Objectives To assess the relationship of left atrial (LA) phasic volumes and LA reservoir function with subclinical cerebrovascular disease in a stroke-free community-based cohort. Background An increase in LA size is associated with cardiovascular events including stroke. However, it is not known whether LA phasic volumes and reservoir function are associated with subclinical cerebrovascular disease. Methods LA minimum (LAVmin) and maximum (LAVmax) volumes, and LA reservoir function, measured as total emptying volume (LAEV) and total emptying fraction (LAEF), were assessed by real-time three-dimensional echocardiography in 455 stroke-free participants from the community-based Cardiovascular Abnormalities and Brain Lesions (CABL) study. Subclinical cerebrovascular disease was assessed as silent brain infarcts (SBI) and white matter hyperintensity volume (WMHV) by brain magnetic resonance imaging (MRI). Results SBI prevalence was 15.4%; mean WMHV was 0.66±0.92%. Participants with SBI showed greater LAVmin (17.1±9.3 vs. 12.5±5.6 ml/m2, p<0.01) and LAVmax (26.6±8.8 vs. 23.3±7.0 ml/m2, p<0.01) compared to those without SBI. LAEV (9.5±3.4 vs. 10.8±3.9 ml/m2, p<0.01) and LAEF (38.7±14.7% vs. 47.0±11.9%, p<0.01) were also reduced in participants with SBI. In univariate analyses, greater LA volumes and smaller reservoir function were significantly associated with greater WMHV. In multivariate analyses, LAVmin remained significantly associated with SBI [adjusted odds ratio (OR) per SD increase: 1.37, 95% confidence intervals (CI) 1.04–1.80, p<0.05] and with WMHV (β=0.12, p<0.01), whereas LAVmax was not independently associated with either. Smaller LAEF was independently associated with SBI (adjusted OR=0.67, 95% CI 0.50–0.90, p<0.01) and WMHV (β=−0.09, p<0.05). Conclusions Greater LA volumes and reduced LA reservoir function are associated with subclinical cerebrovascular disease detected by brain MRI in subjects without history of stroke. LAVmin and LAEF, in particular, are more strongly associated with SBI and WMHV than the more commonly measured LAVmax, and their relationship with subclinical brain lesions is independent of other cardiovascular risk factors.

Objectives We sought to assess the association between the presence of a septal pouch in the left atrium and ischemic stroke. Background Recently, a new anatomical entity, named a left septal pouch (LSP), was described in a pathology study. It was suggested that the presence of LSP may favor the stasis of blood and possibly result in thromboembolic complications. However, the embolic potential of a LSP is not known. Methods The association between LSP and risk of stroke was assessed using a population-based case-control study design. The presence of LSP was assessed by transesophageal echocardiography in 187 patients over age 50 with first-ever ischemic stroke (96 men, mean age 70.6 ± 9.0 years) and in 157 control subjects matched to patients by age, sex, and race/ethnicity. The association between LSP and risk of stroke was assessed after adjustment for other stroke risk factors. Results Patients with LSPs were younger (67.5 ± 9.1 vs. 69.6 ± 8.8; p=0.046) and had a lower proportion of hypertension (68.0% vs. 80.3%; p=0.01). There were no difference in the prevalence of LSP between stroke patients and control subjects (28.9% vs. 29.3%; p=0.93). The subgroup of 69 patients (36.9%) with crytptogenic stroke showed a similar prevalence of LSP (31.9% vs. 29.3%; p=0.70). Multivariable analysis showed that the presence of LSP was not associated with ischemic stroke (OR 1.09, 95% CI 0.64 to 1.85) or cryptogenic stroke (OR 1.41, 95% CI 0.71 to 2.78). Conclusions This study does not demonstrate evidence for association of the presence of LSP with ischemic stroke, or with cryptogenic stroke. The stroke risk associated with LSP may still require further evaluation in the younger stroke populations. The possibility that associated cofactors that may turn LSP from an innocent bystander into a causative mechanism for stroke remain to be elucidated.

Direct measurement of multiple VC areas using 3D transesophageal echocardiography allows for assessing MR severity in patients with multiple jets, particularly for MR degrees greater than mild and in cases of more than 2 jets, for which geometric assumptions may be challenging.

