[The classification of coronary lesion from Society for Cardiac Angiography and Intervention predicts better results of coronary angioplasty than the one from American College of Cardiology/American Heart Association Coronary Disease]. / La clasificación de lesiones coronarias de la Society for Cardiac Angiography and Interventions predice mejor el éxito de la angioplastia coronaria que la del American College of Cardiology/American Heart Association.

BACKGROUND: The classification of coronary lesion complexity, using the American College of Cardiology/American Heart Association (ACC/AHA) is a predictor of balloon angioplasty success. Stents have improved results even in complex lesions. AIM: To compare the ACC/AHA and the new Society for Cardiac Angiography (SCA&I) coronary lesion scores as predictors of angioplasty success. PATIENTS AND METHODS: Ali consecutive angioplasty procedures (n = 346, 456 lesions, 47% stents) were prospectively analyzed from August 1996 to March 1999. Coronary lesions were classified using the ACC/AHA and SCA&I scores. Angiographic success was assessed and its multivariate predictors determined with logistic regression analysis. RESULTS: According to the ACC/AHA score, angiographic success was 97, 92.7, 93.3, and 82.3% in A, Bl, B2 and C lesions respectively (p = 0.013). There only were significant differences in success between C and A, Bl or B2 lesions. According to the SCA&I score success was achieved in 97.3, 97.9, 75.8 and 33.3% in nonCP, CP, nonCO and CO lesions respectively (P < 0.001). With the SCA&I score statistically significant differences in angiographic success were found for all lesion score comparisons, except between nonCP and CP lesions. No other variables had predictive value for angiographic success. CONCLUSIONS: Coronary angioplasty angiographic success is better predicted by the new SCA&l lesion score than with the ACC/AHA lesion classification in a group of patients with frequent use of stents.

Effect of rotational atherectomy in noncalcified atherosclerotic plaque: a volumetric intravascular ultrasound study.

OBJECTIVES: This study used pre-rotational and post-rotational atherectomy volumetric intravascular ultrasound analysis to determine whether rotational atherectomy causes ablation of non-calcified atherosclerotic plaque. BACKGROUND: Rotational atherectomy is currently the preferred treatment for heavily calcified coronary lesions. However, the mechanism of lumen enlargement in noncalcified lesions has not been studied in detail. Intravascular ultrasound allows detailed, cross-sectional imaging of the coronary arteries in vivo. The normal coronary artery wall, the major components of the atherosclerotic plaque and the quantitative changes in vessel, lumen and plaque cross-sectional areas and volumes that occur as a result of the atherosclerotic disease process and during transcatheter therapy can be studied in a manner otherwise not possible. METHODS: Eighteen noncalcified native vessel lesions in 18 patients were imaged before and after rotational atherectomy using intravascular ultrasound systems incorporating motorized transducer pullback through a stationary imaging sheath. External elastic membrane, lumen and plaque plus media cross-sectional areas were measured every 1 mm of lesion length (for a total of 10 image slices), and external elastic membrane, lumen and plaque plus media volumes were calculated using Simpson's rule. RESULTS: After rotational atherectomy, the minimal lumen cross-sectional area increased from 1.37 +/- 0.50 to 2.99 +/- 0.60 mm2 (mean value +/- 1 SD, p < 0.0001). Lumen volume increased from 23.2 +/- 9.0 to 38.0 +/- 8.0 mm3 (p < 0.0001) as a result of a decrease in plaque plus media volume (from 102.2 +/- 50.9 to 85.8 +/- 47.7 mm3, p < 0.0001), with no change in total vessel (external elastic membrane) volume (125.3 +/- 54.2 to 123.8 +/- 52.9 mm3, p = 0.119). CONCLUSIONS: Rotational atherectomy effectively ablates noncalcified plaque in non-calcium-containing lesions.

Patterns and mechanisms of in-stent restenosis. A serial intravascular ultrasound study.

