Acetylcholine testing helps evaluate coronary spasm

By David Douglas

Intracoronary acetylcholine (ACH) provocation testing is a valid and safe means of assessing coronary vasomotor function in patients with anginal symptoms, according to German and UK researchers.

As Dr. Peter Ong told Reuters Health by email, "We believe that ACH testing should be performed in patients with chest pain and unobstructed coronary arteries for four major reasons."
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Testing, continued Dr. Ong, may allow determination of vasospastic angina as the cause of the chest pain, reassure the patient that a cause for the chest pain has been found, facilitate initiation of appropriate medical therapy (calcium channel blockers and nitrates), and avoid further unnecessary invasive procedures.

In a February 26 online paper in Circulation, Dr. Ong of Robert-Bosch-Krankenhaus in Stuttgart, Germany, and colleagues note that despite its apparent utility, ACH testing is rarely used in Europe and the U.S.

To further evaluate the method, the investigators studied patients who underwent diagnostic coronary angiography for suspected myocardial ischemia. All had unobstructed arteries defined as coronary stenosis of less than 50%. The ACH test was conducted directly after diagnostic coronary angiography in 847 patients.

In all, 35% of patients complained of chest pain at rest, 22% had pain on exertion, and 24% had pain under both circumstances. Troponin positive acute coronary syndrome was seen in 4%.

In 117 patients, the ACH test was negative (no symptoms, no ECG changes, no epicardial spasm) and in 242 patients the test was inconclusive.

The overall frequency of epicardial spasm, defined as a greater than 75% diameter reduction with angina and ischemic ECG-shifts, was 33.4%. That of microvascular spasm (angina and ischemic ECG-shifts without epicardial spasm) was 24.2%.

Epicardial spasm was most often diffuse and located in the distal coronary segments. No fatal or irreversible non-fatal complications occurred, however nine patients had minor complications. These were most commonly symptomatic bradycardia, which was seen in six patients.

Given these findings, the researchers conclude that the test should be employed in order to help find functional causes for angina in patients with unobstructed coronary arteries and also may be of value in patients presenting with symptoms other than angina pectoris such as syncope or heart failure.

Commenting on the findings by email, Dr. Scott Kinlay, author of an accompanying editorial, told Reuters Health, "True 'variant angina' due to coronary vasospasm is quite rare (less than 5% of patients with angina). This is when a proximal (beginning) part of a coronary artery occludes or nearly occludes with spasm. This results in no blood flow to a large part of the heart and precipitates symptoms and ECG changes similar to a heart attack."

"Fortunately, this is reversible in most cases, and when the spasm abates or is treated by nitroglycerin, the artery relaxes, opens up again and normal blood flow resolves," added Dr. Kinlay, of Veterans Affairs Boston Healthcare System and Brigham and Women's Hospital. "There is no way to diagnose this . . . accurately without cardiac catheterization and a test for abnormal vasoconstriction such as described in the Ong paper."

He went on to say, "Many more patients in the Ong paper had vasoconstriction of more distal segments of coronary artery (near the ends of the artery). This is an abnormal response and quite common particularly in patients who do not have their risk factors well controlled (e.g. those who are not on good cholesterol treatment, have poorly controlled blood pressure control, or continue to smoke). This response may contribute to angina symptoms especially if it is superimposed on even a mild narrowing in the artery due to the accumulation of cholesterol in the artery wall."

"This is because moderate vasoconstriction on top of a mild narrowing leads to more significant narrowing in the artery and impaired blood flow leading to angina," he said. "This is not true variant angina with coronary spasm, as it is not associated with the specific ECG changes and symptom pattern of this condition. However, it is an abnormal response that impairs the quality of life of patients."

Summing up, Dr. Kinlay observed, "The importance of the Ong paper is that it reminds us that arteries are not static pipes, but dynamic organs that regulate blood flow by changing their size. In coronary disease, and particularly with poor risk factor control, abnormal vasoconstriction (whether it is true variant angina or other patterns of vasoconstriction) can contribute to angina symptoms. Vasodilator medications (e.g. nitrates, calcium channel blockers) can also help counteract this effect. So even if the angiogram appears 'normal' or only mildly diseased, vasoconstriction may be the principle cause of angina symptoms in some patients. Intensive control of the risk factors for atherosclerosis and in some cases vasodilator medications are arguably more important in this situation."

However, as he pointed out in his editorial, "Testing for vasomotor function should be used cautiously in patients at higher risk of adverse events . . . and operators should have interventional equipment and skills to treat severe vasospasm with intracoronary vasodilators and obstructive disease with percutaneous coronary intervention."

SOURCE: http://bit.ly/1qPNgJM and http://bit.ly/1izqvWB

Circulation 2014.

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