Author + information
- Massimo Fineschi, MD and
- Tommaso Gori, MD, PhD* ()
- ↵*Department of Cardiology, University Medical Center, Langenbeckstr. 1, 55131 Mainz, Germany
Dr. Cannon is to be complimented on his important contributions in the description of the elusive pathophysiology of microvascular angina. We would like to contribute to his otherwise excellent review (1) recently published in the Journalby making mention of another condition that also depends on an impairment in the regulation of coronary microvascular resistances and that, therefore, should be included among the “microvascular angina” syndromes. This condition, known as the coronary slow-flow phenomenon (CSFP), is increasingly recognized as a separate clinical entity along with the “classic” coronary syndrome X based on 3 degrees of evidence: 1) the coronary syndrome X and the CSFP differ mechanistically; 2) the CSFP has typical clinical features that differ strikingly from those of coronary syndrome X; and, finally, 3) its prognosis is not as benign as that traditionally described for coronary syndrome X.
Although a number of formal definitions have been proposed, the CSFP essentially consists of a delay in the progression of the contrast injected in the coronary vasculature during coronary angiography. Importantly, invasive studies have demonstrated that, compatible with the delayed opacification, resting coronary artery resistances are abnormally elevated in these patients; in striking contrast with “classic” coronary syndrome X, however, these resistances respond normally to vasodilator stimuli such as papaverine and adenosine and during exercise (2,3). As such, abnormalities in the regulation of microvascular tone occur only in resting conditions in patients with the CSFP, and while coronary syndrome X is characterized by an impaired coronary flow reserve, the CSFP is associated with a normal, or even supranormal, one (3). In line with this abnormality, while coronary syndrome X patients typically experience angina under stress, the CSFP is more commonly associated with rest angina. Further, while there is general agreement that coronary syndrome X occurs more commonly in post-menopausal women, the CSFP has been typically found in young male smokers (4). Finally, and most importantly, life-threatening arrhythmias and sudden cardiac death have been described in these patients (5).
A number of issues still need to be clarified with regard to the pathogenesis, clinical presentation, therapy, and outcome of the CSFP. Despite these unsolved issues, the CSFP (or coronary syndrome Y, given the proposed role of neuropeptide Y ) should be finally recognized the status of separate clinical entity within the framework of microvascular angina, and computation of the Thrombolysis In Myocardial Infarction frame count should become a routine procedure. Further, microvascular angina should not be considered a single condition with a homogeneous pathophysiology and clinical pattern. Recognizing this complexity will probably help to explain many of the controversies well described by Dr. Cannon.
- American College of Cardiology Foundation