JAPANESE CIRCULATION JOURNAL
Online ISSN : 1347-4839
Print ISSN : 0047-1828
ISSN-L : 0047-1828
48 巻, 6 号
選択された号の論文の11件中1~11を表示しています
  • FONTAINE G, FRANK R, TNET L, GUIRAUDON G, CABROL C, CHOMETTE G, GROSGO ...
    1984 年 48 巻 6 号 p. 515-538
    発行日: 1984/06/20
    公開日: 2008/04/14
    ジャーナル フリー
    Arrhythmogenic right ventricular dysplasia (ARVD) is a recently individualised clinical entity which sometimes presents with episodes of ventricular tachycardia (VT). These attacks may be resistant to anti-arrhythmic therapy and new therapeutic approaches have been developed for the treatment of this condition. These new methods are mainly surgical, based on the analysis of electrical activation of the heart in sinus rhythm and during VT. This approach has increased our understanding of the physiophathology of VT, not only in the context of ARVD, but also in the most commonly encountered clinical setting of VT, after myocardial infarction. Electrophysiological study of the epicardial activation of the dysplastic zones has demonstrated the presence of delayed potentials recorded after the end of the QRS complex. This can be explained by the histopathology of these issues. ARVD is characterised histologically by partial degeneration of the myocardial wall. Most of the muscle fibers are replaced by fatty tissue in the middle of which some healthy fibers survive. These changes are mainly observed in the intramyocardial and subepicardial layers, the subendocardium being almost normal. Strands of isolated muscle fibers within the non-conducting fatty degeneration may lead to very delayed activation with respect to the adjacent healthy tissues. The propagation of activation is delayed as it passes through this plexiform structure and in the zones adjacent to healthy muscle were reentry phenomena may arise. In ARVD, these changes are mainly located over the right ventricle, so explaining the right ventricular origin of most forms of VT observed in this condition. However, we have also observed a case which suggested an isolated arrhythmogenic left ventricular dyplasia. Epicardial mapping localizes the point of origin of VT in zones situated between the slow and normally conducting tissues. Simple ventriculotomy, a full thickness section of the ventricular wall, at the point of epicardial breakthrough of the VT prevents recurrence in the great majority of patients. The same pathophysiological concepts may be applied to VT complicating myocardial infarction but in this situation the myocardial fibers capable of slowly conducting the activation are isolated with in the fibrous tissue in the border zone of the infarct. The point of origin of VT is usually within the interventricular septum with a point of epicardial breakthrough which could be located some distance away. Different surgical techniques have been developed to deal with this condition. Encircling endocardial ventriculotomy isolates the arrhythmogenic zone from the rest of the healthy tissues by tracing an incision all around the arrhythmogenic border zone. Subendo-cardial excision could be performed at the point of origin of the abnormal activation. Cryoablation seems a less aggressive procedure. These new surgical techniques of managing resistant VT complicating myocardial infarction have given improved results by comparison with previous methods (aneurysm-ectomy, myocardial revascularization) which were not based on electrophy-siological concepts. More selective techniques like close chest ventricular tachycardia fulguration is a promising method currently on the way of development to manage recurrent VT of any etiology with minor damage to myocardial function.
  • MINORU HORIE, HIROFUMI YASUE, SHINGO OMOTE, AKINORI TAKIZAWA, MASAO NA ...
    1984 年 48 巻 6 号 p. 539-545
    発行日: 1984/06/20
    公開日: 2008/04/14
    ジャーナル フリー
    In 31 patients with transmural myocardial infarction in whom coronary arteriography was performed within 8 hours after the onset of symptoms, we examined (1) the effect of restoration of coronary blood flow on serum CPK time-activity curve and (2) the relationship between cumulative CPKr and the left ventricular function in the chronic phase. We divided 31 patients into 2 groups: Group A consists of 19 patients in whom coronary reperfusion was established. Group B consists of 12 patients whose coronary artery remained occluded. In group A, the time required to reach peak serum CPK activity was significantly shorter than in group B. when comparing CPKr with percent abnormally contracting segment (%ACS) in 2 groups, correlation between CPKr and %ACS was not good, but it revealed linear relation in both group A and B. CPKr divided by & ACS(CPK%ACS) was significant higher in group A than in group B. We concluded that reperfusion of infarct-related coronary artery changes serum CPK time-activity curve resulting in earlier appearance of peak serum CPK and that infarct size cannot be estimated by from level alone.
