Letter by Ong et al Regarding Article, “Coronary Artery Spasm: A 2009 Update”
To the Editor:
We read with great interest the clinician update “Coronary Artery Spasm: A 2009 Update” by Stern and Bayes de Luna.1 The topic of coronary vasospasm is clinically important, and the authors should be congratulated for bringing coronary vasospasm to the attention of the readers of Circulation. However, the authors stress that the diagnosis of coronary vasospasm as the cause of resting angina requires demonstration of transient ST elevation. Furthermore, the authors suggest that pharmacological testing should be done only under special conditions and with extreme care. We strongly disagree with both statements.
Although the described combination of transient ST elevation and resting chest pain makes the diagnosis of coronary spasm highly likely, such observations are extremely rare in clinical practice, supporting the false impression in the cardiology community that coronary vasospasm is a rare entity. We recently demonstrated that coronary vasospasm is a frequent cause of chest pain in patients undergoing coronary angiography for a presumed acute coronary syndrome.2 One third of these patients had no culprit lesion, and half of them had coronary vasospasm as the underlying cause of their resting angina. However, none of the patients with coronary vasospasm had ST elevation with chest pain during telemetry in the coronary care unit.
Over the past years, awareness of coronary vasospasm as a major pathogenetic factor in many aspects of ischemic heart disease has decreased in the cardiology community, as correctly noted by Stern and Bayes de Luna. Stenting of lesions causing 50% obstruction has become common in patients with resting angina, assuming that symptoms were triggered by plaque instability. Although the cause of resting angina in the absence of high-grade lesions may be coronary vasospasm, this concept is largely ignored by the cardiology community. An improved understanding of the mechanisms leading to resting chest pain without severe coronary lesions can be achieved only if some form of functional testing becomes part of the cardiac catheterization in such patients. “Seeing is believing”: The provocation of coronary vasospasm associated with ECG changes (usually not ST elevation but ST depression) and an impressive reproduction of the patient’s symptoms not only will reassure the patient that indeed the heart was the source of the chest pain but also will help the cardiologist understand how common the phenomenon of coronary vasospasm is even in the white patient population. We perform >500 functional tests per year using increasing doses of acetylcholine in patients with chest pain but without severe coronary lesions without complications. The most important procedural aspect for the safety of the test is the graded increase in acetylcholine dose. This technique avoids the life-threatening spasm that may occur if an initial dose of 100 μg is injected into the left coronary artery of a patient with severe vasospastic angina.
In summary, we believe that the article by Stern and Bayes de Luna may be misleading by stating that the typical patient with coronary vasospasm will have ST elevation that can be observed in a 12-lead ECG or on Holter monitoring during the attack. Only functional testing (which is a very safe procedure) during coronary angiography will demonstrate that coronary vasospasm is frequent. It should be suspected in many patients with angina but no severe coronary lesions.