Do Patients Maintain Proper Long-Term Cardiopulmonary Fitness Levels After Cardiac Rehabilitation? A Retrospective Study Using Medical Records

Objective@#To examine whether patients who participated in a cardiac rehabilitation (CR) program after hospitalization for acute coronary syndrome maintained cardiorespiratory fitness (CRF) in the community. @*Methods@#We conducted a retrospective study including 78 patients who underwent percutaneous coronary intervention or coronary artery bypass graft surgery at our hospital’s cardiovascular center and participated in a CR program and a 5-year follow-up evaluation. Patients were divided into a center-based CR (CBCR) group, participating in an electrocardiography-monitored exercise training in a hospital setting, and a home-based CR (HBCR) group, receiving aerobic exercise training and performed self-exercise at home. @*Results@#No significant differences were found between groups (p>0.05), except the proportion of non-smokers (CBCR 59.5% vs. HBCR 31.7%; p=0.01). In both groups, the maximal oxygen consumption (VO2max) increased significantly during the first 12 weeks of follow-up and remained at a steady state for the first year, but it decreased after the 1-year follow-up. Particularly, VO2max at 5 years decreased below the baseline value in the HBCR group. In the low CRF group, the CRF level significantly improved at 12 weeks, peaked at 1 year, and was still significantly different from the baseline value after 5 years. The high CRF group did not show any significant increase over time relative to the baseline value, but most patients in the high CRF group maintained relatively appropriate CRF levels after 5 years. @*Conclusion@#Continuous support should be provided to patients to maintain optimal CRF levels after completing a CR program.

Do Patients Maintain Proper Long-Term Cardiopulmonary Fitness Levels After Cardiac Rehabilitation? A Retrospective Study Using Medical Records

Objective@#To examine whether patients who participated in a cardiac rehabilitation (CR) program after hospitalization for acute coronary syndrome maintained cardiorespiratory fitness (CRF) in the community. @*Methods@#We conducted a retrospective study including 78 patients who underwent percutaneous coronary intervention or coronary artery bypass graft surgery at our hospital’s cardiovascular center and participated in a CR program and a 5-year follow-up evaluation. Patients were divided into a center-based CR (CBCR) group, participating in an electrocardiography-monitored exercise training in a hospital setting, and a home-based CR (HBCR) group, receiving aerobic exercise training and performed self-exercise at home. @*Results@#No significant differences were found between groups (p>0.05), except the proportion of non-smokers (CBCR 59.5% vs. HBCR 31.7%; p=0.01). In both groups, the maximal oxygen consumption (VO2max) increased significantly during the first 12 weeks of follow-up and remained at a steady state for the first year, but it decreased after the 1-year follow-up. Particularly, VO2max at 5 years decreased below the baseline value in the HBCR group. In the low CRF group, the CRF level significantly improved at 12 weeks, peaked at 1 year, and was still significantly different from the baseline value after 5 years. The high CRF group did not show any significant increase over time relative to the baseline value, but most patients in the high CRF group maintained relatively appropriate CRF levels after 5 years. @*Conclusion@#Continuous support should be provided to patients to maintain optimal CRF levels after completing a CR program.

Flexor Carpi Radialis Tendon Rupture due to Repetitive Golf Swing

Flexor carpi radialis (FCR) muscle is located in the forearm anteriorly that runs through a synovial fibro-osseous tunnel in the forearm. We described a case of FCR tendon rupture due to repetitive overuse injury. A 55-year-old man, right-hand dominant, presented with right forearm pain and swelling which started 3 days ago while playing amateur golf. Focal tenderness and bruising over volo-ulnar region of the right forearm were examined. Plain radiographs showed soft tissue edema around lesion area and no detectable fracture. Ultrasonography showed multiple hypoechoic lesions suspected as hematoma of the flexor muscle group. After done magnetic resonance imaging, he was diagnosed with rupture of FCR tendon at proximal origin and strain of flexor digitorum superficialis and palmaris longus muscle. He received compressive dressing and restriction of wrist range of motion for three weeks. Two months later, remaining traces of lesions were observed at the follow-up ultrasonography and the pain disappeared.

Activin Receptor-Like Kinase 5 Inhibitor Attenuates Fibrosis in Fibroblasts Derived from Peyronie's Plaque

