Quantitative Angiographic Studies Research Articles

Intimal hyperplasia thickness at follow-up is independent of stent size: A serial intravascular ultrasound study

The purpose of this study was to determine whether the thickness of the intimal hyperplasia (IH) layer that accumulates within Palmaz-Schatz stents is dependent on stent size. Intravascular ultrasound (IVUS) and quantitative angiographic (QCA) studies were performed after stent implantation and at follow-up (5.4 ± 3.8 months) in 161 patients with 177 lesions treated with 221 Palmaz-Schatz stents. Stent and lumen cross-sectional area (CSA) were measured. IH CSA and thickness at follow-up were calculated and compared with stent CSA and circumference. Maximum IH CSA and thickness were measured at the smallest follow-up lumen CSA; mean IH CSA and thickness was averaged over the length of the stent. Maximum IH CSA measured 4.8 ± 2.4 mm 2, and mean IH CSA measured 2.8 ± 2.2 mm 2. Maximum IH thickness (at the smallest follow-up lumen CSA) measured 0.60 ± 0.36 mm, and mean IH thickness (over the length of the stent) measured 0.30 ±0.19 mm. There was a weak, but significant correlation between mean and maximum IH CSA versus stent CSA (r = 0.215, p < 0.0001 and r = 0.355, p < 0.0001, respectively). However, there was no correlation between mean or maximum IH thickness versus stent CSA (r = 0.018, p = 0.643 and r = 0.056, p = 0.463, respectively) or stent circumference (r = 0.002, p = 0.956 and r = 0.069, p = 0.361, respectively). IH thickness was found to be independent of the stent size. This explains the known higher frequency of restenosis in smaller stents compared with larger stents.

701-5 Endovascular Stents Reduce Restenosis by Eliminating Geometric Arterial Remodeling: A Serial Intravascular Ultrasound Study

Previous studies have shown that (1) stents reduce restenosis, (2) stents do not recoil, and (3) geometric remodeling may be an important contributing factor in restenosis. Therefore, to understand the mechanisms by which stents reduce restenosis, we analyzed serial (post-intervention and follow-up @ 5.0 ± 2.9 months) intravascular ultrasound and quantitative angiographic studies in 33 stented lesions and compared the results to 135 nonstented lesions treated with various devices (30 PTCA, 57 directional and 26 rotational atherectomy, and 22 excimer laser angioplasty). Post-intervention and followup external elastic membrane (EEM), stent, and lumen areas were used to calculate (1) plaque area, (2) late lumen loss (Δ lumen area), (3) geometric remodeling (Δ EEM area or Δ stent area in stented lesions and Δ EEM area in nonstented lesions), and (4) tissue growth Δ (stent-lumen) area in stented lesions and Δ plaque area in nonstented lesions. Stent Non-stent p Post-intervention EEM area (mm 2 ) 29.3 ± 118 204 ± 65 &lt; 0.0001 Lumen area (mm 2 ) 8.5 ± 39 6.1 ± 2.4 &lt; 0.0001 Plaque area (mm 2 ) 20.9 ± 9.3 14.3 ± 5.7 &lt; 0.0001 Angiographic % diameter stenosis 9 ± 18 19 ± 14 0.0011 Follow-up EEM area (mm 2 ) 27.7 ± 9.5 187 ± 6.0 &lt; 0.0001 Lumen area (mm 2 ) 6.5 ± 4.4 35 ± 3.0 &lt; 0.0001 Plaque area (mm 2 ) 22.0 ± 8.0 15.2 ± 5.5 &lt; 0.0001 Angiographic % diameter stenosis 36 ± 18 51 ± 26 0.005 Restenosis # (%) 8(23%) 77(57%) 0.0017 Late lumen loss (mm 2 ) 2.4 ± 2.6 2.6 ± 2.7 NS Remodeling (mm 2 ) 02 ± 13 1.7 ± 2.9 0.0061 Tissue growth (mm 2 ) 2.2 ± 2.4 1.0 ± 2.3 0.0076 Geometric remodeling is less (0.2 ± 1.3 vs 1.7 ± 2.9 mm 2 ) and tissue growth is greater (2.2 ± 2.4 vs 1.0 ± 2.3 mm 2 ) in stented lesions than in nonstented lesions. Stents reduce restenosis by achieving a better primary (post-procedural) result and by eliminating geometric remodeling. The elimination of geometric remodeling offsets a stent-related increase in plaque mass (tissue growth or neointimal hyperplasia) to prevent restenosis.

Absence of detectable delayed elastic recoil 24 hours after percutaneous transluminal coronary angioplasty

During percutaneous transluminal coronary angioplasty (PTCA), part of the constraints developed by the inflated balloon beyond the value needed for splitting or fracturing the atherosclerotic plaque are absorbed by the elastic components of the arterial wall to be restored after balloon deflation. The return of these elastic components to their unstrained dimensions (elastic recoil) results in the loss of a significant part of the theoretical maximal gain in lumen diameter achieved during balloon inflation. Although the contribution of elastic recoil to the residual stenosis of coronary segments immediately after PTCA appears well established, 1–3 controversy remains regarding the possible contribution of some progressive or delayed recoil to the restenosis observed in 17 to 47% of patients several weeks or months after PTCA. 4 Morphologic studies of restenosis sites after PTCA have suggested that chronic recoil could be a mechanism of late luminal narrowing, independent of intimai fibrous proliferation. 4–5 However, quantitative angiographic studies in small populations did not show a further reduction in minimal lumen diameter of dilated coronary segments during the first 24 hours after successful PTCA. 1,2 The present study was designed to evaluate in a large group of patients whether gradual or delayed elastic recoil could result in a further luminal narrowing during the first 24 hours after successful PTCA. Alt angiographic data were obtained under standardized conditions, including local infusion of nitrates, to minimize the influence of vasomotor tone.

