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Review
. 2004 Apr;90(4):457-63.
doi: 10.1136/hrt.2003.020594.

Angina pectoris and normal coronary arteries: cardiac syndrome X

Filippo Crea  1 , Gaetano A Lanza
Affiliations
Review

Angina pectoris and normal coronary arteries: cardiac syndrome X

Filippo Crea et al. Heart. 2004 Apr.
No abstract available

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Figures

Figure 1
Figure 1
Proposed pathophysiological mechanism of syndrome X. Coronary microvascular dysfunction might be limited to pre-arterioles, functionally defined as 100–500 μm vessels interposed between large epicardial arteries and arterioles (responsible for metabolic regulation of coronary blood flow), supplying small myocardial regions scattered throughout the myocardium. An inappropriate constriction and/or impaired pre-arteriolar dilation, in response to metabolic or pharmacological arteriolar dilatation, would cause ischaemia in small myocardial regions surrounded by areas with a normal microvascular function, exhibiting normal, or even compensatory increased myocardial contractility, which would limit regional (and global) contractile abnormalities. In this setting, metabolic markers of ischaemia released from small myocardial areas would be diluted in the coronary blood circulation, thus making their detection difficult using traditional approaches. Of note, a sustained compensatory release of adenosine from myocardial ischaemic regions might contribute to limit the degree of ischaemia. Yet adenosine might by itself induce chest pain (because of its algogenic effect mediated by A1 receptor stimulation on cardiac pain receptors), ischaemia-like ST changes (because of its electrophysiological effect mediated by A1 receptor stimulation on myocardial fibres), and even exacerbate subendocardial ischaemia through a steal mechanism. Modified from Maseri et al.
Figure 2
Figure 2
Cardiac production of oxidative hydroperoxides (ROOHs) (left panel) and conjugated dienes (CD) (right panel) after atrial pacing in patients with syndrome X. The production of these oxidative lipoperoxide products during pacing, in the presence of ST segment depression and angina, is indicative of an ischaemia–reperfusion damage similar to that observed during balloon vessel occlusion in patients with obstructive coronary stenosis undergoing coronary angioplasty. There is no evidence of oxidative product release during atrial pacing in subjects without any history of angina pectoris (controls). Measures are obtained in blood samples from coronary sinus. t0  =  base; t1, t5, t15  =  1, 5, and 15 minutes after atrial pacing or coronary angioplasty. *p < 0.01 and †p < 0.05 v baseline. Modified from Buffon et al.
Figure 3
Figure 3
Radionuclide images obtained three hours after the injection of 123I-metaiodobenzylguanidine (MIBG) from a healthy subject (left panel) and from a patient with syndrome X (right panel). Cardiac MIBG uptake was normal (arrows) in the control subject, but it was totally absent (question mark) in the syndrome X patient, despite normal lung and liver MIBG uptake, consistent with a severe impairment of cardiac sympathetic function. Modified from Lanza et al.
Figure 4
Figure 4
Changes in time to platelet aggregation induced by exercise in patients with obstructive coronary artery disease (CAD), in patients with syndrome X, and in matched healthy controls. Platelet aggregation, measured using the PFA-100 method, with collagen and adenosine diphosphate as activating stimuli, does not change in controls, but it increases in CAD patients. In contrast, platelet aggregation decreases in syndrome X patients. Ex, exercise. *p < 0.01, †p < 0.001, and ‡p < 0.0001 versus pre-exercise. Modified from Lanza et al.
See this image and copyright information in PMC

References

    1. Cannon RO, Epstein SE. “Microvascular angina” as a cause of chest pain with angiographically normal coronary arteries. Am J Cardiol 1988;61:1338–43. ▸ This study summarises the earlier evidence of coronary microvascular dysfunction in patients with angina and normal coronary arteries. - PubMed
    1. Maseri A, Crea F, Kaski JC, et al. Mechanisms of angina pectoris in syndrome X. J Am Coll Cardiol 1991;17:499–506. ▸ This article reviews the evidence in favour and against an ischaemic origin of syndrome X. The authors then propose a novel pathogenetic hypothesis, which explains why transient myocardial ischaemia may occur in syndrome X in the absence of regional wall motion abnormalities and inconsistent detection of metabolic markers of ischaemia. - PubMed
    1. Buchthal SD, den Hollander JA, Merz CNB, et al. Abnormal myocardial phosphorus-31 nuclear magnetic resonance spectroscopy in women with chest pain but normal coronary angiograms. N Engl J Med 2000;342:829–35. - PubMed
    1. Chauhan A, Mullins PA, Taylor M, et al. Both endothelium-dependent and endothelium-independent function is impaired in patients with angina pectoris and normal coronary angiograms. Eur Heart J 1997;18:60–8. - PubMed
    1. Cannon RO, Camici PG, Epstein SE. Pathophysiological dilemma of syndrome X. Circulation 1992;85:883–92. ▸ This study reviews literature data which challenge the notion that myocardial ischaemia is actually responsible for chest pain and ST segment changes in syndrome X patients. - PubMed

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