@article {1292, title = {Association of annular calcification and aortic valve sclerosis with brain findings on magnetic resonance imaging in community dwelling older adults: the cardiovascular health study.}, journal = {J Am Coll Cardiol}, volume = {57}, year = {2011}, month = {2011 May 24}, pages = {2172-80}, abstract = {

OBJECTIVES: The objective of this study was to investigate the associations of mitral annular calcification, aortic annular calcification, and aortic valve sclerosis with covert magnetic resonance imaging (MRI)-defined brain infarcts.

BACKGROUND: Clinically silent brain infarcts defined by MRI are associated with increased risk for cognitive decline, dementia, and future overt stroke. Left-sided cardiac valvular and annular calcifications are suspected as risk factors for clinical ischemic stroke.

METHODS: A total of 2,680 CHS (Cardiovascular Health Study) participants without clinical histories of stroke or transient ischemic attack underwent brain MRI in 1992 and 1993, 1 to 2 years before echocardiographic exams (1994 to 1995).

RESULTS: The mean age of the participants was 74.5 {\textpm} 4.8 years, and 39.3\% were men. The presence of any annular or valvular calcification (mitral annular calcification, aortic annular calcification, or aortic valve sclerosis), mitral annular calcification alone, or aortic annular calcification alone was significantly associated with a higher prevalence of covert brain infarcts in unadjusted analyses (p < 0.01 for all). In models adjusted for age, sex, race, body mass index, physical activity, creatinine, systolic blood pressure, total cholesterol, high-density lipoprotein cholesterol, smoking, diabetes, coronary heart disease, and congestive heart failure, the presence of any annular or valve calcification remained associated with covert brain infarcts (risk ratio: 1.24; 95\% confidence interval: 1.05 to 1.47). The degree of annular or valvular calcification severity showed a direct relation with the presence of covert MRI findings.

CONCLUSIONS: Left-sided cardiac annular and valvular calcifications are associated with covert MRI-defined brain infarcts. Further study is warranted to identify mechanisms and determine whether intervening in the progression of annular and valvular calcification could reduce the incidence of covert brain infarcts as well as the associated risk for cognitive impairment and future stroke.

}, keywords = {Aged, Aortic Valve Stenosis, Brain, Brain Infarction, Calcinosis, Cohort Studies, Female, Humans, Magnetic Resonance Imaging, Male, Mitral Valve Stenosis, Retrospective Studies}, issn = {1558-3597}, doi = {10.1016/j.jacc.2011.01.034}, author = {Rodriguez, Carlos J and Bartz, Traci M and Longstreth, W T and Kizer, Jorge R and Barasch, Eddy and Lloyd-Jones, Donald M and Gottdiener, John S} } @article {6335, title = {Residential relocation by older adults in response to incident cardiovascular health events: a case-crossover analysis.}, journal = {J Environ Public Health}, volume = {2014}, year = {2014}, month = {2014}, pages = {951971}, abstract = {

OBJECTIVE: We use a case-crossover analysis to explore the association between incident cardiovascular events and residential relocation to a new home address.

METHODS: We conducted an ambidirectional case-crossover analysis to explore the association between incident cardiovascular events and residential relocation to a new address using data from the Cardiovascular Health Study (CHS), a community-based prospective cohort study of 5,888 older adults from four U.S. sites beginning in 1989. Relocation was assessed twice a year during follow-up. Event occurrences were classified as present or absent for the period preceding the first reported move, as compared with an equal length of time immediately prior to and following this period.

RESULTS: Older adults (65+) that experience incident cardiovascular disease had an increased probability of reporting a change of residence during the following year (OR 1.6, 95\% confidence interval (CI) = 1.2-2.1). Clinical conditions associated with relocation included stroke (OR: 2.0, 95\% CI: 1.2-3.3), angina (OR: 1.6, 95\% CI: 1.0-2.6), and congestive heart failure (OR: 1.5, 95\% CI: 1.0-2.1).

CONCLUSIONS: Major incident cardiovascular disease may increase the probability of residential relocation in older adults. Case-crossover analyses represent an opportunity to investigate triggering events, but finer temporal resolution would be crucial for future research on residential relocations.

