Prinzmetal's angina
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These studies suggest that Prinzmetal's angina is caused by coronary artery spasms mediated by alpha-adrenergic receptors and endothelial dysfunction, and can be effectively managed with calcium antagonists like diltiazem, nifedipine, and verapamil.
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Understanding Prinzmetal's Angina: Mechanisms, Diagnosis, and Treatment
Mechanisms of Prinzmetal's Angina
Coronary Artery Spasm and Alpha-Adrenergic Receptors
Prinzmetal's angina, also known as variant angina, is primarily caused by a temporary increase in coronary vascular tone, leading to a significant but transient reduction in the luminal diameter of the coronary arteries. This condition is often mediated by alpha-adrenergic receptors, which can induce severe spasms in the coronary arteries. Studies have shown that the administration of epinephrine and propranolol can trigger these spasms, resulting in ST-segment elevation on an ECG. The spasm typically occurs at a single focal site and can affect both normal and diseased vessels.
Role of Parasympathomimetic Agents
Parasympathomimetic agents like methacholine and pilocarpine can also induce anginal attacks in patients with Prinzmetal's angina. These agents have been used in clinical settings to provoke coronary arterial spasms, which are then documented through coronary arteriograms and left ventriculograms. This highlights the role of the autonomic nervous system in the pathogenesis of the condition, where enhanced parasympathetic activity at rest can trigger sympathetic nerve stimulation, leading to coronary artery spasms.
Diagnosis of Prinzmetal's Angina
Transient ST-Segment Elevation
The hallmark of Prinzmetal's angina is the transient ST-segment elevation observed during an anginal attack. This elevation is a critical diagnostic criterion and differentiates it from other forms of angina that are typically induced by physical exertion.
Ergonovine Provocation Test
The most sensitive and specific diagnostic test for Prinzmetal's angina is the administration of ergonovine intravenously. This test involves administering incremental doses of ergonovine until a positive result is achieved, indicated by the presence of symptoms and associated ST-segment elevation. Nitroglycerin is used to rapidly reverse the effects if a refractory spasm occurs.
Treatment of Prinzmetal's Angina
Calcium Channel Blockers and Nitrates
Medical therapy for Prinzmetal's angina primarily involves the use of vasodilator drugs, including nitrates and calcium channel blockers. Diltiazem, a calcium entry blocker, has been shown to significantly reduce the frequency of anginal attacks and nitroglycerin consumption. In a multiclinic controlled trial, diltiazem reduced angina frequency by up to 68% and was well-tolerated by patients . Verapamil, another calcium channel blocker, has also been effective in resolving anginal attacks, even in cases complicated by ventricular tachycardia and fibrillation.
Avoidance of Beta-Blockers and Aspirin
Beta-blockers and large doses of aspirin are contraindicated in patients with Prinzmetal's angina. These medications can exacerbate the condition by increasing coronary artery spasm.
Surgical Interventions
Surgical treatments, such as aortocoronary bypass grafting, have shown limited success in providing long-term relief from anginal attacks. Many patients experience a recurrence of symptoms postoperatively, suggesting that surgical intervention may not be the most effective approach for this condition .
Conclusion
Prinzmetal's angina is a unique form of angina characterized by transient coronary artery spasms leading to ST-segment elevation. The condition is primarily diagnosed through the observation of these transient changes and can be effectively managed with calcium channel blockers and nitrates. Understanding the underlying mechanisms, including the role of alpha-adrenergic receptors and the autonomic nervous system, is crucial for the effective treatment and management of this condition.
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