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Biomedical subjects

K Imataka

Publications and source records attributed to K Imataka.

At least 73 records · Page 4Linked to original sources
PubMed1984

Carotid bruits and their clinical significance.

Vascular murmurs were routinely sought over the carotid arteries in 1,777 outpatients of 40 years of age or older who attended the cardiovascular clinic of our institute, and carotid bruits were heard in 82 patients (4.6%). The prevalence of carotid bruits increased with age from 5/467 (1.1%) in patients aged 40 to 49 years to 26/150 (17.3%) in those aged 70 to 79 years. Calcification of the carotid arteries was examined by posteroanterior films of the cervical spine in 447 patients 60 years of age or older and carotid calcification was found in 20 (42.6%) of 47 patients with carotid bruits and in 50 (12.5%) of 400 patients without them. The incidence of carotid calcification in the former group was 3.4 times that in the latter (p less than 0.01), although the incidences of hypertension and glucose intolerance were not related to the presence or absence of carotid bruits. A history of cerebral bleeding or infarction was found in 19 (23.2%) of 82 patients with carotid bruits, as compared with 64 (3.8%) of 1,695 patients without them (p less than 0.01). However, the location of the cerebrovascular lesions did not necessarily correlate with the laterality of the carotid bruits. These results indicate that patients with carotid bruits show an increased risk of stroke and that these bruits are a general and non-focal sign of severe atherosclerotic cerebrovascular disease.

Adult↗
PubMed1984

[A case of huge neurofibroma expanding extra- and intracranially through the enlarged jugular foramen--CT scan findings and surgical approach].

The surgical approach to the jugular foramen has been considered to be very difficult and troublesome, because of the location in which important structures, such as the internal jugular vein, internal carotid artery and lower cranial nerves, converge in the narrow deep space. A case of huge neurofibroma, which extended from the tentorium cerebelli through the dilated jugular foramen to the level of the vertebral body of C3 was presented. A 12-year-old girl was admitted with complaints of visual disturbance and palsy of the V-XII cranial nerves of the left side. Plain skull film showed prominent widening of the cranial sutures and enlargement of the sella turcica. Horizontal CT scan with contrast showed symmetrical ventricular dilatation and a heterogeneously enhanced mass, which was situated mainly in the left CP angle. Coronal CT scan with contrast revealed a huge mass and enlarged jugular foramen, through which the tumor extended to the level of the vertebral body of C3. Occlusion of the sigmoid sinus and the internal jugular vein of the left side was noticed in the vertebral angiography. Two-stage approach, the first one for removal of the intracranial tumor and the second one for extracranial tumor, was performed for its huge tumor. Several authors have reported excellent surgical approaches for the tumors situated in the jugular foramen. By our approach, modifying Gardner's original one, a wide operative field was obtained to remove the tumor around the jugular foramen with success. Our approach for the jugular foramen was described with illustrations.

Adolescent↗
PubMed1983

Evaluation of methods for estimating infarct size by myosin LC2: comparison with cardiac enzymes.

The relationship between histologically determined infarct size and release or peak levels of circulating cardiac enzymes and myosin light chain 2 (LC2) was studied. Myocardial infarction was produced by ligating the left anterior descending coronary artery in 18 conscious closed-chest dogs. Creatine phosphokinase (CPK), cytosolic and mitochondrial isozymes of aspartate transaminase (sAST and mAST) in the plasma, and LC2 in the serum were measured serially until 10 days after infarction, when infarct size was determined histologically [range 4.0-38.8% of the left ventricular weight (%LV)]. Infarct size correlated most closely with LC2 release (r = 0.82, P less than 0.001) and less closely with peak sAST (r = 0.59, P less than 0.01), peak mAST (r = 0.49, P less than 0.05), peak CPK (r = 0.22), and CPK release (r = 0.14). The correlation between infarct size and CPK release was improved by limiting the analysis to the dogs with infarct size of less than 20% LV (n = 11, r = 0.53, P less than 0.1). Because, among cardiac enzymes and LC2, CPK activity decayed most rapidly in the lymph fluid when incubated in vitro, degeneration of CPK in the lymph stream may contribute to the nonlinear relationship between infarct size and CPK release.

