Doctor of Medicine, Yokohama City University (2003)
Peter Fitzgerald, Postdoctoral Faculty Sponsor
This study sought to determine the additional clinical value of gait speed to Framingham risk score (FRS), cardiac function, and comorbid conditions in predicting cardiovascular events in patients with ST-segment elevation myocardial infarction.There is growing evidence that gait speed is inversely associated with all-cause mortality, particularly cardiovascular mortality, among the elderly.We undertook a single-center prospective observational study of gait speed in 472 patients with ST-segment elevation myocardial infarction in Japan, between 2001 and 2008. Gait speeds were measured using a 200-m course before discharge in all patients, and we followed up cardiovascular events, which consist of cardiovascular deaths, nonfatal myocardial infarctions, and nonfatal ischemic strokes.During the 2,596 person-years of follow-up, 83 patients (17.6%) experienced cardiovascular events. Cardiovascular events increased across decreasing tertiles of gait speed (fastest tertile: n = 5, 3.2%; middle tertile: n = 20, 12.6%; slowest tertile, n = 58, 36.7%). By multiple adjusted Cox proportional hazards analysis, gait speed was a significant and independent predictor of cardiovascular events (hazard ratio for increasing 0.1 m/s of gait speed: 0.71, 95% confidence interval [CI]: 0.63 to 0.81, p < 0.001). The addition of gait speed to the model incorporating FRS, B-type natriuretic peptide levels, and comorbidity index improved reclassification (net reclassification index: 32.8%, 95% CI: 17.4 to 48.3, p < 0.001) and the C-statistics with a reasonable global fit and calibration (C-statistics: from 0.703 [95% CI: 0.636 to 0.763] to 0.786 [95% CI: 0.738 to 0.829]).Among patients with ST-segment elevation myocardial infarction, slow gait speed was significantly associated with an increased risk of cardiovascular events. (Gait Speed for Predicting Cardiovascular Events After Myocardial Infarction; NCT01484158).
View details for DOI 10.1016/j.jacc.2013.02.020
View details for Web of Science ID 000318910300006
View details for PubMedID 23500222
To assess the mechanism of long-term LDL-C-lowering effect of ezetimibe-plus-statin.Coronary artery disease patients whose LDL-C ? 70 mg/dL after treatment with atorvastatin 10 mg/day or rosuvastatin 2.5 mg/day were randomly assigned to receive ezetimibe 10 mg/day + statin (n = 78) or double-dose statin (n = 72) for 52 weeks.Greater LDL-C reduction was observed and maintained until 52 weeks in ezetimibe-plus-statin, while LDL-C levels re-increased after 12 weeks in double-dose statin. Although lathosterol/TC increased, campesterol/TC decreased more in ezetimibe-plus-statin. In contrast, lathosterol/TC unchanged and campesterol/TC increased, increasing campesterol/lathosterol ratio for 52 weeks in double-dose statin. Plasma PCSK9 levels were higher in double-dose statin than in ezetimibe-plus-statin at 12 weeks, but similar at 52 weeks.Although the difference in PCSK9 between 2 groups was transient, that in both campesterol and lathosterol persisted until 52 weeks. These results demonstrated simultaneous inhibition of cholesterol absorption and synthesis provides stable and greater decrease in LDL-C levels.
View details for DOI 10.1016/j.atherosclerosis.2012.07.036
View details for Web of Science ID 000309261400028
View details for PubMedID 22892323
Ezetimibe-plus-statin therapy has been reported to provide greater reduction in low-density lipoprotein cholesterol (LDL-C) level than statin monotherapy. The aim of the present study was to evaluate the relationship between LDL-C lowering effect and baseline cholesterol absorption and synthesis markers in patients with coronary artery disease (CAD).A total of 171 patients with CAD whose LDL-C level was ? 100 mg/dl after treatment with atorvastatin (10mg/day) or rosuvastatin (2.5 mg/day) for 4 weeks were assigned to additionally receive ezetimibe (10mg/day) plus a statin or a double dose of statin for 12 weeks. The decreases in LDL-C (-30.0 ± 15.6 mg/dl vs. -19.2 ± 14.2 mg/dl) and the ratio of campesterol, an absorption marker, to total cholesterol levels (-1.35 ± 0.90 µg/mg vs. 0.33 ± 0.74 µg/mg) were greater in the ezetimibe-plus-statin group (P<0.05, respectively). The decrease in LDL-C level in the ezetimibe-plus-statin group was greatest in patients with baseline levels of higher absorption and lower synthesis markers and smallest in patients with baseline levels of lower absorption and higher synthesis markers (-34.3 ± 15.6 mg/dl vs. -21.5 ± 16.7 mg/dl, P<0.05). The decrease in LDL-C did not differ, irrespective of baseline levels of cholesterol absorption and synthesis markers, in the double-dose statin group, and was similar to that in patients with lower absorption and higher synthesis markers in the ezetimibe-plus-statin group.Ezetimibe-plus-statin therapy may be useful for lowering LDL-C level, irrespective of baseline levels of cholesterol absorption and synthesis markers.
View details for DOI 10.1253/circj.CJ-11-0391
View details for Web of Science ID 000295428200034
View details for PubMedID 21817821