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 < 0.05; nifedipine/isosorbide dinitrate, 3.1 ± 4.0 chest pains per week and 5.5 ± 6.6 ST segment deviations per week, p < 0.05). In all respects, verapamil/isosorbide dinitrate and nifedipine/isosorbide dinitrate were similar to one another. Thus, in patients with very frequent episodes of variant angina, a calcium antagonist/isosorbide dinitrate combination is much more effective than isosorbide dinitrate alone in reducing the frequency of angina and ischemic ECG alterations.     

Reflex heart rate and blood pressure changes during ST segment elevation in patients with variant angina

Responses of heart rate and blood pressure to transient myocardial ischemia were analyzed in patients with variant angina. Heart rate changes during ST segment elevation were examined by means of a Holter ECG monitoring system. All 27 ST segment elevations from 10 patients with anterior ischemia were accompanied by an increase in heart rate by 12 ± 2 bpm (mean ± SEM, p < 0.001) at peak ST segment elevation. With inferior ischemia in nine patients, heart rate decreased significantly by 4 ± 1 bpm (n = 28, p < 0.001). However, 9 of these 28 ST segment elevations showed a biphasic response of heart rate, that is, an initial increase and subsequent decrease. Such heart rate changes were not different between ST segment elevations with and without chest pain. With chest pain systolic blood pressure rose in anterior ischemia by 42 ± 5 mm Hg (n = 10, p < 0.001) but fell in inferior ischemia by 22 ± 8 mm Hg (n = 7, p < 0.05). We conclude that a different cardiovascular reflex occurs in response to inferior versus anterior ischemia and it is independent of chest pain.     

不稳定性心绞痛冠状动脉造影和血运重建的可行性探讨

目的研究不稳定性心绞痛的临床及介入心脏病学诊疗,并探讨其诊疗指引。方法分析包括初发型、恶化型、卧位型、变异型、中间综合征共63例不稳定性心绞痛患者的临床介入心脏病学诊疗资料,患者均行选择性冠状动脉造影。结果37例患者冠状动脉造影显示冠脉狭窄,占58.7％,其中70.3％狭窄程度大于50％,43.8％为多支冠脉狭窄。年龄、性别、病程、血脂在冠脉狭窄与非狭窄患者之间的差别无统计意义,但伴高血糖或高血压的患者冠脉狭窄发生率明显高于不伴高血糖或高血压患者。另冠脉狭窄中67.5％患者24小时动态心电图示ST下移≥0.2mV。26例冠脉狭窄大于50％的患者作了介入治疗后心绞痛消失。结论不稳定性心绞痛尤其伴高血压、高血糖或24小时动态心电图ST下移≥0.2mV患者多数有冠脉器质性狭窄,甚至为多支冠脉狭窄,其次不稳定性心绞痛易发生急性心肌梗死或猝死的潜在的病理解剖基础,应尽早行冠脉造影以便进一步治疗,必要时行介入治疗,三支病变拟行冠状动脉旁路移植术。     

Holter monitor ST segment evaluation in hospitalized patients with unstable angina

The correlation of angina attacks with ST segment changes detected during ambulatory Holter monitoring was evaluated in patients with unstable angina. Forty hospitalized patients had one to three 24-hour Holter recordings each. Twenty-three patients had a cardiac catheterization, confirming significant coronary artery disease. The Holter recordings, scanned blindly by computer, were evaluated for ST segment shifts (defined as +/- 1.5 mm from baseline, lasting 60 seconds or longer). Angina attacks were carefully logged. Over the total forty patient experience, only 15 of 74 (20.3%) angina attacks had corresponding ST segment shifts on the Holter recordings. Nine of 34 (26.5%) angina attacks in the 23 patients who had a cardiac catheterization had corresponding ST segment shifts. A total of 159 ST segment shifts were recorded on these forty patients, but only 15 (9.4%) ST shifts corresponded to a time when the patients were actually experiencing angina attacks. The performance of the test procedure was quantified by use of Youden's J statistic. The aggregate J, over all patients, was 0.203 (J = 1.0 is perfect, J = 0.0 is useless). When consideration was restricted to patients with cardiac catheterization, the aggregate experience J was 0.263. Dealing with only the patients who had angina attacks during the monitoring, and computing the J statistic for each individual patient, the resulting mean J statistic was 0.146, with SEM = 0.0731. The Holter monitoring worked reasonably well in only 2 of the 14 patients who gave clear tests of the procedure. In an attempt to improve the performance of the procedure, 21 Holter recordings in eight patients were reread for ST segment shifts of only +/- 1 mm from baseline, lasting 30 seconds or longer. In these eight patients with rescanned Holter recordings, only five of 17 (29.4%) angina attacks resulted in an ST segment shift. In conclusion, ambulatory Holter recordings proved not to be a suitable method of documenting ST segment shifts during angina attacks in this study.     