  • JUN SASAKI, TOMOKI KAWANO, YASUSHI SASAKI, YASUYUKI ISHIHARA, TEIZO SA ...
    1984 年 48 巻 6 号 p. 546-551
    発行日: 1984/06/20
    公開日: 2008/04/14
    ジャーナル フリー
    The concentrations of lipids and apolipoproteins in serum following onset of acute myocardial infarction were measured periodically in eleven patients for 28 days. Significant and sustained decrease in the concentration of HDL-cholesterol was observed by the seventh days post-infarction and remained low throughout the remainder of the study. The concentration of apo A-I and apo A-II assayed by electroimmunoassay was significantly low by 4th and 5th days post-infarction, remained low until day 10 and then began to increase but were not back to the initial values by 28 days post-infarction. Apo B, C-I, C-II, C-III, and E levels remained unchanged throughout the course. The concentrations of total cholesterol, triglycerides tended to fall reaching the lowest levels on day 7 and 10, but were not significant. The concentration of serum phospholipids level tended to decrease and fall significantly by day 7 and 10. The concentration of the free fatty acids in the serum was elevated during the first 2 days post-infarction and was within the normal range throughout the remainder of the study.
  • KIYOTAKA KAKU, YUZO HIROTA, GEN SHIMIZU, KOICHI FURUBAYASHI, KEISHIRO ...
    1984 年 48 巻 6 号 p. 552-558
    発行日: 1984/06/20
    公開日: 2008/04/14
    ジャーナル フリー
    To evaluate the effect of contrast material on left ventricular (LV) function, LV pressure and its first derivative were continuously monitored during and after LV cineangiography with Mikro-tip&oR; angiocatheters in 15 normal subjects (Group 1) and patients with coronary artery disease (CAD)0 without LV asynergy (Group 2, n=10), with mild asynergy (Group 3, n=12) and severe asynergy (Group 4, n=13). In all 4 groups, systolic hypotension, decrease of negative dP/dt, and prolonged time constant of LV pressure fall (T) were observed in 30 seconds after dye injection, and all these parameters returned to the control value in 2 minutes. LV end-diastolic pressure (EDP) began to elevate at one minute, reached its peak at 2 minutes, and stayed elevated for 7 minutes. Although significant decrease in LV systolic pressure was seen, indexes of LV contractility, peak positive dP/dt and (dP/dt)/DP40, showed increase in all groups. NO different directional changes of these parameters were observed among 4 groups. The degree of LVEDP elevation was parallel to the diastolic elastic stiffness constant (K) in Group 1 (r=0.64, (p<0.05). It is concluded that systolic hypotension and prolonged relaxation are only transient, and elevation of LVEDP after the contrast material injection seems to be the effect of only acute volume overload.
  • HIROSHI NONOGI, SHIGETAKE SASAYAMA, TSUNETARO SAKURAI, CHUICHI KAWAI, ...
    1984 年 48 巻 6 号 p. 559-566
    発行日: 1984/06/20
    公開日: 2008/04/14
    ジャーナル フリー
    To detect the left ventricular boundary in the intravenous ventriculography, we used a subtraction technique for background suppression. Images containing contrast medium and reference mask images were transfered to a computer through a flying spot scanner and stored on the digital disc. Stored reference mask images were subtracted from the digitized contrast images. The resulting images were then electronically enhanced to extract the left ventricular (LV) image. The LV boundary was delineated with an algorithm we have developed and the volume of the LV cavity was calculated automatically. The validity of this method was compared with data obtained from conventional left ventriculogram (LVG). In 11 patients, values for end-diastolic volume (EDV), end-systolic volume (ESV) and ejection fraction (EF) calculated from the intravenous LVG were correlated closely with those from the conventional LVG (128±38 (SD) vs 133±39 ml, r=0.95; 50±28 vs 53±30 ml, r=0.98; 63±10 vs 62±12%, r=0.96, respectively). Nine patients with valvular regurgitation were followed up serially after valve replacement. EDV index fell significantly after corrective surgery (145±50 to 81±33 ml/m2, p<0.02), whereas, EF was affected variably depending upon the preoperative state (58±13 to 61±11%, not significant). Thus, this method is less invasive than conventional LVG and has successfully allowed for sequential determination of ventricular function on an outpatient basis.
  • HAKUO TAKAHASHI, ISAO IYODA, HIDEAKI YAMASAKI, KAZUO TAKEDA, HIROSHI O ...
