age of 37. Also in 10 subjects horizontal or downsloping ST segment depression (range 1-2 mm) was recorded, usually in association with tachycardia (135 +/- 10.5 beats/min). Nine of these exercised on a bicycle ergometer, and widespread ST segment depression was observed in eight. Thus ST segment changes, which are often interpreted as myocardial ischaemia in patients with ischaemic heart disease, are commonly seen in 24 hour electrocardiographic monitoring of healthy volunteers.

Alternans of the ST segment of T wave. A sign of electrical instability in Prinzmetal's angina.

In an effort to determine the incidence of ventricular arrhythmias associated with ST segments alternans, the patterns of ST segment and T-wave electrical alternans (STEA) were analyzed in 93 patients during spontaneous Prinzmetal's angina. Twenty-eight of 93 patients, or 30% (Group I), showed STEA during episodes of ST segment elevation. SIxty-five of 93 patients, or 70% (Group II), showed no alternans during episodes of ST segment elevation. In Group I, ventricular arrhythmias, defined as all ventricular ectopic activity greater than 5 beats per minute and complex Lown grades III to V, occurred during 52 of 55 episodes, or 95%; whereas in Group II, ventricular arrhythmias occurred in only 51 of 125 episodes, or 41% (p less than 0.01). The difference in the incidence of ventricular fibrillation (VF) or ventricular tachycardia (VT) in the two groups was more striking. VT or VF occurred in 20 of 55 in Group I (36%) versus 5 of 125 in Group II (4%). Although there were no significant differences in age or sex between Group I and II patients, there was a significant difference in the magnitude of the maximum ST segment elevation (5 mm in Group I versus 3 mm in Group II, p less than 0.01). This study demonstrates that the occurrence of STEA and T wave alternans frequently heralds the onset of ventricular arrhythmias in Prinzmetal's angina. Both the arrhythmias and the alternans occur during the time of maximal ST segment elevation.