Abstract 2799: Procollagen Type III Amino-terminal and Carboxyl-terminal Telopeptide of Collagen type I but not Carboxyl-terminal Propeptide Type I are Associated with Heart Failure in the Elderly; The Cardiovascular Health Study

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Eddy Barasch ◽  
John S. Gottdiener ◽  
Gerard Aurigemma ◽  
DW Kitzman ◽  
Jing Han ◽  
...  

Background: The presence of excess myocardial matrix fibrosis (MF) contributes to alteration in the left ventricular (LV) diastolic and eventually, systolic performance. The increased collagen-derived serum peptides associated with collagen synthesis (procollagen type III aminoterminal peptide-PIIINP-, carboxyl-terminal propeptide type I -PIP-) and degradation (carboxyl-terminal telopeptide of collagen type I -CTIP-) have been shown in a number of small studies to correlate with histologic assessment of MF. While the prevalence of heart failure (HF), especially diastolic (D)HF increases with aging, no large studies evaluate the association of MF with DHF or systolic (S) HF in the elderly. Aims: To determine the association between the 3 biomarkers of MF turnover Methods: In 880 participants (ppt), mean age 77 ± 6 yrs, 52 % males, 79 % white, enrolled in the Cardiovascular Health Study, a prospective community based study of individuals > 65 yrs of age , serum levels of PIIINP, PIP and ICTP were measured by radioimmunoassay; 179 had HF with normal LVEF (DHF), 131 had HF with LVEF ± 55%, (SHF), 287 controls (no HF) and 283 healthy ppts. Results: Logistic regression models using a progressive number of adjustment variables are illustrated in the table . The ROC curves showed for CTIP the AUC =0.69; p<0.0001 and for PIIINP, AUC = 0.66, p<0.0001. The comparison of two ROC curves = NS. Model 1: unadjusted model Model 2: adjusted by age, gender and race Model 3: model 2+ adjustment for LVH, hypertension, diabetes, CHD, any ACE inhibitor, potassium-sparing agents alone, any diuretic, serum creatinine, cystatin C Conclusions: 1. PIP was not associated with SHF or DHF. 2. Even when adjusted for multiple potential confounders, there is still a strong association between CTIP, PIIINP and DHF as well as SHF. 3. The lack of association between PIP and HF might be a characteristic of this age group where possible PIIINP, reflecting the poorly cross-linked collagen, predominates .

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Eddy Barasch ◽  
John S Gottdiener ◽  
Jing Han ◽  
Gerard P Aurigemma ◽  
Dalane W Kitzman ◽  
...  

Background: Significant changes in the cardiac anatomy, morphology and function occur with aging. Increased collagen deposition in the myocardial matrix has been associated with prevalent heart failure (HF) in the elderly. The relation between age with serum level of procollagen type III aminoterminal peptide-PIIINP-, carboxyl-terminal propeptide type I -PIP-, reflecting collagen synthesis, and carboxyl-terminal telopeptide of collagen type I -CITP-marker of collagen type I degradation, is largely unknown in healthy free-living elderly individuals. Aim: To determine the relation between age with serum biomarkers of fibrosis (SBF) in a large group of community-dwelling elderly individuals. Methods: In 880 participants (ppts), mean age 77 ± 6 yrs, 52 % males, 79 % white, enrolled in the Cardiovascular Health Study, serum levels of PIIINP, PIP and CITP were measured; 179 had HF with normal LVEF (DHF), 131 had HF with LVEF < 55% (SHF), 287 controls (no HF), and 283 healthy ppts. Kruskal-Wallis test, one-way ANOVA, chi-square test and Spearman correlation were performed as appropriate. Results: SFB values and the main demographic variables are displayed in the table . The association between age with the 3 SBF for the entire study population were: PIP: r = 0.13 (p <0.0001), CITP: r = 0.13, p < 0.0001, PIIINP: r = 0.04, p = 0.20. For the individuals groups, the associations were: PIP with DHF (r = 0.25, p=0.001), CITP with DHF (r = 0.15, p =0.05), controls (r= 0.27, p < 0.0001) and healthy control groups (r = 0.19, p = 0.001). PIIINP was associated with age only in the control group (r = 0.12, p = 0.04). No association was found between age and SBF in the SHF group.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Eddy Barasch ◽  
John S Gottdiener

