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T Nanke

Publications and source records attributed to T Nanke.

6 recordsLinked to original sources
PubMed1999

Development of a new analytical method for the electrocardiogram using short-time first Fourier transforms.

To detect the minute electric potential inside the QRS complex, a new frequency domain method was designed using short-time First Fourier Transforms (SFFT) and high-frequency sampling (oversampling). SFFT improved the frequency resolution by oversampling that was applied to this analysis. The electric potential data of 15,000 points received weighted, running average processing and was subtracted from the original waveform to reduce the low-frequency component. The data in a segment of 160 ms, including QRS, was processed by frequency analysis with the SFFT computation routine. The ECG of healthy individuals was analyzed by this method and its usefulness evaluated. The processing waves of the X-axis, Y-axis, and Z-axis of a representative normal subject were formed into 3 groups of peak electric potential. SFFT enabled the detection of the structure inside the QRS complex without signal averaging, and is considered capable of evaluating the process of excitement inside the QRS complex in the various heart diseases.

Adult↗
PubMed1995

[A study on frequency characteristics of filter for detecting high frequency components of QRS complex and its application to the intraventricular conduction system].

A method to detect the high frequency component of QRS complex was developed and the mode of intraventricular conduction was analyzed from its sequential changes. An originally developed subtraction method was used to diminish the transient phenomenon related to phase shift and to obtain easily changeable filtering characteristics. The subjects included normal healthy persons (N), persons having right or left bundle branch block (R and L) and ventricular premature contraction of R or L type (VR and VL). Three components, initial low, mid high and terminal low amplitude were obtained in the N group. In the R group, mid component was lower and duration of the terminal component was longer than in the N group. In the L group, mid and terminal components were not clearly discriminated. Further, their amplitudes were low and duration of each component was markedly prolonged. In the VR and VL groups, the amplitude of the initial component was low and its duration was prolonged. From these findings, the excitation wave through the normal conduction system was short in duration and relatively high in amplitude and includes high frequency component. As contrasted, the duration was prolonged and the amplitude was low in conduction disturbance, seen in bundle branch block or ventricular premature contraction. Thus, the mode of intraventricular conduction could be defined by this newly developed method.

Adult↗
PubMed1991

[Alcohol-induced variant angina and considerations of its mechanism: a case report].

A 64-year-old man had episodes of angina pectoris several hours after ingestion of alcohol. Otherwise, anginal attacks never occurred. He was diagnosed as having variant angina based on the typical ST elevation in leads II, III and aVF during the anginal attacks. We performed an alcohol challenge test on his 4th admission day. He was given 540 ml of "sake" at 6:00 p.m. and anginal attacks with ST elevations occurred 9.5 hours after its ingestion. The peak value of plasma ethanol was 136 mg/dl at 9:00 p.m. and it returned to 0 when angina occurred. By alcohol ingestion, urinary excretion of Mg increased in association with a slight decrease in serum Mg. The ratio of serum Ca to Mg was increased from 4.0 at the control state before taking alcohol to 4.5 at the occurrence of anginal attack. Mg content in red blood cells and in plasma catecholamines did not differ between before and after ingesting alcohol. We concluded that the change in the extracellular Ca-Mg equilibrium may contribute to the mechanism of alcohol-induced variant angina.

Aged↗
PubMed1990

[Inhibition of vasospastic angina by alcohol ingestion].

A 66-year-old man having a long history of angina on effort has started to show frequent episodes of angina at rest since 6 months ago. He noticed that chest pain was uncommon after taking alcohol. A variant form of angina pectoris (variant angina) was diagnosed by documentation of typical ST elevation during anginal attack and also by inducing coronary arterial spasm with intracoronary administration of ergonovine maleate. Ambulatory ECG monitoring revealed frequent ST elevation during sleep. Since the history suggested that alcohol ingestion could be effective for preventing variant angina, this effect was examined by giving 540 ml of "sake" in the evening. Variant angina was inhibited, while plasma ethanol was detected. The plasma ethanol reached its peak value as 152 mg/dl at 10 o'clock pm and returned to zero after 12 hours. When ethanol disappeared in the plasma, variant angina recurred again. Although the precise mechanism for inhibition of variant angina by alcohol ingestion is not clear, alcohol or its metabolite such as acetaldehyde seems to be able to inhibit coronary arterial spasm.

Aged↗