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PubMed1986

The long-term outcome of patients who suffered and survived an acute myocardial infarction in the midst of recurrent attacks of variant angina.

Twenty-one patients, ranging in age between 28 and 59 years, who survived hospitalization for an acute myocardial infarction in association with repetitive attacks of variant angina, were followed prospectively for 59.1 +/- 5.1 (SEM) (range 17-120) months. Four patients died, one of sudden death 17 months after admission, one of congestive heart failure at 33 months, and two of cancer at 43 and 45 months of follow-up. Three patients had four new myocardial infarctions at 22, 32, 33, and 61 months of follow-up. Six patients were readmitted for angina or other cardiac reasons. Twelve patients remained asymptomatic throughout the follow-up and one more patient was asymptomatic before and after his recurrent myocardial infarction. No relapse of variant angina was documented. Thus, the long-term course of patients with variant angina culminating in acute myocardial infarction is relatively benign, despite the highly unstable features of their initial presentation.

Angina Pectoris, Variant↗
PubMed1998

High-density lipoprotein particles are large in patients with variant angina.

OBJECTIVE: Dyslipidemia in patients with coronary vasospasm may be characterized by low level of high-density lipoprotein (HDL)-cholesterol as well as apolipoprotein (apo) A-I but not high level of low-density lipoprotein-cholesterol. This study sought to examine the HDL particle size in patients with variant angina. METHODS: The HDL particle size was examined by analyzing serum lipid levels in 38 patients with variant angina to compare with those of 40 control subjects and 30 normocholesterolemic patients with stable effort angina. Also, actual HDL size distribution was assessed by electrophoresis. RESULTS: The HDL-cholesterol, apoA-I and apoA-II levels were all lower (P < 0.01 for each) in patients with variant angina and patients with stable effort angina as compared with control subjects. The apoA-II level was lower (P < 0.01) in patients with variant angina than in patients with stable effort angina. The apoA-I/apoA-II ratio was lower (P < 0.01) in patients with stable effort angina, but not in patients with variant angina as compared with control subjects. In contrast, the HDL-cholesterol/apoA-I ratio was higher in patients with variant angina than in control subjects (P < 0.01) and also patients with stable effort angina (P < 0.01). The slope of the regression line, comparing HDL-cholesterol and apoA-I levels, was greater in patients with variant angina than in control subjects (P < 0.05) and patients with stable effort angina (P < 0.05), suggesting an increase in larger HDL particles. Native polyacrylamide gel electrophoresis revealed that HDL particles in patients with variant angina were skewed towards larger sizes compared with control subjects (P < 0.01) and patients with stable effort angina (P < 0.01). The abnormal serum lipid values were normalized in the patients with variant angina after the medical treatment and inactivation of the coronary spasm. CONCLUSION: High HDL-cholesterol/apoA-I levels associated with low serum HDL-cholesterol and apoA-I levels were characteristic in patients with variant angina, in whom HDL particles were large, cholesterol-rich and possibly malfunctioning.

Angina Pectoris, Variant↗
PubMed1980

Prinzmetal's angina. Aternating ST-segment deviation in anterior and inferior electrocardiographic leads during the same episode of pain.

A 60-year-old man had recurrent episodes of spontaneously occurring pain in the chest which were associated with ST-segment elevation consistent with Prinzmetal's angina. The simultaneous elevation of the S-T segment in anterior and inferior electrocardiographic leads with initial ST-segment depression followed by elevation in high lateral leads suggested that heightened vascular reactivity in variant angina may involve multiple coronary vessels during the same episode of vasospasm.

Aged↗
PubMed1991

[A case of sleep apnea syndrome with variant angina].

A 56-year-old male was admitted because of respiration arrest during sleep, and precordial crushing sensation which repeatedly occurred early in the morning. He had been hypertensive and aware of daytime sleepiness for ten years. After admission, all night polysomnography was recorded a total of four times. Apnea index was 37.5 times/hour, and central type apnea was predominant. The diagnosis of sleep apnea syndrome was made. In the early morning of the fourteenth day after admission, the patient developed anterior chest pain associated with ST elevation in leads II, III, and aVF of the electrocardiogram. Thus, the case was thought to be complicated by variant angina. There were no anginal attacks during the all night polysomnography recordings. However, a causal relationship between the sleep apnea and variant anginal attacks was suspected. Since both the sleep apnea and the variant anginal attacks tended to occur during the stages of REM sleep, and they are both related to changes in activity of the autonomic nervous system. It was considered that hypoxemia following sleep apnea and/or the hyperventilation after the apneic episodes might be the cause of the variant anginal attacks.

Angina Pectoris, Variant↗
PubMed1983

U wave inversion during attacks of variant angina.

