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To determine whether heart rate recovery (HRR) following an exercise tolerance test (ETT) is correlated with a changing ratio of peak oxygen consumption (VO2) and maximal metabolic equivalents (METmax).
A total of 60 acute myocardial infarction (AMI) patients who underwent ETT at both assessment points - 3 weeks (T0) after the AMI attack and 3 months after T0 (T1) were included. After achieving a peak workload, the treadmill was stopped with a 5-minute cooldown period, and the patients recovered in a comfortable and relaxed seated position. HRR was defined as the difference between the maximal heart rate (HRmax) and the HR measured at specific time intervals - immediately after the cool down period (HRR-0) and 3 minutes after the completion of the ETT (HRR-3).
HRR-0 and HRR-3 increased over time, whereas VO2max and METmax did not show significant changes. There was a positive correlation between HRR at T0 and the exercise capacity at T0. HRR at T0 also showed a positive correlation with the exercise capacity at T1. There was no significant correlation between HRR measured at T0 and the change in the ratio of VO2max and METmax, as calculated by subtracting VO2max and METmax obtained at T0 from those obtained at T1, divided by VO2max at T0 and multiplied by 100.
Post-exercise HRR measured at 3 weeks after the AMI onset can reflect the exercise capacity 3 months after the first ETT. However, it may be difficult to correlate post-exercise HRR at T0 with the degree of increase in cardiopulmonary exercise capacity in patients with AMI.
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To evaluate the effects of cardiac rehabilitation (CR) on functional capacity in obese and non-obese patients who have suffered acute myocardial infarction (AMI).
Overall, 359 patients who have suffered AMI, and were referred for CR after percutaneous coronary intervention from 2010 to 2015 and underwent an exercise tolerance test before and after phase II CR were included in this study. The patients were divided into two groups: obese group with body mass index (BMI) ≥25 kg/m2 (n=170; age, 54.32±9.98 years; BMI, 27.52±2.92 kg/m2) and non-obese group with BMI <25 kg/m2 (n=189; age, 59.12±11.50 years; BMI 22.86±2.01 kg/m2). The demographic characteristics and cardiopulmonary exercise capacity of all patients were analyzed before and after CR.
There were significant changes in resting heart rate (HRrest) before and after CR between the obese and non-obese groups (before CR, p=0.028; after CR, p=0.046), but other cardiopulmonary exercise capacity before and after CR was not different between the groups. HRrest (p<0.001), maximal metabolic equivalents (METs, p<0.001), total exercise duration (TED, p<0.001), and maximal oxygen consumption (VO2max, p<0.001) improved significantly in the obese and non-obese groups after CR. No difference in the change in the cardiopulmonary exercise capacity rate was detected between the groups.
CR may improve functional capacity in patients who suffered AMI regardless of their obesity.
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To quantify changes in cardiopulmonary function using a lower body positive pressure supported (LBPPS) treadmill during the exercise tolerance test (ETT) in healthy subjects before applying the LBPPS treadmill in patients with gait problems.
We evaluated 30 healthy subjects who were able to walk independently. The ETT was performed using the Modified Bruce Protocol (stages 1–5) at four levels (0%, 40%, 60%, and 80%) of LBPPS. The time interval at each level of the LBPPS treadmill test was 20 minutes to recover to baseline status. We measured systolic blood pressure, diastolic blood pressure, peak heart rate (PHR), rating of perceived exertion (RPE), metabolic equivalents (METs), and oxygen consumption rate (VO2) during each LBPPS condition.
Systolic blood pressure increased as the LBPPS level was increased (40% to 80%). PHR, RPE, METs, and VO2 were negatively associated with the LBPPS condition, although they were not always significant different among the LBPPS levels. The equation from a random effect linear regression model was as follows: VO2 (mL/kg/min)=(2.75×stage)+(–0.14×LBPPS level)+11.9 (r2=0.69).
Detection of the changes in physiological parameters during a submaximal ETT using the LBPPS system may be helpful for applying the LBPPS treadmill in patients who cannot perform the ETT due to gait problems, even at submaximal intensity.
