Cyclic flow variations(CFVs) is defined as morphological evidence of wide flow velocity variations in the Doppler signals due rapid spontaneous changes showing cyclic reduction and abrupt reperfusion of blood flow velocity seen in the critically stenotic arteries. Since first development of the CFVs model using dog by Folts and Uchida, it has been widely used as exellent experiemental model for study of the Acute ischemic heart disease syndrome including unstable angina. Nowadays it has been well documented that these CFVs are closely associated with temporal platelet aggregation and followed thrombus formation at the stenotic arterial lesion with endothelial or medial injury and subsequent release of various chemical mediators, eg. thromboxan A2 and serotonin. Also the CFVs can be seen in some patients of coronary artery stenosis during underwent PTCA, femoral artery stenosis and carotid or cerebral artery stenosis as well as in animal models. Moreover, CFVs has been thought to be the natural preconditioning in the unstable angina.

We tried to make the CFVs model using left anterior descending coronary artery (LAD) in 6 dogs. Pericardial cradle was made through 5th intercostal thoracotomy. The LAD was isolated carefully and critically stenosed by plastic constrictor and Doppler velocimeter probe was placed under the constrictor. After then intimal and medial layer of the LAD was damaged by a forcep. After appearing of CFVs, we observed and recorded for an hour. Myeloperoxide(MPO) activity in the ischemic and non-ischemic area of the myocardium were studied and compared after sacrifice.

CFVs was found in all 6 dogs within an hour. The mean frequency of the CFVs was 9.8±4.45 times/hour. The mean coronary blood flow was 5.7±2.7 ml/min. And MPO activity was 1.47±0.5 units/g tissue in the ischemic myocardium and 0.49±0.27 units/g tissue in the non-ischemic area with statistical significance(p<0.005).

CFVs model using various animal models and arterial sites can widely provide usefulness to document pathophysiology and pharmacologic mechanism in human acute ischemic heart disease syndromes.