| Background:Our previous studies found that reverse redistribution(RR) in 201T1 myocardial perfusion scintigraphy was one of the characters in patients with coronary artery spasm(CAS).Being non-invasive criteria by combining of the rest chest pain,negative ECG exercise test and RR in 201T1 myocardial perfusion scintigraphy,the sensitivity and the specificity for diagnosing CAS were 98%and 90%,respectively.However,the mechanism of RR is not clarified.Objective:This study was aimed to explore the possible mechanism of RR in thallium-201(201T1) myocardial perfusion scintigraphy by comparing the changes of plasma endothelin- 1(ET- 1 ),nitric oxide(NO) levels,ET- 1/NO ratio,coronary artery blood flow and myocardial blood flush during stress tests in patients with CAS.Materials and methods1.Study population The patients who underwent ECG exercise tests and were proposed to receive 201T1 myocardial perfusion scintigraphy were included.According to the final diagnosis,the patients were divided into following three groups.(1) control group(n=30):①A normal presentation on 201T1 myocardial perfusion scintigraphy.②Coronary heart disease(CHD) was clinically excluded.(2) CAS group(n=30):①RR was present on 201T1 myocardial perfusion scintigraphy.②With rest chest pain.③And a negative ECG exercise tests.④No angiographic stenosis(≥50%) was found by coronary artery angiography (CAG).(3) CHD group(n=30):①Ischemic perfusion defect on 201T1 myocardial perfusion scintigraphy.②Consistent with Denomination and Diagnosis Standard for Ischemic Heart Disease by International academy of Cardiology and International Association of Cardiology as well as WHO Clinic Denomination Standardization Associated Experts Group in 1979.③CAG showed stenosis of 50%or above in one or more vessels.2.Methods(1) 201T1 myocardial perfusion scintigraphyVasodilators like Calcium channel blockers and long-acting nitrates were discontinued for 24 h,short-acting nitrates for at least 12h before 201T1 myocardial perfusion scintigraphy.Dipyridamole was injected intravenously at a rate of 0.14mg/kg·min for 4min.Followed by intravenous 111 MBq of 201T1,the initial images were taken at 10 min,and the delay images at 3h,after the injection.Semi-quantitative intergration was used in the analysis,the left ventricle was divided into 9 portions:apical,anterior,basal anterior,anterolateral,posterolateral, ante-septal,post-septal,inferior,and posterior segments.Each segment was assessed using a five-point scoring system(0=normal;1=slightly reduced perfusion; 2=moderaterly reduced perfusion;3=severely reduced perfusion;4=no perfusion). The summed different score(SDS) was calculated as the difference between summed stress score and summed rest score.Myocardial ischemia was assigned if SDS≥2. Conversely,RR was defined if SDS≤-2.(2) Detection of ET-1 and NO:Venous blood was collected before stress test, immediately and 3h after stress test.NO was measured by nitrate reductase method, and ET-1 was measured by the homogeneous competitive radioimmuno assay method.(3) Coronary angiography and dipyridamole testEighteen patients with CAS were undergone coronary angiography and dipyridamole test.Coronary angiography was performed with conventional methods. In particularly,at least four projections for left coronary artery and two perpendicular projections for right coronary artery were taken during CAG.Nitroglycerin and other vascular dilators were prohibited during CAG After the initial CAG,dipyridamole was injected intravenously at a rate of 0.14mg/kg·min for 4min,and then repeated CAG.Anlysis of images:Coronary artery diameters,corrected TIMI frame count (CTFC) and TIMI myocardial perfusion grade(TMPG) were calculated automatically by the software and compared between RR related vessels and non-RR related vessels.Results1.comparison of blood ET-1,NO and the ratio of ET-1/NO during 201T1 myocardial perfusion scintigraphy.