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Biomedical subjects

M Yamaki

Publications and source records attributed to M Yamaki.

At least 163 records · Page 9Linked to original sources
PubMed1985

Body surface distributions of ST segment changes after exercise in effort angina pectoris without myocardial infarction.

To investigate the sites of exercise-induced ST segment changes on the body surface in effort angina pectoris without myocardial infarction, we performed 87-lead ECG mapping in 61 patients before and 1.5 and 5 minutes after treadmill exercise. ST segment depression most often occurred in the left anterior chest leads and ST segment elevation developed mainly in the right upper chest leads. There was a good correlation between the number of lead points that showed ST segment depression (nSTd) and the number of those that showed ST segment elevation (nSTe) 1.5 minutes after exercise (r = 0.92). From 1.5 to 5 minutes after exercise, changes in nSTd for individual patients correlated well with changes in nSTe (r = 0.89). It was suggested that the ST segment elevation observed in this study directly reflected the subendocardial ischemia of the left ventricle. In patients with one-vessel disease (n = 32), there was wide overlap in the sites of ST segment changes among patients with left anterior descending artery disease (n = 19), those with left circumflex artery disease (n = 6), and those with right coronary artery disease (n = 7). These findings should lead to a better understanding of exercise-induced ST segment changes for the diagnosis of coronary artery disease.

Adult↗
PubMed1985

Noninvasive assessment of left ventricular wall motion abnormalities by QRS isointegral maps in previous anterior infarction.

In order to determine to what extent left ventriculographic abnormalities can be predicted from ECG changes in myocardial infarction (MI), 87 unipolar ECGs were simultaneously recorded in 22 patients with previous anterior MI with no conduction defects. We adopted a QRS isointegral mapping technique for analyzing body surface mapping data. Particular attention was given to the area where the QRS time-integral value was less than the lower limit (mean minus two standard deviations) of the normal, and this area was designated as the departure area. Left ventricular wall motion was assessed by left ventriculography and correlated with the departure area. The departure area demonstrated a close correlation with the left ventricular ejection fraction (r = -0.93) and the extent of asynergy (r = 0.74). It is suggested that the departure area reflects the loss of electromotive force due to MI. We conclude from this study that the QRS isointegral map is a useful method for evaluating left ventricular function in patients with anterior MI.

Adult↗
PubMed1985

Characterization of a rat tRNA gene cluster: comparison of nucleotide sequences of the gene for tRNALeu newly found in repeating units.

In the rat, DNA carrying a cluster of the genes for tRNAAsp, tRNAGly, and tRNAGlu, aligned in that order, is repeated about 10 times. Seven DNA clones corresponding to the independent repeating units were isolated from a rat gene library. Nucleotide sequence analysis of these clones revealed the presence of a fourth tRNA gene, the gene for tRNALeu, in the cluster. The tRNALeu gene is located about 600 base pairs (bp) upstream from the tRNAAsp gene and its polarity differs from those of the other three tRNA genes. Among the repeating units, the nucleotide sequence of tRNALeu is conserved to a relatively high degree.

Animals↗
PubMed1985

Detection of local abnormalities in ventricular activation sequence by body surface isochrone mapping in patients with previous myocardial infarction.

Body surface isochrone mapping was performed in 36 normal subjects and in 85 patients with previous myocardial infarction. Eighty-seven unipolar electrocardiograms distributed over the anterior chest and the back were recorded simultaneously. For each lead, activation time was measured as the time from the onset of QRS to the peak of the R wave. The lead points where R waves were not observed were designated the "no R wave area" (NR area). Isochrone maps of normal subjects had a consistent pattern, with isochrone lines extending from the right upper anterior chest to the left anterior chest and then to the back. NR area was small and was located only on the right upper chest or the upper back. On the isochrone maps of patients with myocardial infarction, abnormal findings were observed; NR area was found in 26 of 28 patients with anterior infarction on the upper to middle anterior chest, in 13 of 22 patients with inferior infarction on the lower chest, and in 24 of 25 patients with anterior and inferior infarction on the upper to lower anterior chest. Activation time was delayed near the NR area (peri-NR area delay) in 37 patients. In patients with apical infarction, an islandlike zone of delayed activation was typically found on the left precordium. These abnormal patterns are considered to indicate local abnormalities in the activation of infarcted myocardium; the NR area indicates dead unexcitable scar, and the peri-NR area delay and islandlike zone of delayed activation indicate partially infarcted myocardium of slow activation. Patients with NR area had greater degree of left ventricular asynergy and lower ejection fraction than those without.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Diagnosis of coronary artery disease by body surface mapping--body surface distribution of exercise-induced ST changes in patients without myocardial infarction.

In 36 patients with effort angina pectoris without myocardial infarction, the sites of exercise-induced ST changes (depression and elevation) on the body surface were investigated. Exercise-induced ST depression was most often seen in left anterior chest leads. The body surface distribution of ST depression failed to identify the obstructed coronary artery. Exercise-induced myocardial ischemia was thought to extend to the greater part of the subendocardial region of the left ventricle. Exercise-induced ST elevation was mainly found on the upper right anterior chest. It has been suggested that these leads face the interior of the left ventricle and the observed ST elevation directly reflects subendocardial ischemia of the left ventricle. This data is important for evaluating ST changes in exercise electrocardiography.

