Author + information
- Richard O. Cannon III, MD* ()
- ↵*National Heart, Lung, and Blood Institute, National Institutes of Health, Translational Medicine Branch, NHLBI, Building 10-CRC, Room 5-3330, 10 Center Drive, Bethesda, Maryland 20892-1454
Drs. Fineschi and Gori propose a new syndrome of coronary microvascular dysfunction, manifest by slow passage of contrast media in coronary arteries of patients presenting with acute chest pain. They suggest “coronary syndrome Y” to distinguish this syndrome from “syndrome X” used by some investigators and clinicians to identify the larger group of patients with angina-like chest pain (rest or effort provoked), ischemic-appearing electrocardiographic response to exercise stress, and normal coronary angiograms.
Consistent with my discussion in the Journal(1), I believe that syndrome Y with the “coronary slow-flow phenomenon” has uncertainties similar to other groups of patients with chest pain despite normal coronary angiograms, whether designated as syndrome X, microvascular angina, or something else. Thus, is this syndrome a primary abnormality of coronary microvascular function or a result of activated platelets and vasoactive debris from plaques in epicardial arteries not apparent on visual assessment of coronary angiograms? From a clinical perspective, what criteria are necessary for diagnosis? Assessment of the flow of contrast media from epicardial arteries into the myocardium is largely subjective and may be confounded by dilation of epicardial arteries due to administration of nitrates before coronary angiography, thus reducing flow velocity at that level of the circulation. Accordingly, what Thrombolysis In Myocardial Infarction frame count could identify patients with this syndrome with acceptable sensitivity and specificity? Are there characteristic electrocardiographic changes to suggest ischemia? Are troponin levels elevated to suggest myonecrosis? Are wall motion abnormalities present on echocardiography? In this regard, intense microvascular constriction, possibly due to neurohormonal activation accompanying psychological or other life stress, has been proposed to account for the Takotsubo syndrome of reversible apical ballooning (recently reviewed by Akashi et al. ), but such striking wall motion abnormalities do not appear with any regularity in reports referenced by Drs. Fineschi and Gori. Can imaging studies such as cardiac magnetic resonance imaging show evidence of endocardial hypoperfusion if performed proximate to an episode of chest pain for patients with recurrent symptoms? Finally, what treatments currently available to clinicians are effective in managing symptoms and preventing pathophysiologic (once defined) features of this new syndrome?
I look forward to additional clinical research that may well legitimize this, and other, syndromes of chest pain with normal coronary arteries and structurally normal hearts.
- American College of Cardiology Foundation
- Cannon R.O. III.
- Akashi Y.J.,
- Goldstein D.S.,
- Barbaro G.,
- Ueyama T.