After myocardial infarction(MI), the heart undergoes extensive myocardial remodeling through the accumulation of fibrous tissue in both the infarcted and noninfarcted myocardium, which distorts tissue structure, incre...After myocardial infarction(MI), the heart undergoes extensive myocardial remodeling through the accumulation of fibrous tissue in both the infarcted and noninfarcted myocardium, which distorts tissue structure, increases tissue stiffness, and accounts for ventricular dysfunction. There is growing clinical consensus that exercise training may beneficially alter the course of post-MI myocardial remodeling and improve cardiac function. This review summarizes the present state of knowledge regarding the effect of post-MI exercise training on infarcted hearts. Due to the degree of difficulty to study a viable human heart at both protein and molecular levels, most of the detailed studies have been performed by using animal models. Although there are some negative reports indicating that post-MI exercise may further cause deterioration of the wounded hearts, a growing body of research from both human and animal experiments demonstrates that post-MI exercise may beneficially alter the course of wound healing and improve cardiac function. Furthermore, the improved function is likely due to exercise training-induced mitigation of reninangiotensin-aldosterone system, improved balance between matrix metalloproteinase-1 and tissue inhibitor of matrix metalloproteinase-1, favorable myosin heavy chain isoform switch, diminished oxidative stress, enhanced antioxidant capacity, improved mitochondrial calcium handling, and boosted myocardial angiogenesis. Additionally, meta-analyses revealed that exercise-based cardiac rehabilitation has proven to be effective, and remains one of the least expensive therapies for both the prevention and treatment of cardiovascular disease, and prevents re-infarction.展开更多
AIM: To examine the contribution of treatment resistant depression(TRD) to mortality in depressed postmyocardial infarction(MI) patients independent of biological and social predictors.METHODS: This secondary analysis...AIM: To examine the contribution of treatment resistant depression(TRD) to mortality in depressed postmyocardial infarction(MI) patients independent of biological and social predictors.METHODS: This secondary analysis study utilizes the Enhancing Recovery in Coronary Heart Disease(ENRICHD) clinical trial data.From 1834 depressed patients in the ENRICHD study,there were 770 depressed post-MI patients who were treated for depression.In this study,TRD is defined as having a less than 50% reduction in Hamilton Depression(HAM-D) score from baseline and a HAM-D score of greater than 10 in 6 mo after depression treatment began.Cox regression analysis was used to examine the independent contributions of TRD to mortality after controlling for the biological and social predictors.RESULTS: TRD occurred in 13.4%(n = 103) of the 770 patients treated for depression.Patients with TRD were significantly younger in age(P = 0.04)(mean = 57.0 years,SD = 11.7) than those without TRD(mean = 59.2 years,SD = 12.0).There was a significantly higher percentage of females with TRD(57.3%) compared to females without TRD(47.4%) [χ2(1) = 4.65,P = 0.031].There were significantly more current smokers with TRD(44.7%) than without TRD(33.0%) [χ2(1) = 7.34,P = 0.007].There were no significant differences in diabetes(P = 0.120),history of heart failure(P = 0.258),prior MI(P = 0.524),and prior stroke(P = 0.180) between patients with TRD and those without TRD.Mortality was 13%(n = 13) in patients with TRD and 7%(n = 49) in patients without TRD,with a mean follow-up of 29 mo(18 mo minimum and maximum of 4.5 years).TRD was a significant independent predictor of mortality(HR =1.995; 95%CI: 1.011-3.938,P = 0.046) after controlling for age(HR = 1.036; 95%CI: 1.011-1.061,P = 0.004),diabetes(HR = 2.912; 95%CI: 1.638-5.180,P < 0.001),heart failure(HR = 2.736; 95%CI: 1.551-4.827,P = 0.001),and smoking(HR = 0.502; 95%CI: 0.228-1.105,P = 0.087).CONCLUSION: The analysis of TRD in the ENRICHD study shows that the effective treatment of depression reduced mortal展开更多
文摘After myocardial infarction(MI), the heart undergoes extensive myocardial remodeling through the accumulation of fibrous tissue in both the infarcted and noninfarcted myocardium, which distorts tissue structure, increases tissue stiffness, and accounts for ventricular dysfunction. There is growing clinical consensus that exercise training may beneficially alter the course of post-MI myocardial remodeling and improve cardiac function. This review summarizes the present state of knowledge regarding the effect of post-MI exercise training on infarcted hearts. Due to the degree of difficulty to study a viable human heart at both protein and molecular levels, most of the detailed studies have been performed by using animal models. Although there are some negative reports indicating that post-MI exercise may further cause deterioration of the wounded hearts, a growing body of research from both human and animal experiments demonstrates that post-MI exercise may beneficially alter the course of wound healing and improve cardiac function. Furthermore, the improved function is likely due to exercise training-induced mitigation of reninangiotensin-aldosterone system, improved balance between matrix metalloproteinase-1 and tissue inhibitor of matrix metalloproteinase-1, favorable myosin heavy chain isoform switch, diminished oxidative stress, enhanced antioxidant capacity, improved mitochondrial calcium handling, and boosted myocardial angiogenesis. Additionally, meta-analyses revealed that exercise-based cardiac rehabilitation has proven to be effective, and remains one of the least expensive therapies for both the prevention and treatment of cardiovascular disease, and prevents re-infarction.
文摘AIM: To examine the contribution of treatment resistant depression(TRD) to mortality in depressed postmyocardial infarction(MI) patients independent of biological and social predictors.METHODS: This secondary analysis study utilizes the Enhancing Recovery in Coronary Heart Disease(ENRICHD) clinical trial data.From 1834 depressed patients in the ENRICHD study,there were 770 depressed post-MI patients who were treated for depression.In this study,TRD is defined as having a less than 50% reduction in Hamilton Depression(HAM-D) score from baseline and a HAM-D score of greater than 10 in 6 mo after depression treatment began.Cox regression analysis was used to examine the independent contributions of TRD to mortality after controlling for the biological and social predictors.RESULTS: TRD occurred in 13.4%(n = 103) of the 770 patients treated for depression.Patients with TRD were significantly younger in age(P = 0.04)(mean = 57.0 years,SD = 11.7) than those without TRD(mean = 59.2 years,SD = 12.0).There was a significantly higher percentage of females with TRD(57.3%) compared to females without TRD(47.4%) [χ2(1) = 4.65,P = 0.031].There were significantly more current smokers with TRD(44.7%) than without TRD(33.0%) [χ2(1) = 7.34,P = 0.007].There were no significant differences in diabetes(P = 0.120),history of heart failure(P = 0.258),prior MI(P = 0.524),and prior stroke(P = 0.180) between patients with TRD and those without TRD.Mortality was 13%(n = 13) in patients with TRD and 7%(n = 49) in patients without TRD,with a mean follow-up of 29 mo(18 mo minimum and maximum of 4.5 years).TRD was a significant independent predictor of mortality(HR =1.995; 95%CI: 1.011-3.938,P = 0.046) after controlling for age(HR = 1.036; 95%CI: 1.011-1.061,P = 0.004),diabetes(HR = 2.912; 95%CI: 1.638-5.180,P < 0.001),heart failure(HR = 2.736; 95%CI: 1.551-4.827,P = 0.001),and smoking(HR = 0.502; 95%CI: 0.228-1.105,P = 0.087).CONCLUSION: The analysis of TRD in the ENRICHD study shows that the effective treatment of depression reduced mortal