Sequential 12 lead electrocardiograms were recorded during angina pectoris induced by ergonovine maleate in 38 patients with variant angina. Transient U wave inversion was observed in 17 patients with ST segment elevation in anterior chest leads, but in only three of 21 patients with ST segment elevation in the inferior leads associated with right coronary artery spasm. In the 17, all of whom had spasm of the left anterior descending coronary artery, the sensitivity of ST segment elevation in V5 was only 41%, and that of U wave inversion 71%. U wave inversion without ST segment elevation occurred during attacks in 35% of patients. During the recovery phase, the sensitivity of U wave inversion was 82% in V4 and 65% in V5, though ST segment elevation was absent in both V4 and V5. Thus, inverted U waves without ST segment elevation often appear in marginal ischaemic zones or during the time of recovery from temporary ischaemia. Detection of inverted U waves should aid in the diagnosis of variant angina when only lead V5 is used as a monitor and when electrocardiograms are recorded only during the recovery phase.

Adult↗
PubMed1980

Relation of coronary arterial spasm to sites of organic stenosis.

Among 63 patients with Prinzmetal's variant angina, coronary arterial spasm responsible for attacks of variant angina was documented arteriographically in 9 patients. In each observed episode (11 attacks in nine patients), coronary spasm producing myocardial ischemia occurred at and was superimposed on a site of preexisting organic stenosis. Measurements of normal portions of "spastic" and "nonspastic" vessels suggested a generalized uniform constriction of all major coronary arteries during attacks, with "spasm" limited to the site of an organic lesion in most cases. In two cases the magnitude of constriction in all vessels was consistent with generalized coronary hypercontractility or spasm. Among 104 patients with organic coronary artery disease and documented single vessel coronary spasm (foregoing 9 patients combined with 95 others from published reports), there were 70 patients with essentially single vessel organic coronary disease in 90 percent of whom the spasm involved the diseased vessel. Of 60 cases abstracted from the literature in which the relation of coronary spasm to the site of organic disease was described, 88 percent had the spasm causing ischemia localized to the site of an organic lesion. Hypotheses attempting to describe the pathophysiologic aspects of coronary spasm in variant angina must account for the intimate association of spasm with sites of organic stenosis in the majority of cases.

Angina Pectoris↗
PubMed1984

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.

Adult↗
PubMed1996

Elevation of the plasma histamine concentration in the coronary circulation in patients with variant angina.

In the present study plasma histamine was found to be elevated in the great cardiac vein in 8 of 11 patients with variant angina but in none of 8 control patients. Although further investigation is required to determine the exact cause-and-effect relation between histamine release and provocation of spontaneous variant anginal attacks, the present study presents clinical evidence that histamine may well be related to episodes of variant angina as suggested in animal studies.

Adult↗
PubMed2001

Estradiol supplementation suppresses hyperventilation-induced attacks in postmenopausal women with variant angina.

OBJECTIVES: We sought to examine whether estradiol (E2) supplementation suppresses anginal attacks in women with variant angina. BACKGROUND: Estrogen is known to improve endothelial function. Coronary spasm plays an important role in the pathogenesis of not only variant angina but also ischemic heart disease in general, and endothelial dysfunction seems to be involved in the pathogenesis of coronary spasm. METHODS: Fifteen postmenopausal women with variant angina (mean age 54.2 years) were given a hyperventilation (HV) test, a provocation test for coronary spasm, in the early morning of day 1 (baseline), day 3 (after 2-day transdermal E2 supplementation, 4 mg) and day 5 (after 2-day placebo administration). We measured the flow-mediated (endothelium-dependent) dilation (FMD) of the brachial artery with the ultrasound technique before each HV test. RESULTS: The anginal attacks with ST segment elevation were induced by HV in all patients on days 1 and 5. However, no attacks were induced on day 3. Supplementation with E2 augmented FMD (3.5 +/- 0.6*, 8.9 +/- 0.7 and 4.0 +/- 0.5* on days 1, 3 and 5, respectively; *p < 0.01 vs. day 3). The serum E2 levels on days 1, 3 and 5 were 22.7 +/- 2.8*, 96.2 +/- 9.2 and 30.7 +/- 7.1* pg/ml, respectively (*p < 0.01 vs. day 3). CONCLUSIONS: The present results demonstrated for the first time, to our knowledge, that E2 supplementation suppresses the HV-induced attacks in women with variant angina, in part because of the improvement of endothelial function.

Angina Pectoris, Variant↗
PubMed1983

Factors influencing the long-term prognosis of treated patients with variant angina.