不稳定型心绞痛并发的室性心动过速及介入治疗对其的影响

目的探讨不稳定型心绞痛并发的室性心动过速(简称室速)特点以及经皮冠状动脉(简称冠脉)介入治疗对其的影响。方法对10例不稳定型心绞痛患者并发的室速,通过心电图观察室速发生前ST段的变化。行冠脉造影及介入治疗,了解室速特点与冠脉病变的关系。通过临床随访包括动态心电图观察室速发作情况。结果6例变异型心绞痛患者并发的室速在冠脉闭塞期出现,均为单一前降支病变;4例混合型心绞痛患者并发的室速,2例出现在ST段压低最深时,另2例则出现ST段逐渐变浅时,均为多支冠脉病变。10例均成功地接受了介入治疗。在10个月至4.1年的随访过程中,10例均未出现室速和临床再狭窄。结论不稳定型心绞痛并发的室速可能是缺血及再灌注损伤引起,ST段下移所致室速的患者冠脉病变可能更为复杂、严重。介入治疗可控制这类室速的发作。     

Submaximal exercise testing after unstable angina

Sixty-one consecutive men, mean age 56 years, who fulfilled criteria for unstable angina and who responded to medical therapy, underwent submaximal exercise testing prior to hospital discharge and at least 3 days after their last episode of angina. Forty-two patients were receiving propranolol at the time of exercise. Submaximal exercise was targeted to 120 beats/minute and strict criteria for the premature termination of each study were followed. Follow-up data were available on 55 patients post-discharge over a period of 6 to 36 weeks.No patient suffered recurrence of unstable angina or myocardial infarction due to the exercise test. Exercise was prematurely terminated by an ischemic response (chest pain and/or ST segment changes) in 34 patients (56%) and by leg fatigue in 13 patients (21%). Only five patients had exercise-induced ventricular ectopic activity, four of whom were not receiving propranolol. Nine patients achieved the target heart rate. Exercise-induced abnormal electrocardiographic changes predicted the postdischarge recurrence of episodes of unstable angina (p < 0.05). Comparison of predischarge submaximal exercise data with postdischarge maximal exercise shows that recovery in cardiovascular function after unstable angina occurs soon after stabilization and prior to the submaximal test.     

Diagnosis of important fixed coronary stenosis in patients with variant angina by exercise tests after treatment with calcium antagonists.

A 12 lead electrocardiogram was recorded during treadmill exercise in 57 patients with variant angina in whom coronary angiography was performed. Thirty six patients performed exercise tests with and without calcium antagonists, and 21 performed them only with calcium antagonists. In 55 patients calcium antagonists had prevented spontaneous attacks of variant angina for more than two days before the test. The other two patients were given a single dose of diltiazem (90 mg) two hours before the test. Exercise testing without calcium antagonists induced ST segment elevation with chest pain in nine patients, ST segment depression in 10 (nine with chest pain), and no important shift of the ST segment in 17. Five patients had severe coronary stenosis (greater than or equal to 75%) and all of them showed positive response. Thirty one patients had no important coronary stenosis and 14 of them showed positive response. The sensitivity of the exercise test in detecting a coronary stenosis greater than or equal to 75% was 100% without calcium antagonists but the specificity was low (55%). When the exercise test was done in patients taking calcium antagonists, only two (specificity 96%) of 48 patients without severe coronary stenosis showed positive response (elevation of ST segment in one and depression in another) whereas all nine patients with severe coronary stenosis had a positive response (depression of ST segment in six and elevation in three (sensitivity 100%). It is concluded that exercise testing with calcium antagonists may be a useful method for detecting severe coronary stenosis in patients with variant angina.     