}, keywords = {Aged, Cardiovascular Diseases, Cross-Over Studies, Female, Humans, Incidence, Life Change Events, Logistic Models, Longitudinal Studies, Male, Prospective Studies, Residence Characteristics, United States}, issn = {1687-9813}, doi = {10.1155/2014/951971}, author = {Lovasi, Gina S and Richardson, John M and Rodriguez, Carlos J and Kop, Willem J and Ahmed, Ali and Brown, Arleen F and Greenlee, Heather and Siscovick, David S} } @article {9917, title = {Association Between Cigarette Smoking~and Subclinical Markers of Cardiovascular Harm.}, journal = {J Am Coll Cardiol}, volume = {85}, year = {2025}, month = {2025 Mar 18}, pages = {1018-1034}, abstract = {

BACKGROUND: Cigarette smoking is a strong risk factor for cardiovascular harm.

OBJECTIVES: The study sought to explore the detailed relationships between smoking intensity, pack-years, and~time since cessation with inflammation, thrombosis, and subclinical atherosclerosis markers of cardiovascular harm.

METHODS: We included 182,364 participants (mean age 58.2 years, 69.0\% female) from 22 cohorts of the Cross Cohort Collaboration with self-reported smoking status, including smoking intensity and/or pack-years, and concurrent subclinical marker measurements. Markers were categorized into 3 domains: inflammation (high-sensitivity C-reactive protein, interleukin-6, glycoprotein acetylation), thrombosis (fibrinogen, D-dimer), and subclinical atherosclerosis (coronary artery calcium, carotid intima-media thickness, carotid plaque, and ankle-brachial index). Utilizing multivariate regression models and restricted cubic splines, we assessed associations of smoking status, intensity, pack-years, time since cessation, and subclinical markers.

RESULTS: A total of 15.3\% of participants currently smoke (mean 16.7 cigarettes/day, mean 30.0 pack-years), and 34.6\% of participants formerly smoked (median 19.0 years since quitting, mean 22.4 pack-years). Participants with a history of smoking showed higher levels of all subclinical markers compared with those who have never smoked, with stronger associations observed in those currently smoke. Among participants who currently smoke, smoking intensity showed a clear dose-response relationship with all markers, except for D-dimer, specifically with incremental 1\% to 9\% higher levels of subclinical markers per 10 cigarettes. After 20 cigarettes, the patterns appeared to plateau for blood markers, while they continued to increase for atherosclerosis markers. Among those who have ever smoked, robust dose-response relationships were observed for pack-years with all subclinical markers, with incremental 1\% to 9\% higher levels per 10 pack-years. The dose-response effects persisted after 20 pack-years for all markers, though with a milder slope. Among participants who smoked formerly, there were substantially lower levels of biomarkers with longer time since quitting, and most markers were not different compared with those who have never smoked by 30 years, except for the coronary artery calcium score, which remained 19\% higher even beyond quitting after 30 years.

CONCLUSIONS: Smoking-relevant parameters show strong and dose-response relationships across 3 domains of subclinical markers of cardiovascular harm. The sensitivity of the tested subclinical markers to small increments in cigarette exposure suggests potential value in the regulation of new and existing tobacco products.

}, keywords = {Aged, Atherosclerosis, Biomarkers, Cardiovascular Diseases, Carotid Intima-Media Thickness, Cigarette Smoking, Cohort Studies, Female, Humans, Male, Middle Aged, Risk Factors}, issn = {1558-3597}, doi = {10.1016/j.jacc.2024.12.032}, author = {Yao, Zhiqi and Tasdighi, Erfan and Dardari, Zeina A and Jha, Kunal K and Osuji, Ngozi and Rajan, Tanuja and Boakye, Ellen and Rodriguez, Carlos J and Matsushita, Kunihiro and Simonsick, Eleanor M and Lima, Jo{\~a}o A C and Widome, Rachel and Cohen, Debbie L and Appel, Lawrence J and Khera, Amit and Hall, Michael E and Judd, Suzanne E and Cole, Shelley A and Vasan, Ramachandran S and Benjamin, Emelia J and Lotufo, Paulo A and Bensenor, Isabela M and El Khoudary, Samar R and Barinas-Mitchell, Emma and Janssen, Imke and Psaty, Bruce M and Eaton, Charles B and Lamonte, Michael J and Cawthon, Peggy M and Orwoll, Eric S and Irvin, Marguerite R and Bhatnagar, Aruni and DeFilippis, Andrew P and El-Shahaway, Omar and Blaha, Michael J} }