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Coronary vasomotion in patients with syndrome X: evaluation with positron emission tomography and parametric
J G Meeder1, P K Blanksma, E E van der Wall
1Department of Cardiology, University Hospital Groningen, The Netherlands.
Insights
Syndrome X patients and those with minimal coronary artery disease exhibit normal endothelial function and vasodilator reserve. Abnormal coronary vasomotion is unlikely the primary cause of Syndrome X, suggesting other mechanisms like sympathetic tone may be involved.
Area of Science:
- Cardiology
- Nuclear Medicine
- Physiology
Background:
- Syndrome X, characterized by angina and ischemia with normal coronary angiography, is often attributed to abnormal coronary vasomotion.
- The precise causative mechanism of Syndrome X remains incompletely understood, necessitating further investigation into micro- and macrocirculation.
- Evaluating endothelial function, vasodilator reserve, and myocardial perfusion heterogeneity is crucial for understanding Syndrome X pathophysiology.
Purpose of the Study:
- To elucidate the causative mechanism of abnormal coronary vasomotion in patients with Syndrome X.
- To evaluate endothelial function, vasodilator reserve, and myocardial perfusion heterogeneity in patients with Syndrome X.
- To differentiate the pathophysiological mechanisms in Syndrome X from those in minimal coronary artery disease.
Main Methods:
- [13N]ammonia positron emission tomography was used to assess myocardial perfusion at rest and during stress.
- Cold pressor stimulation was employed to evaluate endothelial function.
- Dipyridamole stress testing was utilized to assess vasodilator reserve.
- Parametric polar mapping with a 480-segment model was used to analyze myocardial perfusion heterogeneity.
Main Results:
- Patients with Syndrome X and minimal coronary artery disease showed normal myocardial perfusion responses during cold pressor stimulation and dipyridamole stress testing.
- Resting myocardial perfusion was elevated in both patient groups compared to healthy volunteers, but this difference was normalized after correcting for rate-pressure product.
- Increased heterogeneity of resting myocardial perfusion was observed in patients with Syndrome X compared to controls.
Conclusions:
- Endothelial dysfunction and impaired vasodilator reserve are not major pathophysiological factors in Syndrome X.
- Abnormal coronary vasomotion is unlikely to be the primary cause of Syndrome X.
- Other mechanisms, such as increased sympathetic tone or focal release of vasoactive substances, may contribute to the pathogenesis of Syndrome X.
Abstract:
The aim of this study was to elucidate further the causative mechanism of abnormal coronary vasomotion in patients with syndrome X. In patients with syndrome X, defined as angina pectoris and documented myocardial ischaemia during stress testing with normal findings at coronary angiography, abnormal coronary vasomotion of either the micro- or the macrocirculation has been suggested as the causative mechanism. Accordingly, we evaluated endothelial function, vasodilator reserve, and perfusion heterogeneity in these patients. Twenty-five patients with syndrome X (definitely normal coronary arteriogram, group A), 15 patients with minimal coronary artery disease (group B) and 21 healthy volunteers underwent [13N]ammonia positron emission tomography at rest, during cold pressor stimulation (endothelial function) and during dipyridamole stress testing (vasodilator reserve). Heterogeneity of myocardial perfusion was analysed by parametric polar mapping using a 480-segment model. In both patient groups, resting perfusion was increased compared to the normal subjects: group A, 127+/-31 ml.min-1.100 g-1; group B, 124+/-30 ml.min-1.100 g-1 normal subjects, 105+/-21 ml.min-1.100 g-1 (groups A and B vs normals, P<0.05). These differences were abolished after correction for rate-pressure product. During cold pressor stimulation, the perfusion responses (ratio of cold pressor perfusion to resting perfusion) were similar among the patients and the control subjects (group A, 1.20+/-0.23; group B, 1.24+/-0.22; normal subjects, 1.23+/-0.14). Likewise, during dipyridamole stress testing, perfusion responses were similar among the three groups (group A, 2.71+/-0.67; group B, 2.77+/-1.29; normal subjects, 2. 91+/-1.04). In group A the heterogeneity of resting perfusion, expressed as coefficient of variation, was significantly different from the volunteers (20.1+/-4.5 vs 17.0+/-3.0, P<0.05). In group B (coefficient of variation 19.4+/-3.9) the difference from normal volunteers was not significant. In this study, patients with syndrome X and patients with minimal coronary artery disease showed normal perfusion responses during cold pressor stimulation and dipyridamole stress testing. Our findings therefore suggest that endothelial dysfunction and impaired vasodilator reserve are of no major pathophysiological relevance in patients with syndrome X. Rather, other mechanisms such as increased sympathetic tone and focal release of vasoactive substances may play a role in the pathogenesis of syndrome X.