Elimination of variable vasomotor tone in studies with repeated quantitative coronary angiography

In quantitative coronary angiographic studies, unintentional changes of coronary vasomotor tone may have a significant influence on the coronary artery diameters, thereby increasing the variability in the measurements. To obtain objective data on these measurement variabilities, two protocols were designed to assess the influences of ionic and nonionic radiographic contrast media on the mean diameters of angiographically normal coronary arteries. The vessel sizes were determined with the CAAS using automated edge detection techniques. In 21 patients (study no. I), coronary angiograms were taken in identical angiographic projections before (control), and immediately following several (at average 7) subsequent diagnostic dye injections administered over a period of about 7 min. The ionic contrast agent diatrizoate 76% induced a coronary dilation of 19 +/- 7% (mean +/- s.d., p less than 0.001; n = 10); the nonionic agent iopromide 370 increased the coronary artery diameters by only 6 +/- 4% (p less than 0.01; n = 11). In another 11 patients (study no. II) coronary angiograms were obtained using the nonionic contrast medium iopamidol 300 at 5, 8, 10 and 11 min after the control acquisition; this protocol was repeated in the same patients with diatrizoate 76%. With iopamidol, coronary diameter changes were not significant at any time; with diatrizoate, however, coronary dilation was measured at 10 min (2 +/- 2%; p less than 0.01) and at 11 min (10 +/- 3%; p less than 0.001). In a third study it was tested, whether standardization of coronary vasomotor tone (e.g. in coronary angiographic follow-up studies) is possible by the induction of a reproducible maximum coronary dilation with nitrocompounds. In 12 patients, the mean diameters of angiographically normal coronary segments were analyzed before and at various times after i.v. administration (over 4 min) of 0.025 mg SIN-1/kg bodyweight. Coronary dilation was maximal at 10 or 15 min after the onset of the SIN-1-infusion (29 +/- 5%; p less than 0.001). 0.8 mg nitroglycerin given s.l. at 15 min did not further dilate the coronary arteries (28 +/- 7%). One hour after SIN-1, coronary dilation still amounted to an average of 24 +/- 8% (p less than 0.001) and became 'maximal' again, when 0.8 mg nitroglycerin was again administered sublingually (28 +/- 8%; p less than 0.001). In conclusion, short-term variability of coronary vasomotor tone induced by ionic radiographic contrast media can be eliminated by the use of nonionic contrast agents and observation of injection intervals of at least 2 min. In quantitative coronary angiographic follow-up studies, as well as during acute interventions (e.g., PTCA), identical baseline vasomotor tone can be achieved by induction of the maximal coronary dilation using nitrocompounds.

A Review of Calcium Antagonists and Atherosclerosis

Many detailed studies have demonstrated that calcium antagonists can suppress development of diet-induced atherosclerosis in the thoracic aorta of animals. A number of possible mechanisms have been proposed based on in vitro work, but the exact mechanism remains unclear. Alteration of serum lipid levels and blood pressure does not appear to be the common pathway. Differing effects between calcium antagonists of different classes indicate that the voltage-dependent calcium channel-blocking action common to all calcium antagonists is not the sole mechanism. Preliminary results of several major quantitative angiographic studies in human coronary artery disease have recently become available and indicate that calcium antagonists are able to retard the progression of existing lesions in humans also. There is also evidence that calcium antagonists may prevent the development of new lesions and, in some cases, induce lesion regression. Longer follow-up and further trials are required to assess the appropriateness of widespread clinical application of these agents in coronary artery disease, to determine the optimal timing for their introduction, and to define their mechanism of action in influencing the natural history of atherosclerosis.

How critical is frame selection in quantitative coronary angiographic studies?

To analyse quantitatively a coronary arterial segment from a cineangiogram, an end-diastolic or neighbouring frame is usually selected. However, different cardiologists may select other (although usually neighbouring) frames, even when the same selection criteria are followed. It is also possible that the frames are selected from different cardiac cycles. In this study the effects of such phase shifts on the reproducibility of the quantitative measurements were studied. In a total of 38 consecutive patient films obtained at a filmspeed of 25 frames s-1, the frame phi demonstrating the severity of a lesion optimally as judged by a senior cardiologist, the three preceding frames, the three following frames and one frame exactly one cycle prior to or following frame phi were selected; frame phi was always chosen in the end-diastolic phase of the cardiac cycle. In each film one coronary arterial segment with a focal lesion was analysed quantitatively in these total of 8 frames with the Cardiovascular Angiography Analysis System (CAAS). No significant differences were found in the mean difference and the standard deviations of the differences (variabilities) in the obstruction diameter, interpolated reference diameter, percent diameter stenosis, extent of the obstruction and area of atherosclerotic plaque obtained in the various frames with respect to frame phi. Therefore, it may be concluded that the selection of a cineframe for quantitative analysis in the end-diastolic phase of the cardiac cycle is not very critical.(ABSTRACT TRUNCATED AT 250 WORDS)