Animals↗
PubMed1983

Fibrillatory wave size in paroxysmal atrial fibrillation.

Little attention has been paid to the atrial fibrillatory waves (f waves) in paroxysmal atrial fibrillation. The present study attempted (1) to compare the f wave size in paroxysmal atrial fibrillation with that in persistent fibrillation, and (2) to examine whether the f wave size can predict the development of persistent from paroxysmal atrial fibrillation. The size of the f waves was measured in 60 patients with paroxysmal atrial fibrillation of non-rheumatic etiology (group A), 87 patients with persistent atrial fibrillation of non-rheumatic etiology (group B), and 34 patients with persistent atrial fibrillation of rheumatic etiology (group C). The f wave size in group A was 1.1 +/- 0.1 mm (mean +/- SE) which was significantly smaller than 1.6 +/- 0.1 mm in group B and 2.2 +/- 0.2 mm in group C (p less than 0.01, respectively). Among patients with paroxysmal atrial fibrillation, persistent atrial fibrillation developed in 9 of 19 patients (47.4%) with f wave size of 1.2 mm or more, and only in 5 of 41 patients (12.2%) with f wave size of less than 1.2 mm. These results indicate that paroxysmal atrial fibrillation generally has smaller f waves than persistent atrial fibrillation, but that the presence of larger f waves indicates potential development of persistent atrial fibrillation.

Atrial Fibrillation↗
PubMed1982

Experimental production of papillary muscle and mitral valve lesions by vagal manipulations in rabbits.

The present paper describes peculiar lesions in papillary muscles and mitral valves produced by vagal manipulations. In the 109 rabbits killed one week after clipping or crushing of their cervical vagi, papillary muscle and mitral valve lesions were found in 53 (48.6%) and 52 (47.7%) hearts respectively. The lesions were identified by visible deposits of colloidal carbon which had been injected intravenously during the first 3 postoperative days. The left ventricular free wall, interventricular septum and right ventricle were free of carbon deposits. The papillary muscles involved were characterized by swelling and increased stiffness which corresponded to degeneration of the myocardial cells and interstitial fibrosis on microscopic observation. Hydroxyproline content of the papillary muscles involved was 1.4 times more than that of normal hearts, while there was no significant difference in hydroxyproline content of either interventricular septum or left ventricular free wall between the manipulated and the normal preparations. Heart murmurs were heard in 23 animals studied. Phonocardiograms revealed mid to late systolic murmurs with or without midsystolic click. These results indicate that the vagus nerve plays an important role in the pathogenesis of some forms of papillary muscle and mitral valve lesions.

Animals↗
PubMed1982

Left atrial enlargement in patients with paroxysmal atrial fibrillation.

The present study was designed to examine whether the left atrium is dilated in paroxysmal atrial fibrillation or not. Left atrial dimension (LAD) on M-mode echocardiogram was (1) 23.3 +/- 0.7 mm (mean +/- S.E.) in 24 normal subjects, (2) 30.5 +/- 0.7 mm in 58 patients without atrial fibrillation who had hypertension and/or ischemic heart disease, (3) 35.5 +/- 0.9 mm in 27 patients with paroxysmal atrial fibrillation of whom 23 had non-rheumatic cardiovascular diseases and 4 had idiopathic atrial fibrillation, (4) 40.5 +/- 1.1 mm in 38 patients with persistent atrial fibrillation of whom 30 had nonrheumatic cardiovascular diseases and 8 had idiopathic atrial fibrillation, and (5) 53.3 +/- 2.0 mm in 17 patients with persistent atrial fibrillation who had rheumatic heart disease. LAD showed a stepwise and significant increase from the first to the fifth group. LAD of patients with paroxysmal atrial fibrillation was not related to either the number or duration of paroxysms. These results indicate that the left atrium is slightly dilated in patients with paroxysmal atrial fibrillation.

Adult↗
PubMed1981

Experimental production of poststenotic dilatation in the carotid arteries of rabbits.

