Factors related to daily step counts of stroke patients during hospitalization in a convalescent rehabilitation ward.

OBJECTIVES: Clarifying the factors related to decreased physical activity in post-stroke patients is essential for effective disease management. This study aimed to examine the factors influencing the amount of daily steps taken by post-stroke patients in a convalescent rehabilitation ward during activities other than rehabilitation (non-rehabilitation steps). MATERIALS AND METHODS: Eighty-nine post-stroke patients (60.8±14.4 years; 55 men) were enrolled. The inclusion criteria were walking independently within the ward and having a walking speed of ≥24 m/min. Data on patient clinical characteristics including age, sex, body mass index, stroke type, hemiparetic side, and time from stroke onset were collected. Stroke impairment and motor and cognitive functional disabilities were assessed using the Stroke Impairment Assessment Set and the Functional Independence Measure, respectively. The non-rehabilitation steps were calculated by subtracting the steps during the rehabilitation activities from the total steps using Fitbit Flex2. RESULTS: The average number of non-rehabilitation steps was 4,523±2,339 steps/day. The hierarchical multiple regression analysis revealed that sex, motor disability, and the interaction term of stroke impairment with cognitive disability were significantly related to non-rehabilitation steps. Simple slope analysis demonstrated that the stroke impairment slope was steeper at lower levels than at higher levels of cognitive disability for non-rehabilitation steps. CONCLUSIONS: In addition to independent effects of sex and motor disability, this study found that stroke impairment and cognitive disability were interactively related to non-rehabilitation steps in post-stroke patients in a convalescent rehabilitation ward. These findings may provide useful information for managing physical activity in post-stroke patients after hospital discharge.

Stretching exercises enhance vascular endothelial function and improve peripheral circulation in patients with acute myocardial infarction.

The purpose of this study was to clarify the acute effects of a single session of stretching exercises on vascular endothelial function and peripheral circulation in patients with acute myocardial infarction. This study evaluated 32 patients (mean age, 66 ± 9 years) who received phase I cardiac rehabilitation after acute myocardial infarction. Five types of stretching exercises were performed on the floor: wrist dorsiflexion, close-legged trunk flexion, open-legged trunk flexion, open-legged lateral trunk bending, and cross-legged trunk flexion. Each exercise entailed a 30-second stretching followed by a 30-second relaxation, and was repeated twice. Low- and high-frequency components (LF and HF) of heart rate variability (LF, 0.04-0.15 Hz; HF, 0.15-0.40 Hz) were analyzed, and HF and LF/HF were used as indices of parasympathetic and sympathetic nervous activities, respectively. Reactive hyperemia peripheral arterial tonometry (RH-PAT) index was measured and used as a parameter for vascular endothelial function. Transcutaneous oxygen pressure (tcPO2) on the right foot and chest was also measured, and the Foot-tcPO2/Chest-tcPO2 ratio was used as a parameter for peripheral circulation. The HF, RH-PAT index, and Foot-tcPO2/Chest-tcPO2 ratio were significantly higher after the exercises than before (P < 0.05, P < 0.01, and P < 0.05, respectively). There was no significant difference in the LF/HF ratio measured before and after stretching exercises. These findings demonstrate that stretching exercises improve vascular endothelial function and peripheral circulation in patients with acute myocardial infarction.

Preoperative skeletal muscle density is associated with postoperative mortality in patients with cardiovascular disease.

OBJECTIVES: Although skeletal muscle density (SMD) is useful for predicting mortality, the cut-off in an acute clinical setting is unclear, especially in patients with cardiovascular disease (CVD). This study was performed to determine the preoperative SMD cut-off using the psoas muscle and to investigate the effect on postoperative outcomes, including sarcopaenia, in CVD patients. METHODS: Preoperative psoas SMD was measured by abdominal computed tomography in CVD patients. Postoperative sarcopaenia was defined according to the criteria of the Asia Working Group for Sarcopaenia. The Youden index was used to test the predictive accuracy of survival models. The prognostic capability was evaluated using multivariable survival and receiver operating characteristic curve analyses. RESULTS: Continuous data were available for 1068 patients (mean age 65.5 years; 63.6% male). A total of 105 (9.8%) deaths occurred during the 1.99-year median follow-up period (interquartile range 0.71-4.15). The psoas SMD cut-off estimated by the Youden index was 45 Hounsfield units with high sensitivity and moderate specificity for all-cause mortality and was consistent in various stratified analyses. After adjusting for the existing prognostic model, EuroSCORE II, preoperative and postoperative physical status, psoas SMD cut-off was predicted for mortality (hazard ratio 2.42, 95% confidence interval 1.32-4.45). The psoas SMD cut-off was also significantly associated with postoperative sarcopaenia and provided additional prognostic information to EuroSCORE II on receiver operating characteristic curve analysis (area under the curve 0.627 vs 0.678, P = 0.011). CONCLUSIONS: Reduced psoas SMD was associated with postoperative mortality and added information prognostic for mortality to the existing prognostic model in CVD patients.

Excessive SBP elevation during moderate exercise discriminates patients at high risk of developing left ventricular hypertrophy from hypertensive patients.

