JAPANESE CIRCULATION JOURNAL
Online ISSN : 1347-4839
Print ISSN : 0047-1828
ISSN-L : 0047-1828
Volume 54, Issue 5
Displaying 1-15 of 15 articles from this issue
  • KANJI IGA, KENJIRO HORI, TADASHI MATSUMURA, GO TOMONAGA, HIROMITSU GEN ...
    1990 Volume 54 Issue 5 Pages 473-477
    Published: May 20, 1990
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The left ventricular filling pattern was studied by pulsed Doppler echocardiography in 13 congestive heart failure patients with normal sinus rhythm. The first study was done when congestive heart failure was present; the second after the signs and symptoms of congestive heart failure disappeared. In 12 of the 13 patients, the peak mitral flow velocity in atrial systole (PFVA) increased after the congestive heart failure disappeared (mean increase from 50.5 cm/sec to 74.8 cm/sec : p = 0.0001, paired t test), and the peak mitral flow velocity in early diastole (PFVE) decreased significantly in all 8 patients in whom secondary mitral regurgitation became less severe after improvement of congestive heart failure (mean decrease from 90.8 cm/ sec to 52.0 cm/sec : p = 0.0001, paired t test). The ratio of PFVA to PFVE (PFVA/PFVE) increased in all cases after the congestive heart failure improved (mean increase from 0.59 to 1.33 : p = 0.0001, paired t test). The PFVA/PFVE is a simple index of left ventricular diastolic function. A PFVA/PFVE greater than one indicates disturbed left ventricular diastolic function. However, when the' PFVA/PFVE is in a normal range for the patients' age ("pseudo-normalization") and is accompanied by impaired left ventricular systolic function in congestive heart failure, markedly increased left ventricular end-diastolic pressure must be considered.
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  • MINORU HORIE, SHUNICHI MIYAZAKI, HIROSHI NONOGI, AKINORI TAKIZAWA, MAS ...
    1990 Volume 54 Issue 5 Pages 478-486
    Published: May 20, 1990
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    To quantify the of early reperfusion on the size of infarcts, an enzyme indicator was developed: myocardial creatine kinese (CK) release tare (Kr), based on a compartment kinetics model. In 59 patients with acute myocardial infraction (MI) who received intracoronary thrombolysis therapy in the acute phase, the Kr showed a good correlation with the flow condition of infarct-related coronary artery and the time required to reach peak enzyme activity. Apparent serum CK disappearance rate (Kd') was estimated by using the method of Norris. The kd' was significantly underestimated in patients without reperfusion, suggesting the presence of prolonged enzyme release from the infarcted area. In 22 of 59 patients, who had a first acute anterior MI(left anterior descending arterial lesion), the correction of cumulative enzyme release by myocardial enzyme release (Kr) resulted in a closer correlation with chronic phase left ventricular function. Thus, kinetic analysed of serum enzyme release provide a useful means to estimate the infarct size during intracoronary thrombolysis therapy.
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  • HIROTAKA ODA, TSUTOMU MIIDA, HIRONORI SATO, NORIO HIGUMA
    1990 Volume 54 Issue 5 Pages 487-492
    Published: May 20, 1990
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    We describe 3 patients with cholesterol embolization after left heart catheterization via the femoral route. The left catheterizations were performed via the femoral route in all reported cases in which cholesterol embolization occurred as a complication of left catheterization. Postmortem examinations revel that PTCA, using the right brachial approach, is the safest method for treatment of intractable angina in patients with evidence of cholesterol embolization.
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  • RYUICHI FUJIWARA, YASUNORI KUTSUMI, TAKIO HAYASHI, SOO SOO KIM, TOSHIH ...
