Fat in the renal sinus (RS), a region of the kidney in which low pressure venous and lymphatic vessels are present, may indirectly influence blood pressure (BP). The purpose of this study was to assess the association between RS fat and control of BP upon receipt of antihypertensive medications. Two hundred-five (205) participants aged 55 to 85 years at risk for cardiovascular (CV) events underwent magnetic resonance imaging assessments of abdominal and RS fat, measurement of blood pressure, and determination of the number of prescribed antihypertensive medications. Multivariable linear regression was used to determine associations between RS fat, blood pressure, and the number of prescribed antihypertensive medications. Abdominal fat averaged (416 ± 160 cm3, median and interquartile range (IQR) of 396 cm3 and 308 to 518 cm3); intraperitoneal (IP) fat averaged (141 ± 73 cm3, median and IQR of 129 cm3 and 86 to 194 cm3); and RS fat averaged (4.6 ± 3.2 cm3, median and IQR of 4.2 cm3 and 2.2 to 6.6 cm3). After accounting for age, gender, height, body mass index (BMI), and IP fat, RS fat correlated with the number of prescribed antihypertensive medications (p=0.010), stage II hypertension (p=0.02), and renal size (p=<0.001). In conclusion, after accounting for other body fat depots and risk factors for hypertension, renal sinus fat volume is associated with the number of prescribed antihypertensive medications and stage II hypertension. These results indicate that further studies are warranted to determine if fat accumulation in the renal sinus promotes hypertension.
Background Limited data exist on the prevalence, associations and prognosis of individuals with asymptomatic left ventricular systolic dysfunction (ALVSD), especially in populations without prior clinical cardiovascular disease (CVD). Methods and Results Kaplan-Meier and Cox proportional hazard analyses were used to assess the association between ALVSD, defined as left ventricular ejection fraction less than 50%, and adjudicated incident congestive heart failure (CHF), all-cause mortality, and CVD events. Out of 5004 participants, 112 participants had CHF, 321 had a CVD event, and 278 died after 9 years of follow-up. The overall prevalence of ALVSD was 1.7%, with a higher prevalence in African Americans (2.6%). ALVSD had worse cardiovascular risk profile and was also associated with increased risk in unadjusted and adjusted models for incident CHF [HR (95%): 12.0(7.04 – 20.3), p<0.0001 and 8.69(4.89 – 15.45), p<0.001 respectively], CVD [HR (95%):3.32(1.98 -5.58), p<0.001 and 2.21(1.30 – 3.73), p=0.003 respectively] and all-cause mortality [HR(95%):3.47(2.03 – 5.94), p<0.0001 and 2.00(1.13-3.54), p=0.017 respectively]. A 10% decrement in LVEF at baseline was associated with increase in risk in unadjusted and adjusted models for clinical CHF [HR (95%CI): 2.17(1.82 -2.63), p<0.0001 and 2.13(1.73 - 2.51), p<0.001 respectively] and all-cause mortality [HR (95%CI): 1.22(1.05 – 1.41), p=0.009 and 1.17(1.00 – 1.36), p=0.047 respectively]. Among the subset of participants with ALVSD, LVMI was particularly informative about risk for incident CHF (c- index = 0.74). Conclusions ALVSD is uncommon in individuals without prior clinical CVD, but is associated with high risk for CHF, CVD, and all-cause mortality. LVMI had good discrimination for incident CHF in MESA participants with ALVSD.
Background:This study was to evaluate the prognostic significance of low gradient severe aortic stenosis (LG SAS) and preserved left ventricular ejection fraction (LVEF) with the integration of echocardiographic and clinical data. Methods:The study included 172 patients with LG SAS (AVAi ≤ 0.6 cm 2 /m 2 , mean aortic pressure gradient < 40 mm Hg) and LVEF (≥ 50%). LV outflow tract diameters were measured at both the aortic valve annulus and 5 mm below the annulus for the measurement consistency. Patients were divided into the low flow LG SAS (LF/LG SAS: SVi < 35mL/m 2 and AVAi ≤ 0.6 cm 2 /m 2 ) and normal-flow LG SAS groups (NF/LG SAS: SVi ≥ 35mL/m 2 and AVAi ≤ 0.6 cm 2 /m 2 ). Echocardiographic findings and clinical data were systematically analyzed with mean follow-up of 3.0 ± 1.6 years.Results: LF/LG SAS had significantly smaller AVAi, lower SVi, a higher prevalence of atrial fibrillation (28% vs 12% P = .01) and diabetes (47% vs 27% P = .007) and lower 3-year cumulative survival than NF/LG SAS. Multivariable analysis showed that dyspnea, renal dysfunction (CI 1.42-3.99, P < .01), left atrial diameter, and SVi were independently associated with an increased risk for all-cause mortality. Aortic valve intervention (AVI) improved survival in LF/LG SAS (68% vs 48%, P < .05) in comparison with medical management (HR: 4.20, CI: 1.12-15.76, P = .03), but only modestly in NF/LG SAS (75% vs 65% P > .05). Conclusion:Outcome of LG SAS was independently associated with clinical characteristics. AVI likely improved outcome of LF/LG SAS who had high-risk clinical characteristics and unfavorable echocardiographic findings. K E Y W O R D Saortic stenosis, aortic valve area, aortic valve intervention, echocardiography, stroke volume
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