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Irene Meissner

Publications and source records attributed to Irene Meissner.

24 records · Page 2Linked to original sources

Endothelial nitric oxide synthase T-786C single nucleotide polymorphism: a putative genetic marker differentiating small versus large ruptured intracranial aneurysms.

BACKGROUND AND PURPOSE: Anecdotal evidence exists for at least 2 subpopulations of intracranial saccular aneurysms, namely, those that may form rapidly and rupture when small versus those that enlarge slowly and may rupture particularly when > or =10 mm in diameter. We sought to determine whether the endothelial nitric oxide synthase (eNOS) T-786C single nucleotide polymorphism (SNP), implicated in cardiovascular disease susceptibility, could facilitate differentiation between small (< or =5 mm) versus large (> or =10 mm) ruptured aneurysms. METHODS: In accordance with institutional guidelines, clinical data were recorded prospectively and genomic DNA was isolated from blood samples obtained from 52 aneurysmal subarachnoid hemorrhage (SAH) patients (cases) and 90 randomly selected controls. Samples were assayed for eNOS gene promoter T-786C SNP with the use of gene microarray technology. Statistical analyses included multiple logistic regression. RESULTS: Although there was no difference in genotype distributions between cases and controls, all 13 patients with large aneurysms were (T/C) heterozygous for the polymorphism, while 9 of 22 patients (41%) with small aneurysms were (T/T or C/C) homozygous (P=0.01). The mean (+/-SD) ruptured aneurysm diameter among all heterozygotes (8.5+/-5.2 mm) was significantly greater than that for C/C (6.0+/-2.3 mm) or T/T (4.7+/-1.8 mm) homozygotes (P=0.04). With the use of multivariate analysis, heterozygosity remained significantly associated with aneurysm size > or =10 mm (P=0.03). CONCLUSIONS: The eNOS T-786C SNP distinguishes genetically between small and large ruptured aneurysms. Although not predictive of SAH in the population at large, our data suggest that among persons with known intracranial aneurysms, eNOS T-786C genotype may be a factor influencing the size at which an aneurysm ruptures, a finding that should be taken into consideration along with other anatomic features of the aneurysm.

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Is aortic dilatation an atherosclerosis-related process? Clinical, laboratory, and transesophageal echocardiographic correlates of thoracic aortic dimensions in the population with implications for thoracic aortic aneurysm formation.

OBJECTIVES: The study determined, in a population-based setting, whether dilatation of the thoracic aorta is an atherosclerosis-related process. BACKGROUND: The role of atherosclerosis in thoracic aortic dilatation and aneurysm formation is poorly defined. METHODS: The dimensions of the thoracic aorta were measured with transesophageal echocardiography in 373 subjects participating in a population-based study (median age 66 years; 52% men). The associations between clinical and laboratory atherosclerosis risk factors, aortic atherosclerotic plaques, and aortic dimensions were examined. RESULTS: Age, male gender, and body surface area (BSA) jointly accounted for 41%, 31%, 38%, and 47% of the variability in diameters of the sinuses of Valsalva, ascending aorta, aortic arch, and descending aorta, respectively. Adjusting for age, gender, and BSA: 1) smoking was associated with a greater aortic arch diameter, and diastolic blood pressure and diabetes were each associated with a greater descending aorta diameter (p < 0.05); 2) atherosclerotic plaques in the descending aorta were associated with a greater descending aorta diameter (0.18 +/- 0.08-mm increase in diameter per 1-mm increase in plaque thickness; p = 0.02); and 3) minor negative associations were noted between atherosclerotic plaques and risk factors for atherosclerosis and the dimensions of the proximal thoracic aorta. Notably, atherosclerosis risk factors and plaque variables each accounted for <2% of the variability in aortic dimensions, adjusting for age, gender, and BSA. CONCLUSIONS: Age, gender, and BSA are major determinants of thoracic aortic dimensions. Atherosclerosis risk factors and aortic atherosclerotic plaques are weakly associated with distal aortic dilatation, suggesting that atherosclerosis plays a minor role in aortic dilatation in the population.

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Lack of association between Chlamydia pneumoniae seropositivity and aortic atherosclerotic plaques: a population-based transesophageal echocardiographic study.