bstructive sleep apnea (OSA) is common, underdiagnosed and associated with cardiovascular diseases such as heart failure, left ventricular (LV) and right ventricular (RV) dysfunction, myocardial infarction, arrhythmias, and systemic and pulmonary hypertension. 1 Previous studies have shown the adverse affects of OSA on both LV and RV functions. 2,3 However, many risk factors for OSA, such as excess weight, male sex and advanced age, are the same as the risk factors for cardiovascular diseases. Proving that OSA actually causes cardiac dysfunction independent of these confounding risk factors is difficult. Early recognition of RV dysfunction before pulmonary arterial (PA) hypertension develops is important for preventing further progression to heart failure and even death. 4 Thus, there is a need for a more detailed analysis of its pathophysiologic importance and for techniques that may supplement available technology in identifying early signs of RV impairment. Editorial p 250Recently, tissue Doppler imaging (TDI) and strain/strain rate (SR) imaging have been shown to be reliable and accurate novel techniques for evaluating global and regional ventricular function. 5 As TDI has the disadvantage of being preload and afterload dependent, a new TDI-derived index of isovolumic myocardial acceleration (IVA) has been validated to be a reliable and relatively load independent measure of cardiac systolic function. 6 Velocity vector imaging (VVI) is a novel method based on 2-dimensional B-mode images. The method involves tracking ultrasonic speckles permitting angle-independent measurement of tissue velocity and deformation. 7 It has been shown to be a reliable method for the quantification of regional contractile dysfunction with the ability to detect subclinical cardiac dysfunction. 8 In this study, VVI and TDI were used to evaluate regional subclinical RV dysfunction in newly diagnosed moderate-to-severe OSA The aims of this study were to evaluate subclinical regional right ventricular (RV) dysfunction in newly diagnosed obstructive sleep apnea (OSA) patients without systemic and pulmonary arterial (PA) hypertension, and to correlate OSA severity to RV dysfunction, using both velocity vector imaging (VVI)-derived strain imaging and tissue Doppler imaging (TDI).

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Although ambulatory blood pressure (BP) is a better predictor of cardiovascular outcomes than office BP, its association with subclinical cerebrovascular disease is not clarified. We investigated the associations of office and ambulatory BP values with subclinical cerebrovascular disease in a population based, predominantly elderly cohort without prior stroke.

Objective To determine the prevalence and correlates of subclinical myocardial inflammation in patients with rheumatoid arthritis (RA). Methods RA patients (n = 119) without known cardiovascular disease underwent cardiac 18‐fluorodeoxyglucose (FDG) positron emission tomography with computed tomography (PET‐CT). Myocardial FDG uptake was assessed visually and measured quantitatively as the standardized uptake value (SUV). Multivariable linear regression was used to assess the associations of patient characteristics with myocardial SUVs. A subset of RA patients who had to escalate their disease‐modifying antirheumatic drug (DMARD) therapy (n = 8) underwent a second FDG PET‐CT scan after 6 months, to assess treatment‐associated changes in myocardial FDG uptake. Results Visually assessed FDG uptake was observed in 46 (39%) of the 119 RA patients, and 21 patients (18%) had abnormal quantitatively assessed myocardial FDG uptake (i.e., mean of the mean SUV [SUVmean] ≥3.10 units; defined as 2 SD above the value in a reference group of 27 non‐RA subjects). The SUVmean was 31% higher in patients with a Clinical Disease Activity Index (CDAI) score of ≥10 (moderate‐to‐high disease activity) as compared with those with lower CDAI scores (low disease activity or remission) (P = 0.005), after adjustment for potential confounders. The adjusted SUVmean was 26% lower among those treated with a non–tumor necrosis factor–targeted biologic agent compared with those treated with conventional (nonbiologic) DMARDs (P = 0.029). In the longitudinal substudy, the myocardial SUVmean decreased from 4.50 units to 2.30 units over 6 months, which paralleled the decrease in the mean CDAI from a score of 23 to a score of 12. Conclusion Subclinical myocardial inflammation is frequent in patients with RA, is associated with RA disease activity, and may decrease with RA therapy. Future longitudinal studies will be required to assess whether reduction in myocardial inflammation will reduce heart failure risk in RA.

Objectives: We investigated right ventricular (RV) structural and functional cardiac alterations in obstructive sleep apnea (OSA) independent of systemic hypertension and their correlation to the severity of OSA. Methods: Forty-one moderate-to-severe OSA but otherwise healthy patients and 30 body mass index-matched control subjects were included. All subjects underwent 24-hour ambulatory blood pressure monitoring, standard and tissue Doppler imaging of the RV. Results: The OSA group had increased RV wall thickness, impaired right ventricular outflow tract fractional shortening (RVOT fs), tricuspid annular plane systolic excursion (TAPSE), RV myocardial performance index (MPI) and RV myocardial acceleration during isovolumic contraction (IVA) (p < 0.001). Apnea hypopnea index (AHI) and mean pulmonary artery (PA) pressure were correlated with all these indices (p < 0.01 for all). RV free wall thickness (p < 0.001) and IVA (p = 0.006) remained significant predictors of AHI after adjusting for age, body mass index, mean PA pressure, RVOT fs, TAPSE and MPI in a multiple stepwise linear regression model. Conclusions: OSA is associated with impaired RV function despite normal systemic blood pressures. The level of RV dysfunction has a direct relationship with the severity of OSA. RV free wall thickness and IVA are independent predictors of AHI in uncomplicated OSA patients.