Coronary arteriography and left ventriculography during spontaneous and exercise-induced ST segment elevation in patients with variant angina

The present study is an angiographic demonstration of coronary artery spasm during both spontaneous and exercise-induced angina in three patients with variant angina. In each case, clinical, ECG, coronary angiographic, and left ventriculographic observations were made at rest, during spontaneous angina, and during exercise-induced angina. The character of chest pain was similar during spontaneous and exercise-induced episodes. ST segment elevation was present in the anterior ECG leads during both episodes. The left anterior descending coronary artery became partially or totally obstructed during both types of attacks. When coronary spasm was demonstrated during both types of attacks, left ventriculography disclosed akinetic or dyskinetic wall motion in the area supplied by the involved artery. In those patients with reproducible exercise-induced ST segment elevation and chest pain, thallium-201 scintigraphy showed areas of reversible anteroseptal hypoperfusion. Thus in selected patients exercise-induced attacks of angina were similar to spontaneous episodes.     

Ventricular arrhythmias during ergonovine-induced episodes of variant angina

Of 95 consecutive patients with active variant angina who underwent ergonovine testing in the coronary care unit while off treatment, 24 (25%) developed serious ventricular arrhythmias: ventricular tachycardia in eight, bigeminy in seven, pairs in five, and frequent ventricular extrasystoles in four. Ergonovine-induced arrhythmias were observed more often in patients with anterior than inferior ST segment elevation (p less than 0.05). ST segment elevation was significantly higher (10.3 +/- 8.1 vs 3.1 +/- 2.1 mm) in patients who developed arrhythmias. All ventricular arrhythmias began within 3 minutes after the onset of ST segment elevation. The intravenous administration of nitroglycerin eliminated arrhythmias in 22 of 24 cases; in only two patients did ventricular arrhythmias develop after the administration of nitroglycerin. Serious ventricular arrhythmias were found during spontaneous variant angina attacks in 14 of 24 patients with ergonovine-induced arrhythmias compared to 16 of 71 patients without ergonovine-induced arrhythmias (p less than 0.001). We conclude that arrhythmias during ergonovine testing are most often caused by ischemia and not reperfusion. Patients with arrhythmias during ergonovine-induced attacks are more likely to have arrhythmias during spontaneous attacks.     

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.     

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.     

The effect of coronary vasospasm on the direction of ST-segment deviation in patients with both hypertrophic cardiomyopathy and vasospastic angina

BACKGROUND: There has been no report of ECG changes during anginal attacks in patients with coexistent hypertrophic cardiomyopathy (HCM) and vasospastic angina. STUDY OBJECTIVES: To elucidate the change in ST-segment during anginal attacks in patients with coexistent HCM and vasospastic angina (the HCM group) in comparison with that of patients with vasospastic angina and no left ventricular hypertrophy (the non-HCM group). DESIGN: Retrospective study. PATIENTS: Twelve patients in the HCM group, and 28 patients in the non-HCM group. MEASUREMENTS: The direction of ST segment shift, either ST-segment elevation or depression, on the ECGs recorded during vasospastic anginal attacks with severe vasoconstriction in the epicardial coronary artery after intracoronary injection of acetylcholine. RESULTS: Age, male gender, and distribution of coronary arteries in which the vasospasm occurred were similar between the two groups. Collateral circulation to the affected arteries was absent in all the study patients. The prevalence of anginal attacks associated with ST-segment elevation was 2.7 times higher in the non-HCM group than in the HCM group (51. 5% [17 of 33 attacks] vs 18.8% [3 of 16 attacks], respectively; p = 0.03). CONCLUSIONS: In the HCM group, myocardial ischemia associated with a transmural injury pattern seen on the ECG, which is represented as ST-segment elevation, seldom develops during vasospastic anginal attacks because of marked left ventricular hypertrophy.     

Prinzmetal's variant angina: Hemodynamic and angiographic observations during pain

Hemodynamic and angiographic data obtained during pain from four patients with Prinzmetal's variant angina are reported. The left ventricular pressure-time index did not increase before or during attacks of angina in three of the four patients; left ventricular systolic performance was impaired during pain in all three. In one of these three patients left ventricular pressure-volume data obtained during angina suggested a reduction in diastolic compliance; in another, pain and S-T segment elevation were present during coronary arterial spasm. The fourth patient had an increase in both arterial blood pressure and heart rate before an attack; in this patient coronary arterial spasm could not be demonstrated during the period of pain and S-T elevation. The data presented suggest that hemodynamic factors that increase the myocardial Oxygen requirements are absent and that coronary arterial spasm is present in some, but not all, patients with variant angina.     