OBJECTIVE: Hypertensive patients show an excessive elevation of SBP during exercise, although optimal blood pressure (BP) control is required to prevent development of left ventricular hypertrophy (LVH). This study examined whether excessive SBP elevation during moderate exercise is associated with new-onset LVH in these patients. METHODS: A total of 143 hypertensive patients without LVH whose BP had been maintained below 140/90 mmHg with antihypertensives performed cycle ergometer exercise test at moderate intensity to assess SBP elevation during exercise (ΔSBP). Left ventricular mass index (LVMI) was assessed by echocardiography once a year to identify new-onset LVH. Patients were divided into three groups according to tertiles of ΔSBP. We examined the associations between ΔSBP and new-onset LVH using the Kaplan-Meier method, log-rank test, and Cox regression analysis. RESULTS: The patients (100 men, 65.3 ±â€Š9.1 years) had resting BP of 126 ±â€Š16/75 ±â€Š11 mmHg. New-onset LVH developed in 47 patients (32.9%) within a follow-up period of 2.5 ±â€Š1.6 years. Higher ΔSBP was significantly associated with higher incidence of LVH (P < 0.001): 12.8, 27.1, and 58.3% in the lowest, middle, and highest tertiles, respectively. In multivariate analysis, ΔSBP was a significant independent determinant of new-onset LVH (hazard ratio for 10 mmHg increase in ΔSBP, 1.45; 95% CI 1.22-1.73; P < 0.001). In comparison with the lowest tertile, the hazard ratios of the middle and highest tertiles for incidence of LVH were 3.16 (95% CI 1.07-9.32) and 6.43 (95% CI 2.35-17.62), respectively. CONCLUSION: Excessive SBP elevation during moderate exercise can be used to identify hypertensive patients at high risk of developing LVH.

Beneficial effects of L- and N-type calcium channel blocker on glucose and lipid metabolism and renal function in patients with hypertension and type II diabetes mellitus.

It has been proved that cilnidipine has N-type calcium channels inhibitory activity as well as L-type calcium channels and inhibits excessive release of norepinephrine from the sympathetic nerve ending. This study was undertaken to compare the efficacy of amlodipine (an inhibitor of L-type calcium channels) and cilnidipine (an inhibitor of both L-type and N-type calcium channels) in patients with hypertension and type II diabetes mellitus. Seventy-seven hypertensive patients were divided into two groups according to presence/absence of type II diabetes mellitus. In these two groups of patients, the effects of amlodipine and cilnidipine on glucose and lipid metabolism and renal function were compared. As for glucose and lipid metabolism, homeostasis model assessment insulin resistance (HOMA-R) level in the non-diabetic group and triglyceride in the diabetes group were significantly lower with cilnidipine than with amlodipine. As regards renal function in the diabetic group, estimated glomerular filtration rate (eGFR) was significantly higher and urinary albumin/creatinine ratio was significantly lower with cilnidipine than with amlodipine. Cilnidipine which inhibits N-type calcium channels is more useful for patients with hypertension and diabetes mellitus from its effects on glucose and lipid metabolism and renal function.

Influence of nifedipine coat-core and amlodipine on systemic arterial stiffness modulated by sympathetic and parasympathetic activity in hypertensive patients.

The aim of this study was to compare the effects of nifedipine coat-core (once daily formulation) and amlodipine on systemic arterial stiffness in patients with hypertension. Study drugs were assigned by the randomized open-label crossover method. After the blood pressure was maintained below 130/85 mm Hg for 8 months by treatment with either drug in 48 hypertensive patients (aged 63.2+/-6.9 years; 64.5% men), they were switched to the other drug for another 8 months. The blood pressure, heart rate, plasma catecholamine level and brachial-ankle pulse wave velocity were measured before and after a bicycle ergometer testing. Heart rate recovery was calculated from the change of the heart rate after treadmill exercise testing. The high-frequency and low-frequency components of the heart rate variability spectrum were analyzed from 24-h Holter electrocardiograms. The change of blood pressure after exercise testing showed no significant difference between the two medications. However, the increases of heart rate, noradrenalin and branchial-ankle pulse wave velocity after exercise were significantly smaller with nifedipine treatment than with amlodipine (P=0.0472, P=0.006 and P=0.0472, respectively). Heart rate recovery was significantly faster with nifedipine treatment (P=0.0280). The nighttime high-frequency component of heart rate variability was significantly larger after nifedipine treatment than after amlodipine (P=0.0259), while the nighttime low/high-frequency ratio was significantly smaller with nifedipine (P=0.0429). Nifedipine reduced functional arterial stiffness and improved heart rate recovery by altering the autonomic activity balance in hypertensive patients.

Comparison of cardiovascular responses between upright and recumbent cycle ergometers in healthy young volunteers performing low-intensity exercise: assessment of reliability of the oxygen uptake calculated by using the ACSM metabolic equation.