BACKGROUND: Studies have suggested that restenosis within Palmaz-Schatz stents results from neointimal hyperplasia or chronic stent recoil and occurs more frequently at the articulation. METHODS AND RESULTS: Serial intravascular ultrasound (IVUS) was performed after intervention and at follow-up in 142 stents in 115 lesions. IVUS measurements (external elastic membrane [EEM], stent, and lumen cross-sectional areas [CSAs] and diameters) were performed, and plaque CSA (EEM lumen in reference segments and stent lumen in stented segments), late lumen loss (delta lumen), remodeling (delta EEM in reference segments and delta stent in stented segments), and tissue growth (delta plaque) were calculated. After intervention, the lumen tended to be smallest at the articulation because of tissue prolapse. At follow-up, tissue growth was uniformly distributed throughout the stent; the tendency for greater neointimal tissue accumulation at the central articulation reached statistical significance only when normalized for the smaller postintervention lumen CSA. In stented segments, late lumen area loss correlated strongly with tissue growth but only weakly with remodeling. Stents affected adjacent vessel segments; remodeling progressively increased and tissue growth progressively decreased at distances from the edge of the stent. These findings were similar in native arteries and saphenous vein grafts and in lesions treated with one or two stents. There was no difference in the postintervention or follow-up lumen (at the junction of the two stents) when overlapped were compared with nonoverlapped stents. CONCLUSIONS: Late lumen loss and in-stent restenosis were the result of neointimal tissue proliferation, which tended to be uniformly distributed over the length of the stent.

Regression of left ventricular hypertrophy in experimental renovascular hypertension: diastolic dysfunction depends more on myocardial collagen than it does on myocardial mass.

OBJECTIVE: To evaluate regression of experimental left ventricular hypertrophy (LVH) in terms of its effects both on myocardial collagen levels and on diastolic stiffness. METHODS: Two-kidney, one clip Goldblatt hypertensive rats were left untreated for 4 weeks (HT4W, n = 12) or 12 weeks (HT12W, n = 11) and compared with rats the treatment of which was started after 4 weeks of hypertension with 30 mg/kg per day losartan for 8 weeks (LOS, n = 12), or 50 mg/l enalapril for 8 weeks (ENA, n = 11). A group of sham-operated rats served as controls (SHAM, n = 9). RESULTS: The blood pressure of the rats increased significantly and LVH developed both after 4 and after 12 weeks of hypertension. Treatment with losartan or enalapril significantly decreased blood pressure and induced complete regression of LVH. Myocardial hydroxyproline concentrations increased in groups HT4W and HT12W (530 +/- 153 and 581 +/- 111 micrograms/g, respectively) relative to that in the SHAM group (421 +/- 22 micrograms/g). None of the treatments induced regression of increased myocardial collagen levels. The slopes of the end-diastolic stress-strain relationships in the isolated beating hearts were significantly higher in HT4W, HT12W and in both treated groups compared with those in the SHAM group, indicating increased diastolic myocardial stiffness. CONCLUSION: Losartan and enalapril treatments decreased blood pressure and induced complete regression of LVH in this model of renovascular hypertension. In contrast, none of the treatments induced regression of increased myocardial collagen levels or reduced the abnormal left ventricular diastolic stiffness. These data suggest that diastolic dysfunction depends more on increased myocardial collagen levels than it does on myocardial mass in this model of pathological LVH.

Mechanisms and immediate and long-term results of adjunct directional coronary atherectomy after rotational atherectomy.