(1) The dynamic changes of plasma ET-1 levels during heart stress test1) Before stress test,the plasma ET-1 level was higher in CAS groups(163.53 ±8.58 pg/ml) than in CHD group(137.73±8.32 pg/ml) and in control group(116.15±6.65 pg/ml,P＜0.01).2) In control group,there were no significant differences in plasma ET-1 levels between different time points(F=0.138,P=0.871 ).3) In CSA group,the plasma ET-1 level went down at immediately after stress test(151±9.15 pg/ml) compared with those before stress test(163.53±8.58 pg/ml,P＜0.01 ),and went up at 3h after stress test(164.76±7.14 pg/ml).There were no significant differences between before and at 3h after stress test(P=0.571).4) In CHD group,the plasma ET-1 level went up at immediately after stress test (147.00±9.68 pg/ml) compared with those before stress test(137.73±8.32 pg/ml, P＜0.01 ),and went down at 3h after stress test(138.25±8.78 pg/ml).There were no significant differences between before and at 3h after stress test(P=0.822).(2) The dynamic changes of serum NO levels during heart stress test1) Before stress test,the serum NO level was higher in control group(70.10±6.90μmol/L) than in CHD group(62.64±7.45μmol/L) and CAS group(60.32±8.20μmol/L,P＜0.01).2) In control group,the serum NO level increased at immediately after stress test (83.14±8.31μmol/L) compared with those before stress test(70.10±6.90μmol/L, P＜0.01 ),and decreased at 3h after stress test(68.06±6.21μmol/L,P＜0.01 ).There were no significant differences between before and at 3h after stress test(P=0.117).3) In CAS group,the serum NO level inceased at immediately after stress test (63.78.±8.30μmol/L) compared with those before stress test(60.32±8.20μmol/L,P＜0.01 ),and decreased at 3h after stress test(46.70±8.79μmol/L) which were lower than those before stress test(P＜0.01).4) In CHD group,the serum NO level increased at immediately after stress test (67.04±7.99μmol/L)compared with those before stress test(62.64±7.45μmol/L, P＜0.01 ),and decreased at 3h after stress test(60.33±7.92μmol/L,P＜0.01 ).There were no significant differences between before and at 3h after stress test(P=0.473).(3) The dynamic changes of ET-1/NO ratio during heart stress test1) Before stress test,the ratio of ET-1/NO was higher in CAS group(2.75±0.39) than CHD group(2.22±0.31) and control group(1.67±0.18,P＜0.01).2) In control group,the ratio of ET-1/NO went down at immediately after stress test(1.40±0.12) compared with those before stress test(1.67±0.18,P＜0.01 ), and went up at 3h after stress test(1.71±0.18,P＜0.01 ).There were no significant differences between before and at 3h after stress test(P=0.562).3) In CAS group,the ratio of ET-1/NO went down at immediately after stress test(2.41±0.36) compared with those before stress test(2.75±0.39,P＜0.01), and went up at 3h after stress test(3.36±0.78,P＜0.01 ) which were higher than those before stress test(P＜0.01).4) In CHD group,there were no significant differences in the ratioes of ET-1/NO between different time points(F=1.168,P= 0.316).2.Comparison on coronary artery diameters,CTFC and TMPG before and after dipyridamole test during CAG.(1) Blood flow was slower in RR related vessels while compared with non-RR related vessels before dipyridamole test.After injection of dipyridamle,with heart rate increasing and blood flow going faster,the coronary artery diameters increased by 16%±8%in RR related vessels and 14%±12%in non-related vessels,respectively.(2) Before dipyridamole test,CTFC was higher in RR related vessels(36±6) than those in non-RR related vessels(29±7,t=2.982,P=0.009).After intravenous dipyridamole injection,CTFC decreased remarkable in RR related vessels(26±7,t =4.466,P=0.001) as well as in non-RR related vessels(25±5,t=2.308,P= 0.038). (3) Before dipyridamole test,TMPG was lower in RR related vessels(2.02±0.39 ) than those in non-RR related vessels(2.56±0.31,t=2.832,P=0.018).After intravenous dipyridamole injection,TMPG increased remarkable in RR related vessels(2.92±0.12,t=2.832,P=0.018) as well as in non-RR related vessels (2.92±0.12,t=4.261,P=0.001).Conclusions1.The abnormal ratio of ET-1/NO indicates endothelial dysfunction which results in a slight coronary artery constriction under rest state in patients with CAS.2.Under the rest state,endothelial dysfunction induces a slight coronary artery constriction in patients with CAS which results in slower blood flow and presents as a perfusion defect in 201T1 myocardial perfusion scintigraphy.However,exercise or dipyridamole induces coronary artery relaxation by changing the ratio of ET-1/NO and increases coronary blood flow which presents as normal myocardial perfusion.It may be one of the possible mechanisms of RR in 201T1 myocardial perfusion scintigraphy in patients with CAS.
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