Failure of ketanserin, a serotonin inhibitor, to prevent spontaneous or ergonovine-induced attacks of variant angina

Six patients hospitalized with active variant angina were treated for 3 days with the serotonin antagonist ketanserin after a 3 day control period on no medication. The number of variant angina episodes per patient per day was 1.52 +/- 1.42 during the control period and 2.05 +/- 2.30 during ketanserin therapy (p = NS). Ergonovine was administered in incremental doses of 0.0125 mg to 0.4 mg in the control period, during intravenous ketanserin administration and after 3 days of oral treatment. All 6 patients developed ST elevation during all 3 ergonovine tests. The ergonovine dose at which ST elevation developed was similar in each of the 3 periods. It is concluded that ketanserin is of no value in the treatment of variant angina and that both spontaneous and ergonovine-induced coronary spasm in man are unlikely to be mediated by a serotonergic mechanism.     

Spontaneous coronary artery spasm in variant angina is caused by a local hyperreactivity to a generalized constrictor stimulus

To assess whether spontaneous coronary artery spasm in patients with variant angina results from local coronary hyperreactivity to a generalized constrictor stimulus or from a stimulus generated only at the site of the hyperreactive segment, the behavior of spastic and nonspastic coronary segments was studied in six patients with variant angina in whom focal coronary spasm developed spontaneously during cardiac catheterization. None of the patients had critical (greater than 50% luminal diameter reduction) organic coronary stenoses. Coronary diameters were measured by computerized quantitative arteriography during control, spontaneous spasm and ergonovine-induced spasm and after intracoronary nitrates were given. During spontaneous spasm, the luminal diameter of spastic and both proximal and distal nonspastic coronary segments was significantly reduced from control values, 64.2%, 13.2% and 14.8%, respectively. Average diameter reduction of unrelated arteries was 12.3%. Ergonovine, which was also administered to four patients, provoked focal spasm at the same site as spontaneous spasm. During intravenous ergonovine, luminal diameter of spastic segments was reduced by 91.5%, that of nonspastic proximal segments by 17.8% and that of nonspastic distal segments by 11.5%. Luminal diameter of unrelated arteries during ergonovine-induced spasm was reduced by 17.7%. Constriction of spastic segments was greater during ergonovine-induced spasm (p less than 0.05), whereas the extent of diameter reduction of nonspastic segments was not significantly different during spontaneous spasm and ergonovine-induced spasm. Intracoronary isosorbide dinitrate dilated spastic and nonspastic coronary segments to a similar extent from control (20.7%, 18% and 16.5%, respectively; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

Wavelet transform analysis of heart rate variability to assess the autonomic changes associated with spontaneous coronary spasm of variant angina

We used Wavelet transform (WT) to investigate whether variation in autonomic tone was associated with spontaneous coronary spasm in patients with variant angina by analysis of heart rate variability (HRV). Twenty-one episodes preceding ST-segment elevation were selected under Holter monitoring in 12 men and 3 women with variant angina. HRV indices were calculated at 10 second intervals with the continuous WT, and analyzed within 30 minutes preceding ST-segment elevation. High frequency (HF; 0.15 approximately 2.00 Hz) increased significantly during the 4 minutes prior to ST-segment elevation, low frequency (LF; 0.04 approximately 0.15 Hz) decreased significantly during the period from 10 to 5 minutes and increased significantly during the 2 minutes prior to ST-segment elevation, the LF/HF ratio decreased significantly during the period from 10 to 3 minutes and increased significantly during the 2 minutes prior to ST-segment elevation. The RR interval decreased significantly during the 2 minutes prior to ST-segment elevation. These results suggest that the acute variation in autonomic tone was associated with spontaneous coronary spasm in patients with variant angina. A reduction in sympathetic activity, then enhancement of vagal activity may play a key role in triggering the spontaneous coronary spasm, and the secondary activation of sympathetic activity may worsen the coronary spasm resulting in the attack.     