Diagnosis of important fixed coronary stenosis in patients with variant angina by exercise tests after treatment with calcium antagonists

A 12 lead electrocardiogram was recorded during treadmill exercise in 57 patients with variant angina in whom coronary angiography was performed. Thirty six patients performed exercise tests with and without calcium antagonists, and 21 performed them only with calcium antagonists. In 55 patients calcium antagonists had prevented spontaneous attacks of variant angina for more than two days before the test. The other two patients were given a single dose of diltiazem (90 mg) two hours before the test. Exercise testing without calcium antagonists induced ST segment elevation with chest pain in nine patients, ST segment depression in 10 (nine with chest pain), and no important shift of the ST segment in 17. Five patients had severe coronary stenosis (greater than or equal to 75%) and all of them showed positive response. Thirty one patients had no important coronary stenosis and 14 of them showed positive response. The sensitivity of the exercise test in detecting a coronary stenosis greater than or equal to 75% was 100% without calcium antagonists but the specificity was low (55%). When the exercise test was done in patients taking calcium antagonists, only two (specificity 96%) of 48 patients without severe coronary stenosis showed positive response (elevation of ST segment in one and depression in another) whereas all nine patients with severe coronary stenosis had a positive response (depression of ST segment in six and elevation in three (sensitivity 100%). It is concluded that exercise testing with calcium antagonists may be a useful method for detecting severe coronary stenosis in patients with variant angina.     

Vasospastic ischemic mechanism of frequent asymptomatic transient ST-T changes during continuous electrocardiographic monitoring in selected unstable angina patients

Asymptomatic episodes of ST segment and/or T wave changes are often reported during Holter monitoring in patients with angina pectoris. However, the interpretation of such changes is debated relative to silent myocardial ischemia. We studied 11 patients admitted to the CCU because of frequent episodes of unstable anginal attacks who had undergone repeated periods of Holter monitoring, characterized by predominantly occurring asymptomatic episodes of ST segment and/or T wave changes associated with less frequent typical anginal attacks. In a total of 89 days of Holter monitoring, the patients evidenced 520 episodes of transient ECG changes including 180 of ST elevation, 73 of ST depression, and 267 of T wave alterations. Only 12% of episodes were symptomatic. Coronary injection during asymptomatic ST-T changes was performed in eight patients. In six it was possible to document spontaneous coronary spasm. In seven patients ergonovine administration induced anginal pain, ST-T changes, and coronary spasm. In all patients the anginal attacks completely disappeared with medical treatment and the asymptomatic episodes were abolished in six and reduced in four. Our findings support the hypothesis that in certain selected unstable anginal patients, transient asymptomatic ECG changes are caused by acute myocardial ischemia.     

Circadian variation in variant angina

Thirteen hospitalized patients with variant angina were studied to assess circadian variation in disease activity. Over 48 hours, all angina attacks were noted, a continuous Holter electrocardiogram was recorded and 2 ergonovine tests were performed 12 hours apart, 1 at 4 AM and the other at 4 PM. Only 2 patients gave a clearcut history of more frequent nocturnal or early morning attacks. During the study period, 1.8 +/- 1.6 AM and 0.62 +/- 1.2 PM angina episodes per patient were reported (p less than 0.02), but a circadian pattern was apparent in only 4 patients. However, Holter analysis revealed 5.3 +/- 13.8 AM and 2.6 +/- 8.5 PM episodes of ST elevation per patient (p less than 0.05) and 8.1 +/- 13.9 AM and 3.2 +/- 8.5 PM episodes of ST elevation, ST depression or T-wave pseudonormalization (p less than 0.01). Ten of 11 patients with Holter abnormalities had more frequent AM than PM attacks (p less than 0.01). ST elevation developed during all 13 of the 4-AM and 12 of 13 of the 4-PM ergonovine tests. In 10 cases the ergonovine threshold at which the attack occurred was lower in the morning, in no case was it lower in the afternoon, and in 3 patients the morning and afternoon doses were identical (p less than 0.01). Thus, circadian variation in disease activity both for spontaneous and provoked attacks is present in most patients with variant angina, even though it is often not clinically apparent.     

