Aim: Cerebral white matter lesions (WML) are known to increase with age, as is left ventricular (LV) diastolic dysfunction with normal contraction. Although aging is a common risk factor, the link between these diseases is not fully understood. The aim was to clarify this relationship, using the ratio between early diastolic mitral inflow and early diastolic mitral annular tissue velocity (E/E'). E/E' measured by tissue Doppler echocardiography offers an indicator of the severity of LV diastolic dysfunction, reflecting both diastolic LV stiffness and diastolic LV filling pressure. Methods:Participants comprised 75 patients aged between 65 and 75 years with normal LV contraction and no signs or history of symptomatic heart failure, ischemic heart diseases, atrial fibrillation, stroke, or cognitive dysfunction. The volume of WML was quantified on brain magnetic resonance imaging. Results:The participants were classified into three groups: Low E/E', E/E' ≤ 8; Middle E/E', 8 < E/E' < 15; and High E/E', E/E' ≥ 15. WML volume was 3.6 ± 3.0 mL in Low E/E', 5.4 ± 6.5 mL in Middle E/E' and 12.0 ± 11.0 mL in High E/E', increasing significantly with increased diastolic LV stiffness (Low vs High, P = 0.034; Middle vs High, P = 0.016). Linear regression analysis showed the positive association between the volume of WML and E/E' ratio (r = 0.377, P = 0.0009). Conclusions:This investigation identified an association between LV diastolic dysfunction and WML. Further investigations are required to clarify whether there is a direct association between the two diseases. Geriatr Gerontol Int 2014; 14 (Suppl. 2): 71-76.Keywords: cerebral white matter lesions, left ventricular diastolic dysfunction, ratio of early diastolic mitral inflow to early diastolic mitral annular tissue velocity.

Impaired renal function was related to higher percentage of lipid volume and lower percentage of fibrous volume in coronary plaque. Our findings may explain the increasing risk of cardiovascular events in patients with renal dysfunction.

Aim: Cerebral white matter hyperintensity (WMH) is highly prevalent in the elderly population, and increases the risk of dementia and stroke. We investigated the relationship between ambulatory blood pressure monitoring levels and quantitatively measured WMH volumes among elderly hypertensive patients with well-controlled blood pressure (BP) to re-evaluated effective hypertension management methods to prevent the progression of WMH. Methods:Participants comprised 84 hypertensive patients aged between 65 and 75 years without symptomatic heart failure, ischemic heart disease, atrial fibrillation, stroke or cognitive dysfunction.Results: Linear regression analysis showed that office BP was not associated with WMH volume increases. Raised night-time systolic BP (P = 0.013) were associated with greater WMH volumes during ambulatory blood pressure monitoring. To clarify the effect of asleep systolic BP on WML volume, we then classified patients into two systolic BP groups as follows: <125 mmHg (n = 47) and ≥125 mmHg (n = 37). Baseline characteristics were almost similar in both groups, except the dipper type of circadian BP variation was significantly common in the group with night-time systolic BP <125 mmHg. However, WMH volume was greater in the group with night-time systolic BP ≥125 mmHg than that in the <125 mmHg group (9.0 ± 8.4 mL vs 4.1 ± 4.3 mL, P = 0.015). Conclusion:Higher night-time systolic BP levels were observed to contribute greater WMH volumes in elderly hypertensive patients. To prevent the progression of WMH, controlling BP on the basis of ambulatory blood pressure monitoring is important. Geriatr Gerontol Int 2015; 15 (Suppl. 1): 59-65.Keywords: ambulatory blood pressure monitoring, cerebral white matter hyperintensity, circadian blood pressure variation, night-time blood pressure, office blood pressure.

