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At least 397 records · Page 22Linked to original sources
PubMed1993

[The role of the vascular endothelium and vasospasm in different coronary syndromes. A common physiopathological base for distinct entities?].

A literature review on the endothelial functions and endothelial dysfunction/lesion, as well as the atherosclerosis role in this process is performed. The several physiological explanations of both acute and chronic coronary syndromes are also reviewed, with particular emphasis to the recent studies on vasospasm mechanisms and its role in the physiopathogeny of variant angina and syndrome X. The role of the endothelial dysfunction/lesion as a common physiopathological basis to all coronary syndromes, is discussed.

Angina Pectoris, Variant↗
PubMed1997

Antianginal effects of YM430, a novel calcium entry-blocking and beta-adrenoceptor-blocking agent in several experimental angina models.

1. We evaluated the antianginal effects of YM430 in several experimental models in vitro and in vivo. 2. In isolated dog coronary artery, YM430 (10(-8)-10(-6) M) inhibited 3,4-diaminopyridine-induced rhythmic contractions with an IC50 value of 59.2 nM. 3. In anesthetized rats, YM430 (10-100 mg/kg PO) inhibited arginine vasopressin-induced ST-segment depression with an IC50 value of 36.6 mg/kg PO. 4. In anesthetized dogs, YM430 (0.3 mg/kg IV) significantly inhibited ST-segment elevation induced by coronary artery occlusion. 5. These findings suggest that YM430 may be of value in the treatment of various types of angina pectoris such as variant and stable angina.

4-Aminopyridine↗
PubMed1990

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.

Adult↗
PubMed1982

[Variant angina non-invasive assessment of coronary morphology].

The predictability of coronary morphology was investigated in 28 patients with variant angina using clinical symptomatology, effectiveness of nifedipine an appropriate ECG changes. Using coronary angiography seven patients had shown normal or not significantly stenosed coronary arteries (group 1), 21 had significant coronary stenoses (greater than 70%) (group 2). Six patients of group 1 showed resting angina only, 11 out of group 2 had in addition exertional angina and 4 had to be assigned clinically to threatening infarct enlargement. Treatment with nifedipine was successful in 6 patients of group 1, however, only in 6 out of 17 patients in group 2. In no case did treatment with nifedipine lead to success in multiple vascular involvement. Normal control ECGs were present in 6 patients of group 1, a pathologic ECG with Q spikes or T inversions was seen in 20 patients of group 2. Results indicate good diagnostic accuracy for normal coronary vessels in the presence of angina at rest, effective treatment with nifedipine and normal control ECGs. Significant coronary stenoses may be assumed when angina at rest and during exertion, ineffective treatment with nifedipine and pathologic control ECGs are demonstrable. Using these parameters prediction of coronary morphology with non-invasive methods was possible in 14 of the 28 patients with variant angina.

Angina Pectoris, Variant↗
PubMed1992

Biphasic changes (initial increase and late decrease) in coronary sinus venous oxygen saturation during anginal attacks induced by intracoronary acetylcholine in patients with variant angina.

In order to evaluate the effects of intracoronary acetylcholine on coronary resistance vessels, oxygen saturation in coronary sinus blood was continuously measured to compare its dynamic changes during intracoronary injection of acetylcholine in both patients with variant angina and control subjects. Group 1 consisted of 6 patients without coronary artery disease. Group 2 consisted of 10 patients with variant angina and spasm in the left anterior descending coronary artery. A fiberoptic reflection oximetry system was used for the continuous measurement of coronary sinus venous oxygen saturation. Acetylcholine (20 micrograms) was injected directly into the left coronary artery over 30 s. In the group 1 patients, coronary sinus venous oxygen saturation was increased from 39 +/- 2% (mean +/- SEM) to 54 +/- 3% at 30 s, continuously climbed to 70 +/- 3% at 60 s and then gradually decreased to 53 +/- 5% at 120 s after the initiation of intracoronary injection of acetylcholine. In contrast, in the group 2 patients, coronary sinus venous oxygen saturation was transiently increased from 39 +/- 2% to 56 +/- 4% at 30 s, reversed, decreased to 52 +/- 4% at 60 s and then rapidly decreased to 36 +/- 3% at 120 s with the onset of chest pain associated with electrocardiographic ischemic changes. Coronary arteriography during attacks demonstrated a total or subtotal occlusion of the left anterior descending coronary artery due to severe spasm in all of the 10 patients. The extent of increases in coronary sinus venous oxygen saturation at 30 s after acetylcholine injection was not significantly different between the two groups (group 1: 15 +/- 4%, group 2: 17 +/- 3%). Heart rate, blood pressure and rate-pressure product were essentially unchanged at 30 s after intracoronary injection of acetylcholine in both groups. These data suggest that in control adult humans, coronary blood flow was increased through dilatation of resistance vessels by acetylcholine, while in patients with variant angina, coronary blood flow was transiently increased by dilatation of resistance vessels, after which it was suddenly decreased by spasm of an epicardial artery induced by this agent. Relaxant responses to acetylcholine of coronary resistance vessels appear to be preserved well in patients with variant angina.

