Angina attack

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Understanding Angina Attacks: Mechanisms, Types, and Management

Mechanisms of Angina Attacks

Coronary Hypothesis and Blood Supply Interference

The coronary hypothesis posits that angina pectoris attacks are due to temporary interference with the blood supply to a part of the heart muscle. This theory is supported by the frequent post-mortem discovery of advanced coronary disease in patients who died from angina pectoris, and the similarity between the symptoms of angina pectoris and coronary occlusion.

Alpha-Adrenergic Receptor-Mediated Coronary Artery Spasm

Prinzmetal's variant angina, a specific type of angina, is often caused by severe spasms of a large coronary artery mediated by alpha-adrenergic receptors. These spasms can be induced by the administration of epinephrine and propranolol, leading to significant ST-segment elevation in the ECG during the attack. This variant form of angina is characterized by pain occurring at rest, often more severe and longer-lasting than typical angina, and is associated with transient ST-segment elevation.

Parasympathomimetic Agents and Coronary Arterial Spasm

In some cases of Prinzmetal's variant angina, anginal attacks can be induced by parasympathomimetic agents such as methacholine. These agents cause coronary arterial spasms, which can lead to complete occlusion even in normal coronary arteries, as evidenced by corresponding ST-segment elevations in the ECG.

Types of Angina

Classical Angina Pectoris

Classical angina pectoris is characterized by recurrent attacks of retrosternal pain triggered by effort or emotional stress and relieved by rest and nitroglycerin. This type of angina is typically associated with atherosclerotic narrowing of the coronary arteries.

Prinzmetal's Variant Angina

Prinzmetal's variant angina differs from classical angina in that it occurs at rest, is not provoked by exercise or emotion, and is often cyclic, recurring at the same time of day or night. This variant is marked by severe pain and transient ST-segment elevation during attacks, which return to normal after the pain subsides.

Triggers and Symptoms

Common Triggers

Angina can be triggered by various factors, including physical exertion, emotional stress, large meals, smoking, and extreme temperatures. These triggers lead to decreased blood flow to the heart, causing chest pain or pressure that may radiate to the arms, jaw, or upper back.

Emotional Stress and Angina

Emotional stress is a well-documented trigger for angina attacks. Historical and contemporary studies have shown a strong link between emotional stress and the onset of anginal pain, with changes in the ECG often observed during emotionally induced attacks.

Management of Angina

Pharmacologic Therapy

The management of angina includes the use of pharmacologic agents such as beta-blockers, nitrates, calcium channel blockers, and ranolazine. In some countries, additional agents like trimetazidine, ivabradine, and nicorandil are also used. These medications aim to reduce the frequency and severity of angina attacks and improve the patient's quality of life.

Revascularization and Advanced Therapies

Revascularization procedures, such as coronary artery bypass grafting, are indicated for high-risk individuals and can improve angina symptoms. However, some patients may experience recurrent angina even after revascularization, necessitating newer therapies like enhanced external counterpulsation, transmyocardial revascularization, and stem cell therapy.

Conclusion

Angina pectoris, characterized by chest pain due to reduced blood flow to the heart, can manifest in various forms, including classical and Prinzmetal's variant angina. Understanding the mechanisms, triggers, and effective management strategies is crucial for improving patient outcomes and quality of life. Pharmacologic treatments and advanced therapies play a significant role in managing this condition, highlighting the need for ongoing research and innovation in the field.