Longevity-associated NADH dehydrogenase subunit-2 237 Leu/Met polymorphism modulates the effects of daily alcohol drinking on yearly changes in serum total and LDL cholesterol in Japanese men.

Reduced nicotinamide adenine dinucleotide (NADH) dehydrogenase subunit 2 237 leucine/methionine (ND2-237 Leu/Met) polymorphism, is reportedly associated with longevity in the Japanese population. The ND2-237Met genotype may exert resistance to atherogenic diseases, such as myocardial infarction or cerebrovascular disorders. To investigate whether ND2-237 Leu/Met polymorphism is associated with yearly changes in serum lipid levels, we conducted a longitudinal study of 107 healthy Japanese male subjects. Analysis of covariance revealed that the interaction between the ND2-237 Leu/Met genotypes and habitual drinking was significantly associated with yearly changes in serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDLC) levels (p=0.036 and p=0.006, respectively). In multiple regression analysis, daily drinking was significantly and positively associated with yearly changes in serum LDLC levels in men with ND2-237Met (p=0.026). After adjusting for covariates, yearly changes in serum LDLC levels were significantly lower in non-daily drinkers with ND2-237Met than in those with ND2-237Leu (p=0.047). These results suggest that ND2-237Met has a beneficial impact on yearly changes in serum LDLC in non-daily drinkers but not in daily drinkers.

A population-based study of arterial stiffness index in relation to cardiovascular risk factors.

We investigated the relation of arterial stiffness, considered an independent predictor of cardiovascular events, to cardiovascular risk factors in a population-based study of 1023 subjects. An Arterial Stiffness Index (ASI) was developed to evaluate arterial stiffness based on an analysis of the pulse wave amplitude pattern acquired from measurements of brachial blood pressure. In control subjects (n = 266) without any major risk factors, the ASI was 46 +/- 11, and increased with age (r = 0.346). The ASI was significantly higher in women ranging from 50 to 54 years of age than in age-matched men. The ASI rose in correlation with the number of risk factors. Subjects with two risk factors showed a significantly higher ASI than those without any risk factors (54 +/- 26 vs. 46 +/- 11). The ASI was significantly increased in diabetic subjects with hypertension in comparison to those without hypertension. Furthermore, hyperlipidemic subjects with hypertension showed significantly higher values than those without hypertension. ASI could be a useful predictor of cardiovascular events in hypertensive subjects with multiple risk factors.

Long-term inhibition of intimal hyperplasia using vascular photodynamic therapy in balloon-injured carotid arteries.

Flexible treatments for intimal hyperplasia after angioplasty are still needed. The aim of this study was to demonstrate the long-term effects of vascular photodynamic therapy with talaporfin sodium on intimal hyperplasia following interventional injury. Intimal hyperplasia was induced by balloon distension injury to the carotid artery in 31 rabbits. Talaporfin, 5.0 mg/kg, was delivered systemically immediately after balloon injury. The injury site was irradiated with a diode laser light of wavelength 664 nm using a fluence of 50 J/cm2 after 30 min. At day 3 and weeks 3, 6, 9, 15, and 25 after photodynamic therapy, the treated artery of each rabbit was excised and examined immunohistochemically. Thirty minutes after talaporfin administration, drug fluorescence was found only in the balloon-injured carotid artery wall. At 3 days, no smooth muscle cells were seen in the media of the photodynamic therapy-treated arterial segments. Intimal hyperplasia developed progressively in the balloon-injured and untreated segments; however, in the segments treated with photodynamic therapy, intimal hyperplasia was markedly suppressed until 25 weeks and the media was repopulated by smooth muscle cells without macrophages. Vascular photodynamic therapy with talaporfin may be used to inhibit restenosis after vascular intervention.