Variant angina pectoris.
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A 66-year-old man having a long history of angina on effort has started to show frequent episodes of angina at rest since 6 months ago. He noticed that chest pain was uncommon after taking alcohol. A variant form of angina pectoris (variant angina) was diagnosed by documentation of typical ST elevation during anginal attack and also by inducing coronary arterial spasm with intracoronary administration of ergonovine maleate. Ambulatory ECG monitoring revealed frequent ST elevation during sleep. Since the history suggested that alcohol ingestion could be effective for preventing variant angina, this effect was examined by giving 540 ml of "sake" in the evening. Variant angina was inhibited, while plasma ethanol was detected. The plasma ethanol reached its peak value as 152 mg/dl at 10 o'clock pm and returned to zero after 12 hours. When ethanol disappeared in the plasma, variant angina recurred again. Although the precise mechanism for inhibition of variant angina by alcohol ingestion is not clear, alcohol or its metabolite such as acetaldehyde seems to be able to inhibit coronary arterial spasm.
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OBJECTIVE: To evaluate the correlation between thrombosis and stability of atherosclerotic plaque within criminal vessels in patients with unstable angina pectoris (UAP) by coronary angioscopy, to explore the clinical pathological basis for acute coronary syndromes (ACS). METHODS: Sixty-eight patients with UAP were enrolled, the patients with post-infarction angina pectoris and variant angina pectoris were excluded. There were 48 males and 20 females, aged from 40 to 73 (average 62.4 +/- 8.6) years. The criminal vessels of there patients were observed by coronary angioscopy during percutaneous coronary intervention (PCI) therapy. RESULTS: There were 68 criminal vessels in 68 patients. Atherosclerotic plaques were observed in all criminal vessels. Among criminal vessels, thrombi and intimae lesions were detected in 63 cases and 46 cases, respectively. Among 68 cases with atherosclerotic plaques, there were 48 cases of yellow plaques (70.5%), 18 cases of light yellow plaques (26.5%) and 2 cases of white plaques (2.94%). Sixty-three thrombi cases were mural and on-occlusive, which included 11 cases of red or mixed thrombi (17.5%) and 52 cases of white or pink thrombi (82.5%). All intimae lesions were accompanied by thrombosis, which included 11 cases of red or mixed thrombi (23.9%) and 35 cases of white or pink thrombi (76.1%). CONCLUSION: The study has shown that the rupture of unstable yellow plaque and its thrombosis were the pathological basis of UAP. Therefore, stabilizing yellow plaque before its rupture may play critical role in prevention and treatment of ACS.
To assess the efficacy and safety of verapamil in variant angina pectoris, we entered 16 patients in a double-blind, randomized trial of nine months, duration. During treatment with verapamil, the frequency of angina fell substantially (12.6 +/- 25.9 chest pains per week with placebo, 1.7 +/- 2.8 pains per week with verapamil, mean +/- S.D.; P less than 0.01), as did the use of nitroglycerin tablets (14.4 +/- 34.4 tablets per week with placebo, 2.1 +/- 3.3 tablets per week with verapamil; P less than 0.05). The number of hospitalizations for clinical instability was significantly lower with verapamil (P less than 0.01). The number of episodes of transient ST-segment deviation during treatment with verapamil was reduced (33.1 +/- 39.3 ST-segment deviations per week with placebo, 7.7 +/- 11.7 deviations per week with verapamil; P less than 0.01). Verapamil caused no side effects forcing a reduction in dosage or a discontinuation. We conclude that verapamil is safe and effective in the therapy of variant angina pectoris.
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