title: Differential progression of complex and smooth stenoses within the same coronary tree in men with stable coronary artery disease.
abstract: OBJECTIVE
  We sought to compare the evolution of complex and smooth stenoses within the same coronary tree in patients with stable coronary artery disease.
  
  
  BACKGROUND
  Progression of coronary stenosis has prognostic significance and may be influenced by local and systemic factors. Stenosis morphology is a determinant of disease progression, but no previous study has systematically assessed progression of complex and smooth stenoses within the same patient.
  
  
  METHODS
  We studied 50 men with stable angina who 1) had one complex coronary stenosis and one smooth stenosis in different noninfarct-related coronary vessels at initial coronary angiography, and 2) had a second angiogram after a median interval of 9 months (range 3 to 24). Patients with lesions > or = 10 mm long, at a major branching point or with > 85% diameter reduction were not included. Coronary lesions were measured quantitatively from comparable end-diastolic frames. Stenosis morphology was determined qualitatively by two independent observers.
  
  
  RESULTS
  All patients remained in stable condition during follow-up. Progression, defined as an increase in diameter stenosis by > or = 15% was seen in only eight complex stenosis (16%) but in no smooth lesions (p < 0.01). The severity of complex stenoses changed more than that of corresponding smooth stenoses (mean +/- 1 SD 5.8 +/- 13% vs. -0.06 +/- 6%, p < 0.01). On average, the annual rate of growth was 11.4 +/- 28% and 1.5 +/- 14% for complex and smooth lesions, respectively (p < 0.01).
  
  
  CONCLUSIONS
  Few coronary stenoses progress rapidly in stable angina. Complex and smooth coronary stenoses progress at different rates within the same coronary tree. complex stenosis morphology itself is an important determinant of progression of stenosis in patients with apparently clinically stable coronary artery disease.
authors.affiliation: Department of Cardiological Sciences, St. George's Hospital Medical School, London, England, United Kingdom.
authors.forename: M R
authors.initials: MR
authors.lastname: Chester
authors.forename: L
authors.initials: L
authors.lastname: Chen
authors.forename: D
authors.initials: D
authors.lastname: Tousoulis
authors.forename: J
authors.initials: J
authors.lastname: Poloniecki
authors.forename: J C
authors.initials: JC
authors.lastname: Kaski
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000000981:diagnostic imaging; D003251:Constriction, Pathologic / Q000097:blood / Q000000981:diagnostic imaging / Q000473:pathology; D017023:Coronary Angiography; D003327:Coronary Disease / Q000097:blood / Q000000981:diagnostic imaging* / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology*; D005500:Follow-Up Studies; D006801:Humans; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D011379:Prognosis
chemical_list: D008055:Lipids