Coronary artery compliance and adaptive vessel remodelling in patients with stable and unstable coronary artery disease

Abstract

Objective-To test the hypothesis that patients with unstable coronary syndromes show accentuated compensatory vessel enlargement compared with patients with stable angina, and that this may in part be related to increased coronary artery distensibility. Design and patients-In 23 patients with unstable coronary syndromes (10 with non-Q wave myocardial infarction and 13 with unstable angina), the culprit lesion was investigated by intravascular ultrasound before intervention. The vessel cross sectional area (VA), lumen area (LA), and plaque area (VA minus LA) were measured at end diastole and end systole at the lesion site and at the proximal and distal reference segments. Similar measurements were made in 23 patients with stable angina admitted during the same period and matched for age, sex, and target vessel. Calculations were made of remodelling index (VA at lesion site ÷ VA at reference site), distensibility index ([( A/A)/ P] × 10 3 , where A is the luminal area change in systole and diastole and P the diVerence in systolic and diastolic blood pressure measured at the tip of the guiding catheter during a cardiac cycle), and stiVness index ([ln(P sys /P dias )]/( D/D), where P sys is systolic pressure, P dias is diastolic pressure, and D is the diVerence between systolic and diastolic lumen diameters). Positive remodelling was defined as when the VA at the lesion was > 1.05 times larger than at the proximal reference site, and negative remodelling when the VA at the lesion was < 0.95 of the reference site. Results-Mean (SD) LA at the lesion site was similar in both groups (4.03 (1.8) v 4.01 (1.93) mm 2 ), while plaque area was larger in the unstable group (13.29 (4.04) v 8.34 (3.6) mm 2 , p < 0.001). Remodelling index was greater in the unstable group (1.14 (0.18) v 0.83 (0.15), p < 0.001). Positive remodelling was observed in 15 patients in the unstable group (65%) but in only two (9%) in the stable group (p < 0.001). Negative remodelling occurred only in two patients with unstable symptoms (9%) but in 17 (74%) with stable symptoms. At the proximal reference segment, the diVerence in LA between systole and diastole was 0.99 (0.66) mm 2 in the unstable group and 0.39 (0.3) mm 2 in the stable group (p < 0.001), and the calculated coronary artery distensibility was 3.09 (2.69) and 0.94 (0.83) per mm Hg in unstable and stable patients, respectively (p < 0.001). The stiVness index was lower in patients with unstable angina (1.95 (0.94) v 3.1 (0.96), p < 0.001). Conclusions-Compensatory vessel enlargement occurs to a greater degree in patients with unstable than with stable coronary syndromes, and is associated with increased coronary artery distensibility. (Heart 2000;84:314-319)

Longitudinal heterogeneity of coronary artery distensibility in plaques related to acute coronary syndrome

“…Recent intravascular ultrasound (IVUS) studies have indicated that culprit lesions in ACS are characterized by large eccentric plaques with an echolucent zone, ulceration, thrombus formation, spotty calcium deposits and more positive remodeling compared with culprit lesions in stable angina pectoris or non-culprit lesions in ACS [4][5][6][7][8][9][10][11][12][13], and that culprit coronary artery walls are more distensible in ACS than in stable angina [14,15]. Coronary artery distensibility has been studied using IVUS imaging and it is reportedly determined by age, diabetes mellitus, and the size or thickness, eccentricity, composition and remodeling of the imaged plaque [14][15][16][17][18][19][20][21][22]. However, how increased vessel distensibility in the ACS-related coronary artery contributes to unstable clinical manifestations has not been elucidated.…”

Relationship Between Arterial and Fibrous Cap Remodeling

“…[5][6][7]28,35,36 Furthermore, previous IVUS studies have consistently demonstrated that lesions with positive remodeling were associated with worse clinical outcomes. 15,19,36 -40 In our present study population, 12-month clinical follow-up did not show any prognostic impact of the arterial and fibrous cap remodeling because of the small sample size and short follow-up period.…”

“…18 On the other hand, negative (inadequate) arterial remodeling or vessel shrinkage is associated with lumen narrowing in a majority of patients with stable angina pectoris. [5][6][7]28,31 Although the exact mechanism for extent and direction of arterial remodeling is not fully understood, it is suggested that intraplaque cytokines such as matrix metalloproteinases may cause disruption of the media and induce subsequent positive arterial remodeling. 9,10 On the other hand, it also is reported that matrix metalloproteinases may cause thinning and ultimate disruption of the fibrous cap, resulting in plaque rupture and acute coronary syndrome or sudden cardiac death.…”

“…[1][2][3][4]28 Lack of this adaptive process may be associated with atherosclerotic lesion progression 29,30 or restenosis after balloon angioplasty. 18 On the other hand, negative (inadequate) arterial remodeling or vessel shrinkage is associated with lumen narrowing in a majority of patients with stable angina pectoris.…”

Molecular magnetic resonance imaging of atherosclerotic vessel wall disease

“…ECM protein expression is associated with neoangiogenesis and unstable plaques [47]. Positive vascular remodeling of coronary atherosclerotic plaques has been found postmortem in the majority of patients with a myocardial infarction [48]. To detect and characterise these mechanisms, an elastin-specific Gd-labeled low-molecular-weight probe (855.95 Da) has been successfully used to target elastin expression in initial stages of coronary artery disease in a mouse and swine model of atherosclerosis (Fig.…”