    1990 Volume 54 Issue 5 Pages 493-500
    Published: May 20, 1990
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The relationship of plasma lipid and apolipoprotein (apo) concentrations and plasma insulin response to oral glucose load to angiographically determined coronary artery disease (CAD) was investigated in 65 normolipidemic (plasma cholesterol <230 mg/dl and plasma triglyceride <150 mg/dl) males. According to the results of coronary angiography, the patients were divided into 2 groups: patients with normal coronary artery, NCA group (n = 21); and patients with coronary artery disease, CAD group (n = 44). No significant differences in concentrations of plasma cholesterol and triglyceride were observed between the CAD and NCA groups. In the CAD group cumulative lifetime tobacco consumption was higher and high density lipoprotein (HDL) cholesterol concentration was lower than those in the NCA group. The variables that correlated with the severity of CAD, defined by the number of lesions and percent stenosis, were levels of plasma apo A-I and apo B. Prevalence of subjects with reduced oral glucose tolerance did not differ between 2 groups. However, hyperinsulinemic response to oral glucose load was present in the CAD group. HDL-cholesterol concentration, the sum of plasma insulin levels and the magnitude of the early insulin response during oral glucose challenge were accurate predictors of the presence of but not the severity of CAD. Multivariate analysis of the data confirmed the independent effect of plasma levels of apo A-I and apo B on the severity of CAD. The present data indicated that plasma levels of apo A-I and apo B were powerful discriminators in the normolipidemic CAD patients and that a high insulin response might be an indicator of enhanced susceptibility to the distinct coronary atherosclerosis.
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  • HISAO TAGUCHI, YASUNORI OHBAYASHI, KENJI HASHIMOTO, MASAHIKO KINOSHITA
    1990 Volume 54 Issue 5 Pages 501-506
    Published: May 20, 1990
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    From among subjects who were examined by submaximal exercise testing in 1987, 54 were selected in order to examine the relationship between the blood pressure response during exercise and the tendency to develop left ventricular hypertrophy. Only those subjects having resting systolic blood pressure values between 120 mmHg and 140 mmHg were selected. The maximum systolic blood pressure during submaximal exercise was highly correlated with the sum of the R wave amplitude in V5 and the S wave amplitude in V1 of the resting ECG (r = 0.496, p>0.001, n = 54), as well as with the left ventricular mass normalized for body surface area (r = 0.609, p<0.005, n = 23). The maximum systolic blood pressure measured during submaximal exercise did not correlate with age or exercise duration. These results suggest that a greater blood pressure response during exercise is related to the tendency to develop left ventricular hypertrophy.
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  • TOMOHIRO OSANAI, HARUO MATSUMURA, TAKASHI KIKUCHI, OSAMU MINAMI, YOSHI ...
    1990 Volume 54 Issue 5 Pages 507-514
    Published: May 20, 1990
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The purpose of this study was to clarify how the metabolism of vascular prostacyclin (PGI2) and thromboxane (TX) A2 in spontaneously hypertensive rats (SHR) is involved in aging and development of hypertension. We removed the aortic walls from 5-week-old and 20 to 25-week-old SHR and age-matched Wistar Kyoto rats (WKY). At 5 weeks of age, there was no significant difference in basal and maximal (arachidonic acid 0.1mM) 6-keto-PGF Production between SHR and WKY, but the TXB2 generation in the SHR aortic wall was markedly enhanced as compared with that in WKY. At 20 to 25 weeks of age, the SHR aortic wall synthesized about I .5 times more 6-keto-PGF In the basal condition and twice as much as in the maximal condition as did the WKY wall. However there was no significant difference in TXB2 production between SHR and WKY. Age-dependent increase of vascular 6-keto-PGF was greater in SHR than in WKY. Moreover, the maximal/basal 6-keto-PGF Production ratio increased with age in SHR, but not in WKY. The synthesis of vascular TXB2 was enhanced with age in WKY, but did not change with age in SHR. These data suggest that not only the enhanced basal generation of vascular 6-keto PGF but also a much greater reservoir of 6-keto-PGF Synthesis in SHR was induced by both hypertension and maturity. The increased production of vascular TXB2 in young SHR may affect the development of hypertension.
