Article

Microvascular Angina and the Continuing Dilemma of Chest Pain With Normal Coronary Angiograms

Translational Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA.
Journal of the American College of Cardiology (Impact Factor: 15.34). 10/2009; 54(10):877-85. DOI: 10.1016/j.jacc.2009.03.080
Source: PubMed

ABSTRACT Since initial reports over 4 decades ago, cases of patients with angina-like chest pain whose coronary angiograms show no evidence of obstructive coronary artery disease and who have no structural heart disease continue to be a common occurrence for cardiologists. Many features of this patient population have remained constant with successive reports over time: a female predominance, onset of symptoms commonly between 40 and 50 years of age, pain that is severe and disabling, and inconsistent responses to conventional anti-ischemic therapy. Because patients may have had abnormal noninvasive testing that led to performance of coronary angiography, investigators have sought to show an association of this syndrome with myocardial ischemia. Abnormalities in coronary flow and metabolic responses to stress have been reported by several groups, findings consistent with a microvascular etiology for ischemia and symptoms, but others have questioned the presence of ischemia, even in patients selected for abnormal noninvasive testing. Despite considerable efforts by many groups over 4 decades, the syndrome remains controversial with regard to pathophysiology, diagnosis, and management.

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    • "In up to 60% of patients undergoing coronary angiography (CAG), no significant obstructive coronary artery disease (CAD) is detected, and these patients with nonobstructive CAD are treated conservatively (Bugiardini and Bairey Merz, 2005; Cannon, 2009; Maddox et al., 2010; Vaccarino et al., 2013). Still, chest pain in patients with normal or near normal coronary arteries is prevalent and recurrent (Jespersen et al., 2013; Mommersteeg et al., 2013), related to increased clinical examinations (Beigel et al., 2013; Rossini et al., 2013), hospitalization (Rossini et al., 2013), major adverse cardiac events (Bugiardini and Bairey Merz, 2005; Jespersen et al., 2012) and mortality (Jespersen et al., 2012; Rossini et al., 2013; Sharaf et al., 2013), which requires further investigation. "
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    • "We hypothesized that serum adipokines might be involved in the development of CSX. CSX is thought to be characterized by myocardial ischemia, caused by endothelial dysfunction in coronary microcirculation (Cannon et al. 1983) and impaired coronary flow reserve (Cannon 2009). A number of studies have confirmed impairment of both endotheliumdependent and endothelium-independent coronary vasodilation exists in CSX (Cannon 2009; Cannon et al. 1985). "
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