PURPOSE: Transforming growth factor-beta1 (TGF-beta1) is the key fibrogenic cytokine associated with Peyronie's disease (PD). The aim of this study was to determine the antifibrotic effect of 3-((5-(6-Methylpyridin-2-yl)-4-(quinoxalin-6-yl)-1H-imidazol-2-yl) methyl)benzamide (IN-1130), a small-molecule inhibitor of the TGF-beta type I receptor activin receptor-like kinase 5 (ALK5), in fibroblasts isolated from human PD plaque. MATERIALS AND METHODS: Plaque tissue from a patient with PD was used for primary fibroblast culture, and we then characterized primary cultured cells. Fibroblasts were pretreated with IN-1130 (10 microM) and then stimulated with TGF-beta1 protein (10 ng/ml). We determined the inhibitory effect of IN-1130 on TGF-beta1-induced phosphorylation of Smad2 and Smad3 or the nuclear translocation of Smad proteins in fibroblasts. Western blot analyses for plasminogen activator inhibitor-1, fibronectin, collagen I, and collagen IV were performed to evaluate effect of IN-1130 on the production of extracellular matrix proteins. RESULTS: The treatment of fibroblasts with TGF-beta1 significantly increased phosphorylation of Smad2 and Smad3 and induced translocation of Smad proteins from the cytoplasm to the nucleus. Pretreatment with IN-1130 substantially inhibited TGF-beta1-induced phosphorylation of Smad2 and Smad3 and nuclear accumulation of Smad proteins. The TGF-beta1-induced production of extracellular matrix proteins was also significantly inhibited by treatment with IN-1130 and returned to basal levels. CONCLUSIONS: Overexpression of TGF-beta and activation of Smad transcriptional factors are known to play a crucial role in the pathogenesis of PD. Thus, inhibition of the TGF-beta signaling pathway by ALK5 inhibitor may represent a promising therapeutic strategy for treating PD.

Establishment of a Cavernous Fibrosis Model in a Rat Using Adenovirus Expressing Transforming Growth Factor-beta1 / 대한남성과학회지

PURPOSE: Transforming growth factor-beta1 (TGF-beta1) has been implicated in cavernous fibrosis due to a variety of causes of erectile dysfunction (ED), such as diabetes mellitus and post-radical prostatectomy. To examine the role of the TGF-beta signaling pathway in cavernous fibrosis, we established a rat model of cavernous fibrosis by using adenovirus expressing TGF-beta1 (ad-TGF-beta1). MATERIALS AND METHODS: Four-month-old male Sprague-Dawley rats received intracavernous injection of ad-TGF-beta1 (1x10(8), 1x10(9), or 1x10(10) virus particles [vp] in 100 microliter of PBS) and the penis was harvested for histologic examination at 10, 20, or 30 days after injection (n=4 per group and per time point). Based on the initial findings, the animals were divided into three groups (n=6 per group): Group 1, age-matched control; Group 2, intracavernous injection of ad-LacZ (1x10(10) vp/100 microliter); and Group 3, intracavernous injection of ad-TGF-beta1 (1x10(10) vp/100 microliter). At 30 days after injection, erectile function was evaluated during electrical stimulation of the cavernous nerve. The penis was then harvested and stained with Masson's trichrome and antibody to smooth muscle alpha-actin. RESULTS: Masson's trichrome staining revealed that intracavernous delivery of ad-TGF-beta1 sufficiently induced cavernous fibrosis in a dose-dependent manner. The fibrotic scars persisted up to 30 days after injection at the highest dosage (1x10(10) vp/100 microliter), whereas no histologic evidence of cavernous fibrosis was found in the control rats or the ad-LacZ-injected rats. The rats receiving ad-TGF-beta1 showed a higher cavernous collagen content and less smooth muscle content than the control rats or ad-LacZ-injected rats. Erectile function was significantly decreased in rats receiving ad-TGF-beta1 compared with that in controls or rats receiving ad-LacZ. CONCLUSIONS: This model induced by ad-TGF-beta1 may play an important role in understanding the pathophysiologic mechanisms of cavernous fibrosis-associated TGF-beta signaling and the development of new therapeutics targeting this pathway.

The Effect of tolterodine Via Oral and Intravenous Administrations on Voiding in Awake Spontaneously Hypertensive Rats as an Overactive Bladder Model

PURPOSE: We investigated the effect of oral or intravenous tolterodine on cystometric parameters in awake spontaneously hypertensive rats (SHRs) as a model of overactive bladder (OAB). The aim of our study was to observe the experimental conditions required to reproduce the clinical pharmacological effects of tolterodine, as seen in humans, to decrease bladder pressure or increase bladder capacity. MATERIALS AND METHODS: We studied the effects of the most widely used antimuscarinic drug, tolterodine, on cystometric parameters via two different administrations (oral and intravenous) in awake SHRs. RESULTS: Oral administration of tolterodine 10 mg/kg(-1) body weight in awake rats did not change any cystometric parameters significantly. Intravenous administration of tolterodine 0.3 mg/kg(-1) body weight significantly decreased basal pressure (BP) and micturition pressure (MP), but showed no effect on micturition interval (MI) or bladder capacity (BC). CONCLUSION: Despite a high dose of tolterodine via an oral or an intravenous route, a decrease in BP or MP was the only effect on cystometrographic parameters in awake rats, whereas MI and BC were not significantly affected. Therefore, it is difficult to reproduce in awake rats as an acute response the cystometric increase in the MI that is observed in humans after chronic administration of antimuscarinic agents.