Strain Measurements During Adenosine Triphosphate Infusion Before and After Percutaneous Coronary Intervention

被引:3
|
作者
Hosaka, Motoko
Takagi, Atsushi [1 ]
Takagi, Tsutomu [2 ]
Ashihara, Kyomi
Hagiwara, Nobuhisa
机构
[1] Tokyo Womens Med Univ, Shinjuku Ku, Tokyo 1628666, Japan
[2] Takagi Cardiol Clin, Kyoto, Japan
关键词
Adenosine; Coronary artery disease; Tissue Doppler imaging; ACUTELY ISCHEMIC-MYOCARDIUM; PHARMACOLOGICAL STRESS ECHOCARDIOGRAPHY; VENTRICULAR DELAYED RELAXATION; ARTERY-DISEASE; DOPPLER-ECHOCARDIOGRAPHY; COLOR KINESIS; TISSUE DOPPLER; WALL-MOTION; VELOCITY; ANGIOPLASTY;
D O I
10.1253/circj.CJ-09-0972
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: In regional myocardial ischemia, contractile delay develops, which can be assessed by measuring time to peak strain (TPS) on tissue Doppler imaging. The aims of the present study were to clarify the usefulness of TPS measurements during adenosine triphosphate (ATP) stress in assessing myocardial ischemia and to evaluate whether prolongation of TPS disappears immediately after percutaneous coronary intervention (PCI) or not. Methods and Results: A total of 26 patients underwent strain measurements before and after PCI. Corrected TPS for heart rate (TPSc) in target regions and in control regions were measured both at baseline and during ATP infusion. TPSc ratio was calculated as a ratio of TPSc during ATP stress to TPSc at baseline. TPSc in the target region significantly increased during ATP infusion before PCI, which was significantly longer than hyperemic TPSc in control regions. Accordingly, TPSc ratio in the target regions before PCI was significantly greater than that in control regions (1.22 +/- 0.17 vs 0.96 +/- 0.09, respectively, P<0.0001). Following PCI, the TPSc ratio in the target regions significantly decreased to 0.98 +/- 0.05 (P<0.0001). Receiver operating characteristic curve analysis provided a cutoff of 1.04 in TPSc ratio for detecting myocardial ischemia with a sensitivity of 93% and specificity of 93%. Conclusions: TPS measurements during ATP stress differentiated target from control myocardium before PCI. The prolongation of TPSc disappeared immediately after PCI. (Circ J 2010; 74: 1600-1608)
引用
收藏
页码:1600 / 1608
页数:9
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