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  • TAKASHI TAKENAKA, YUJI OGAWA, KATSUYUKI TOBISE
    1990 Volume 54 Issue 5 Pages 515-523
    Published: May 20, 1990
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The mechanism of progressive pulmonary hypertension induced by monocrotaline (MCT) remains controversial. To determine whether or not functional changes in pulmonary arterial smooth muscle contribute to the development of pulmonary hypertension, we examined the reactivity of isolated pulmonary artery segments 7, 14 and 21 days after a single subcutaneous injection of MCT. In Ca2+ -free buffer, pulmonary arteries from MCT-treated rats contracted when CaCl2 was added without any other stimulation. The pulmonary artery exposed to MCT also exhibited hyperreactivity to KCl and 5-hydroxytryptamine. These functional changes in the pulmonary artery preceded the elevation of right ventricular systolic pressure and right ventricular hypertrophy. The contraction in response to Ca2+ suggests that the pulmonary artery of rats given MCT may be contracted in situ. Vasoconstriction due to these alterations may play an important role in the development of pulmonary hypertension according to this model.
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  • ISSEI KOMURO, MASAHIKO KURABAYASHI, YOSHIKAZU SHIBAZAKI, YUICHI KATOH, ...
    1990 Volume 54 Issue 5 Pages 526-534
    Published: May 20, 1990
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Pressure overload induces cardiac hypertrophy and reexpression of contractile protein isogenes. To ascertain the molecular mechanism of these events, we examined the expression of cellular oncogenes and the early change in the translational activity of specific cardiac mRNA by two-dimensional gel electrophoresis of in vitro translational products. Pressure overload increased the expression levels of c-fos, c-myc, and c-Ha-ras genes. The relative predominance of 8 species out of over 400 translational products was increased by pressure overload while that of 2 translational products was decreased. We cloned four pressure-overload-responsive CDNA clones by differential dot blot hybridization. The expression pattern of each CDNA clone in the pressure-overloaded hearts was similar to that in fetal hearts. To examine whether mechanical stimuli directly induce specific gene expression in the heart, we cultured rat neonatal cardiocytes in elastic silicone dishes and stretched these adherent cells. Myocytes stretching stimulated amino acid uptake and expression of the c-fos gene, which was blocked by protein kinase C inhibitors. These results suggest that there are some early responsive genes in cardiac hypertrophy and that mechanical loading directly stimulates gene expression possibly via protein kinase C activation.
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  • MASATSUGU HORI, NOBUAKI NAKATSUBO, TOSHIFUMI KAGIYA, KUNIMITSU IWAI, H ...
    1990 Volume 54 Issue 5 Pages 535-539
    Published: May 20, 1990
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    It is reported that Na+ influx contributes to stretch-induced cardiac hypertrophy. Na influx may also be involved in cardiac hypertrophy induced by catecholamine. In the present study, to test whether Na+/H+ exchange plays an important role in norepinephrine-induced cardiac hypertrophy, the effect of Na+/H+ exchange inhibitor, amiloride on protein systhesis was studied in cultured neonatal rat cardiomyocytes in serum free medium. [3H]Phenylalanine uptake was determined 24 and 48 hours after administration of norepinephrine with and without amiloride. In the control, norepinephrine increased [3H]phenylalanine uptake in a dose dependent manner (10-5-10-7 M). Prazosin (10-7 M) and amiloride (10-5-10-4M) significantly attenuated the norepinephrine mediated protein synthesis. These results indicate that α1-adrenergic stimulation enhances the protein synthesis through activation of Na+/H+ exchange. Therefore, Na+ influx and/or PH increase may play a key role in cardiac hypertrophy.