OBJECTIVES: The objective of this study was to examine the relationship between Chlamydia pneumoniae seropositivity and aortic atherosclerotic plaques in the general population. BACKGROUND: Seroepidemiologic studies suggest that C pneumoniae infection plays a role in the pathogenesis of atherosclerosis. METHODS: Transesophageal echocardiography was performed in 385 subjects (median age 66 years, range 51 to 101 years; 53% men), a sample of the Olmsted County (Minnesota) population. The association between C pneumoniae immunoglobulin (Ig) G antibody titers and aortic atherosclerotic plaques was examined. RESULTS: Chlamydia pneumoniae IgG antibodies (titers >or=1:16) were detected in 287 subjects (74.5%): low titers (1:16 to 1:32) in 58 (15.1%), intermediate titers (1:64 to 1:128) in 144 (37.4%), and high titers (>or=1:256) in 85 subjects (22.1%). Antibody titers were not associated with the presence of aortic plaques after adjustment for age, gender, and smoking status (p = 0.64). Compared with titers <1:16, the adjusted odds ratios for aortic plaques were 1.46 (95% confidence interval [CI] 0.63 to 3.42) for low titers, 1.32 (95% CI 0.68 to 2.55) for intermediate titers, and 0.94 (95% CI 0.42 to 2.07) for high titers. Among the subgroup with plaques, antibody titers were not associated with the presence of plaques >or=4 mm thick (p = 0.99), plaques >or=6 mm (p = 0.49), or mobile debris (p = 0.71), after adjustment for age and smoking. CONCLUSIONS: Chlamydia pneumoniae IgG antibody titers are not associated with the presence or severity of aortic atherosclerosis in the general population. These observations do not support a role for C pneumoniae infection in the initiation or progression of atherosclerosis.

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Relation of coronary artery disease and cerebrovascular disease with atherosclerosis of the thoracic aorta in the general population.

The association between clinical coronary artery disease, cerebrovascular disease, and aortic atherosclerosis has not been examined in the general population. Transesophageal echocardiography was performed in 581 subjects, a random sample of the Olmsted County (Minnesota) population aged >/=45 years, participating in the Stroke Prevention: Assessment of Risk in a Community (SPARC) study. The frequency and severity of atherosclerosis of the thoracic aorta were determined in the population and the association between clinical coronary artery disease, cerebrovascular disease, and aortic atherosclerosis was examined. Previous myocardial infarction, angina pectoris, and coronary artery bypass surgery were significantly associated with aortic atherosclerosis, adjusting for age and gender (p </=0.01). Among subjects with atherosclerosis, these manifestations were associated with complex atherosclerosis (plaques >4-mm thick, ulcerated plaques, or mobile debris), adjusting for age and gender (p <0.05). Age, smoking, pulse pressure, previous myocardial infarction (odds ratio [OR] 4.67; 95% confidence interval [CI] 1.42 to 15.40), and coronary artery bypass surgery (OR 5.12; 95% CI 1.01 to 26.01) were independently associated with aortic atherosclerosis. Among subjects with atherosclerosis, age, smoking, pulse pressure, hypertension treatment, and coronary artery disease (OR 2.50; 95% CI 1.18 to 5.30) were independently associated with complex atherosclerosis. Weak associations were observed between previous ischemic stroke, transient ischemic attack, and aortic atherosclerosis, associations that were not significant after age- and gender-adjustment (p >0.2). Thus, coronary artery disease is strongly associated with aortic atherosclerosis and complex atherosclerosis in the general population. Cerebrovascular disease is weakly associated with aortic atherosclerosis, thereby questioning the overall importance of aortic atherosclerosis in the pathogenesis of cerebrovascular events in the general population.

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Are left atrial appendage flow velocities adequate surrogates of global left atrial function? A population-based transthoracic and transesophageal echocardiographic study.

BACKGROUND: Left atrial appendage (LAA) contraction velocities are used frequently as surrogates of global left atrial (LA) function, but the validity of this approach has not been confirmed. OBJECTIVE: The objective of our study was to assess the relationship between LAA flow velocities and multiple global LA variables. METHODS: The correlations between LAA contraction velocities and global LA variables (difference between maximal and minimal LA volumes, mitral inflow A velocity, atrial ejection force, mitral annulus late diastolic [a'] velocity, pulmonary vein atrial reversal velocity) were assessed in 349 subjects participating in the Stroke Prevention: Assessment of Risk in a Community study (age, 67 +/- 11 years; 53% men; all subjects in sinus rhythm), who were examined with transthoracic and transesophageal echocardiography. RESULTS: The correlations between LAA contraction velocities and multiple global LA variables were poor or nonsignificant. The best correlations, albeit weak, were between LAA velocities and mitral annulus a' velocities (r = 0.32 and r = 0.35 for correlations with septal and lateral annulus a' velocities, respectively, P <.001). Low LAA contraction velocities (lowest 10%, velocities <56 cm/s) were not sensitive in detecting low values (lowest 10%) of LA variables (sensitivity <0.2 for most LA variables). In a subgroup of subjects with lower left ventricular ejection fraction (< or =50%), the correlations between LAA velocities and LA variables were not apparently better than those in the total population. LAA velocities correlated negatively with LAA orifice diameter (r = -0.29, P =.002). The correlations between LAA velocities and global LA variables remained poor after correcting for LAA orifice size. CONCLUSION: LAA contraction velocities correlate poorly with multiple LA variables. Therefore, LAA flow velocities should not be used as surrogates of global LA function.

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