OBJECTIVES: The purpose of this study was to confirm the mechanisms and the immediate and long-term results of rotational atherectomy and adjunct directional coronary atherectomy. BACKGROUND: Rotational atherectomy is best suited for treating calcific stenoses, but the ability of rotational atherectomy alone to optimize lumen dimensions in large vessels is limited; this is only partly improved by adjunct balloon angioplasty. METHODS: We treated 165 lesions in 163 patients by use of rotational atherectomy and adjunct directional coronary atherectomy. Quantitative angiography and intravascular ultrasound were used for lesion analysis. A matched comparison with 208 lesions treated with rotational atherectomy and adjunct coronary angioplasty was performed. Patients were then followed up for at least 9 months, and target-lesion revascularization was assessed. RESULTS: In the 61 lesions imaged sequentially, lumen area increased from 1.7 +/- 0.8 (mean +/- 1 SD) to 3.9 +/- 1.1 mm(2) after rotational atherectomy, owing to a decrease in plaque plus media area from 16.8 +/- 5.0 to 15.2 +/- 5.2 mm(2) (both p < 0.0001). After adjunct directional coronary atherectomy, lumen area increased even more to 6.7 +/- 2.0 mm(2) (vs. 5.1 +/- 1.4 mm(2) after adjunct coronary angioplasty, p < 0.0001) as a result of both vessel expansion (18.8 +/ 5.3 to 20.8 +/- 5.7 mm(2)) and additional plaque removal (to 14.1 +/- 5.0 mm(2), all p < 0.0001). The total arcs of calcium decreased from 207 +/- 107 degrees to 166 +/- 93 degrees after rotational atherectomy and to 145 +/- 87 degrees after directional coronary atherectomy. Overall, procedural success was 96%, and final diameter stenosis was 15 +/- 17%. Target-lesion revascularization was 23%. The only independent predictor of target-lesion revascularization was a larger overall atherectomy index (84% vs. 59%, p = 0.048). CONCLUSIONS: There is a synergistic relationship between rotational atherectomy and directional coronary atherectomy in the treatment of calcific lesions. The immediate results show a high procedural success--lumen dimensions were larger and late target-lesion revascularization was lower in lesions treated with rotational atherectomy and directional coronary atherectomy than in those treated with rotational atherectomy and adjunct balloon angioplasty.

Small stent size and intimal hyperplasia contribute to restenosis: a volumetric intravascular ultrasound analysis.

OBJECTIVES: The purpose of this study was to use volumetric intravascular ultrasound analysis of Palmaz-Schatz stents to assess the in-stent restenotic process. BACKGROUND: By reducing lesion elastic recoil and chronic arterial remodeling, stents improve the long-term results of coronary angioplasty. However, stents are prone to the development of neointimal hyperplasia. Angiographic studies of stent restenosis have suggested that these hyperplastic responses are the cause of in-stent restenosis; however, it is difficult to visualize the radiolucent Palmaz-Schatz stent by angiography. Intravascular ultrasound provides detailed cross-sectional imaging of the coronary arteries, especially the intense metallic reflection of endovascular stents. METHODS: Forty-four patients with 60 Palmaz-Schatz stents underwent intravascular ultrasound imaging at follow-up ([mean +/- SD] 8.8 +/- 7.2 months after implantation). Thirty-four stents were placed in saphenous vein grafts and 26 in native coronary arteries; 30 were placed in restenotic lesions. Intravascular ultrasound with automatic transducer pullback at 0.5 mm/s allowed measurement of stent, lumen and intimal hyperplasia cross-sectional areas at 1-mm axial increments within the stents. Using Simpson's rule, stent, lumen and intimal hyperplasia volumes were calculated. Patterns of in-stent restenosis were then identified. RESULTS: Restenotic stents had smaller stent volumes (120 +/- 41 vs. 147 +/- 43 mm3, p = 0.016) and lumen volumes (62 +/- 28 vs. 118 +/- 42 mm3, p < 0.0001) but larger intimal hyperplasia volumes (58 +/- 36 vs. 29 +/- 18 mm3, p < 0.001) than nonrestenotic stents. A focal restenosis pattern was more common (20 [77%] of 26) than a diffuse restenosis pattern (6 [23%] of 26). Stents with focal restenosis and stents with diffuse restenosis had equally small stent volumes (120 +/- 44 vs. 120 +/- 31 mm3, respectively, p = NS); however, stents with diffuse restenosis had larger intimal hyperplasia volumes (84 +/- 30 vs. 50 +/- 34 mm3, p < 0.05). Focal restenosis was most commonly located at the central articulation (45%); the location of focal restenosis was related to the focal accumulation of neointimal tissue. CONCLUSIONS: Stent volume and magnitude and distribution of intimal hyperplasia are important in the development of in-stent restenosis. Stent volume was smaller and intimal hyperplasia volume greater in restenotic stents. Stent restenosis is more commonly focal in nature and located at the central articulation.