The impact of patient age on carotid atherosclerosis results from the Munich carotid biobank

Transkript

1 Klinik und Poliklinik für Vaskuläre und Endovaskuläre Chirurgie Interdisziplinäres Gefäßzentrum Klinikum rechts der Isar (MRI) der TU München (TUM) Headline bearbeiten The impact of patient age on carotid atherosclerosis results from the Munich carotid biobank J. Pelisek, H. Wendorff, C. Wendorff, H.-H. Eckstein

2 Age?? 2

3 Study design Carotid plaques from 832 patients ( ) (Munich Biobank) Inclusion criteria Sufficient quality of plaque tissue for histological characterization Availability of patient history and clinical data Exclusion criteria Insufficient quality of plaque tissue No patient data Included 764 carotid patients

4 Methods Tissue material fixed in formalin and embedded in paraffin Plaque segmentation (3-4 mm): (3-5)x Plaque classification according to AHA (H. Stary , 2000) V VI VII complex pl.(cp) Neurological symptoms, plaque stability Semi-quantitative IHC-analysis: Cellularity, calcification, collagen content, infiltrates Plaque composition clinically relevant (worst) section: 1. Instability, 2. Classification CP>VI>V>VII, 3. Inflammation 4. Collagen amount

5 Patient demographic data In total (n=764) Asymptomatic patients (n=472) Symptomatic patients (n=292) Age (years) 69.9 ± ± ± 9.4 Gender (males) 71.5% 73.1% 68.8% Hypertension 86.0% 86.0% 86.0% Hyperlipidemia 54.6% 60.2% 45.5% Diabetes mellitus 26.4% 26.9% 25.7% Chronic kidney disease 8.0% 8.7% 6.8% Coronary heart disease 10.9% 10.8% 11.0% Peripheral artery disease 5.2% 6.8% 2.7% Smoking 48.6% 55.7% 37.0% Neurological symptoms 38.2% - -

6 Results

7 Regression analysis: Increasing age and carotid plaque morphology Plaque classification (AHA) (V VI VII CP) Asymptomatic patients Symptomatic patients Beta P Beta P Plaque stability Collagen content Calcification Cellularity Inflammation Neovascularisation Adjusted for: gender, hypertension, smoking, diabetes mellitus, chronic kidney disease, coronary heart disease, intake of statins

8 Subgroup analysis Age vs. AHA classification type V P=0.008 n: n: P=0.129 type VI type VII complex plaque Asymptomatic patients Statistics: Kruskal-Wallis-test P<0.001 Symptomatic patients

9 Subgroup analysis Age vs. plaque vulnerability P=0.248 P=0.596 unstable unstable stable stable Asymptomatic patients Statistics: Chi-Quadrat test P<0.001 Symptomatic patients

10 Asymptomatic p. Symptomatic p. Statistics: Kruskal-Wallis-test Y-axis: semi-quantitative IHC analysis 1 = maximal observed histological feature Klinik für Vaskuläre und Endovaskuläre Chirurgie - Interdisziplinäres Gefäßzentrum Subgroup analysis Age vs. plaque composition Histological feature Histological feature Calcium deposition Cellularity Inflammation P=0.091 P=0.020 P=0.047 P=0.406 P=0.665 P=0.783

11 Age?? 11

12 Summary Changes in carotid plaque morphology during aging Asymptomatic patients Symptomatic patients Plaque severity ( complex pl.) increased (65 75 y.) increased (60 80 y.) Unstable plaques increasing (30 60%) no changes, high (60-70%) Calcification increasing until 75 y. no changes Cellularity decreasing until 65 y. no changes Inflammation decreasing until 65 y. no changes

13 Klinik und Poliklinik für Vaskuläre und Endovaskuläre Chirurgie Interdisziplinäres Gefäßzentrum Klinikum rechts der Isar (MRI) der TU München (TUM) Headline bearbeiten Thank you

14 Patient demographic data

15 Summary - Plaque complexity/severity Asymptomatic patients: Symptomatic patients: - Calcium deposition Asymptomatic patients: Symptomatic patients: - Cellularity and inflammation Asymptomatic patients: Symptomatic patients: increased between years increased between years increases until 75 years no changes with age decreases until 65 years no changes with age - Plaque stability Asymptomatic patients: decreases with age (30% 60%) Symptomatic patients: no changes with age (but high 70%)

16 Patient demographic data Parameter in total (n=764) Asymptomatic (n=472) Symptomatic (n=292) Age (years) 69.9 ± ± ± 9.4 Gender (males) 71.5% 73.1% 68.8% Hypertension 86.0% 86.0% 86.0% Hyperlipidemia 54.6% 60.2% 45.5% Diabetes mellitus 26.4% 26.9% 25.7% Chronic kidney disease 8.0% 8.7% 6.8% Coronary heart disease 10.9% 10.8% 11.0% Peripheral occlusive disease 5.2% 6.8% 2.7% Smoking 48.6% 55.7% 37.0% Neurological symptoms 38.2% - - ASA/clopidogrel 85.3% 86.4% 83.6% ACE inhibitor 27.6% 28.2% 26.7% Beta-blocker 36.0% 38.1% 32.5% Diuretics 13.9% 13.6% 14.4% Statins 68.7% 69.7% 67.1%

17 Study design 832 Carotid plaques ( ) (Biobank) Inclusion criteria Patients with carotid artery stenosis >70% undergoing CEA in our clinic Sufficient quality of plaque tissue for histological characterization Availability of patients history and clinical data Exclusion criteria Methods Malignancy Insufficient quality of plaque tissue no morphological characterization possible Tissue material fixed in formalin and embedded in paraffin within 24 hours Plaque segmentation (3-4 mm) 3-5 segments per Plaque / staining Characterization Plaque classification according to AHA (H. Stary , 2000), neurological symptoms, plaque stability Cellularity, calcification, collagen content, infiltrates, neovessels Plaque composition: clinically relevant (worst) case / average case

18 Asymptomatic patients Symptomatic patients Klinik für Vaskuläre und Endovaskuläre Chirurgie - Interdisziplinäres Gefäßzentrum Subgroup analysis Age vs. plaque composition Semi-quantitative IHC analysis: low content mean content high content P=0.107 Semi-quantitative IHC analysis: 0 (+) (+) (++) (++) (+++) P=0.689

19 Subgroup analysis Age vs. plaque vulnerability and clinical symptomatic *

20 Results