运动诱发ST段抬高的临床意义

对５例运动诱发暂时性ＳＴ段抬高的原因及其与血管病变的关系进行分析，提出劳力型心绞痛患者运动诱发ＳＴ段抬高的临床意义不同于变异型心绞痛患者，对前者在近期内施行经皮冠状动脉腔内成形术（ＰＴＣＡ）是安全和有效的。运动诱发ＳＴ段抬高恢复正常后，相邻导联的ＳＴ段压低仍持续存在，提示其缺血相关血管有严重阻塞性病变。     

Two electrocardiographic patterns with or without transient T-wave inversion during recovery periods of variant anginal attacks

Continuous electrocardiographic recordings during anginal attacks in patients with variant angina were reviewed. Twenty-seven attacks in 15 patients were associated with transient T-wave inversion during recovery periods of angina (type A), while in another 69 attacks in 28 patients there was no T-wave inversion (type B). In none of the patients was there an ischemic T-wave inversion during angina-free periods. Both the maximum elevation (0.79 +/- 0.57 mV) and duration (5.3 +/- 1.2 min) of ST-segment deviation of type A attacks were significantly higher and longer than those of type B (0.44 +/- 0.27 mV, 2.8 +/- 1.4 min). Ten patients who had both type A and type B attacks one time or the other were selected for further evaluation. In these 10, the duration of ST-segment elevation was significantly longer during type A attacks (5.2 +/- 1.2 min, n = 18) than during type B attacks (2.7 +/- 1.2 min, n = 20) but there was no significant difference in the maximum ST-segment elevation. Giant U-wave inversion appeared in 15% of the type A attacks, but never in type B. Therefore, the T-wave abnormality related to ischemic episodes in patients with variant angina seems to be associated with more severe ischemia of longer duration than milder episodes of transient ischemia.     

Precordial ST-segment elevation caused by right coronary artery occlusion

Among 57 consecutive patients undergoing percutaneous transluminal coronary angioplasty (PTCA) of the right coronary artery, eight patients showed precordial ST-segment elevation in leads V1-3 during the procedure. The mechanism of this ST elevation was investigated reviewing the coronary angiographic findings. All patients had angina pectoris, but none had evidence of myocardial infarction. The balloon inflation time was limited to 60 sec, and 12 lead electrocardiograms were recorded every 15 sec. In the eight patients who had precordial ST-segment elevation, six had the anatomically dominant right coronary artery, and two had proportioned (balanced) left and right coronary arteries. Six patients, however, had functionally dominant left coronary arteries because of good collaterals supplying the right coronary artery from the left coronary artery. Thus, functionally, six had the dominant left coronary artery, one had proportioned coronary supply, and only one had the dominant right coronary artery. In all eight patients, the most proximal portion of the right coronary artery was occluded during PTCA, obstructing both the conus branches and the right ventricular branches. This often induced precordial ST-segment elevation in cases with the functionally dominant left or proportioned coronary artery. This ST-segment elevation seemed to represent right ventricular ischemia, as the inferior wall was protected from ischemia by good collaterals. However, precordial ST-segment elevation was rare in the functionally dominant right coronary artery even when the most proximal portion of the right coronary artery was occluded. This fact seemed due to masking of electrocardiographic manifestations of right ventricular ischemia by the dominant electrical forces of inferior wall ischemia.     

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 less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transient changes in left ventricular mechanics during attacks of Prinzmetal's angina: an M-mode echocardiographic study

M-mode echocardiograms were recorded in 12 patients with Prinzmetal's angina during 29 episodes of transient myocardial ischemia at rest (18 spontaneous and 11 ergonovine-induced). At peak ST segment elevation a regional mechanical impairment was observed in the interventricular septum during 23 episodes of angina and in the posterior wall during six episodes. In the 18 spontaneous episodes the left ventricular ischemic wall, when compared to the basal state, was found to have a significant reduction in motion (-76.3 +/- 9.1%) (mean +/- SEM), in diastolic thickness (-11.7 +/- 2.5%), and in percent systolic thickening (-88.0 +/- 5.6%). Increase in left ventricular end-diastolic diameter (+13.1 +/- 2.1%) and decrease in percent fractional shortening (-38.1 +/- 3.7%) were also observed. When ST segment was back to the isoelectric line, a transient overshoot in regional left ventricular function was observed. In induced episodes statistically significant changes could be detected by M-mode echocardiography even before appearance of ST segment elevation and anginal pain. No significant difference was found in type or degree of mechanical impairment between induced and spontaneous episodes. Therefore, in patients with Prinzmetal's angina: (1) M-mode echocardiography allows detection of mechanical changes due to transient myocardial ischemia; and (2) mechanical impairment occurs earlier than clinical (pain) and electrocardiographic (ST segment elevation) signs of transmural ischemia.     

