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Invasive coronary reactivity testing for non-obstructive chest pain is criticized as an unproven research tool that does not justify its risks and expenses.
To the Editor: Dr Phan and colleagues presented 2 interesting patients with chest pain and normal coronary angiograms, speculating that for one patient the symptoms were due to microvascular coronary dysfunction and, for the other, due to abnormal cardiac nociception. I do not believe they have justified their conclusion that both patients illustrate the value of coronary reactivity testing. Indeed, the details of their diagnostic investigations are a reminder of the old saw that a well person is one who has not been completely worked up. The first patient, with cardiac syndrome X, had already had a negative radionuclide perfusion stress test (usually positive in this syndrome) and 2 normal coronary angiograms before commencing the workup discussed by the authors, which included repeat coronary angiography and insertion of an intracoronary flow wire followed by intracoronary infusion of vasoactive agents. The authors dismissed the negative stress test as reflecting the insensitivity of that test, although lack of specificity of the coronary reactivity testing is equally plausible. They justified the risks of the invasive evaluation by pointing out that patients with microvascular coronary dysfunction have an increased risk for adverse events, although no treatment has been demonstrated to reduce that risk. The 1 article cited to support an improved prognosis with treatment refers to hypertensive patients with abnormal brachial artery flow-mediated vasodilatation; whether these findings would apply to a nonhypertensive patient with microvascular coronary dysfunction is unknown. The second patient, a woman diagnosed with abnormal cardiac nociception, had normal coronary reactivity testing but had severe chest pain during flow-wire manipulations and infusions, requiring 2 doses of 25 μg of fentanyl for relief. She was treated with “reassurance and low-dose imipramine . . . ” and “has not sought additional testing at 18-month follow-up.” There is no evidence that the testing led to more effective therapy for this patient. I believe it would be a mistake to conclude that the coronary reactivity testing described by Phan et al is anything more than a research tool. Although the authors provided interesting theoretical explanations for the chest pain in their 2 patients, the diagnostic studies resulted in empirical, not tailored, therapy with no proven benefits in terms of symptom relief or prognosis. They therefore have not justified the increased risk and expense of the procedure.
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Steven W. Seiden (2009) studied this question.
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