TY - JOUR
T1 - Types of change in coronary stenosis severity and their relative importance in overall progression and regression of coronary disease. Observations from the FATS trial
AU - Brown, B. G.
AU - Hillger, B. L.
AU - Zhao, X. Q.
AU - Poulin, D.
AU - Albers, J. J.
AU - Kwiterovich, P. O.
AU - Ross, R.
AU - Smirnov, V. N.
AU - Buchwald, H.
PY - 1994/1/1
Y1 - 1994/1/1
N2 - Background and Methods. Quantitative angiographic coronary intervention trials typically average measurements of coronary stenosis change in order to make a single composite estimate of mean change per patient. This obscures the relative importance of certain mechanisms of progression or regression. We have examined the contributions of, and the effect of therapy on, five different types of lesion change as observed in 1034 proximal coronary lesions and 1316 total lesions, measured at baseline and 2.5 years later in the Familial Atherosclerosis Treatment Study (FATS). Results. On average, proximal lesions progressed by 2.10 percent stenosis (%S) during treatment with a modest conventional (CONV) lipid-lowering program, and regressed by -0.85%S with niacin plus colestipol (N + C) and by -0.75%S with lovastatin plus colestipol (L + C) (p = 0.003). Among the CONV patients, the mean 2.10%S change was the sum of (1) +0.24%S due to progression of two lesions to total occlusion, (2) 0.00%S due to regression (recanalization) of total occlusions, (3) +0.11%S due to worsening of initially 'normal' segments, (4) -0.01%S due to late regression of previously dilated (PTCA) lesions and (5) 1.76%S from incremental change in nonoccluded lesions. Mechanisms 1 and 3 were unaffected by intensive therapy. Mechanism 5 was the principal mediator of the therapeutic benefit; significant but less striking benefits were mediated through mechanisms 2 and 4. Baseline lesion severity is an important determinant of the frequency of progression and regression, and of therapeutic benefit. Conclusions. Incremental progression/regression, total occlusion or its recanalization, new lesion formation, and regression of PTCA restenosis may contribute to mean stenosis change in native vessels in patients with coronary disease. Three of these mechanisms are favorably altered by intensive lipid-lowering therapy in FATS. Outcome also depends strongly on the mix of stenosis severity among lesions at baseline. These findings have important implications for the design and interpretation of angiographic trials.
AB - Background and Methods. Quantitative angiographic coronary intervention trials typically average measurements of coronary stenosis change in order to make a single composite estimate of mean change per patient. This obscures the relative importance of certain mechanisms of progression or regression. We have examined the contributions of, and the effect of therapy on, five different types of lesion change as observed in 1034 proximal coronary lesions and 1316 total lesions, measured at baseline and 2.5 years later in the Familial Atherosclerosis Treatment Study (FATS). Results. On average, proximal lesions progressed by 2.10 percent stenosis (%S) during treatment with a modest conventional (CONV) lipid-lowering program, and regressed by -0.85%S with niacin plus colestipol (N + C) and by -0.75%S with lovastatin plus colestipol (L + C) (p = 0.003). Among the CONV patients, the mean 2.10%S change was the sum of (1) +0.24%S due to progression of two lesions to total occlusion, (2) 0.00%S due to regression (recanalization) of total occlusions, (3) +0.11%S due to worsening of initially 'normal' segments, (4) -0.01%S due to late regression of previously dilated (PTCA) lesions and (5) 1.76%S from incremental change in nonoccluded lesions. Mechanisms 1 and 3 were unaffected by intensive therapy. Mechanism 5 was the principal mediator of the therapeutic benefit; significant but less striking benefits were mediated through mechanisms 2 and 4. Baseline lesion severity is an important determinant of the frequency of progression and regression, and of therapeutic benefit. Conclusions. Incremental progression/regression, total occlusion or its recanalization, new lesion formation, and regression of PTCA restenosis may contribute to mean stenosis change in native vessels in patients with coronary disease. Three of these mechanisms are favorably altered by intensive lipid-lowering therapy in FATS. Outcome also depends strongly on the mix of stenosis severity among lesions at baseline. These findings have important implications for the design and interpretation of angiographic trials.
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U2 - 10.1111/j.1749-6632.1994.tb17337.x
DO - 10.1111/j.1749-6632.1994.tb17337.x
M3 - Article
C2 - 7695184
AN - SCOPUS:0028913839
SN - 0077-8923
VL - 748
SP - 407
EP - 417
JO - Annals of the New York Academy of Sciences
JF - Annals of the New York Academy of Sciences
ER -