    1984 年 48 巻 6 号 p. 567-574
    発行日: 1984/06/20
    公開日: 2008/04/14
    ジャーナル フリー
    To determine the importance of the renal nerves in DOCA-salt hypertension, either renal denervation or a sham-operation was carried out on both DOCA-salt-treated and non-DOCA-treated rats. The systolic blood pressure of the non-DOCA rats remained within normotensive levels, in which the difference in blood pressure levels between the renal denervated and the sham-operated groups was not significant. On the other hand, the blood pressure of the rats treated with DOCA, and having intact renal nerves, began to rise by the end of the first week and rose consistently thereafter, whereas, in the renal denervated DOCA-salt rats, the blood pressure started to rise by the second week and then proceeded to increase gradually. The differences between the sham and the denervated rat groups were significant throughout the four weeks. The mean arterial pressure, directly measured from the caudal artery of conscious rats during the fourth week of this study, was 166±7 mmHg in the sham-operated and 129±4 mmHg in the renal-denervated rats (the data having an 1% significant difference). To test the effects of renal denervation on the natriuresis, pentobarbital-anesthetized rats wee infused intravenously with physiological saline. The renal denervated rats which had received DOCA excreted more sodium than did the sham-operated rats. When the rats were later anesthetized with urethane to allow intracisternal injections of hypertonic saline, the mean blood pressure in renal denervated rat groups was again lower than that of the sham-denervated rat groups. However, subsequent intracisternal injections of 5% saline produced similar pressor responses as well as tachycardia in both DOCA groups. In comparing the non-DOCA with the COCA-treated group, it was found that the degree of pressor response was significantly greater in the latter group. Finally, renal denervation was confirmed by measuring the norepinephrine content of the kidney in the fourth week of the study; the level was significantly lower in the renal denervated than in the sham-operated group. These results suggest that intact renal nerves are important in the development of the DOCA-salt hypertension. ]the depressor effects of renal denervation are not brought about by the elimination of direct vasoconstriction of renal vasculature, but rather as a result of long lasting effects on renal function.
  • KAZUTAKA NISHIMURA, HIDEKAZU SHIMIZU, TATSUO KOKUBU
    1984 年 48 巻 6 号 p. 575-579
    発行日: 1984/06/20
    公開日: 2008/04/14
    ジャーナル フリー
    Prokallikrein was activated by trypsin and by α-chymotrypsin, but not by proteases, such as plasmin, thrombin, urokinase, carboxypeptidase B, papain, elastase, pepsin, and cathepsin D. Moreover, rat fresh serum did not activate prokallikrein. Maximum activation of prokallikrein by trypsin was obtained at the concentration of 10 μg to 1 mg per ml in PBS and that by α-chymotrypsin was at the concentration of 5 mg per ml. The enzymic properties of trypsin-activated and α-chymotrypsin-activated kallikreins were identical with those of active kallikrein in the kidney.
  • YO YASUDA, SENRI HIRAKAWA, MICHIO ARAKAWA, KENJIRO KAMBARA, JUNPEI IIN ...
    1984 年 48 巻 6 号 p. 580-590
    発行日: 1984/06/20
    公開日: 2008/04/14
    ジャーナル フリー
    Pulmonary extravascular water volume was obtained as the lung thermal volume (LTV) in mongrel dogs (n=3) by double indicator dilution method, using negative heat and indocyanine green. We used a technic of one injection site (right atrium) and two sampling sites, i.e. pulmonary artery trunk and aortic root. In 13 dogs, cardiac outputs determined simultaneously from thermodilution curves in pulmonary artery trunk, aortic root and from dye dilution curve in aortic root, were in a good agreement with a coefficient of variation of ±12%. Lung thermal volume measured twice within a period of 5 minutes in 17 dogs, gave closely similar values with a coefficient of variation of ±9%. Lung thermal volume was 5.7±1.1 ml/kg (mean ±SD) and corresponding "weighted lung water" (WLW), which was measured by destructive, direct method, was 5.0± 1.0 ml/kg, the ratio of LTV to WLW(LTV/WLW) being 1.2±0.2 in control state. LTV/WLW ratio was 1.2±0.2 in 11 dogs loaded with dextran, and 1.1±0.1 in 6 dogs loaded with alloxan. Thus the lung thermal volume slightly exceeded WLW. In order to evaluate the extent to which the thermal diffusion into the left ventricular wall would cause LTV to slightly overestimate the pulmonary extravascular water volume, dye dilution curves and thermodilution curves were recorded simultaneously in the left atrium (LA) and aortic root (Ao) in a total of 25 runs in 5 dogs. The ratio of LTV obtained in LA to that in Ao was 0.9±0.1 (mean±SD). It was concluded that the pulmonary extravascular water volume was overestimated, by about 10% due to the thermal diffusion into the left ventricular wall.
