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PubMed1989

Effect of magnesium on anginal attack induced by hyperventilation in patients with variant angina.

To examine whether or not magnesium suppresses coronary spasm, the effect of magnesium infusion on anginal attacks induced by hyperventilation was studied in 20 patients with variant angina. In all patients, anginal attacks associated with ischemic ST segment changes on the electrocardiogram were repeatedly induced by hyperventilation. The study was performed in the early morning successively for 3 days. On days 1 and 3 (control studies), 50 minutes before the hyperventilation test, a 5% glucose solution was infused as a placebo. On day 2 (magnesium study), 50 minutes before the hyperventilation test, magnesium sulfate (0.27 mM/kg body wt) was infused during a 20-minute period. During the control studies, anginal attack was induced by hyperventilation in all 20 patients, whereas during the magnesium study, anginal attack was induced by hyperventilation in only six (30%) of the 20 patients (p less than 0.001 vs. control studies). The changes in arterial blood pH and PCO2 caused by hyperventilation were not significant between the control study and the magnesium study. Mean serum magnesium concentration increased from 2.2 +/- 0.2 to 6.0 +/- 0.5 mg/dl immediately after infusing magnesium and was 4.5 +/- 0.6 mg/dl before the hyperventilation test during the magnesium study. We conclude that magnesium suppresses anginal attacks induced by hyperventilation in patients with variant angina.

Aged↗
PubMed1980

Significance of thromboxane A2 in myocardial ischemia in patients with coronary artery disease.

To examine plasma levels of vasoconstrictive prostanoid (thromboxane A2) in patients with coronary artery disease, amounts of its product, thromboxane B2, in acidic lipid extracts from plasma were determined by a radioimmunoassay. Peripheral venous samples were obtained in 14 normal subjects and 12 patients with coronary artery disease, and simultaneous aortic and coronary sinus blood samples were obtained at rest, during pacing, and after pacing in eight cases who were subjected to atrial pacing stress test. Mean thromboxane B2 levels in peripheral venous blood in 14 normal subjects were found to be 243 +/- 96 pg/ml. Of nine cases with angina pectoris on effort (angiographically documented severe coronary artery stenosis), five exhibited increased thromboxane B2 levels in peripheral plasma. Three cases of a variant form of angina pectoris exhibited pronounced increases in peripheral thromboxane B2 levels. Of eight cases subjected to atrial pacing stress test, three exhibited marked increases in thromboxane B2 levels in coronary sinus effluent at peak pacing, two of which were accompanied by typical anginal pain during the test. These findings suggest that increased thromboxane A2 production may be associated with altered thromboxane metabolism. This may occur because of altered interactions between functions of vascular wall and blood platelets within coronary circulation in patients with coronary artery disease.

Angina Pectoris↗
PubMed1990

The relationship between growth of atherosclerotic plaques, variant angina and sudden death.

Clinico-pathological findings are described in two patients with typical variant angina who died suddenly during an ischemic attack. In both cases, detailed pathologic examination of the coronary arteries disclosed severe focal atherosclerosis of the anterior descending coronary artery. The only distinctive histological finding was new intimal proliferation of smooth muscle cells enmeshed within mucoid substance, superimposed on the old fibrous cap of the plaque. These findings agree with experimental and clinical data which suggest that coronary vasospasm may be related to growth of atherosclerotic plaques. This study provides histological evidence that progression of an atherosclerotic plaque may underlie variant angina and sudden death.

Angina Pectoris, Variant↗
PubMed1979

Coronary artery spasm during exercise in patients with variant angina.

Seven patients with typical variant angina without coronary stenoses greater than 50% developed angina and ST-segment elevation during treadmill exercise testing. In all cases the ST-segment elevation occurred in the same leads during exercise testing as during spontaneous attacks at rest. Five of the patients had developed spontaneous coronary spasm during coronary arteriography, in each case in the artery corresponding to the site of ST-segment elevation. In five patients, thallium was injected during the exercise test during which angina and ST-segment elevation occurred. In each case, a large perfusion defect not present at rest was found in the zone corresponding to the site of ST-segment elevation. These findings suggest that coronary artery spasm may occur during exercise in patients with variant angina.