OBJECTIVES: To clarify (1) differences in cardiovascular response during low-intensity exercise in the upright versus the recumbent position, and (2) whether the oxygen uptake (V o 2 ) calculated by the American College of Sports Medicine (ACSM) metabolic equation reflects the actual V o 2 at low-intensity testing. DESIGN: Repeated-measures comparison study. SETTING: University research laboratory. PARTICIPANTS: Thirty-one healthy, young volunteers (age, 23+/-2y). INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Blood pressure, rate pressure product (RPP), V o 2 , oxygen pulse, carbon dioxide output (V co 2 ), and ventilatory equivalent (V e ) were measured during graded exercise testing using upright and recumbent cycle ergometers. The estimated V o 2 was calculated by using the ACSM metabolic equation. RESULTS: Systolic blood pressure, RPP, V o 2 , oxygen pulse, V co 2 , and V e at 15 or 30W were significantly higher in the recumbent position than in the upright one ( P <.05), however, no significant differences were observed at 50 and 70W. The estimated V o 2 during exercise was significantly higher than the actual one, at every level of intensity, from 15 to 70W ( P <.05). CONCLUSIONS: Cardiovascular responses should be carefully monitored even during low-intensity exercise using a recumbent cycle ergometer. The V o 2 estimated using the ACSM metabolic equation did not reflect the actual V o 2 during low-intensity exercise at 70W or less.

Adaptation to low-intensity exercise on a cycle ergometer by patients with acute myocardial infarction undergoing phase I cardiac rehabilitation.

BACKGROUND: The adaptation of patients with acute myocardial infarction (AMI) to a phase I rehabilitation program has not been widely assessed. METHODS AND RESULTS: Forty-two male patients (62+/-8 years) with AMI were classified as exercise tolerant (group A, n=25) or excessive response (systolic blood pressure (SBP) increase >30 mmHg during exercise; group B, n=17). Hemodynamic parameters during exercise using a cycle-ergometer were monitored for the first 3 days. The power of low- and high-frequency components (LF: 0.05-0.2 Hz; HF: 0.2-1 Hz) was analyzed by heart rate variability. Anxiety status was assessed using the Spielberger's State-Trait Anxiety Inventory. Patients in group B were significantly older, had lower cardiac function and a longer hospitalization than group A (p<0.05, respectively). The excessive elevation of SBP on Day 1 decreased and became <30 mmHg on Day 3 in group B. The decreases in HF during exercise on Days 1 and 3 were significantly smaller in group B than in group A (p<0.05 and p<0.05, respectively). The LF/HF ratio on Day 1 was significantly higher in group B than in group A (p<0.05). In group B, the anxiety score before exercise was significantly higher than that at the time of discharge (p<0.05), whereas there was no change in group A. CONCLUSION: Factors influencing a significant elevation of blood pressure during phase I rehabilitation are age, physical deconditioning, imbalance of autonomic nervous activity and anxiety.

Protective effect of urinary trypsin inhibitor on myocardial mitochondria during hemorrhagic shock and reperfusion.

OBJECTIVE: To examine the mitochondrial function in the myocardium after hemorrhagic shock and reperfusion and to evaluate the protective effect of urinary trypsin inhibitor (UTI) on mitochondria. DESIGN: Animal experiment. SETTING: University research laboratory. SUBJECTS: Wistar rats receiving 50,000 units/kg/hr of UTI (n = 27; UTI group) and control rats (n = 26; control group). INTERVENTIONS: Rats were subjected to low-perfusion ischemia with the left ventricular systolic pressure maintained at 50 mm Hg for 60 mins by bleeding, followed by a 60-min reperfusion by transfusion of shed blood. UTI was infused continuously from 10 mins before bleeding. Cardiac function was measured before bleeding, after bleeding, and after transfusion; at each determination point, the myocardial contents of adenosine triphosphate (ATP), creatine phosphate (P-Cr), pyruvate (Pyr), and lactate (Lac) were measured enzymatically. The cytosolic phosphorylation potential (PP) as well as the redox potential of the oxidized form of nicotinamide adenine dinucleotide/reduced form of nicotinamide adenine dinucleotide couple in mitochondria (Eh(NAD+/NADH)) and change of Gibbs free energy in ATP hydrolysis (deltaG(ATP hydrolysis) energy) were calculated. MEASUREMENTS AND MAIN RESULTS: Cardiac function decreased during hemorrhagic shock but improved significantly in the UTI group after transfusion compared with the control group. Lac and the Lac/Pyr ratio were significantly lower in the UTI group than in the control group after transfusion. ATP and P-Cr were significantly higher in the UTI group than in the control group after transfusion. PP (x10(3) M-1), Eh(NAD+/NADH) (x - 1 mV), and deltaG(ATP hydrolysis) (x - 1 kcal/mol) were 1.9 +/- 0.4, 266 +/- 4, and 9.7 +/- 0.2, respectively, in the control group and 4.0 +/- 0.9, 274 +/- 5 and 13.0 +/- 0.2, respectively, in the UTI group after transfusion (p <.001, p <.001, and p <.001, respectively). CONCLUSIONS: In reperfusion after hemorrhagic shock, oxidative phosphorylation in myocardial mitochondria is impaired and energy production remains reduced, even after reperfusion. UTI contributed to the recovery of cardiac function after reperfusion, probably by reducing the severity of mitochondrial dysfunction during a state of shock and by maintaining energy production.