Intravenous administration of anisodamine is effective on variant angina
To the editor: A 60-year-old man presented to our emergency department in November 2012, due to an episode of chest pain associated with angina-linked syncope attacks. His past medical history was notable for drug-controlled hypertension (nifedipine 30 mg/d). On physical examination following the 30 minutes after chest pain, he was asymptomatic, with vital signs in the normal range, and an unremarkable chest X-ray. ECG was also carried out and showed sinus bradycardia rhythm (Figure 1A). The morning after initial presentation, the patient experienced acute onset of chest pain, lasting for a total of 30 minutes. An emergency ECG was performed and showed 3 mm ST-segment elevation in the inferior leads and specular antero-lateral ST depression (Figure 1B). The patient was immediately transferred to the catheterization laboratory for coronary angiography. The angiography revealed absence of significant coronary artery disease with minimal plaque disease in left and right coronary arteries. Because the patient had already been prescribed calcium antagonist and nitrate, we started intravenous infusion of anisodamine (10 μg/s) to him about 8 h/d for 14 days. During 1 year follow-up, he was symptom free without any syncope attack, and both the ECG and echocardiography were normal.
Variant angina is a form of acute coronary syndrome characterized by recurrent angina at rest associated with >2 mm elevation of ST-segment; with normalization of the ST-segment after relief of pain without degenerating into myocardial infarction. The pathogenesis of vasospasm is still unclear and several mechanisms and precipitating factors have been proposed, including increased sympathetic tone, enhanced oxidative stress, magnesium deficiency, augmented Rho-kinase activity, sodium-hydrogen exchange, genetic susceptibility, cigarette smoking, and low-grade inflammation.1
Long-term management of variant angina depends on the status of the coronary arteries. Several reports confirmed the clinical benefits of calcium antagonists and nitrates, and therefore, they were the most commonly used drugs.3
However, there were reports of recurrence of cardiac arrest in spite of being on a combination of nitrates and calcium channel blocker, which was the same as the case we represented.
Since 1980s, many basic and clinical studies in China have proved that anisodamine can produce significant effects on relieving microvascular spasm, improving and dredging the coronary microcirculation, anti-platelet aggregation, decreasing blood viscosity, and increasing the tolerance of myocardium to ischemia in patients with microcirculatory disorder.4
The previous studies found that intracoronary administration of 1 000 μg anisodamine was effective in reversing coronary no-reflow phenomenon during primary percutaneous coronary intervention (PCI) in ST elevation myocardial infarction (STEMI) patients and this effect may be due to improving coronary microcirculation. To the best of our knowledge, we described the first case of variant angina treated with anisodamine. It is encouraging based on the effective and safe results. Nevertheless, longer periods of follow-up are required to confirm that symptoms do not recur. Perhaps the administration of anisodamine could be an optional treatment for variant angina in proper patients.
Hou Xumin and Jiang Jinqi
Department of Cardiology (Hou XM), Department of Emergency (Jiang JQ), Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai 200030, China
Correspondence to: Dr. Jiang Jinqi, Department of Emergency, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai 200030, China (Email: email@example.com)
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