Background: The fibrillar myocardial extracellular matrix is mainly composed of type I and III fibrillar collagen and their turnover are reflected in the serum level of carboxyl-terminal propeptide type I (PIP) and procollagen type III aminoterminal peptide (PIIINP). The prognostic value of these biomarkers in elderly individuals with heart failure (HF) or other cardiovascular disease (CVD) and in healthy subjects is largely unknown. Aim: To determine the predictive value of PIP, its degradation metabolite, carboxyterminal telopeptide of procollagen type I (CTIP), and PIIINP serum level for the incident CV morbidity and mortality in a nested case control study of community-dwelling elderly individuals enrolled in the Cardiovascular Health Study (CHS). Methods: In 880 participants (ppts) enrolled in the CHS (mean age 77 ± 6 yrs, 52 % males, 79 % white), 310 with HF, 287 controls (no HF but other CVD) and 283 healthy ppts, serum levels of PIIINP, PIP and CTIP were measured by radioimmunoassay. The number of incident CV disease and death were recorded. Wilcoxon rank sum test, Kruskal-Wallis test, and Cox proportional hazards regression were used as appropriate. Results: Age, gender and race and fully adjusted analyses are presented in the table : Conclusions: In this large elderly cohort, there is a strong association between CTIP, PIIINP and incident CVD and death. Elevated CTIP level increases the risk of death more than 50% and of symptomatic PVD by almost two-fold. Whereas PIIINP has a lower predictive power than CTIP, PIP was not associated with incident CVD or death. Serum CTIP and PIIINP have a good prognostic value for both incident CVD and death in elderly individuals with or without known CV disease.


Stroke ◽  
2001 ◽  
Vol 32 (suppl_1) ◽  
pp. 363-363
Author(s):  
Charles B Bernick ◽  
Lewis H Kuller ◽  
Will T Longstreth ◽  
Corinne Dulberg ◽  
Teri A Manolio ◽  
...  

P136 Objective: Silent infarcts seen on cranial MRI scans are a risk factor for subsequent clinical stroke in the elderly. This study examines the type of clinical strokes seen in those with silent infarcts. Methods: Cranial MRI examination was completed on 3324 Cardiovascular Health Study (CHS) participants aged 65+ who were without a prior history of clinical stroke. Incident strokes were identified over an average follow-up of 4 years and classified as hemorrhagic or ischemic. Ischemic strokes were further subdivided into lacunar, cardioembolic, atherosclerotic or other/unknown. Results: Silent MRI infarcts >3mm were found in approximately 28% (n=923). Of these, 7% (n=67) subsequently had a clinically evident stroke. The characteristics of the silent MRI infarcts in those who sustained an incident stroke were as folows: 56 had only subcortical infarcts, of which 55 were <20mm; 4 had only cortical infarcts; and 7 had both cortical and subcortical infarcts. Of those with only subcortical silent MRI infarcts, 16% (n=9) went on to a hemorrhagic stroke and 84% (n=47) sustained an ischemic stroke. The ischemic strokes were subtyped as 12 cardioembolic, 3 lacunar, 2 atherosclerotic and 30 unknown/other. Considering only those with cortical silent infarcts, either alone or in combination with subcortical infarcts, there was 1 hemorrhagic stroke and 10 ischemic strokes. Half of the ischemic strokes were cardioembolic and half were unknown type. Conclusion: Elderly individuals with silent subcortical infarcts who go onto subsequent stroke may be at risk not only for lacunar infarcts but also cardioembolic or hemorrhagic strokes.


1998 ◽  
Vol 79 (05) ◽  
pp. 912-915 ◽  
Author(s):  
Mary Cushman ◽  
Frits R. Rosendaal ◽  
Bruce M. Psaty ◽  
E. Francis Cook ◽  
J. Valliere ◽  
...  

SummaryCoagulation factor V Leiden is a risk marker for venous thrombosis. For arterial thrombosis no large study to date has included population-based elderly patients. The Cardiovascular Health Study is a longitudinal study of 5,201 men and women over age 65. With 3.4-year follow-up, we studied 373 incident cases of myocardial infarction (MI), angina, stroke, or transient ischemic attack (TIA), and 482 controls. The odds ratios for each event with heterozygous factor V Leiden were: MI, 0.46 (95% CI 0.17 to 1.25); angina, 1.0 (95% CI 0.45 to 2.23); stroke, 0.77 (95% CI 0.35 to 1.70); TIA, 1.33 (95% CI 0.5 to 3.55); any outcome, 0.83 (95% CI 0.48 to 1.44). Adjustment for cardiovascular risk factors did not change relationships. In older adults factor V Leiden is not a risk factor for future arterial thrombosis.