Holter ECG study of the electrocardiographic phenomena in Prinzmetal angina attacks with emphasis on the study of ventricular arrhythmias

The ECG phenomena in 20 outpatients (121 episodes) suffering from variant angina with transient ST segment elevation greater than 1.5 mm. (Prinzmetal angina) were studied by Holter monitoring. The most important changes in the ECG morphology were: a) increased height of the R wave in all cases, b) the S wave decreased or disappeared, c) the ST segment elevation varied from 1.5 to 38 mm, d) the TQ interval was ascending in 78 episodes, e) there was a double alternance of ST-TQ in 20 episodes and f) the first modification of the ECG was an increase of the T wave height. Arrhythmias were seen in 19 patients (44 episodes). The most frequent were premature ventricular contractions. The prevalence and importance of the ventricular arrhythmias were statistically related to the duration of the episodes (p less than 0.005), the degree of the ST segment elevation (p less than 0.005), the presence of ST-TQ alternance (p less than 0.005) and the presence of increased R wave greater than 25% (p less than 0.025).     

Repeat treadmill exercise testing: Variability of results in patients with angina pectoris

To assess the reproducibility and individual variability of ECG treadmill exercise test results, we evaluated 23 patients with coronary artery disease and stable exertional angina by means of two control exercise tests performed on different days within a 1 week period. In addition, each control test was followed on the same day by a single dose of placebo or active agent determined in a randomized double-blind manner and the exercise test was repeated. When the mean exercise test results from the control tests on days 1 and 2 were compared, there was a significant increase in exercise duration to angina (7.4 ± 3.2 to 9.0 ± 3.3 minutes, p < 0.05), ST segment depression (7.8 ± 3.9 to 9.6 ± 3.6 minutes, p < 0.01), and maximal exercise (9.7 ± 3.7 to 11.0 ± 4.1 minutes, p < 0.01). In addition, when the mean exercise results on the control test were compared to those on the postplacebo test on the same day, similar increases in exercise duration were observed at each end point (p < 0.01). Individual differences of more than 2 minutes in exercise duration between the two control tests and between the control and postplacebo tests in time to angina, ST segment depression, and maximal exercise were frequent (26% to 33% of patients). However, the mean rate-pressure products on the two control tests performed on days 1 and 2 and on the control and postplacebo tests performed on the same day did not differ at angina, ST segment depression, and maximal exercise. Therefore, we conclude that patients demonstrate considerable variability in the time to angina, ST segment depression, and maximal exercise but not in rate-pressure product at these end points.     

Effects of atrial pacing on QT dispersion in patients with coronary artery disease without angina pectoris and ST segment depression.

The aim of this study was to investigate QT dispersion during atrial pacing in patients with coronary artery disease (CAD) without clinical ischemia, such as angina pectoris and ST segment depression. Thirteen patients with normal coronary arteries and 42 patients with CAD (12 with single-vessel, 16 with two-vessel and 14 with three-vessel disease) having no angina pectoris or ST segment depression during atrial pacing with maximum rate of 120/minute were enrolled in the study. Twelve-lead surface ECGs were recorded at 100 mm/second paper speed before pacing, at maximum pacing rate, and during the recovery period for measurement of QT interval parameters. Corrected QTd (QTcd) increased from 43.4 +/- 8.1 to 49.3 +/- 9.5 ms (p < 0.05) in the control group, from 46.1 +/- 8.1 to 74.3 +/- 7.7 ms (p < 0.0001) in the single-vessel disease group, from 48.5 +/- 10.4 to 93.8 +/- 22.1 ms in the two-vessel disease group (p < 0.0001), and from 49.7 +/- 13.6 to 128.5 +/- 31 ms (p < 0.0001) in the three-vessel disease group at peak atrial pacing period. A positive correlation was found between the severity of CAD and QTcd (r = 0.49, p < 0.0001). It was found that pacing-induced QTc dispersion identifies coronary disease extent, even when there is no ST depression or T wave inversion during pacing.     