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In atherosclerosis, plaque vulnerability is strongly related to rupture, and vulnerable plaques contain numerous inflammatory cells, particularly macrophages, suggesting that inflammation is closely associated with plaque instability. Recently, it has been suggested that F-18 fluorodeoxyglucose (FDG) on positron emission tomography (PET) is a useful technique for detection of local inflamed atherosclerotic lesions. We therefore examined the effects of atorvastatin on F-18-FDG accumulations in atherosclerotic plaques at common carotid and ascending aorta. A total of 20 patients with dyslipidemia but not treated with medication were enrolled and imaged using F-18-FDG -PET and CT for baseline measurement. They were randomized to receive 20-mg or 5-mg atorvastatin after imaging and F-18-FDG -PET and CT were checked again 6 months later. Changes in the standard uptake value (SUV) of F-18-FDG-accumulation rate (plaque/integral plasma) between baseline and follow-up were evaluated. After atorvastatin treatment, serum C-reactive protein (CRP) levels, low-density lipoprotein (LDL) cholesterol levels and malondialdehyde-modified LDL (MDA-LDL) cholesterol levels were significantly reduced (CRP levels: from 1277±704 mg/dl to 609±314 mg/dl, p < 0.0001, LDL cholesterol levels: from 154±29 mg/dl to 98±29 mg/dl, p < 0.0001, MDA-LDL cholesterol levels: 178.4±70.8 IU/l to 125.4±49.7 IU/l, p < 0.0001, respectively). The maximum SUV significantly decreased at follow-up (common carotid arteries: from 1.36 ±0.13 g/dl to 1.28 ±0.22 g/dl, p = 0.047, ascending aorta: from 1.63 ±0.20 g/dl to 1.53 ±0.16 g/dl, p = 0.032, respectively). Notably, the decrease in the SUV was well correlated with reduction of serum CRP levels (common carotid arteries: r = 0.52, ascending aorta: r = 0.47, respectively), LDL cholesterol levels (common carotid arteries: r = 0.46, ascending aorta: r = 0.43, respectively) and MDA-LDL cholesterol levels (common carotid arteries: r = 0.47, ascending aorta: r = 0.43, respectively). Six-month atorvastatin treatment had anti-inflammatory effects and decreased SUV detected by F-18-FDG -PET, which might represent regression of aortic vulnerability.

Background: The left main coronary artery (LMCA) is an important target of atherosclerotic plaque accumulation. The purpose of this study is to investigate the relationship between metabolic syndrome and plaque characteristics at LMCA. Methods: We enrolled 63 consecutive patients with stable angina who underwent percutaneous coronary intervention (PCI). Using intravascular ultrasound (IVUS), cross-sectional area (CSA), lumen area and plaque area were checked at LMCA undergoing PCI for the left anterior descending coronary artery or left circumflex coronary artery but not LMCA. Total plaque volume at LMCA was also checked by IVUS. The tissue characteristics of coronary plaque at LMCA was analyzed and quantified using integrated backscatter (IB) IVUS. The patients were devided into the two groups who had metabolic syndrome (n = 34) or not (n = 39). We evaluated the relationship between plaque burden at LMCA and metabolic syndrome. Results: Patients with metabolic syndrome had significantly larger plaque area and CSA at minimum lumen area (MLA) of LMCA than patients without metabolic syndrome (10.8 ± 3.7mm2 vs 8.2 ± 4.4 mm2, p = 0.01, 25.8 ± 5.0mm2 vs 23.1 ± 5.4 mm2, p = 0.04, respectively). About total plaque volume at LMCA, patients with metabolic syndrome had also significantly larger volume than patients without metabolic syndrome (53.8 ± 24.7mm3 vs 39.8 ± 21.2 mm3, p = 0.021, respectively). Furthermore, the lipid component of plaque volume at LMCA using IB-IVUS was significantly larger in patients with metabolic syndrome than without metabolic syndrome (25.7 ± 12.1mm3 vs 19.3 ± 11.6 mm3, p = 0.038, respectively). Conclusion: These findings suggest that patients with metabolic syndrome have not only larger plaque but also lipid-rich plaque at LMCA than without metabolic syndrome. IVUS and IB-IVUS Parameter at LMCA

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