Associations of the Alpha-Actinin Three Genotype with Bone and Muscle Mass Loss among Middle-Aged and Older Adults.

Bone and muscle mass loss are known to occur simultaneously. The alpha-actinin three (ACTN3) genotype has been shown to potentially affect bone and muscle mass. In this study, we investigated the association between the ACTN3 genotype and bone and muscle mass loss in community-dwelling adults aged ≥ 60 years. This study was a cross-sectional analysis of data from 295 participants who participated in a community health checkup. The ACTN3 genotypes were classified as RR, RX, or XX types. Bone mass loss was defined as a calcaneal speed of sound T-score of <−1.32 and <−1.37, and muscle mass loss was defined as an appendicular skeletal muscle index of <7.0 kg/m2 and <5.7 kg/m2 in men and women, respectively. The percentages of XX, RX, and RR in the combined bone and muscle mass loss group were 33.8%, 30.8%, and 16.7%, respectively, with a significantly higher trend for XX. Multinomial logistic regression analysis showed that XX had an odds ratio of 3.00 (95% confidence interval 1.05−8.54) of being in the combined bone and muscle mass loss group compared to the RR group (covariates: age, sex, grip strength, and medications). The ACTN3 genotype of XX is associated with a higher rate of comorbid bone and muscle mass loss. Therefore, ACTN3 genotyping should be considered for preventing combined bone and muscle mass loss.

Modification of treatment strategies over a period of 14 years has markedly reduced cardiac events among post-myocardial infarction patients.

Recent trends in the treatment of post-myocardial infarction (MI) patients and the factors accounting for the improvement in outcome are presented. A total of 6,602 post-MI patients (5,320 males, 1,282 females; 58.9 +/- 10.4 years of age) enrolled between 1986 and 1999 were followed up for an average of 12.6 +/- 16.3 months. The incidence of cardiac events, which included fatal and nonfatal recurrent MIs, sudden death and death by congestive heart failure, was highest (44.9 events/1,000 person year) in 1986-1987, but decreased steadily to 22.5 events/1,000 person year by 1997-1999 (Trend p<0.0001). This trend accompanied the increased use of coronary thrombolysis, percutaneous transluminal coronary angioplasty and coronary artery bypass graft surgery, increased prescription of antiplatelet agents (51.5%-83.4%), lipid-lowering agents (29.8%-52.6%) and angiotensin-converting enzyme inhibitors (5.3%-->41.0%), and reduced prescription of calcium antagonists (68.5%-41.0%) and nitrates (60.7%-->45.7%). These changes in treatment have led to a decreased incidence of angina pectoris, wall motion abnormalities and abnormal Q waves on electrocardiograms. The decline in the incidence of cardiac events among post-MI patients in the 14 years between 1986 and 1999 reflects implementation of new therapeutic modalities proven to be effective in clinical trials and in daily practice.

Pravastatin reduces the incidence of cardiac events among patients with myocardial infarction.

We retrospectively compared the incidence of cardiac events in myocardial infarction (MI) patients treated in our departments between 1990 and 1999 with pravastatin or without cholesterol-lowering agents. Our aim was to evaluate the efficacy of pravastatin in the secondary prevention of MI. Cardiac events--defined as fatal or nonfatal recurrent MI, sudden cardiac death, and death from congestive heart failure--occurred in 8 (2.2%) of 356 MI patients treated with pravastatin (17.1 cases/1.000 person x year) and in 39 (5.6%) of 700 MI patients not treated with cholesterol-lowering agents (54.3 cases/1000 person x year), which represented a significant decline among those taking pravastatin (P < 0.05, odds ratio: 0.39, 95% (CI: 0.18-0.84). Likewise, total mortality was significantly lower among patients treated with pravastatin (18 cases, 5.1%; 38.4 cases/1,000 person x year vs 77 cases, 11.0%; 107.2 cases/1,000 person x year, P < 0.01, odds ratio: 0.43, 95% CI: 0.25-0.73). Subgroup analysis revealed a significantly lower incidence or cardiac events in the pravastatin group for 6 of the items among 53 patient characteristics, and was lower but not significant for 45 items and was greater but not significant only for 2 items. Furthermore, multivariate analysis confirmed pravastatin to be a useful factor for preventing the occurrence of cardiac events in MI patients (P < 0.05, odds ratio: (0.44, 95% CI: 0.20-0.95), and Kaplan-Meier curves also showed pravastatin to significantly reduce the incidence of both cardiac events and total mortality. These findings are consistent with those previously reported by several large-scale clinical trials carried out in Western countries, and demonstrate that pravastatin is useful for secondary prevention of MI in Japanese patients.