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The new imaging and regional dyssynchrony analysis methods provide quantitative assessment of resynchronization analogous to that previously obtained only by tagged magnetic resonance imaging. This could provide a useful noninvasive method for both identifying candidates and following long-term therapy.

At >18 mos after acute myocardial infarction, the exercise maintenance rate in our patients remains high, and exercise maintenance may be one of the factors contributing to improvement of health-related quality of life and leisure-time objective physical activity level.

SUMMARYThe present study was undertaken to investigate the relationship between the extent of impaired chronotropic response and cardiac output during exercise, and exercise tolerance in patients with chronic heart failure. The subjects consisted of 24 patients (mean 60.1 ± 14.0 years) who had mild chronotropic incompetence. Cardiopulmonary exercise testing was performed in all patients, and heart rate (HR), anaerobic threshold (AT), maximum oxygen uptake (peak VO 2 ), slope of the regression line relating the ventilatory equivalent to carbon dioxide output (VE/VCO 2 slope), and exercise time were measured. Cardiac output (CO) was measured by a thoracic bioimpedance method and cardiac index (CI) was calculated. Plasma norepinephrine (NE) was measured at rest and immediately after the exercise test. The changes in HR, NE, and CI from the resting state to immediately after exercise were calculated as ∆HR, ∆NE, and ∆CI, respectively. The ∆NE was converted to a logarithmic scale and ∆HR/log∆NE was used as a parameter of HR response to sympathetic nerve stimulation. The results were as follows: HR and NE in the resting state had no correlation with AT and with peak VO 2 . ∆HR/log∆NE correlated positively with both AT and peak VO 2 , and negatively with the VE/VCO 2 slope. ∆HR/ log∆NE correlated positively with peak CI, %∆CI, and ∆CI/exercise time. The data suggest that one of the mechanisms of low exercise tolerance in chronic heart failure patients was due to an inadequate increase in CO response against exercise caused by an impaired HR response to increased NE. (Jpn Heart J 2003; 44: 515-525)

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The cerebral circulatory dynamics were evaluated before and after intra-arterial administration of fasudil hydrochloride in 20 patients with angiographic vasospasm after subarachnoid hemorrhage (SAH). The region of interest time-density curves obtained before and after intra-arterial administration of fasudil hydrochloride were compared in the proximal portion of the middle cerebral artery in the early arterial phase, the distal portion of the middle cerebral artery in the late arterial phase, and the transverse sinus in the venous phase. In the early arterial phase, the time to peak and the time to halfpeak were significantly reduced. In the late arterial phase and venous phase, the time to peak was significantly reduced. These results suggest that intra-arterial administration of fasudil hydrochloride induced dilation of the proximal arteries, and improved cerebral microcirculation. The present study suggests that intra-arterial administration of fasudil hydrochloride is effective as a treatment for vasospasm following SAH.

SUMMARYWe investigated the correlations between exercise intolerance and the plasma levels of neurohormonal factors and proinflammatory cytokines in chronic heart failure (CHF) patients.Sixty-two CHF patients who underwent cardiopulmonary exercise testing (CPX) were enrolled in this study. Peak oxygen uptake (peak VO 2 ) and the plasma concentrations of noradrenaline (NA), brain natriuretic peptide (BNP), and soluble tumor necrosis factor receptors I and II (TNFR-I and -II) were all measured during the CPX. The patients were divided into three groups according to their peak VO 2 ; a severe exercise intolerance group (severe group; peak VO 2 < 18 mL/min/kg), moderate exercise intolerance group (moderate group; 18 ≤ peak VO 2 ≤ 24), and mild exercise intolerance group (mild group; peak VO 2 > 24).There were no significant differences in left ventricular ejection fraction (EF) among the three groups. NA and BNP both increased gradually in parallel with the worsening of exercise intolerance (NA, 211.5 ± 75.7 pg/mL, 331.8 ± 163.7, 441.9 ± 202.9, respectively; BNP, 37.9 ± 25.4 pg/mL, 148.9 ± 117.1, 247.9 ± 150.0, respectively). TNFR-I and II were significantly higher in the severe group than in the moderate group (1746.1 ± 950.7 versus 1085.2 ± 370.5 pg/mL and 2855.3 ± 1550.9 versus 2047.7 ± 648.7 pg/mL, respectively), while the values in the moderate group were not significantly different from those in the mild group. EF showed no significant correlations with NA, BNP, TNFR-I, or TNFR-II, whereas peak VO 2 exhibited significant negative correlations with NA (r = −0.50, P < 0.0001), BNP (r = −0.53, P < 0.0001), TNFR-I (r = −0.50, P < 0.0001), and TNFR-II (r = −0.45, P < 0.0001).It is concluded that NA and BNP rise in parallel with the degree of exercise intolerance, while TNFR-I and -II rise only when exercise intolerance reaches severe levels. (Int Heart J 2005; 46: 1049-1059

We have previously reported that chronic sleep deprivation causes a deficiency of intracellular magnesium (Mg) and decreased exercise tolerance. The aim of this study was to clarify whether oral administration of Mg could be effective in restoring the exercise tolerance that is decreased by chronic sleep deprivation. A bicycle ergometer cardiopulmonary exercise test was performed by 16 healthy volunteers (mean age 21.9 years). They were divided into 2 groups: 8 received doses of 100 mg of Mg orally per day for 1 month (Mg group) and the remaining 8 received no Mg and served as the control group. The study conditions were designed as follows: (1) the usual state (good sleep); and (2) the sleep-deprived state (sleeping time up to 60% less than the usual state for 1 month). The ratio of intracellular Mg content of the sleep-deprived state to the usual sleep state was significantly higher in the Mg group (p<0.05) than the untreated control group. There was no difference between the sleep-deprived state and the usual state with regard to anaerobic threshold and peak oxygen uptake in the Mg group, whereas both of these decreased in the sleep-deprived state in the control group. These results indicate that decreased exercise tolerance observed in the sleep-deprived state could be improved by oral Mg administration.