To determine the prognosis of variant angina and the factors influencing it, 169 consecutive patients hospitalized in our coronary unit were followed for a mean of 15.3 months (range 1 to 68). Survival at 1, 2, and 3 years was 95%, 90%, and 87%, respectively; survival without myocardial infarction was 80%, 78%, and 75%. Twenty of the 22 myocardial infarctions and eight of the 14 deaths occurred within the first 3 months. Mantel-Haenszel log-rank analysis demonstrated that coronary disease, ventricular function, and the degree of disease activity were significant interdependent variables that influenced both survival and survival without infarction. At 1, 2, and 3 years, survival for patients with multivessel disease was 81%, 76%, and 66%; for patients with one-vessel disease, 97%, 92%, and 92%; and for patients without stenoses greater than or equal to 70%, 98% at each year (p = .0003). Survival without infarction at 1 year was 88% in patients with no stenoses greater than or equal to 70% and 82% in patients with single-vessel disease; it did not change thereafter in either group, but was 62%, 58%, and 50% at 1, 2, and 3 years in patients with multivessel disease (p = .001). Treatment did not influence survival in any subgroup (only 14 patients died overall) or survival without infarction in patients with multivessel disease. However, in patients without multivessel disease, treatment with nifedipine, diltiazem, and verapamil improved survival without infarction compared to treatment with perhexiline maleate or long-acting nitrates alone (92% vs 67% at 1, 2, and 3 years; p less than .005). Thus in addition to preventing angina, nifedipine, diltiazem, and verapamil appear to reduce complications in patients with variant angina without multivessel disease.

Adult↗
PubMed1980

Coronary artery spasm.

Variant angina with ST elevation indicates transmural myocardial ischaemia and is due to spasm of a large epicardial coronary artery. Spasm occurs in arteries with varying degrees of fixed obstruction, giving rise to different clinical profiles of variant angina. However, coronary angiography is required to differentiate between those with minor coronary disease, and those with significant (greater than 70%) obstruction. In patients with minor coronary disease or normal arteries, beta-blockers are contraindicated, and treatment with calcium antagonist vasodilators should be commenced after documentation of spontaneous or ergonovine induced spasm. Patients with significant fixed coronary obstructions require bypass grafting if technically feasible. The role of coronary spasm is not confined to variant angina, as it causes angina at rest with ST depression, and may also cause myocardial infarction and sudden death.

Angina Pectoris↗
PubMed2005

Vasospastic angina and microvascular angina are differentially influenced by PON1 A632G polymorphism in the Japanese.

BACKGROUND: Ethnicity and smoking are well-known risk factors for the pathogenesis of coronary vasospasm. Oxidative stress induced by smoking plays a crucial role in coronary vasospasm, but is not enough to account for the pathogenesis of coronary vasospasm, indicating that genetic factors are strongly involved. METHODS AND RESULTS: The study group comprised 162 vasospastic angina patients (VSAs), 61 microvascular angina patients (MVAs) and 61 non-responders (NRs) diagnosed by acetylcholine provocation test. Four polymorphisms of the oxidative stress related genes, cytochrome b-245, alpha polypeptide gene (CYBA) C242T and A640G, paraoxonase 1 gene (PON1) A632G, phospholipase A2 group VII gene (PLA2G7) G994T were genotyped. Allele frequency of PON1 632-G was significantly higher in both the VSA with dominant fashion and the MVA with recessive fashion compared with NR. This association was strongly influenced by gender in the MVA only. There were no significant associations between the other polymorphisms and coronary vasospasm. In addition, the allele frequency of PON1 632-G in the Japanese was higher than in Caucasians. CONCLUSIONS: There was a significant association between PON1 A632G polymorphism and MVA as well as VSA, but the impact of this on VSA and MVA is different in the Japanese.

Acetylcholine↗
PubMed1981

Prinzmetal's variant angina)(PVA). Circadian variation in response to hyperventilation.

The study reports on the outcome of hyperventilation tests in a 57-year-old male with Prinzmetal's variant angina, formerly often complicated by ventricular fibrillation. It was found that hyperventilation for a period of 6 min after a delay of 4 to 6 min was followed by the development of ST-elevation and pain, but only when the test was performed in the morning, whereas the outcome of tests performed later in the day were negative. Pretreatment with calcium blockers, nifedipine or verapamil proved effective in preventing the anginal response to the test, also when it was performed in the morning. It is concluded that hyperventilation performed in the early morning, but not later in the day, may prove to be an effective and safe procedure for provoking Prinzmetal's variant angina, and that hyperventilation may be useful in the evaluation of the efficacy of drug therapy.

Angina Pectoris↗
PubMed1981

Coronary artery spasm during exercise: treatment with verapamil.

Six patients who had documented coronary spasm and no coronary artery with organic obstruction greater than 50% developed angina and ST-segment elevation on exercise testing. Oral verapamil, 160-480 mg/day, prevented exercise-induced ischemia in all patients and increased maximal work capacity from 611+/- 250 kpm to 808 +/- 160 kpm (p less than 0.02). In two patients, a relationship between the prevention of exercise-provoked ischemia and the plasma concentration of verapamil was demonstrated, and in one of these, the relationship had a diurnal pattern. Patients with variant angina may develop coronary spasm on effort and often respond to verapamil.

Angina Pectoris↗