Impact of moderate to vigorous intensity physical activity on change in renal function in patients after acute myocardial infarction.

Acute myocardial infarction (AMI) is associated with a decline in renal function. This study aimed to investigate the impact of engaging in moderate to vigorous intensity physical activity (MVPA) for more than 30 min per day on changes in renal function during the first 3 months after AMI onset. A prospective, observational study was conducted, enrolling 87 patients (75 men; average age, 65.2 ± 12.5 years) who had experienced AMI. The cystatin C-based estimated glomerular filtration rate (eGFRcys) was collected at and 3 months after discharge. Daily MVPA was measured using triaxial accelerometers at a threshold of 3.0 Metabolic equivalent of the task for 3 months. Generalized estimating equations (GEE) were applied to evaluate the longitudinal association between the number of days per week of MVPA for 30 min or more and within-patient changes in eGFRcys. The patients were categorized into three groups based on their MVPA engagement days: 0 days (n = 20), 1-2 days (n = 14), and 3-7 days (n = 53) groups. After adjusting for potential confounding variables, GEE analysis revealed that the eGFRcys slope over 3 months was significantly higher in the 3-7 days group than in 0 days group (B = 2.9, (95% confidence interval: 1.5-4.2), p < 0.001). Similar results were obtained when MVPA time thresholds were set to 40 and 60 min. These findings suggest a significant positive effect of engaging in MVPA for 30 min or more for 3-7 days per week in the improvement of renal function after AMI onset.

Association between physical activity and changes in renal function in patients after acute myocardial infarction: A dual-center prospective study.

BACKGROUND: Acute myocardial infarction (AMI) causes a decline in renal function. This study aimed to elucidate the longitudinal association between physical activity levels and changes in renal function up to 6 months after the onset of AMI. METHODS: In this dual-center prospective observational study, 73 AMI patients (67 men; average age, 65.0±11.7 years) were enrolled from 2017 to 2019. Blood biochemistry, urinalysis, and physical function tests were conducted at discharge and 3 and 6 months post-discharge. The renal function was evaluated based on cystatin C-based estimated glomerular filtration rate (eGFRcys). The number of steps was recorded for 6 months post-discharge. Generalized estimating equation (GEE) models were used to test the longitudinal association between physical activity levels and within-patient changes in eGFRcys. Both GEE models with a follow-up period of 3 and 6 months were constructed to assess the effects of the passage of time. RESULTS: Patients were stratified into the low (n=36; 2903±1187 steps/day) and high groups (n=37; 7988±3192 steps/day) based on the median number of steps. Both GEE models at the 3- (p=0.027) and 6-month follow-up (p=0.034) showed a significant positive association between the physical activity levels and within-patient changes in eGFRcys. The changes in eGFRcys at 6 months were -0.3 mL/min/1.73 m2 and +4.4 mL/min/1.73 m2 among the low and high group participants, respectively. CONCLUSIONS: There was a significant positive association between physical activity and renal function changes after the onset of AMI, which persisted when the follow-up period was extended from 3 to 6 months. Our findings support the importance of interventions that enable maintaining high physical activity levels as a strategy for preserving renal function in AMI patients.

Association between physical activity and change in renal function in patients after acute myocardial infarction.

BACKGROUND: Combined renal dysfunction worsens the subsequent prognosis in patients after acute myocardial infarction (AMI). Therefore, establishing a therapeutic modality to maintain or improve renal function in AMI patients is necessary. This study aimed to elucidate the association between physical activity level and change in renal function in such patients. DESIGN: Prospective and observational study. METHODS: We enrolled 41 patients (35 men; average age, 67.5 ± 12.6 years) after AMI onset. Blood biochemistry, urinalysis, and physical function tests were conducted at discharge and 3 months after discharge. Renal function was evaluated based on cystatin C based-estimated glomerular filtration rate (eGFRcys). The number of steps was recorded for 3 months post-discharge. Generalized estimating equations (GEE) was used to test the association between physical activity level and within-patient changes in eGFRcys. RESULTS: Patients were stratified into low (n = 21; number of steps, 2335 ± 1219 steps/day) and high groups (n = 20; number of steps, 7102 ± 2365 steps/day). eGFRcys significantly increased from baseline to after 3 months in the high group (76.5 ± 13.8 to 83.2 ± 16.0 mL/min/1.73 m2, q = 0.004), whereas no significant change was observed in the low group (65.1 ± 15.9 to 62.2 ± 20.2 mL/min/1.73 m2, q = 0.125). Result of GEE adjusted for potential confounding variables showed a significant positive association between physical activity level and within-patient changes in eGFRcys (p = 0.003). Changes in eGFRcys was -2.9 mL/min/1.73 m2 among low group versus +6.7 mL/min/1.73 m2 among high group. CONCLUSIONS: Physical activity level was positively associated with changes in renal function, demonstrating that high physical activity may suppress renal function decline in patients after AMI.

