[Two surgical cases of severe valvular heart disease with cardiac cachexia (author's transl)].
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Biomedical subjects
Publications and source records attributed to H Kishida.
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Data from 11 cardiology institutes in Japan were examined to determine the effectiveness of drug therapy, especially with calcium antagonists, on variant angina. The subjects were 243 males and 43 females, most of whom were 40-59 years old. Coronary artery lesions were found in 92 of 162 patients (56.7%) in whom cinecoronary arteriograms were done. The efficacy rates of nifedipine, diltiazem and verapamil were 94.0%, 90.8% and 85.7%, respectively. Regardless of the presence or absence of organic coronary artery lesions, the drugs were effective in 92.3% of the patients with normal or nearly normal coronary arteries and in 82.6% of those with stenosis of more than 50% of the luminal diameter. These findings suggest that the drugs are effective through their antispasmodic actions.
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We studied the non-membrane potential-dependent effect of K+ on (dV/dt)max and threshold potential in guinea pig and cat ventricular myocardium. Membrane potential (MP) was changed uniformly in segments (length less than or equal to 1.0 mm) of papillary muscles by applying extracellular polarizing current pulses across a single sucrose gap. Control [K+]o was 5.4 mM and test [K+]o values were 2.0, 10.0, 11.5, 13.0, 16.2, 20, 22, and 24.0 mM. Each muscle was studied under four conditions: (1) control [K+]o and unaltered (control level) resting MP (Em); (2) one of the test [K+]o values and the unaltered (test level) Em; (3) the same test [K+]o and Em held at the control level; (4) control [K+]o and Em held at the test level. At all [K+]o greater than or equal to 11.5 mM, (dV/dt)max showed a decrease significantly (P less than 0.01) greater than the corresponding MP-dependent decrease in both guinea pig and cat myocardium. This non-MP-dependent decrease averaged 7.5% at 11.5 mM, 26.5% at 13.0 mM, 37.2% at 16.2 mM, and 22.7% at 20.0 mM. At [K+]o greater than or equal to 20.0 mM, (dV/dt)max was predominantly slow-channel-dependent; it was increased by hyperpolarization to -110 mV at [K+]o = 20 and 22 mM but not at [K+]o = 24mM. Threshold potential became progressively less negative with increasing [K+]o, but this effect was dependent only on MP. The membrane input resistance (rm) was determined by two opposing factors: at a given [K+]o, rm increased with depolarization; and at a given MP, rm decreased with increasing [K+]o. Our study shows that non-MP-dependent depression of (dV/dt)max in the ventricular myocardium occurs at [K+]o concentrations that may be encountered in vivo.
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Two hundred and twenty patients were selected for testing with the patient-activated Pocket Electrocardiography (PECG) because angina pectoris and similar diagnoses could not be excluded. They were selected during a 30-month period from the population of approximately 12,000 new patients visiting a general medical clinic at Nippon Medical School Hospital. The test confirmed the preliminary diagnosis in 79.1%; 9.6% were not confirmed and 11.3% did not have an attack during the PECG examination. The PECG examination is useful in the differential diagnosis of angina pectoris, cardiac neurosis, phantom arrhythmia, and arrhythmia when the routine ECG examinations are essentially negative.
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