Preservation of myocardial function during ischemia with intracoronary perfluoroocytlbromide (Oxygent).

UNLABELLED: The effects of intracoronary infusion (24 ml/min) of oxygenated perfluoroocytlbromide (PFOB) or autologous blood on regional myocardial function and hemodynamics were studied during a 2 min perfused occlusion in nine open chest dogs to determine if a PFOB infusion could prevent the myocardial dysfunction observed during the balloon occlusion of percutaneous transluminal coronary angioplasty (PTCA). Regional myocardial function was measured with sonomicrometers in the ischemic and non-ischemic zone to determine segment length and percent of systolic shortening (% delta L). Without infusion, the ischemic zone in each animal developed akinesis during a 20 sec coronary occlusion. Each animal underwent a 2 min infusion of blood and PFOB at 24 ml/min. During the 2 min perfused occlusion, the blood ischemic zone % delta L of 14.4 +/- 3.1 versus a PFOB % delta L of 23.4 +/- 2.9. % delta L of blood and PFOB were not as significantly different from control (P less than .05 PFOB vs. blood). The bromine ion in PFOB results in a radiodense compound. Adequate images of the canine left ventricle and coronaries were obtained using DSA. CONCLUSION: (1) PFOB infusion maintains normal myocardial function during perfused coronary inclusion. (2) PFOB may be used as an oxygen carrying contrast agent to obtain DSA images.

Quantification of absolute luminal diameter by computer-analyzed digital subtraction angiography: an assessment in human coronary arteries.

Determination of absolute lumen diameters has been shown to be useful in predicting the functional importance of a coronary stenosis. In this study, both single-plane and orthogonal biplane digital subtraction angiograms were obtained in human cadaver coronary arteries. A single absolute diameter was calculated at the site of greatest narrowing in 20 segments by two automated computerized algorithms. Minimum and maximum diameters at the site of the stenosis were measured from pathologic sections prepared after pressure fixation. Method 1, which determines the edges by means of the first derivative of the videodensity curve, derived absolute diameters that fell between the pathologic minimum and maximum in 10 of 20 segments. Method 2, which determines the edges by an average of the first and second derivatives of the videodensity change, derived absolute diameters that fell between the pathologic minimum and maximum diameters in 15 of 20 segments. Method 1 correlated well with the maximum pathologic diameter (r = .76) and less well with the minrmum pathologic diameter (r = .67). Method 2 correlated very well with the maximum pathologic diameter (r = .79) and also correlated well with the minimum pathologic diameter (r = .74). As would be expected, the computerized algorithms tended to overestimate the minimum pathologic diameter and to underestimate the maximum pathologic diameter. In six segments, two orthogonal views were analyzed; no further accuracy was discernible over single-plane determinations. Thus quantitative coronary angiography by digital subtraction angiography is sufficiently accurate to be of use in the measurement of the severity of a coronary stenosis.

Assessment of coronary artery stenoses by digital subtraction angiography: a pathoanatomic validation.

Automated computer assessment of coronary stenoses from digital subtraction angiographic images comparing geometric and videodensitometric algorithms was performed. Digital subtraction angiograms were acquired on a 512 X 512 X 8 bit pixel matrix at 8 frames/second. Fifteen segments from nine human cadaver coronary arteries, with lesions ranging from 0% to 97%, were analyzed. Hand injections of radiopaque dye were made during the pulsatile infusion of saline solution at physiologic pressures and flows. Individual frames best demonstrating a lesion were digitally magnified and the stenosis was measured; the operator identified only the segment of interest. The artery was then injected with a rapidly hardening gel during the same rate of infusion as that used during image acquisition. Histologic sections were cut at 2 mm intervals after fixation and elastic stains applied. Photographs of the section comparable to the site determined from the angiogram were taken, and hand planimetry by a blinded investigator was performed. There was an excellent correlation between histopathology and videodensitometry (r = 0.93; p less than 0.0001). The two geometric algorithms studied also had very good correlations (r = 0.90 and 0.84) with pathology. Two experienced angiographers, despite excellent agreement with each other, had lower correlations with pathology than any of the three computer algorithms studied (r = 0.79 and 0.83, respectively), although this difference did not attain statistical significance. This in vitro model simulating in vivo conditions validates the use of automated videodensitometric and geometric computer algorithms to interpret coronary angiography and assess severity of stenosis.

Videodensitometric quantitation of aortic regurgitation by digital subtraction aortography using a computer-based method analyzing time-density curves.

To assess the clinical role of computer analysis of time-density curves in the evaluation of aortic regurgitation (AR), digital subtraction aortography (DSA) and cineaortography were performed sequentially in 17 patients with varying degrees of AR (1+ to 4+) and in 4 control patients. DSA was performed at a rate of 30 frames/s on a 512 X 512 X 8 bit pixel matrix using the same total volume and injection rate, but with half the amount of contrast agent as standard cineaortography. A 30 X 30 pixel area of interest was identified in the aorta above the valve plane and in the left ventricle where the AR stream was seen. The density of both areas of interest and the ratio of left ventricular/aortic area of interest density was calculated in each frame and then plotted vs time. The ratio at the end of injection (LVd/Aod) had an excellent correlation with cineaortography (chi 2 = 19, p less than 0.001), ranging from 0 to 0.2 in patients with no AR, 0.2 to 0.5 in those with 1+ AR, 0.5 to 0.7 in those with 2+ AR, 0.7 to 0.9 in those with 3+ AR and more than 0.9 in those with 4+ AR. Thus, quantitative assessment of AR by computer analysis of time-density curves derived from DSA is a new and objective technique with significant clinical potential.