Mental arithmetic stress testing in patients with coronary artery disease

A mental arithmetic stress test was performed by 122 consecutive patients undergoing diagnostic coronary arteriography. Twenty-two patients showed significant ST segment abnormalities during the test (group 1). Of these patients, 20 performed a bicycle exercise test, which was positive in all of them. Seventy patients had a negative mental stress but a positive exercise test (group 2), whereas in 30 patients both tests were negative (group 3). There were no patients with a positive mental stress test and a negative exercise test. Mental stress induced a significant increase in heart rate and systolic blood pressure in the three groups of patients. Group 1 patients, however, achieved higher values of double product during mental stress and had a shorter exercise duration than group 2 and group 3 patients. The extent of coronary artery disease (CAD) was similar in groups 1 and 2, while group 3 patients had a significantly lower prevalence of two or more vessel disease. To investigate the pathogenetic mechanism of mental stress-induced myocardial ischemia, great cardiac vein flow was measured by means of the thermodilution technique in four patients with isolated left anterior descending artery disease, who showed ST segment depression in anterior leads in response to mental stress. In three patients without vasospastic angina the calculated coronary resistance decreased during mental stress, as a result of a normal vasodilatory response to the increased myocardial oxygen consumption induced by the test. By contrast, in one patient with variant angina, coronary resistance increased suggesting coronary vasoconstriction. Our findings demonstrate that mental arithmetic stress testing may induce significant ST segment abnormalities in patients with CAD. Such patients respond to mental stress with a disproportionate increase in myocardial oxygen consumption and have decreased exercise capacity. Although coronary resistance generally decreases during mental stress-induced myocardial ischemia, coronary vasoconstriction may occur in patients with variant angina.     

Nocturnal angina: precipitating factors in patients with coronary artery disease and those with variant angina

Factors precipitating nocturnal myocardial ischaemia were investigated in 10 patients with frequent daytime and nocturnal angina pectoris. Eight patients had fixed obstructive coronary artery disease or a low exercise threshold or both before the onset of ischaemia. Two patients had variant angina with normal coronary arteries and negative exercise tests. During sleep the electrocardiogram, electroencephalogram, electro-oculogram, electromyogram, chest wall movements, nasal airflow, and oxygen saturation were continuously measured. Forty two episodes of transient ST segment depression were recorded in the eight patients with coronary artery disease and 26 episodes of ST segment depression and elevation in the two patients with variant angina and normal coronary arteries. All episodes of ST segment depression in the former group of patients were preceded by an increase in heart rate as a result of arousal and lightening of sleep, bodily movements, rapid eye movement sleep, or sleep apnoea (one episode). In contrast, in the variant angina group no increase in heart rate, arousal, or apnoea preceded 23 of the 26 episodes of ST segment change. Thus increase in myocardial oxygen demand was important in precipitating nocturnal angina in patients with coronary artery disease and reduced coronary reserve. In the patients with coronary spasm these factors did not often precede the onset of nocturnal myocardial ischaemia.     

Nocturnal angina: precipitating factors in patients with coronary artery disease and those with variant angina.

Factors precipitating nocturnal myocardial ischaemia were investigated in 10 patients with frequent daytime and nocturnal angina pectoris. Eight patients had fixed obstructive coronary artery disease or a low exercise threshold or both before the onset of ischaemia. Two patients had variant angina with normal coronary arteries and negative exercise tests. During sleep the electrocardiogram, electroencephalogram, electro-oculogram, electromyogram, chest wall movements, nasal airflow, and oxygen saturation were continuously measured. Forty two episodes of transient ST segment depression were recorded in the eight patients with coronary artery disease and 26 episodes of ST segment depression and elevation in the two patients with variant angina and normal coronary arteries. All episodes of ST segment depression in the former group of patients were preceded by an increase in heart rate as a result of arousal and lightening of sleep, bodily movements, rapid eye movement sleep, or sleep apnoea (one episode). In contrast, in the variant angina group no increase in heart rate, arousal, or apnoea preceded 23 of the 26 episodes of ST segment change. Thus increase in myocardial oxygen demand was important in precipitating nocturnal angina in patients with coronary artery disease and reduced coronary reserve. In the patients with coronary spasm these factors did not often precede the onset of nocturnal myocardial ischaemia.     