Myocardial ischemia in patients with fixed occlusive coronary artery disease secondary to vasospasm in the “normal” vessel

Seven patients with significant fixed occlusive coronary artery disease had coronary artery spasm in a “normal” vessel. All patients had one or more episodes of rest angina and six had exertional angina as well. Four sustained previous myocardial infarction. During spontaneous angina, five patients had ST-segment elevation in the inferior electrocardiographic leads. One patient had ST-segment elevation in anterior leads. During angiography, spasm was demonstrated in the right coronary artery in three patients and in the left anterior descending coronary artery in one patient. This study emphasizes the interaction of fixed and vasospastic disease and has strong implications concerning the management of patients with ischemic heart disease.     

Diurnal variation in left ventricular function: a study of patients with myocardial ischaemia, syndrome X, and of normal controls

Angina can occur in the early morning. The mechanism of this is unclear and both haemodynamic changes and coronary artery spasm may be important. The purpose of this study was to investigate the diurnal variation in pulmonary artery diastolic pressure (an indirect measure of left ventricular filling pressure) in six normal subjects, 18 patients with coronary artery disease, five with variant angina, and six with syndrome X. A transducer tipped catheter and a simple recording system were used to record ambulatory pulmonary artery diastolic pressure for 24 hours. Variation in pulmonary artery diastolic pressure was related to the timing of episodes of ST segment depression and elevation by simultaneously recording a frequency modulated electrocardiogram. Episodes of ST segment change occurred predominantly in the early morning (midnight to 6 am) in variant angina (eight out of 14 episodes) whereas in syndrome X all episodes were recorded during the day. In coronary artery disease both painful and painless episodes were distributed throughout the day, with 10 out of 67 episodes occurring between midnight and 6 am. A similar diurnal variation in pulmonary artery diastolic pressure was seen in the groups--that is, values were low during the day and higher at night, with the maximum values between midnight and 6 am. The 24 hour median pulmonary artery diastolic pressure was higher in patients with coronary artery disease than in the control group and those with syndrome X. The finding that pulmonary artery diastolic pressure, and therefore left ventricular end diastolic pressure, is greatest in the early morning may represent the background haemodynamic state in which other factors lead to myocardial ischaemia during these hours.     

Diurnal variation in left ventricular function: a study of patients with myocardial ischaemia, syndrome X, and of normal controls.

Angina can occur in the early morning. The mechanism of this is unclear and both haemodynamic changes and coronary artery spasm may be important. The purpose of this study was to investigate the diurnal variation in pulmonary artery diastolic pressure (an indirect measure of left ventricular filling pressure) in six normal subjects, 18 patients with coronary artery disease, five with variant angina, and six with syndrome X. A transducer tipped catheter and a simple recording system were used to record ambulatory pulmonary artery diastolic pressure for 24 hours. Variation in pulmonary artery diastolic pressure was related to the timing of episodes of ST segment depression and elevation by simultaneously recording a frequency modulated electrocardiogram. Episodes of ST segment change occurred predominantly in the early morning (midnight to 6 am) in variant angina (eight out of 14 episodes) whereas in syndrome X all episodes were recorded during the day. In coronary artery disease both painful and painless episodes were distributed throughout the day, with 10 out of 67 episodes occurring between midnight and 6 am. A similar diurnal variation in pulmonary artery diastolic pressure was seen in the groups--that is, values were low during the day and higher at night, with the maximum values between midnight and 6 am. The 24 hour median pulmonary artery diastolic pressure was higher in patients with coronary artery disease than in the control group and those with syndrome X. The finding that pulmonary artery diastolic pressure, and therefore left ventricular end diastolic pressure, is greatest in the early morning may represent the background haemodynamic state in which other factors lead to myocardial ischaemia during these hours.     