Arterial dilatation distal to a stenosis has been known as poststenotic dilatation (PSD). This paper describes arterial constriction enough to produce PSD, time course of PSD, structural changes of the dilated segments and influence of hypertension on the development of PSD. These problems were studied in 2 experimental protocols. In protocol I, 87 carotid arteries of 45 rabbits were constricted by silver clip of 0.65 to 2.0 mm in diameter. The arterial diameter was measured at the sites both proximal and distal to the constriction after 3 days to 8 weeks. In protocol II, 22 carotid arteries of 12 rabbits with experimental one-or two-kidney Goldblatt hypertension were constricted and the development of PSD was compared with age matched controls. Remarkable PSD developed in arteries with moderate stenosis of 45 to 60% constriction. The degree of dilatation expressed as ratio of distal to proximal diameter reached about 1.5 at the end of the second week and remained unchanged thereafter. Destruction of the elastic fibers with intimal hyperplasia was observed in the dilated segments even at the early stages of the PSD. Both mild and severe stenosis failed to produce prominent PSD. In protocol II, the PSD averaged 1.18 +/- 0.05 (mean +/- SE) in hypertensive, and 1.32 +/- 0.03 in normotensive animals (p less than 0.05). The result suggests that chronic hypertension decreases the distensibility of the arteries.

Animals↗
PubMed1981

Clinical features of paroxysmal atrial fibrillation. An observation of 94 patients.

During the past 10 years we experienced 234 patients with atrial fibrillation of whom 94 patients (40.2%) showed a paroxysmal form. Underlying diseases of these 94 patients were hypertension and/or coronary heart disease in 51 (54.3%), rheumatic valvular disease in 3 (3.2%), hyperthyroidism in 2 (2.1%), and miscellaneous diseases in 15 patients (16.0%). Idiopathic atrial fibrillation was found in the remaining 23 patients (24.5%). Frequency of paroxysm was variable. paroxysm occurred only once or twice in 35 patients (37.2%) and more than 21 times in 20 patients (21.3%). Duration of a single paroxysm ranged from less than 24 hours in 49 patients (52.1%) to more than 15 days in 7 patients (7.4%). Atrial fibrillation became permanent in 19 (25.3%) of 75 patients who had been observed for a period of more than 1 year.

Adult↗
PubMed1981

Elevation of serum creatine phosphokinase during pindolol treatment.

We observed elevation of serum CPK in hypertensive patients under pindolol treatment. In this report, we showed a representative patient and compared serum CPK values in 56 patients under pindolol treatment to those in 64 patients under propranolol treatment. Mean serum CPK values in the patients under pindolol treatment and propranolol treatment were 117.0 +/- 12.6 (S.E.) and 50.8 +/- 3.8 IU/liter, respectively (p less than 0.01). Although the mechanism of elevation of serum CPK cannot be well understood, we should be careful in clinical evaluation of serum CPK during pindolol treatment.

Creatine Kinase↗
PubMed1981

[Hemodynamic responses to supine bicycle exercise in juvenile hypertensive subjects: an echocardiographic assessment (author's transl)].

Six juvenile hypertensive patients were studied by supine bicycle ergometer exercise during continuous echocardiographic recording. Thirteen normotensive young men were also studied for the control. Left ventricular end-diastolic dimensions (Dd) during exercise was significantly increased from 28.8 +/- 0.5 mm/m2 to 29.7 +/- 0.6 mm/m2 in normotensives, but the increase in Dd was not observed in hypertensives. Effects of propranolol on changes in Dd during exercise were almost equal in two groups. Left ventricular end-systolic dimensions (Ds) were decreased during exercise in both groups. After propranolol administration, Ds in hypertensives was significantly increased from 18.8 +/- 1.0 mm/m2 to 19.4 +/- 1.1 mm/m2 at rest, and during the following exercise it reached to 19.7 +/- 1.1 mm/m2, whereas Ds in normotensives was decreased during exercise even after propranolol. Peripheral vascular resistance at rest was almost equal between the two groups, but in hypertensives the reduction during exercise was restricted. These results suggest that sympathetic activities of cardiovascular system are accentuated in juvenile hypertensive subjects.

Adult↗