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   <subfield code="a">Enhancement of coronary reactive hyperemia in patients with ischemic myocardial tolerance during angioplasty</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Takahiro Tanaka, Hiroshi Nonogi, Shunichi Miyazaki, Yoichi Goto, Akira Itoh, Satoshi Daikoku, Yusuke Yamamoto]</subfield>
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   <subfield code="a">Summary: The purpose of this study was to elucidate the effect of repeated brief coronary occlusions on reactive hyperemia during percutaneous transluminal coronary angioplasty (PTCA) in patients with or without ischemic tolerance. Seventeen patients undergoing PTCA for chronic stable angina were studied. Patients with well developed collateral vessels were excluded. After successful predilatation, coronary flow velocity was recorded with the use of a Doppler flow guide wire, and reactive hyperemia was assessed immediately after each of two 2-min coronary occlusions followed by 2 mins of reperfusion. The intracoronary electrocardiogram (icECG) was recorded via the flow guide wire placed in the center of the ischemic zone. Patients were divided into two groups: those who showed a reduction of ST elevation in the icECG recorded at the time of the second coronary occlusion (group I), and those who showed no difference in ST elevation between the two occlusions (group II). There were no significant differences in blood pressure, heart rate, or baseline coronary flow velocity between the two groups before the first occlusion, but the ST elevation at the time of the first coronary occlusion was greater in group I than in group II (8.9 ± 6.2 versus 1.1 ± 2.0mm,P &lt; 0.01). Reactive hyperemia was significantly greater after the second coronary occlusion than after the first in group I (22.1 ± 15.8 versus 30.4 ± 21.0cm/s,P &lt; 0.05), but it did not change in group II (25.6 ± 13.0 versus 23.5 ± 11.2cm/s NS). Reactive hyperemia was enhanced in patients with ischemic tolerance who showed a reduction in ST elevation in the icECG. These results suggest that observed reactive hyperemia does not necessarily reflect the severity of ischemia.</subfield>
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   <subfield code="a">Springer-Verlag, 1996</subfield>
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   <subfield code="a">Reactive hyperemia</subfield>
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   <subfield code="a">Angioplasty</subfield>
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   <subfield code="a">Ischemia</subfield>
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   <subfield code="a">Preconditioning</subfield>
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   <subfield code="a">Tanaka</subfield>
   <subfield code="D">Takahiro</subfield>
   <subfield code="u">Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, 5-7-1 Fujishirodai, 565, Suita, Osaka, Japan</subfield>
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   <subfield code="a">Nonogi</subfield>
   <subfield code="D">Hiroshi</subfield>
   <subfield code="u">Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, 5-7-1 Fujishirodai, 565, Suita, Osaka, Japan</subfield>
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   <subfield code="a">Miyazaki</subfield>
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   <subfield code="u">Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, 5-7-1 Fujishirodai, 565, Suita, Osaka, Japan</subfield>
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   <subfield code="u">Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, 5-7-1 Fujishirodai, 565, Suita, Osaka, Japan</subfield>
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   <subfield code="a">Itoh</subfield>
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   <subfield code="u">Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, 5-7-1 Fujishirodai, 565, Suita, Osaka, Japan</subfield>
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   <subfield code="a">Daikoku</subfield>
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   <subfield code="u">Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, 5-7-1 Fujishirodai, 565, Suita, Osaka, Japan</subfield>
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   <subfield code="u">Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, 5-7-1 Fujishirodai, 565, Suita, Osaka, Japan</subfield>
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   <subfield code="g">11/5(1996-09-01), 242-247</subfield>
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