Clinical, laboratory, and transesophageal echocardiographic correlates of interatrial septal thickness: a population-based transesophageal echocardiographic study.
BACKGROUND
The determinants of interatrial septal (IAS) thickening ("lipomatous hypertrophy"), a common echocardiographic finding in the elderly, are poorly defined. The objective of this study was to determine the clinical, laboratory, and transesophageal echocardiographic correlates of IAS thickening in the general population.


METHODS
The thickness of the IAS was measured by transesophageal echocardiography in 384 patients (median age: 66 years; range: 51-101 years; 53% men) participating in a population-based study (Stroke Prevention: Assessment of Risk in a Community). The associations between atherosclerosis risk factors, clinical cardiovascular disease, aortic atherosclerotic plaques, and IAS thickness were examined.


RESULTS
Age and body surface area (BSA) were significantly associated with IAS thickness (median: 6 mm; range: 2-17 mm). IAS thickness increased by 12.6% per 10 years of age (95% confidence interval: 9.0-16.4%) adjusting for sex and BSA, and increased by 7.0% per 0.1 m 2 BSA (confidence interval: 5.0-9.2%) adjusting for age and sex. Overall, age, sex, and BSA accounted for 22.5% of the variability in IAS thickness. Current smoking (20.4% increase in IAS thickness in current smokers) and hypertension treatment (8.5% increase in treated patients) were associated with increased IAS thickness, adjusting for age, sex, and BSA ( P < .05), but these two risk factor variables jointly explained only an additional 2.3% of the variability in IAS thickness beyond the variability explained by age, sex, and BSA. Clinical coronary artery and cerebrovascular disease, atrial arrhythmias, and aortic atherosclerotic plaques were not associated with IAS thickness, adjusting for age, sex, and BSA ( P > .3).


CONCLUSIONS
IAS thickening is an age-associated process. Atherosclerosis risk factors are weakly associated with IAS thickening, whereas atherosclerotic vascular disease is not.
Agmon
Yoram
Y
Division of Cardiovascular Diseases and Internal Medicine, Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
Meissner
Irene
I
Tajik
A Jamil
AJ
Seward
James B
JB
Petterson
Tanya M
TM
Christianson
Teresa J H
TJ
O'Fallon
W Michael
WM
Wiebers
David O
DO
Khandheria
Bijoy K
BK
D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D001145:Arrhythmias, Cardiac / Q000150:complications / Q000000981:diagnostic imaging; D050197:Atherosclerosis / Q000150:complications / Q000000981:diagnostic imaging; D015992:Body Mass Index; D001830:Body Surface Area; D002097:C-Reactive Protein / Q000378:metabolism; D017548:Echocardiography, Transesophageal; D005260:Female; D005500:Follow-Up Studies; D006325:Heart Atria / Q000000981:diagnostic imaging* / Q000473:pathology*; D006346:Heart Septum / Q000000981:diagnostic imaging* / Q000473:pathology*; D006400:Hematocrit; D006801:Humans; D006984:Hypertrophy / Q000000981:diagnostic imaging; D018836:Inflammation Mediators / Q000378:metabolism; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D012720:Severity of Illness Index; D012737:Sex Factors
D018836:Inflammation Mediators; D002097:C-Reactive Protein