Abstract 1645: Cardiac adrenergic nerve function and microvascular dysfunction in patients with Cardiac Syndrome X
Background. In patients with cardiac syndrome X (CSX), angina chest pain is believed to be caused by coronary microvascular dysfunction (CMVD). A severe impairment on myocardial scintigraphy of cardiac uptake of 123I-metaiodobenzylguanidine (MIBG), an analogue of norepinephrine was previously reported, suggesting a dysfunction of cardiac adrenergic nerve fibres. It is unknown, however, whether abnormal cardiac MIBG uptake correlates with CMVD in CSX patients.
Methods. We enrolled 20 consecutive patients (58±7 years, 8 men) with a diagnosis of CSX. Planar and SPECT (MIBG) myocardial scintigraphy was performed in all patients. Cardiac MIBG uptake was measured by the heart/mediastinum (H/M) ratio and by a SPECT regional cardiac MIBG uptake defect score (higher values=lower uptake). MIBG data were compared to those obtained in a control group of 10 healthy subjects (53±5 years, 4 men). Coronary flow response (CFR) to adenosine in the left anterior descending coronary artery (LAD) was assessed in CSX patients using high-resolution transthoracic ultrasound Doppler recording, and was expressed as the ratio between maximal coronary flow velocity at peak adenosine infusion (140 μg/kg/min for 120 seconds) and coronary flow velocity at rest.
Results. No control subject showed any significant defects in cardiac MIBG uptake. In contrast MIBG defects were observed in all patients, with 2 (10%) showing no cardiac MIBG uptake at all. Compared to controls, CSX patients showed a significantly lower H/M ratio (1.66±0.14 vs. 2.2±0.3, P<0.001) and a higher MIBG defect score (35±31 vs. 4±2, P=0.004). In CSX patients, however, no significant correlation was found between CFR to adenosine in the LAD coronary artery and MIBG H/M ratio (r=0.09; P=0.72) or SPECT MIBG uptake score in the LAD territory (r=−0.02; P=0.93).
Conclusion. Our data confirm the significant impairment of cardiac MIBG uptake in patients with CSX, suggesting abnormalities in cardiac adrenergic nerve function. These abnormalities, however, do not seem to be of major relevance in decreasing the vasodilator CFR to adenosine in these patients. However, whether they may influence the response to other kinds of vasoactive (dilator or constrictor) stimuli needs to be addressed in appropriate studies.