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OBJECTIVES:We investigated whether there is increased temperature in non-culprit lesions, and the correlation of clinical syndrome with heat production of non-culprit lesions. BACKGROUND: There is a controversy regarding whether there is widespread inflammation involving non-culprit lesions, or whether inflammatory involvement is limited to the culprit lesion. Coronary thermography assesses the local inflammatory involvement in atherosclerotic lesions. METHODS: We included patients suffering from stable angina(SA) or acute coronary syndrome(ACS). All patients had two or more angiographically detectable lesions at different arteries. Culprit lesions should be identified in all patients. Patients with chronic total occlusions and multiple significant lesions at the culprit vessel were excluded. We measured at each non-culprit lesion the temperature difference(Δ T) between the atherosclerotic plaque and the proximal vessel wall temperature. RESULTS: The study population included 42 patients: 23 with SA, 19 with ACS. The Δ T in non-culprit lesions was 0.08± 0.07° C. Patients with ACS had a higher temperature difference in non-culprit lesions compared with patients with SA(ACS 0.11± 0.08° C vs. SA 0.05± 0.06° C; p < 0.01). The mean value of Δ T in nonculprit lesions was higher in the untreated group compared with the treated group with statins(0.11± 0.10° C vs. 0.06± 0.05° C; p=0.05). CONCLUSIONS: The results of this study show that heat is generated in non-culprit lesions. Moreover, in patients with ACS, temperature difference is increased compared with patients with stable angina.
OBJECTIVES: We investigated whether there is increased temperature in non-culprit lesions, and the correlation of clinical syndrome with heat production of non-culprit lesions. METHODS: We included patients suffering from stable angina (SA) or acute coronary syndrome (ACS). All patients had two or more angiographically detectable lesions at Different arteries. Culprit lesions should be identified in all patients. Patients with chronic total occlusions and multiple significant lesions at the culprit vessel were excluded. We measured at each non-culprit lesion the temperature difference (ΔT) between the atherosclerotic plaque and the proximal vessel wall temperature. RESULTS: The study population included 42 patie Patients with ACS had a higher temperature difference in non-culprit lesions compared with patients with SA (ACS 0.11 ± 0.08 ° C vs. SA 0.05 ± 0.06 ° C; p <0.01). The mean value of ΔT in nonculprit lesions was higher in the untreated group compared with the treated group with statins (0.11 ± 0.10 ° C vs. 0.06 ± 0.05 ° C; p = 0.05). CONCLUSIONS: The results of this study show that heat is generated in non-culprit lesions. Moreover, in patients with ACS, temperature difference is increased compared with patients with stable angina.