A 43-year-old woman comes to the office due to occasional chest discomfort over the past year. She describes the pain as a midline pressure or squeezing sensation that lasts 10-15 minutes and is sometimes accompanied by sweating. The patient has no history of hypertension or diabetes mellitus but is a smoker. Ambulatory ECG monitoring shows transient ST-segment elevations in the anteroseptal leads during an episode of chest pain at night. Coronary angiography reveals no atherosclerotic stenosis, but the administration of acetylcholine elicits similar chest pain and ECG changes. Which of the following best explains the coronary intervention findings in this patient?

Question

A 43-year-old woman comes to the office due to occasional chest discomfort over the past year.  She describes the pain as a midline pressure or squeezing sensation that lasts 10-15 minutes and is sometimes accompanied by sweating.  The patient has no history of hypertension or diabetes mellitus but is a smoker.  Ambulatory ECG monitoring shows transient ST-segment elevations in the anteroseptal leads during an episode of chest pain at night.  Coronary angiography reveals no atherosclerotic stenosis, but the administration of acetylcholine elicits similar chest pain and ECG changes.  Which of the following best explains the coronary intervention findings in this patient?

Quizplus · Accepted Answer

11ec160b_3ba3_bb70_9249_c7014e850742_MD0001_00 This patient with episodes of recurrent chest discomfort that spontaneously resolve within 10-15 minutes most likely has vasospastic angina (formerly called Prinzmetal angina). It results from coronary endothelial dysfunction and autonomic imbalance that lead to intermittent coronary vasospasm and myocardial ischemia. Affected patients are usually young (eg, age <50) and lack typical risk factors for coronary artery disease (CAD) (eg, hypertension, diabetes mellitus); however, smoking is a strong risk factor, likely because it contributes to endothelial dysfunction. Symptoms of vasospastic angina are thought to be triggered by excess vagal tone, and they occur most commonly at night when vagal tone is at a peak. The diagnosis is made by ambulatory ECG demonstrating ST-segment elevation during an episode of chest discomfort and coronary angiography revealing an absence of obstructive atherosclerotic CAD. Because of the pathophysiology of the disorder, both acetylcholine and ergot alkaloids (eg, dihydroergotamine) provoke symptoms and may also aid in diagnosis, as follows: Acetylcholine normally stimulates endothelial muscarinic receptors to cause vasodilation via increased release of nitric oxide. However, a deficiency of endothelial nitric oxide in affected patients causes increased vagal tone to instead trigger vasoconstriction and precipitate vasospastic symptoms. Ergot alkaloids activate 5-HT₂ serotonergic receptors to cause vasoconstriction. Normally, the vasoconstriction is somewhat offset by endothelial release of vasodilatory prostaglandins, but this response is lacking in affected patients due to endothelial dysfunction. (Choices A and C) Peripheral endothelial function is typically intact in patients with vasospastic angina. As a result, acetylcholine is expected to cause peripheral vasodilation, which decreases venous return (due to venodilation). Systemic vascular resistance is also decreased, which can lower systemic blood pressure and somewhat reduce coronary artery perfusion pressure. However, this is unlikely to cause myocardial ischemia in the absence of obstructive CAD. (Choice D) Acetylcholine has a negative inotropic effect, reducing cardiac contractility and myocardial oxygen demand. (Choice E) Increased heart rate can increase myocardial oxygen demand and may exacerbate angina symptoms in patients with obstructive CAD, but it is unlikely to cause myocardial ischemia in the absence of CAD. In addition, acetylcholine directly slows heart rate, counteracting any reflex tachycardia caused by peripheral vasodilation. Educational objective: Vasospastic angina is the result of intermittent coronary vasospasm caused by endothelial dysfunction and autonomic imbalance. Although acetylcholine normally stimulates vasodilation, it triggers coronary vasospasm in affected patients due to a deficiency of vasodilatory endothelial nitric oxide. __________ References: Provocative testing for coronary reactivity and spasm. (http://www.ncbi.nlm.nih.gov/pubmed/24201078)

A 43-Year-Old Woman Comes to the Office Due to Occasional