Coronary Disease↗
PubMed1985

The clinical significance of exercise-induced ST-segment elevation in previous anterior myocardial infarction.

To investigate the mechanism of exercise-induced ST elevation in previous anterior myocardial infarction, exercise body surface mapping was performed on 22 patients with anterior myocardial infarction. ST elevation was compared with the findings of exercise radionuclide ventriculography and exercise thallium-201 myocardial perfusion imaging. ST-segment was quantified by the integral of ST-segment voltage. The maximal value of ST segment integral out of the 87 leads on the body surface was defined as ST max. The percent of change in ST max after exercise was closely correlated to the decrease in ejection fraction (r = 0.76). Furthermore, 9 of the 12 patients with increased ST max after exercise had exercise-induced regional wall motion abnormalities mainly in the apical and anterolateral segments, while other 10 patients without increased ST max did not (p less than 0.01). There was no difference in % change of ST max a) between anterior reversible defect (+) group and the (-) group; b) between inferior reversible defect (+) group and the (-) group; c) between single vessel (isolated left anterior descending artery stenosis) group and the multivessel group. This fact indicated that exercise-induced ST elevation did not result from the exercise-induced myocardial ischemia of the infarctional segment or the remote non-infarctional segment. We concluded that exercise-induced ST elevation in previous anterior myocardial infarction is mainly due to the aggravation of anterior wall motion abnormalities induced by exercise.

Adult↗
PubMed1984

Purification of the muscarinic acetylcholine receptor from porcine atria.

The muscarinic acetylcholine receptor from porcine atria has been purified 100,000-fold to homogeneity by solubilization in digitonin/cholate and sequential chromatography on wheat germ agglutinin-agarose, diethylaminoethylagarose, hydroxylapatite, and 3-(2'-aminobenzhydryloxy)tropane-agarose. The yield of purified receptor was 4.3% of that found in the membrane fraction, and the purified receptor bound 11.1-12.8 nmol of L-[3H]quinuclidinyl benzilate per mg of protein, corresponding to a binding component Mr of 78,400-90,000. The purified receptor preparation consisted of two polypeptides in approximately equimolar amounts when examined on silver-stained sodium dodecyl sulfate/polyacrylamide gels. The larger polypeptide (Mr 78,000 on 8% polyacrylamide gels) was specifically alkylated with [3H]propylbenzilylcholine mustard, whereas the smaller polypeptide (Mr 14,800) was not labeled. The possibility that the small polypeptide is a contaminant fortuitously appearing in equimolar amounts with the large polypeptide cannot be ruled out at this time. The purified preparation was highly stable, with no measurable change in the number of ligand binding sites or the gel pattern after 1 month's storage on ice. Scatchard analysis showed a single class of binding sites for the antagonist L-[3H]quinuclidinyl benzilate with a dissociation constant of 61 +/- 4 pM. Equilibrium titration experiments demonstrated that the antagonist L-hyoscyamine displaced L-[3H]quinuclidinyl benzilate from a single class of sites (Kd = 475 +/- 30 pM), whereas the agonist carbamoylcholine interacted at two populations of sites (53% +/- 3% high affinity, Kd = 1.1 +/- 0.3 microM; 47% +/- 3% low affinity, Kd = 67 +/- 14 microM). The ligand binding data were very similar to that for the membrane-bound receptor, suggesting that the receptor has not been altered radically during purification.

Animals↗
PubMed1984

Determination of the left ventricular asynergic site by QRST isointegral mapping in patients with myocardial infarction.

QRST isointegral maps were made from 87 body surface ECGs in 41 patients with prior myocardial infarction. To evaluate the abnormalities of QRST isointegral maps, a deviation map was constructed from a deviation index, which expressed the deviation of the QRST time-integral value from the normal value at each lead point. Patients were divided into 3 groups according to the asynergic site on left ventriculograms: patients with anterior wall asynergy (n = 13), those with inferior wall asynergy (n = 13) and those with both anterior and inferior asynergies (n = 15). A consistent deviation map pattern was obtained in each group regardless of the QRS duration. Consequently, the deviation map was considered to be a practical method of identifying the asynergic site in patients with myocardial infarction, especially in those with intraventricular conduction disturbances. It is suggested that the deviation map can reveal abnormally altered intrinsic ventricular recovery properties resulting from a loss of the electromotive force of the infarcted myocardium.

Adult↗
PubMed1984

Attenuation of exercise-induced R wave increase after diltiazem in effort angina pectoris.

Body surface mapping was used to study the effects of diltiazem on exercise-induced QRS amplitude changes in 7 patients with stable effort angina pectoris. Body surface areas showing R or S amplitude changes (greater than 0.2 mV) after treadmill exercise were calculated. After the administration of 90 mg of diltiazem, the R increased area was significantly smaller than that without diltiazem (p less than 0.02), although the same workload was performed. It was suggested that diltiazem diminished the exercise-induced myocardial ischemia and this improvement of ischemia resulted in the reduction of the R increased area after exercise.

Adult↗