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  • NOBUAKIRA TAKEDA, IZURU NAKAMURA, TADANARI OKUBO, MAKOTO NAGANO
    1990 Volume 54 Issue 5 Pages 540-546
    Published: May 20, 1990
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Alterations of myocardial contractility and energetics were examined in cardiac hypertrophy induced by different types of cardiac overload. Myocardial contractility was estimated by isometric contraction of isolated left ventricular papillary muscles. Myocardial energetics were assessed from ventricular myosin isoenzyme patterns obtained by pyrophosphate gel electrophoresis. Cardiac hypertrophy was induced by endurance swim-training and sustained pressure-overload by abdominal aortic constriction or volume-overload created by an arteriovenous shunt. In swim-trained hypertrophied myocardium, isometric developed tension (T) and dT/dtmax showed a tendency to increase and response of dT/dtmax to isoproterenol increased significantly as compared with sedentary rats. Training shifted the left ventricular myosin isoenzyme pattern toward VM-1, which has the highest ATPase activity. In pressure- or volume-overloaded myocardium, dT/dtmax decreased significantly and mechanical response to isoproterenol also decreased (or tended to decrease in volume-overloaded hearts) as compared with the respective sham-operated controls. In pressure- or volume-overloaded hearts, left ventricular myosin isoenzyme pattern shifted toward VM-3, which has the lowest ATPase activity. These results indicate that alterations in myocardial contractility, mechanical catecholamine responsiveness and myocardial energetics in hypertrophied myocardium do not always display the same trend, but are greatly influenced by the causes or duration of cardiac overload.
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  • YUZO HIROTA, GEN SHIMIZU, KATSUHISA ISHII, JUNYA KUSUKAWA, YOSHIO KITA ...
    1990 Volume 54 Issue 5 Pages 547-553
    Published: May 20, 1990
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Left ventricular (LV) midwall mechanics were evaluated in normal, pressure overload due to hypertension, and volume overload hearts due to aortic (AR) and mitral regurgitations (MR) using a 2 shell compartment model of ellipsoid revolution. While ejection fraction (EF) was in the normal range, midwall fractional shortening (MFS) was depressed with low end-diastolic and end-systolic stress in hypertrophied hearts with pressure overload. Not only LV volumes but also LV systolic pressure and wall thickness were increased in AR. LV enddiastolic pressure was elevated, and EF and MFS were reduced in patients with AR and congestive heart failure (CHF). In patients with MR and CHF, pulmonary capillary wedge pressure was elevated, LV volumes were enlarged and end-systolic stress was high, but LV wall thickness and MFS remained in the normal range. It is concluded from this observation that: l) myocardial contractility is already depressed with normal systolic function in hypertrophied ventricle with pressure overload. 2) AR can be considered to be the disease of both pressure and volume overload, and symptoms of CHF are the result of depressed myocardial contractility. 3) MR is the disease of pure volume overload. Myocardial contractility is well preserved even with the presence of severe CHF in MR.
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  • TETSU YAMAKADO, TAKASHI NAKANO
    1990 Volume 54 Issue 5 Pages 554-562
    Published: May 20, 1990
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    To investigate left ventricular (LV) systolic and diastolic function in cardiac hypertrophy, we analysed LV pressure (catheter tip-manometer) and simultaneously performed cineangiography in 24 patients with systemic hypertension (HT), 25 patients with, hypertrophic cardiomyopathy (HCM) and 25 normal subjects. We digitized LV cineangiograms frame by frame and computed volume and its derivatives, wall thickness and circumferential wall stress. LV systolic pump function was normal or supernormal in HT and HCM. However, myocardial contractility assessed by end-systolic wall stressvolume relation was depressed in HCM whereas it is normally maintained in HT. LV diastolic function was also impaired in HCM and even in HT despite normal systolic function. The LV hypertrophy group showed significantly prolonged time constant of isovolumic relaxation, increased time from end-systole to the peak filling rate, and upward shift of the diastolic pressure-volume relationship. The characteristic findings of LV diastolic function in LV hypertrophy, therefore, can be summarized as impaired isovolumic relaxation, delayed early diastolic filling and decreased diastolic distensibility. The mechanisms of abnormal systolic and diastolic function may include myocardial ischemia and/or calcium overload in hypertrophied myocardium, but further study will be needed to clarify these problems.