  • AKIRA KOBAYASHI, JUN KAMIYA, TESUO YAMASHITA, KYOICHI ISHIZAKA, HIDEHA ...
    1984 年 48 巻 6 号 p. 591-595
    発行日: 1984/06/20
    公開日: 2008/04/14
    ジャーナル フリー
    The accumulation of intermediates subsequent to impaired oxidation of free fatty acids has been suggested as a cause of cellular damage in ischemic myocardium. Many reviews have supported the theory that glucose-insulin-potassium (GIK) solution has a beneficial effect on the ischemic myocardium. We evaluated the effects of GIK solution on intermediates of free fatty acid metabolism in ischemic myocardium. The left coronary artery was occluded for 40 minutes in twelve dogs. In six dogs, 10 minutes before coronary artery occlusion, GIK solution (50 per cent of glucose, 50 units/liter of regular insulin, 50 mEq/ liter of potassium) was given at the rate of 0.1 ml/kg per minute until the time of excision of the hear. In the ischemic area, adenosine triphosphate (ATP) level in the GIK group (3.80±1.34 μmole/g) was significantly higher than that in the control group (2.04±0.68, p<0.05). The free carnitine level was significantly increased was GIK in both ischemic and nonischemic areas (p<0.05). In the control group, the long chain acyl coenzyme A (CoA) level in the ischemic area (23.0±7.0 nmole/g) was significantly higher than that in the nonischemic area (1.71±3.5, p< 0.05). On the other hand, GIK prevented the increase in the long chain acyl CoA in the ischemic area (17.8±5.6). This study suggests that GIK has a protective effect on ischemic myocardium, probably by preventing the accumulation of long chain acyl CoA by improving free fatty acid metabolism.
  • HISATSUNE OOTSUBO, HITONOBU TOMOIKE, KIKUO SAKAI, KATSUHIKO NOGUCHI, A ...
    1984 年 48 巻 6 号 p. 596-601
    発行日: 1984/06/20
    公開日: 2008/04/14
    ジャーナル フリー
    The epicardial coronary artery plays an important role not only as a conduit artery but also as a locus of coronary spasm. Accordingly, diameter change of the large epicardial coronary artery of the in situ canine heart was continuously measured by ultrasonic dimension gauge technique and the effects of alpha adrenergic stimulation on the caliber were studied. After the intravenous administration of phenylephrine the aortic pressure increased by 28 mmHg. however, the left circumflex coronary artery diameter decreased by 3.4% (p<0.01). Norepinephrine and sciatic nerve stimulation after propranolol (1 mg/kg) induced coronary vasoconstriction by 1.3 (p<0.025) and 2.5% (p<0.05) against the obvious increases of aortic pressure by 16 and 19 mmHg, respectively. Thus alpha adrenergic stimulation, in situ in dogs, was shown to directly constrict the large epicardial coronary artery.
  • SHUMPEI OKUBO, CHIKAO YUTANI, MASASHI HORIMOTO, NOBUKO TSUSHIMA, AKIRO ...
    1984 年 48 巻 6 号 p. 602-609
    発行日: 1984/06/20
    公開日: 2008/04/14
    ジャーナル フリー
    A 75-year-old man complaining of dyspnea and having sings of postcapillary pulmonary hypertension was diagnosed as pulmonary veno-occlusive disease and confirmed at autopsy. This is the oldest case ever reported. Almost all the small veins 2 mm or less in external diameter were partially or nearly completely occluded by intimal fibrous tissue, and the obstructive changes in the pulmonary arteries were much more limited. Pulmonary veno-occlusive disease is a rare, almost inevitably fatal disease of unknown etiology which has only recently been separated clearly from primary pulmonary hypertension as a distinct entity. Chest roentgenogram finding suggesting postcapillary pulmonary hypertension is a clue to a diagnosis and differentiates this from two other causes of clinical primary pulmonary hypertension, that is, recurrent pulmonary embolism and plexogenic pulmonary arteriopathy.
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