@article {1391, title = {Cardiovascular physiology in premotor Parkinson{\textquoteright}s disease: a neuroepidemiologic study.}, journal = {Mov Disord}, volume = {27}, year = {2012}, month = {2012 Jul}, pages = {988-95}, abstract = {

Changes in cardiovascular physiology in Parkinson{\textquoteright}s disease (PD) are common and may occur prior to diagnostic parkinsonian motor signs. We investigated associations of electrocardiographic (ECG) abnormalities, orthostasis, heart rate variability, and carotid stenosis with the risk of PD diagnosis in the Cardiovascular Health Study, a community-based cohort of older adults. ECG abnormality, orthostasis (symptomatic or asymptomatic), heart rate variability (24-hour Holter monitoring), and any carotid stenosis (>=1\%) by ultrasound were modeled as primary predictors of incident PD diagnosis using multivariable logistic regression. Incident PD cases were identified by at least 1 of the following: self-report, antiparkinsonian medication use, and ICD-9. If unadjusted models were significant, they were adjusted or stratified by age, sex, and smoking status, and those in which predictors were still significant (P <= .05) were also adjusted for race, diabetes, total cholesterol, low-density lipoprotein, blood pressure, body mass index, physical activity, education level, stroke, and C-reactive protein. Of 5888 participants, 154 incident PD cases were identified over 14 years of follow-up. After adjusting models with all covariates, those with any ECG abnormality (odds ratio [OR], 1.45; 95\% CI, 1.02-2.07; P = .04) or any carotid stenosis (OR, 2.40; 95\% CI, 1.40-4.09; P = .001) at baseline had a higher risk of incident PD diagnosis. Orthostasis and heart rate variability were not significant predictors. This exploratory study suggests that carotid stenosis and ECG abnormalities occur prior to motor signs in PD, thus serving as potential premotor features or risk factors for PD diagnosis. Replication is needed in a population with more thorough ascertainment of PD onset.

}, keywords = {Aged, Antiparkinson Agents, Cardiovascular Physiological Phenomena, Carotid Stenosis, Cohort Studies, Data Interpretation, Statistical, Dizziness, Electrocardiography, Female, Heart Rate, Hospitalization, Humans, Longitudinal Studies, Male, Movement Disorders, Neurologic Examination, Parkinson Disease, Risk, Ultrasonography}, issn = {1531-8257}, doi = {10.1002/mds.24979}, author = {Jain, Samay and Ton, Thanh G and Perera, Subashan and Zheng, Yan and Stein, Phyllis K and Thacker, Evan and Strotmeyer, Elsa S and Newman, Anne B and Longstreth, Will T} } @article {1354, title = {Markers of inflammation in prevalent and incident Parkinson{\textquoteright}s disease in the Cardiovascular Health Study.}, journal = {Parkinsonism Relat Disord}, volume = {18}, year = {2012}, month = {2012 Mar}, pages = {274-8}, abstract = {

BACKGROUND: Studies demonstrate existence of inflammation in prevalent Parkinson{\textquoteright}s disease (PD). We assessed associations of baseline levels of inflammatory markers with prevalent PD at baseline (1989) and incident PD identified over 13 years of follow-up of the Cardiovascular Health Study.

METHODS: Blood samples at baseline were measured for fibrinogen, interleukin-6, tumor necrosis factor-α, C-reactive protein, albumin, and white blood cells. The analysis included 60 prevalent and 154 incident PD cases.

RESULTS: Risk of prevalent PD was significantly higher per doubling of IL-6 among women (odds ratio [OR]=1.5, 95\% confidence interval [CI]: 1.0, 2.4) and WBC among men (OR: 2.4, 95\% CI: 1.2, 4.9) in multivariate models. Risk of incident PD was not associated with higher levels of any biomarker after adjusting for age, smoking, African American race, and history of diabetes. Inverse associations with incident PD were observed per doubling of C-reactive protein (OR=0.9; 95\% CI: 0.8, 1.0) and of fibrinogen among women (OR=0.4; 95\% CI: 0.2, 0.8).

CONCLUSIONS: Although inflammation exists in PD, it may not represent an etiologic factor. Our findings suggest the need for larger studies that measure inflammatory markers before PD onset.

}, keywords = {Aged, Aged, 80 and over, Albumins, Biomarkers, C-Reactive Protein, Enzyme-Linked Immunosorbent Assay, Female, Fibrinogen, Humans, Incidence, Inflammation, Interleukin-6, Leukocyte Count, Male, Parkinson Disease, Prevalence, Risk Factors, Tumor Necrosis Factor-alpha}, issn = {1873-5126}, doi = {10.1016/j.parkreldis.2011.11.003}, author = {Ton, Thanh G N and Jain, Samay and Biggs, Mary L and Thacker, Evan L and Strotmeyer, Elsa S and Boudreau, Robert and Newman, Anne B and Longstreth, W T and Checkoway, Harvey} } @article {6188, title = {Enhancing case ascertainment of Parkinson{\textquoteright}s disease using Medicare claims data in a population-based cohort: the Cardiovascular Health Study.}, journal = {Pharmacoepidemiol Drug Saf}, volume = {23}, year = {2014}, month = {2014 Feb}, pages = {119-27}, abstract = {

PURPOSE: We sought to improve a previous algorithm to ascertain Parkinson{\textquoteright}s disease (PD) in the Cardiovascular Health Study by incorporating additional data from Medicare outpatient claims. We compared our results to the previous algorithm in terms of baseline prevalence and incidence of PD, as well as associations with baseline smoking characteristics.

METHODS: Our original case ascertainment used self-reported diagnosis, antiparkinsonian medication, and hospitalization discharge International Classification of Diseases-Ninth version code. In this study, we incorporated additional data from fee-for-service Medicare claims, extended follow-up time, review of hospitalization records, and adjudicated cause of death. Two movement disorders specialists adjudicated final PD status. We used logistic regression models and controlled for age, sex, African American race, and education.

RESULTS: We identified 75 additional cases but reclassified 80 previously identified cases as not having PD. We observed significant inverse association with smoking status (odds ratio = 0.42; 95\% confidence interval (CI) = 0.22, 0.79), and inverse linear trends with pack-years (p = 0.005), and cigarettes per day (p = 0.019) with incident PD. All estimates were stronger than those from the previous algorithm.

CONCLUSIONS: Our enhanced method did not alter prevalence and incidence estimates compared with our previous algorithm. However, our enhanced method provided stronger estimates of association, potentially due to reduced level of disease misclassification.

}, keywords = {Aged, Aged, 80 and over, Algorithms, Antiparkinson Agents, Cohort Studies, Databases, Factual, Female, Hospitalization, Humans, Incidence, Logistic Models, Male, Medicare, Parkinson Disease, Prevalence, Prospective Studies, Smoking, Time Factors, United States}, issn = {1099-1557}, doi = {10.1002/pds.3552}, author = {Ton, Thanh G N and Biggs, Mary Lou and Comer, Diane and Curtis, Lesley and Hu, Shu-Ching and Thacker, Evan L and Searles Nielsen, Susan and Delaney, Joseph A and Landsittel, Douglas and Longstreth, William T and Checkoway, Harvey and Jain, Samay} }