Quantitative assessment of coronary stenosis by harmonic power Doppler with a simple pulsing sequence and vasodilator stress in patients
Yuichiro Takagi, MD*,
Koji Ohmori, MD, PhD*,*,
Kazushi Yukiiri, MD, PhD*,
Isao Kondo, MD, PhD*,
Yang Yu, MD, PhD*,
Akira Oshita, MD, PhD*,
Hiroto Takeuchi, MD, PhD*,
Katsufumi Mizushige, MD, PhD, FACC* and
Masakazu Kohno, MD, PhD*
* Second Department of Internal Medicine, Kagawa Medical University, Kagawa, Japan
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Figure 1 Principle of the model. At long pulsing intervals (PIs), complete replenishment of the imaging field (boxes) results in a plateau in contrast intensity (CI) in the frame–CI curve (bottom). After the onset of short PI imaging (from frame no. 0), the microbubble concentration in the imaging field was gradually decreased until a constant level was reached, which can be fit to the decay function. Circles in boxes represent microbubbles; open circles are those to be disrupted during each frame. The arrow in the first box indicates the flow direction, whereas the inverted triangles indicate the advancing fronts of the flow.
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Figure 2 Representative recordings from a normal coronary territory. Opacification in the anterior septum was decreased frame by frame until the fourth frame and was constant thereafter (top row). The magnitude of decay was less during infusion of adenosine triphosphate (ATP) (bottom row) than at baseline. The numbers indicate the frame numbers after the onset of short pulsing interval imaging.
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Figure 3 Representative recordings from a territory of a severely stenosed coronary artery. Opacification in the anterior septum was decreased frame by frame until the eighth frame and was constant thereafter at a relatively higher level (top row). The magnitude of decay was greater during hyperemia by adenosine triphosphate (ATP) (bottom row) than at baseline. The numbers indicate the frame numbers after the onset of short pulsing interval imaging.
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Figure 4 The contrast intensity (CI)–frame number curves from the anterior interventricular septum in the patient shown in Figure 2 (left panel) and the patient in Figure 3 (right panel). The alteration in CI fit well with the decay function both at baseline (solid circles) and during adenosine triphosphate (ATP) infusion (open circles) in both territories. Although the magnitude of decay was less during ATP infusion than at baseline in a normal coronary territory (left), it was greater in a severely stenosed coronary territory (right).
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Figure 5 Plots of the myocardial contrast echocardiography-derived myocardial blood flow velocity (MBFV) index at baseline (open circles) and during hyperemia (solid circles) against quantitative coronary angiography (QCA)-derived percent diameter stenosis. The dotted line denotes the average value at baseline, whereas the solid line indicates the regression line for the data during hyperemia (y = 15.5{1 – Exp(0.019[x – 109.8])}, r = 0.53, p < 0.01). ATP = adenosine triphosphate.
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Figure 6 Plots of the myocardial contrast echocardiography-derived myocardial blood flow velocity (MBFV) reserve against quantitative coronary angiography (QCA)-derived percent diameter stenosis. A significant inverse correlation was noted.
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Figure 7 Correlation of myocardial contrast echocardiography-derived myocardial blood flow velocity (MBFV) reserve with fractional flow reserve (FFR). The MBFV reserve exhibited a good negative correlation with the functional severity of coronary stenosis.
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