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  • SUSUMU NAKANO, KAZUHIRO TANIGUCHI, TOMOHIDE KAWAMOTO, MASATAKA MITSUNO ...
    1990 Volume 54 Issue 5 Pages 563-567
    Published: May 20, 1990
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Pre- and postoperative left ventricular (LV) mass and myocardial contractile state were evaluated in 62 patients with aortic regurgitation (AR) and in 20 patients with aortic stenosis (AS). Preoperatively, there was a significant inverse correlation between LV mass and end-systolic wall stress (ESS)/end-systolic volume index in AR patients and AS patients. In patients with preoperative LV mass exceeding 250 g/m2, ejection fraction failed to return to normal postoperatively, despite reduction in ESS close to the normal controls. Our results indicated that myocardial function was irreversible even in postoperative unloading conditions, when preoperative LV mass exceeded 250 g/m2 in AR patients as well as AS patients.
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  • YASURO SUGISHITA, KEIJI IIDA, KIMIHIKO YUKISADA
    1990 Volume 54 Issue 5 Pages 568-574
    Published: May 20, 1990
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    To investigate the clinical roles of mechanical and non-mechanical factors in hypertensive hypertrophy, 125 patients with essential hypertension, 20 with hypertrophic cardiomyopathy (HCM) and 20 with dilated cardiomyopathy (DCM), were studied using echocardiography. The hypertensive patients were separated into 3 groups: those with left ve, ntricular (LV) hypertrophy (H), those without hypertrophy (H(-)) and those with dilatation (D). Group H patients were separated into 3 subgroups: those with subnormal LV end-systolic wall stress (ESS) (HI), those with normal ESS and mild hypertrophy (HIIA), and those with normal ESS and severe hypertrophy (HIIB). The inotropic response to isoproterenol infusion (0.02 μg/kg/min for 5 min) was measured by the increase of fractional shortening (FS) corrected for the decrease of ESS (ΔFS/ΔESS). After antihypertensive treatment for 4.4 1.7 years, echocardiography was repeated. ΔFS/ΔESS was significantly larger in Hl and HCM than in HIIA, was significantly larger in HIIA than in HIIB in which it was significantly larger than in D and DCM. After the treatment, LV mass decreased significantly except in HI. In conclusion, hypertensive hearts are regulated by mechanical and non-mechanical factors. Non-mechanical factors, for example the function of beta-adrenergic receptors in myocardium, have a variety of influences on myocardium, causing a broad spectrum of clinical features and courses.
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  • MIKIO ARITA, SETSUKO FUJIWARA, YUJI UENO, MASAHIKO SHIOTANI, YOSHINARI ...
    1990 Volume 54 Issue 5 Pages 575-580
    Published: May 20, 1990
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The effects of various antihypertensive treatments on the echocardiographic and electrocardiographic findings of left ventricular (LV) hypertrophy were studied in 75 patients with essential hypertension. The hemodynamic effects of the therapy during exercise were also compared. LV mass by echocardiogram was significantly reduced by β-blockade and angiotensin converting enzyme inhibition (ACEI), but only slightly reduced by Ca channel blockade. QRS high voltage criteria of LV hypertrophy by electrocardiogram were reduced by all 3 of these antihypertensive treatments. At submaximal exercise, the pressor responses were attenuated by captopril, but not influenced by metoprolol or nifedipine. The increase in plasma norepinephrine by exercise was significantly suppressed after captopril, but was somewhat augmented after metoprolol or nifedipine. These observations indicate that the responses of hemodynamics and sympathetic nervous activity to exercise are different after the treatment byβ-blocker, Ca channel blocker or ACEI, in spite of the equal antihypertensive effect. However, it is suggested that the regression of LV hypertrophy might be induced by antihypertensive therapy, though the different grade by the individual drug.
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