Publication | Open Access
Role of Autonomic Nervous System in the Pathogenesis of Prinzmetal's Variant Form of Angina
459
Citations
16
References
1974
Year
HypertensionCardiovascular PharmacologyPharmacotherapyCardiovascular ToxicityCoronary Artery DiseasePre-clinical PharmacologyAutonomic Nervous SystemThrombosisNeurologyCardiologyPercutaneous Coronary InterventionHeart RateAutonomic SystemVascular PharmacologyVascular BiologyPharmacologyTen PatientsCardiovascular DiseasePhysiologyEndothelial DysfunctionParasympathetic Nervous SystemVariant FormCardiovascular PharmacodynamicsMedicine
Parasympathetic overactivity at rest is thought to trigger coronary spasm in Prinzmetal's angina by stimulating sympathetic nerves and activating alpha‑adrenergic receptors in large coronary arteries. The authors tested methacholine, atropine, epinephrine, isoproterenol, propranolol, and phenoxybenzamine in ten patients, and performed a Master’s triple two‑step test and selective coronary arteriography on all subjects. Methacholine provoked attacks while atropine and phenoxybenzamine suppressed them, epinephrine induced attacks in two patients, propranolol had no effect, the triple two‑step test and isoproterenol infusion did not trigger attacks despite tachycardia,.
In ten patients with Prinzmetal's variant form of angina the effects of various drugs were assessed: subcutaneous injection of methacholine (10 mg), atropine (0.7 mg), and epinephrine (0.7 mg); intravenous infusion of isoproterenol (20-25 µg/min); and in the three of the above patients who were having recurrent spontaneous attacks at the time of the examination, oral administration of atropine (0.6-1.2 mg), propranolol (30-90 mg), and phenoxybenzamine (10 mg in one patient). Master's triple two-step test and selective coronary arteriography were done on all the patients. In the three patients who were having spontaneous attacks at the time of the examination, the administration of methacholine induced the attacks and that of atropine suppressed the attacks. Epinephrine induced the attacks in two patients and propranolol was without effect in suppressing the attacks. Phenoxybenzamine (in one patient) suppressed the attacks. Neither Master's triple two-step test nor isoproterenol infusion precipitated the attacks, though heart rate increased to more than 110 beats/min and 160 beats/min respectively in all the patients. Coronary arteriograms were normal in seven of the ten patients. It is concluded that enhanced activity of the parasympathetic nervous system, which occurs at rest, is involved in the initiation of the attack by stimulating the sympathetic nerve which in turn probably induces coronary arterial spasm by way of activating alpha (vasoconstrictor) receptors present in the large coronary arteries.
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