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.     

Limited efficacy of magnesium for the treatment of variant angina.

Some patients with variant angina show both ST segment elevation at rest and exercise-induced ST segment elevation. Magnesium deficiency has also been observed in patients with variant angina. This study investigated the correlation between the degree of magnesium deficiency and the efficacy of intravenous administration of magnesium in patients with variant angina. Fifteen patients with angiographically confirmed variant angina were assessed for magnesium deficiency and whether intravenous administration of magnesium (19.2 mEq/l) suppressed exercise-induced ST segment elevation. All 15 patients were studied with a magnesium retention test (0.2 mEq/kg over 4 hr) to analyze magnesium deficiency. In our study, magnesium retention rate in patients with variant angina was not higher than that of controls (57 +/- 24% vs 45 +/- 10%, NS). All 15 patients had anginal attacks during accelerated exercise combined with hyperventilation after placebo infusion, whereas only 8 patients had anginal attacks after magnesium administration. ST segment elevation occurred in 14 patients after placebo infusion, but in only 4 patients after magnesium administration. There were no correlations between disease activity, degree of magnesium deficiency or failure of suppression of ST elevation by the intravenous administration of magnesium. Intravenous administration of magnesium can suppress exercise-induced coronary spasms in some patients with variant angina, but the degree of magnesium deficiency did not correlate with the suppressions of exercise-induced ST elevation after magnesium administration. Intravenous administration of magnesium had limited efficacy in patients with variant angina and exercise-induced ST segment elevation.     

Continuous electrocardiographic recording in Prinzmetal's variant angina pectoris: A report of four cases

Four patients with Prinzmetal''s variant angina pectoris were subjected to continuous electrocardiographic recording. In three of them several episodes of ST segment elevation unaccompanied by pain were recorded. In one patient, identical electrocardiographic alterations were observed both in presence or in absence of pain, while in the others a good correlation was evident between pain and severity of the electrocardiographic abnormalities. In two patients transmural myocardial infarction complicated the course of the angina. In contrast to the classical findings, in these patients the attacks of chest pain did not cease after the infarction, but became more frequent and severe. The electrocardiographic alterations of the anginal episodes occurred in the same myocardial areas involved by the infarction, so that a reversible superposition of electrocardiographic signs of acute ischaemia on those of recent necrosis was observed.Continuous electrocardiographic recording provided the best means of investigation of these patients with the variant form of angina pectoris.     

Comparison of serum lipid values in variant angina pectoris and fixed coronary artery disease with normal subjects

Lipid and apolipoprotein (apo) levels in patients with variant angina were examined and compared with patients with coronary artery disease (CAD) and normal subjects (control). Cholesterol and triglyceride levels in plasma, lipoprotein fractions and several apolipoproteins were measured in 108 men (90 of whom had undergone coronary angiography): 22 had variant angina, 56 had fixed CAD (effort angina and old myocardial infarction) and 30 were normal subjects. Patients with variant angina showed more severe atherosclerotic lesions than the control group, but less severe lesions than the patients with fixed CAD. In comparison with lipid and apolipoprotein, high density lipoprotein cholesterol, apo AI and apo AII decreased significantly in control, variant angina and fixed CAD groups, respectively. Additionally, stepwise discriminant analysis revealed that apo AI was the best discriminator among the 3 groups or between variant angina or fixed CAD and the control group. Variant angina and fixed CAD patients could be discriminated from the control subjects by an apo AI level of 135 and 126 mg/dl, with 71% (p less than 0.025) and 73% (p less than 0.005) accuracy, respectively. By these criteria 77% of the patients with variant angina and 73% of the patients with fixed CAD were precisely discriminated. Discrimination between variant angina and fixed CAD patients, however, was not practical, even if the best discriminator was used. Thus, the apo AI level is useful in discriminating patients with variant angina and fixed CAD from normal subjects. Therefore, symptomatic patients with low apo AI levels should be aggressively examined.