Attenuation of ischemic myocardial injury and dysfunction by cardiac fibroblast-derived factor(s).

Fibroblasts, the majority of non-cardiomyocytes in the heart, are known to release several kinds of substances such as cytokines and hormones that affect cell and tissue functions. We hypothesized that undefined substance (s) derived from cardiac fibroblasts may have the potential to protect against ischemic myocardium. To assess our hypothesis, using rats, we investigated: (1) the effect of cardiac fibroblast-conditioned medium (CM) on the viability of hypoxic cardiomyocytes in vitro, (2) the effect of CM on left ventricular (LV) function in global ischemia-reperfusion in an ex vive model, (3) the mechanism underlying cardioprotection by CM. Seventy-two hours after starting a hypoxic culture, the viability of cardiomyocytes was higher (P < 0.05) in the CM treated group (41.4%) compared to the control (20.5%). In Langendorff's preparation, 30 min after ischemia-reperfusion, LV end-diastolic pressure was lower, and LV developed pressure and -LVdP/dt were higher (P < 0.01 or P < 0.05) in the CM group than in the control, although coronary flow did not differ between the two groups. Pretreatment with a protein kinase C inhibitor or a mitochondrial ATP-sensitive K+ channel blocker attenuated these changes of LV function in the CM group. Such cardioprotection was achieved by a fraction of the CM having a molecular weight (MW) > 50,000, but not by that of the CM with a lower MW. In addition, a specific antibody against hepatocyte growth factor (HGF, MW is 84,000) did not reduce the cardioprotection afforded by CM. There may be an unknown cardioprotective substance other than HGF in rats, which mimics ischemic preconditioning and has MW > 50,000.

Characteristics of death of neonatal rat cardiomyocytes following hypoxia or hypoxia-reoxygenation: the association of apoptosis and cell membrane disintegrity.

Irreversibly injured cardiomyocytes are positive for terminal deoxynucleotidyl transferase nick end-labeling (TUNEL), making it controversial as to whether TUNEL-positive cardiomyocytes induced by hypoxia-reoxygenation are apoptotic (secondarily necrotic) or primarily necrotic. We investigated the relationship between plasma membrane integrity and DNA fragmentation in hypoxic-reoxygenated cardiomyocytes. Cardiomyocytes were prepared from neonatal rat heart and exposed to hypoxia. The plasma membrane integrity was assessed by propidium iodide (PI) staining. The mode of DNA fragmentation was assessed by TUNEL and in situ polymerase chain reaction ligation assay. Furthermore, caspase-3 activity was measured in hypoxic-reoxygenated cardiomyocytes. Reoxygenation for 24 h after 3-8 h of hypoxia increased TUNEL positivity. However, the appearance of PI-positivity preceded that of TUNEL at various time points following reoxygenation. In contrast, TUNEL-positive but PI-negative cells were rarely found. In the hypoxic-reoxygenated cells, caspase-3 activity was increased, and PI- and TUNEL-positive cardiomyocytes possessed a sufficient number of double-strand DNA breaks with single-base 3'-OH terminals. In cardiomyocytes subjected to hypoxia-reoxygenation, the appearance of TUNEL positivity was delayed in comparison to membrane disintegrity, but in these cells caspase-3 has been activated and the mode of DNA fragmentation was apoptosis-specific. Thus, hypoxia-reoxygenation induces apoptosis associated with cell membrane disintegrity in cardiomyocytes.