Multivessel coronary artery spasm.

A 60-year-old patient with variant angina was shown to have myocardial ischemia in two different regions supplied by separate major coronary arteries. Neither artery had significant coronary atherosclerotic obstruction. Ventricular fibrillation was noted during ST-segment elevation in anteroseptal leads. The attacks of pain and arrhythmias disappeared during nifedipine therapy.     

Inappropriate microvascular constriction produced transient ST-segment elevation in patients with syndrome X

Objectives. The aim of this project was to study the responsible site(s) and underlying cardiac disease(s) of patients with transient ST-segment elevation and normal coronary angiograms.Background. Transient ST-segment elevation has been demonstrated in patients with variant angina or unstable angina. In those patients, epicardial coronary arteries, not microvessels, are always the responsible site for the transient ST-segment elevation.Methods. This study consisted of three cases with a transient ST-segment elevation and normal coronary angiograms. Treadmill testings were performed before coronary angiography in all cases. Coronary angiography was undertaken during the control state and during ST-segment elevation and, when possible, a Doppler guide wire was positioned in the left anterior descending artery (LAD). Coronary responses to vasodilators were observed. Finally, cardiac biopsy was performed and pathologic observation was conducted.Results. All three cases had significant ST-segment depression during treadmill testing in II, III, aVF and V_4–6leads; however, no angiographic coronary stenosis was demonstrated and vasospasm was not provoked. A transient ST-segment elevation associated with chest pain was observed in V_1–5leads, but normal coronary angiograms during ST-segment elevation were observed in every case. Coronary blood flow (CBF) velocity profile remained normal during ST-segment elevation. In one case, vasodilator responses to the LAD during ST-segment elevation were also measured. A 0.5 mg intracoronary injection of nitroglycerin increased CBF velocity (220%), but ST-segment elevation was not normalized and chest pain persisted. A 10 mg intracoronary injection of papaverine (PVN) further increased CBF velocity up to 340%, and this normalized ST-segment elevation and relieved chest pain quickly. Either endothelium-dependent coronary flow reserve (CFR) measured with a 100 μg intracoronary infusion of acetylcholine, or flow-dependent CFR by a 10 mg intracoronary injection of PVN was reduced in one of two cases measured. Pathologic findings supported syndrome X as the underlying cardiac disease in all cases.Conclusions. These findings suggested a new clinical implication involving transient ST-segment elevation mimicking variant angina and normal coronary angiograms in patients with syndrome X. The major responsible site for this phenomenon was suggested to be coronary arterioles of less than 200 μm in diameter.     

Hyperventilation and ergonovine tests in Prinzmetal's variant angina pectoris in men

Hyperventilation and ergonovine tests were carried out in a group of 30 patients with variant angina to assess the sensitivity of the 2 tests and to correlate the response with spontaneous disease activity. Hyperventilation produced a positive response in 83% (25 of 30) and ergonovine in 93% (28 of 30) of the patients. After hyperventilation 22 of 25 showed ST-segment elevation, 2 ST depression and 1 T-wave pseudonormalization; after ergonovine ST-segment elevation developed in 23 patients, ST depression in 4 and T-wave pseudonormalization in 1. In all cases the electrocardiographic changes occurred in the same leads as during the spontaneous attacks. The incidence of chest pain and ventricular arrhythmias was similar during both tests; spontaneous remission of ischemia, however, was more frequent (48 vs 14%) after hyperventilation than after ergonovine. Acute ischemia developed at a mean of 218 +/- 112 seconds after the end of hyperventilation in 19 of 25 positive tests; at that time double product was not significantly different from basal values. The sensitivity of hyperventilation was similar (95 vs 100%) to ergonovine in the patients with greater than or equal to 1 daily attack, while in those with less than 1 daily attack the sensitivity of hyperventilation decreased to 55% compared to 77% with ergonovine. Thus, in variant angina the sensitivity of both tests correlates with disease activity. Hyperventilation is a safe provocative test with a sensitivity similar to ergonovine in patients with active disease; however, in patients with sporadic attacks hyperventilation has a lower sensitivity than ergonovine and therefore a limited diagnostic value.