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Spontaneous cervical epidural hematoma (SCEH) is an uncommon cause of acute nontraumatic myelopathy. SCEH presenting as Brown-Sequard syndrome is extremely rare. A 65-year-old man had motor weakness in the left extremities right after his mother's funeral. He received thrombolytic therapy under the impression of acute cerebral infarction at a local hospital. However, motor weakness of the left extremities became aggravated without mental change. After being transferred to our hospital, he showed motor weakness in the left extremities with diminished pain sensation in the right extremities. Diagnosis of SCEH was made by cervical magnetic resonance imaging. He underwent left C3 to C5 hemilaminectomy with hematoma removal. It is important for physicians to be aware that SCEH can be considered as one of the differential diagnoses of hemiplegia, since early diagnosis and management can influence the neurological outcome. We think that increased venous pressure owing to repetitive Korean traditional deep bows may be the cause of SCEH in this case.
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To investigate the effect of combined therapy of exercise and nootropic agent on cognitive function in a focal cerebral infarction rat model.
Forty 10-week old male Sprague-Dawley rats were subjected to photothrombotic cerebral infarction of the left parietal lobe. All rats were randomly divided into 4 groups: group A was photothrombotic cerebral infarction rats without any treatment (n=10); group B was photothrombotic cerebral infarction rats with swimming exercise (n=10); group C was photothrombotic cerebral infarction rats with oral administration of acetyl-L-carnitine (n=10); group D was photothrombotic cerebral infarction rats with swimming exercise and oral administration of acetyl-L-carnitine (n=10). Cognitive function was evaluated using the Morris water maze test on the 1st day, and the 1st, 2nd, and 4th week after the induction of cerebral infarction. The activity of superoxide dismutase (SOD) and the level of malondialdehyde (MDA) in the hippocampus were measured. The neuronal cells of the hippocampus were histopathologically evaluated.
The escape latency was shorter in groups B, C, and D than in group A. However, the differences were not statistically significant at the 1st, 2nd and 4th week. The activity of SOD was the highest in group D. The level of MDA was the lowest in group D. We observed more normal neuronal cells in groups B, C, and D.
The combined therapy of exercise and nootropic agent was helpful in ameliorating oxidative stress in the focal cerebral infarction rat model. However, the effect did not translate into improvement of cognitive function.
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A 53-year-old man abruptly developed headache and unconsciousness. Brain computed tomography (CT) and CT angiography showed subarachnoid hemorrhage, intraventricular hemorrhage, and multiple tortuous vascular structures on the brain stem and upper cervical spinal cord. Four-vessel angiography displayed intradural ventral arteriovenous fistula, supplied by the left vertebral and occipital arteries. Drainage was via both sigmoid sinus and cervical venous plexus. He had been treated with transarterial coil embolization of the left vertebral artery. Subsequently, he suffered from left hemiplegia and cognitive problem. Brain magnetic resonance (MR) and MR angiography performed 4 weeks later revealed multiple infarctions on the left cerebellum, left upper cervical spinal cord, and both medial thalamus, as well as occlusion of the left vertebral artery with reduction in varix size. After rehabilitative management, his muscle strength and cognitive function improved. We report a very rare case of dural arteriovenous fistula on the brain stem and upper cervical spinal cord.
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A 49-year-old man received prolotherapy in the upper cervical region at a local medical clinic. Immediately after the procedure, he felt a sensation resembling an electric shock in his right upper and lower extremities, and continuously complained of numbness and discomfort in the right hemibody. He visited our clinic a week later. Upon physical examination, there were no significant abnormal findings. The visual analog scale was 60 points. T2-weight magnetic resonance images of the cervical spine showed a 0.7 cm sized bright oval spot on the right side of the spinal cord at the level of C4-C5 disc, suggesting spinal cord injury. There were no definite electrodiagnostic abnormalities. Digital infrared thermal images showed moderately decreased surface temperature on lateral aspect of the right forearm and dorsum of the right hand compared with the other side. Considering that very rare complications like spinal cord injury may develop after prolotherapy, we suggest that special interventions such as prolotherapy be performed by professional experts.
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