Adult↗
PubMed1984

Platelet aggregation in variant angina: its relation to plasma catecholamines.

We concurrently measured plasma catecholamine levels and platelet aggregation in patients with variant angina, effort angina and old myocardial infarction. Platelet aggregability was lower in variant angina than in effort angina and old myocardial infarction. Plasma concentrations of epinephrine and norepinephrine in the variant angina group showed higher values than those in the effort angina group and the old myocardial infarction group. Moreover, there was a statistically significant negative correlation between plasma catecholamine concentration and ADP-induced platelet aggregation. These findings suggest that the lower platelet aggregation is related to the higher concentration of plasma catecholamine in variant angina.

Adenosine Diphosphate↗
PubMed1994

Beneficial effects of smoking cessation on the short-term prognosis for variant angina--validation of the smoking status by urinary cotinine measurements.

To examine whether smoking cessation would improve the short-term prognosis for patients with variant angina, 37 smokers with variant angina who were discharged after the complete disappearance of angina by medical treatment with calcium blockers were advised to stop smoking and were followed-up for 1 year. Urinary cotinine radioimmunoassay was used to evaluate their current smoking status. Patients with a urinary cotinine concentration above 50 ng/ml were classified as current smokers. The prevalence of smokers was underestimated by self-reports (11% by self-reports vs. 35% by urinary cotinine measurements after 3 months; 17% by self-reports vs. 36% by urinary cotinine measurements after 1 year). The presence of angina during the first 3 months was significantly (P < 0.05) more prevalent in those who continued to smoke (8/13, 62%) than in those who succeeded in smoking cessation (5/24, 21%) when the current smoking status was determined by urinary cotinine measurements. Smoking cessation definitely improved the prognosis for variant angina even during a relatively short follow-up period.

Angina Pectoris, Variant↗
PubMed1995

Susceptibility of plasma low density lipoprotein to cupric ion-induced peroxidation in patients with variant angina.

OBJECTIVES: The purpose of this study was to investigate the peroxidative susceptibility of plasma low density lipoprotein in patients with active variant angina and to compare it with that in subjects without coronary spasm. BACKGROUND: Oxidized or modified low density lipoprotein can impair endothelium-dependent vasoregulation and has atherogenic properties; it may be related to the genesis of coronary artery spasm by potentiating agonist-induced vasoconstriction. METHODS: The sensitivity of plasma low density lipoprotein for cupric ion (Cu2+)-induced peroxidation was examined. Low density lipoprotein was isolated from plasma in 112 patients: 21 with active variant angina, 18 with inactive variant angina without anginal attacks during the preceding 6 months, 39 with significant organic coronary artery stenoses but without rest angina and 34 control subjects without coronary artery disease. Lipid peroxidation products in low density lipoprotein were assayed as thiobarbituric acid-reactive substances before and after incubation with various concentrations of Cu2+ at 37 degrees C for 24 h. RESULTS: Significantly higher levels of generation of thiobarbituric acid-reactive substances from plasma low density lipoprotein after incubation with Cu2+ were seen in patients with active variant angina than in patients in the other three groups. The dose-response curve of low density lipoprotein peroxidation induced by Cu2+ shifted to the left in this group as compared with the curve in the other three groups. The vitamin E (alphatocopherol) content of low density lipoprotein fraction in these patients was significantly lower than that in the other groups. After > or = 6 months of an angina-free period in five patients with active variant angina, thiobarbituric acid-reactive substances induced by 0.5 mumol/liter Cu2+ in low density lipoprotein were significantly decreased and vitamin E content was significantly increased. CONCLUSIONS: These results indicate that vitamin E-deficient plasma low density lipoprotein in patients with active variant angina is highly susceptible to peroxidative modification.

Analysis of Variance↗