ABC | Volume 111, Nº3, September 2018

Original Article Marino et al Adiponectin and IVUS-VH Coronary Plaque Characteristics Arq Bras Cardiol. 2018; 111(3):345-353 Table 2 – Association of adiponectin plasma levels with segment intravascular ultrasound characteristics in the total study cohort, acute coronary syndrome and stable angina patients IVUS characteristics Unadjusted Model p Multivariable model* p Beta ‡ (95% CI) Beta ‡ (95% CI) All patients (n = 570) Segment plaque Burden -0.40 (-2.04 – 1.23) 0.62 -0.95 (-2.74 – 0.85) 0.30 Dense calcium fraction % 1.35 (0.27 – 2.44) 0.001 0.36 (-0.86 – 1.58) 0.56 Necrotic core fraction % 0.43 (-0.71 – 1.58) 0.46 0.39 (-0.92 – 1.70) 0.56 Fibrofatty tissue fraction % -0.62 (-1.51 – 0.27) 0.17 -0.46 (-1.46 – 0.55) 0.37 Fibrous tissue fraction % -1.17 (-2.81 – 0.48) 0.17 -0.29 (-2.16 – 1.58) 0.76 ACS patients (n = 309) Segment plaque Burden 0.03 (-2.27 – 2.33) 0.98 -0.89 (-3.42 – 1.63) 0.49 Dense calcium fraction % 2.53 (0.92 – 3.78) 0.001 1.10 (-0.50 – 2.70) 0.18 Necrotic core fraction % 0.56 (-1.12 – 2.24) 0.51 0.23 (-1.69 – 2.16) 0.81 Fibrofatty tissue fraction % -1.47 (-2.78 – -0.15) 0.029 -0.99 (-2.49 – 0.50) 0.19 Fibrous tissue fraction % -1.45 (-3.78 – 0.89) 0.22 -0.35 (-3.00 – 2.30) 0.80 SAP patients (n = 261) Segment plaque Burden -0.71 (-3.00 – 1.58) 0.54 -0.87 (-3.46 – 1.73) 0.51 Dense calcium fraction % 0.39 (-1.25 – 2.01) 0.64 -0.41 (-2.28 – 1.47) 0.67 Necrotic core fraction % 0.24 (-1.29 – 1.77) 0.76 0.57 (-1.20 – 2.35) 0.52 Fibrofatty tissue fraction % 0.38 (-0.80 – 1.57) 0.52 0.01 (-1.32 – 1.34) 0.99 Fibrous tissue fraction % -1.01 (-3.31 – 1.30) 0.39 -0.17 (-2.82 –2.48) 0.90 *Adjusted for age, gender, diabetes, hypertension, and C-reactive protein (CRP). Additionally adjusted for indication for coronary angiography in the total cohort. †Logarithmically transformed. ‡ Beta per unit increase in ln-transformed adiponectin concentration. IVUS: intravascular ultrasound; CI: confidence interval of 95%; ACS: acute coronary syndrome; SAP: stable angina pectoris; CRP: C-reactive protein. Table 3 – Association of adiponectin with presence of virtual histology intravascular ultrasound-derived high-risk lesions in the total cohort, acute coronary syndrome and stable angina patients Unadjusted Model p Multivariable model* p OR† (95% CI) OR† (95% CI) Total cohort (n = 570) TCFA 1.11 (0.84 – 1.49) 0.44 1.23 (0.88 – 1.71) 0.23 TCFA PB ≥70% 0.88 (0.57 – 1.37) 0.55 0.81 (0.50 – 1.33) 0.42 Lesion with MLA ≤ 4.0 mm 2 0.84 (0.62 – 1.14) 0.25 0.70 (0.49 – 1.00) 0.052 Lesion with PB ≥70% 1.02 (0.72 – 1.44) 0.93 0.93 (0.63– 1.39) 0.73 ACS patients (n = 309) TCFA 0.85 (0.58 – 1.26) 0.42 0.90 (0.58 – 1.42) 0.66 TCFA PB ≥70% 0.90 (0.57 – 1.42) 0.66 0.77 (0.37 – 1.58) 0.48 Lesion with MLA ≤ 4.0 mm 2 1.13 (0.74 – 1.74) 0.57 0.87 (0.53 – 1.44) 0.59 Lesion with PB ≥70% 1.25 (0.76 – 2.07) 0.38 1.08 (0.60 – 1.94) 0.80 SAP patients (n = 261) TCFA 1.54 (0.99 – 2.38) 0.057 1.78 (1.06 – 3.00) 0.030 TCFA PB ≥70% 0.86 (0.48 – 1.52) 0.60 0.87 (0.45 – 1.69) 0.68 Lesion with MLA ≤ 4.0 mm 2 0.62 (0.40 – 0.97) 0.035 0.55 (0.32 – 0.93) 0.025 Lesion with PB ≥70% 0.86 (0.54 – 1.39) 0.54 0.85 (0.49 – 1.47) 0.56 *Adjusted for age, gender, diabetes, hypertension, and C-reactive protein (CRP). Additionally adjusted for indication for coronary angiography in the total cohort. OR: odds ratio; CI: confidence interval of 95%; TCFA: thin-cap fibroatheroma; PB: plaque burden; MLA: minimal luminal area; ACS: acute coronary syndrome; SAP: stable angina pectoris. †Odds ratio per unit increase in ln-transformed biomarker concentration Another cohort with median follow-up of 2.5 years found that higher adiponectin levels were associated with future cardiovascular death or nonfatal myocardial infarction in SAP patients (n = 1130), but found no association in ACS patients (n = 760). 22 Our results, demonstrating an association of adiponectin with death in SAP patients, comply with these findings. The lack of statistical significance for this association in ACS patients in our study may, in part, have been caused by a limited number of clinical events. Moreover, pathophysiological differences may possibly have contributed to the difference 349