Acetylcholine↗
PubMed1993

Clinical characteristics of patients with spontaneous remission of variant angina.

To determine the factors influencing the spontaneous remission of variant angina, clinical characteristics were examined in 75 Japanese patients with variant angina. Spontaneous remission was defined as an absence of angina at rest for at least 3 months after withdrawal of treatment with calcium antagonists. This remission occurred in 12 patients (16%) (remission group), while angina persisted despite treatment with calcium antagonists and nitrates in 33 patients (44%) (persistent angina group). The remaining 30 patients (40%) were angina-free under treatment with calcium antagonists and/or nitrates (angina-free on treatment group). The prevalence of significant coronary artery stenosis (> 75%) was significantly higher in the remission group than in the persistent angina group (44% vs 7%, p < 0.05). The prevalence of cessation of smoking was significantly higher in the remission group than in the persistent angina group (92% vs 39%, p < 0.01). Age, gender, other coronary risk factors, disease activity of variant angina and site of myocardial ischemia during anginal attacks were not statistically different among the 3 groups. There data indicate that remission of variant angina occurs more frequently in patients with than in those without significant coronary artery stenosis and that cessation of smoking is an important factor for remission of variant angina.

Adult↗
PubMed1982

Verapamil: a selective antagonist of constrictor substances in dog coronary artery: implications for variant angina.

1. Canine circumflex coronary artery ring segments were contracted in vitro by ergometrine, serotonin, phenylephrine, noradrenaline (with propranolol) and a thromboxane A2 analogue, U46619. 2. Ergometrine was classified as a serotonin agonist since concentration-response curves were competitively inhibited by methysergide but not by alpha-adrenoceptor antagonists. 3. Glyceryl trinitrate (IC50 18.6 nmol/l) relaxed the coronary rings precontracted with serotonin, phenylephrine or U46619. In contrast (+/-)-verapamil (0.1-10 mumol/l) was more effective against serotonin than phenylephrine or noradrenaline and was almost inactive against U46619. 4. In a blood perfused left anterior descending coronary artery preparation external diameter was measured by sonomicrometry. Serotonin, U46619 and ergometrine infusions (i.a.) decreased diameter by up to 18% without causing spasm (zero lumen diameter). Lowering the perfusion pressure from 90 to 60 mmHg increased the fall in diameter during serotonin infusions. 5. The negative inotropic potency of verapamil against noradrenaline induced beta-adrenergic stimulation in guinea-pig left atria was compared with the vasodilator potency of verapamil in noradrenaline constricted dog coronary artery rings. Verapamil was eighteen times more potent in cardiac muscle than in coronary smooth muscle. 6. This apparent tissue selectivity of verapamil was confirmed in anaesthetized dogs where plasma concentrations of verapamil 50-150 ng/ml (in the therapeutic range) lowered blood pressure and heart rate and increased P-R interval without greatly reducing the constrictor response to serotonin in the coronary artery. 7. These studies suggest that inhibition of constrictor responses in large coronary vessels may not be an important site of action of verapamil in patients with variant angina.

Angina Pectoris, Variant↗
PubMed1998

[Usefulness of intracoronary injection of acetylcholine and ergonovine in patients with variant angina].

The correlation was examined between the angina-producing arteries predicted to be responsible for the sites of ST segment elevation during spontaneous ischemic attacks and the arteries in which spasm was induced by intracoronary injection of either acetylcholine or ergonovine in patients with variant angina. From 1991 January to 1996 June, 42 patients with variant angina, 40 men and 2 women with a mean age of 61.6 years old, underwent the acetylcholine provocation test within 2 weeks of observation of the last ST segment elevation. After discontinuation of antianginal agents for at least 24 hours, a bolus of acetylcholine was injected in incremental doses of 20, 50 micrograms (occasionally 80 micrograms) into the right coronary artery and of 20, 50 and 100 micrograms incrementally into the left coronary artery to provoke coronary spasm. Intracoronary injection of ergonovine was added in nine patients, in whom intracoronary injection of acetylcholine failed to document coronary spasm on the arteries predicted to be responsible for the sites of ST segment elevation during anginal attacks. Ergonovine was injected in total doses of 40 micrograms into the right coronary artery and of 64 micrograms into the left coronary artery. Positive spasm was defined as induction of more than 99% reversible stenosis. The correlation between the arteries predicted to be responsible for the sites of ST segment elevation during attacks and the vessels in which spasm was induced by acetylcholine test was 78.6% for all patients and 80.0% for all sites of ST segment elevation. By adding the ergonovine test after the acetylcholine test, the correlation increased to 95.2% for all patients and 95.6% for all sites of ST segment elevation. The correlation observed agrees with previous studies in which the ergonovine test was performed in patients without induced spasm by intracoronary injection of acetylcholine and that the super-imposed ergonovine test is useful for diagnosing patients with variant angina.

Acetylcholine↗