2019 ◽  
Vol 74 (4) ◽  
pp. 501-509 ◽  
Author(s):  
Dominik Steubl ◽  
Petra Buzkova ◽  
Pranav S. Garimella ◽  
Joachim H. Ix ◽  
Prasad Devarajan ◽  
...  

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3448-3448
Author(s):  
Neil A Zakai ◽  
Benjamin French ◽  
Alice Arnold ◽  
Anne Newman ◽  
Linda F. Fried ◽  
...  

Abstract Introduction: Anemia is associated with increased morbidity and mortality in the elderly, though the risk factors for and the consequences of hemoglobin (HGB) decline are poorly characterized. Methods: We studied 5201 men and women ≥65 participating in the Cardiovascular Health Study. The cohort was followed biannually and had baseline and repeat hemograms 3 years later. HGB decline was defined as >1g/dL HGB drop, or incident anemia at 3 years by WHO criteria. Results: 4006 participants survived to 3 years and had two HGB measures. The median HGB change was −0.2g/dL (IQR-0.8, 0.1). 961 (24%) participants had a >1g/dL HGB drop and 335 (8%) developed incident anemia. The left side of the table presents adjusted logistic regression models of baseline risk factors for HGB decline. Those with baseline cardiovascular disease (CVD), diabetes and kidney disease were more likely to develop >1g/dL HGB drop while only baseline kidney disease was associated with incident anemia. The table also shows the adjusted risk of HGB decline with concurrent development of co-morbid conditions. A >1g/dL drop in HGB was more likely in those who concurrently developed incident CVD, hypertension or inflammation. Incident anemia was more likely in participants with concurrent development of kidney disease or inflammation. Both incident anemia and a HGB drop >1g/dL were associated with subsequent 9-year mortality adjusting for age, race, gender, year 3 HGB, hypertension, CVD, diabetes, and renal disease; HRs (95% CI) 1.4 (1.2, 1.6) and 1.2 (1.1, 1.4) respectively. Discussion: Among studied factors, baseline CVD, diabetes and kidney disease were risk factors for >1g/dL HGB drop while only baseline kidney disease was a risk factor for incident anemia. Incident CVD and hypertension were associated concurrently with >1g/dL HGB drop while kidney disease was associated with concurrent incident anemia. Inflammation development was the strongest risk factor accompanying HGB decline. HGB decline, especially a 1g/dL drop, was associated with subsequent mortality irrespective of HGB concentration. These data suggest that small HGB changes not captured by the WHO anemia criteria are associated with poor health outcomes and that inflammation is a major correlate of HGB decline in the elderly. Table: Risk Factors for HGB Decline in Age-, Race-, Gender, and Baseline HGB-Adjusted Logistic Regression Models Baseline Risk Factors for HGB Decline Risk of HGB Decline with Concurrent Conditions HGB Drop >1g/dL Incident Anemia HGB Drop >1g/dL Incident Anemia CVD 1.2 (1.1, 1.4) 1.0 (0.8, 1.3) 1.3 (1.1, 1.6) 1.0 (0.7, 1.3) Hypertension 1.1 (0.99, 1.3) 1.1 (0.8, 1.2) 1.4 (1.1, 1.7) 1.1 (0.8, 1.5) Diabetes 1.3 (1.1, 1.5) 1.1 (0.8, 1.4) 0.9 (0.6, 1.4) 0.8 (0.4, 1.7) Kidney Disease (GFR <60ml/min/1.73m2) 1.2 (1.0, 1.3) 1.3 (1.1, 1.7) 1.1 (0.8, 1.4) 1.5 (1.0, 2.1) Inflammation CRP ≥10mg/dL or WBC≥15×109/mm3 1.0 (0.8, 1.3) 1.3 (0.99 1.8) 2.3 (1.8, 2.8) 2.3 (1.8, 3.0)


2004 ◽  
Vol 13 (2) ◽  
pp. 61-68 ◽  
Author(s):  
Sunil T. Mathew ◽  
John S. Gottdiener ◽  
Dalane Kitzman ◽  
Gerard Aurigemma ◽  
Julius M. Gardin

2010 ◽  
Vol 65A (11) ◽  
pp. 1242-1249 ◽  
Author(s):  
D. B. Welmerink ◽  
W. T. Longstreth ◽  
M. F. Lyles ◽  
A. L. Fitzpatrick

Sign in / Sign up

Export Citation Format

Share Document