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Effect of cold stimulation on myocardial perfusion. An investigation using thallium-201 scintigraphy
Insights
Cold stimulation can cause myocardial perfusion abnormalities in patients with coronary artery disease, those with normal coronary arteries, and even healthy individuals. This finding suggests cold pressor tests are unreliable for diagnosing coronary heart disease.
Area of Science:
- Cardiology
- Nuclear Medicine
- Physiology
Background:
- Coronary artery disease diagnosis often relies on stress tests.
- Cold stimulation is a potential stressor for evaluating myocardial perfusion.
Purpose of the Study:
- To investigate the impact of cold stimulation on myocardial perfusion.
- To assess if cold stimulation can differentiate between coronary artery disease, atypical chest pain, and normal subjects.
Main Methods:
- Thallium-201 scintigraphy was employed in three groups: documented coronary artery disease, chest pain without coronary disease, and healthy volunteers.
- Scintigrams were analyzed visually and numerically using circumferential profiling.
- Hemodynamic responses were monitored via double product.
Main Results:
- Transient perfusion defects occurred in patients with coronary artery disease, those with normal coronary arteries, and healthy volunteers.
- No significant difference in hemodynamic responses was observed between subjects with or without perfusion defects.
- Cold stimulation induced perfusion abnormalities across all study groups.
Conclusions:
- Cold stimulation can provoke myocardial perfusion abnormalities in individuals with and without coronary heart disease.
- The cold pressor test is not a reliable method for differentiating coronary heart disease from other chest pain syndromes or normal states.
- Results suggest a spectrum of coronary vasomotor responsiveness to cold stress.
Abstract:
Thallium-201 scintigraphy was used to investigate the effects of cold stimulation on myocardial perfusion in 12 patients with documented coronary artery disease (group 1), nine with chest pain but without evidence of structural coronary artery disease (group 2), and 10 normal volunteers (group 3). The scintigrams were assessed both visually and numerically using a circumferential profile technique. Transient perfusion defects were identified by both techniques in six subjects in group 1, three in group 2, and two in group 3. The haemodynamic responses (assessed by the double product) of subjects with or without transient perfusion defects were not significantly different. Thus cold stimulation can provoke abnormalities of myocardial perfusion not only in patients with coronary heart disease but also in those with structurally normal coronary arteries and in some normal subjects. These results may reflect a spectrum of coronary vasomotor responsiveness to cold stimulation in both normal and ischaemic populations, and it is concluded that cold pressor techniques cannot be relied on to differentiate patients with coronary heart disease from those with atypical chest pain syndromes or even from normal subjects.