Biomedical subjects

Kae Itoh

Publications and source records attributed to Kae Itoh.

4 recordsLinked to original sources

PubMed2005

Reversible ventricular dysfunction takotsubo cardiomyopathy.

BACKGROUND: Recently, many cardiologists have recognized the existence of a rapidly reversible form of heart failure of unknown origin characterized by a takotsubo-shaped, dyskinetic left ventricle on left ventriculography. AIM: To determine the detailed clinical features of takotsubo cardiomyopathy. METHODS: Thirteen elderly patients (11 women and 2 men with a mean age of 75.3 years) who had normal coronary arteries and takotsubo-like left ventricular dysfunction were prospectively enrolled in this study. RESULTS: Cardiac enzymes did not increase significantly, but the mean plasma norepinephrine level was very high on admission (0.98 microg/l). Coronary angiography revealed normal coronary arteries in all patients, but left ventriculography showed apical akinesis combined with basal hyperkinesis, i.e., a takotsubo (Japanese octopus fishing pot)-shaped ventricle. Left ventricular wall motion normalized within a mean of 16.9 hospital days in 12 patients, but 1 patient died of acute renal failure on hospital day 7. Cardiac events did not recur during a follow-up period of 0.5 to 5 years. CONCLUSION: Takotsubo cardiomyopathy seems to be a new type of acute heart failure, which generally has a good prognosis and does not recur. Myocardial damage by catecholamine overload, adrenoceptor hypersensitivity, and changes of catecholamine dynamics due to stress may cause this condition.

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PubMed2005

Relationship between exercise intolerance and levels of neurohormonal factors and proinflammatory cytokines in patients with stable chronic heart failure.

We 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 VO2) 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 VO2; a severe exercise intolerance group (severe group; peak VO2 < 18 mL/min/kg), moderate exercise intolerance group (moderate group; 18 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 VO2 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.

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PubMed2003

Relationship between impaired chronotropic response, cardiac output during exercise, and exercise tolerance in patients with chronic heart failure.

The 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 VO2), slope of the regression line relating the ventilatory equivalent to carbon dioxide output (VE/VCO2 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 deltaHR, deltaNE, and deltaCI, respectively. The deltaNE was converted to a logarithmic scale and deltaHR/log deltaNE 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 VO2. DeltaHR/log deltaNE correlated positively with both AT and peak VO2, and negatively with the VE/CO2 slope. DeltaHR/log deltaNE correlated positively with peak CI, %deltaCI, and deltaCI/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.

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PubMed2003

[Different effects of exercise training in patients with myocardial infarction with or without diabetes mellitus].

OBJECTIVES: This study investigated whether myocardial infarction patients with diabetes mellitus had lower heart rate reserve to exercise by measuring the increment in heart rate (HR) divided by the increment of norepinephrine (NE) concentration from rest to peak exercise (delta HR/log delta NE). The difference in exercise training effects was also investigated. METHODS: The 148 patients after myocardial infarction were divided into two groups, the DM group (n = 34) and the non-DM group (n = 114). Cardiopulmonary exercise testing was performed in each subject at 1 and 3 months after the onset. Blood samples were taken at rest and immediately after peak exercise, rest brain natriuretic peptide, rest and peak norepinephrine were analyzed. Exercise training was performed from 1 to 3 months after the onset. RESULTS: Resting heart rates were significantly higher in the DM group than in the non-DM group both at 1 and 3 months although peak heart rates were not significantly different. Peak oxygen uptake were lower in the DM group both at 1 and 3 months after onset of myocardial infarction compared to the non-DM group. End-tidal carbon dioxide pressure was lower and the rate of increase of minute ventilation to carbon dioxide output was higher in the DM group. Plasma brain natriuretic peptide was higher in the DM group. delta HR/log delta NE was 19.4 +/- 4.0 in the DM group and 22.2 +/- 5.6 in the non-DM group (p < 0.01), and increased in only the non-DM group. delta HR/log delta NE was more closely correlated with peak oxygen uptake in the DM group than in the non-DM group. CONCLUSIONS: Impaired response to exercise training may be caused, in part, by impaired heart rate reserve to exercise in patients with diabetes mellitus.

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