[Assessment of the significance of coronary collateral vessels using thallium-201 myocardial imaging].
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Biomedical subjects
Publications and source records attributed to H Fukuzaki.
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To investigate the relationship between regional contractile dynamics and regional myocardial lesions of the left ventricular wall in patients with hypertrophic cardiomyopathy (HCM), autopsy findings of 11 patients were compared with their ante mortem echocardiographic findings. The regional systolic wall thickenings (%RWT) of the interventricular septum (IVS) and left ventricular posterior wall (LVPW) obtained using M-mode echocardiography were converted into % normalized RWT (%NRWT) by the averaged %RWT in 15 normal subjects. The %NRWT was compared with the wall thickness obtained by echocardiography and/or autopsy, and histological findings, such as the myocardial fibrosis ratio, disarray area ratio, and mean myocyte diameter. 1. There were no significant correlations among wall thickness of the left ventricle, the myocardial fibrosis ratio, the disarray area ratio, and the mean myocyte diameter of each segment. 2. The %NRWT in 22 segments of the 11 patients with HCM was not significantly related to the echocardiographic wall thickness at end-systole, the autopsy wall thickness, the mean myocyte diameter and the disarray area ratio, but that correlated significantly with the echocardiographically-determined wall thickness at end-diastole (r = -0.53, p less than 0.02), and with the myocardial fibrosis ratios (r = -0.59, p less than 0.005). 3. The %NRWT in the IVS was significantly less than that in the LVPW. The %NRWT in all segments of the LVPW was significantly related to the myocardial fibrosis ratios (r = -0.80, p less than 0.005), but was not related to the wall thicknesses or the disarray area ratios.(ABSTRACT TRUNCATED AT 250 WORDS)
To clarify the influence of cardiac function of myocardial histologic lesions on the prognosis of hypertrophic cardiomyopathy (HCM), most recent echocardiographic findings of 30 deceased patients were reviewed. In 12 patients, histological sections from the left ventricular transverse plane made at necropsy were examined. According to the main causes of death, patients were categorized into four groups as sudden death (17 cases), heart failure death (four cases), embolic death (four cases), and non-cardiac death (five cases). 1. Clinically, atrial fibrillation and heart failure (NYHA III, IV) were frequently observed in heart failure and embolic groups. 2. Echocardiographically, left ventricular wall thickness did not differ among the four groups, but percent fractional shortening was significantly smaller in heart failure group than in non-cardiac group, and left ventricular end-diastolic dimension (LVDd) and left atrial dimension were significantly greater in heart failure group than in non-cardiac group. The normalized rapid filling rate was less in heart failure, embolic, sudden death and non-cardiac groups in that order. 3. Histopathologically, the mean myocyte diameter (MD) and percent area of disarray (%D) did not differ among the four groups, but % area of massive fibrosis (MF) greater than 2 mm2 was larger in heart failure, embolic, sudden death and non-cardiac groups in that order, especially in heart failure group. 4. Comparison of echocardiographic and histopathological findings: Though MD and %D did not correlate with any echocardiographic indices, %MF correlated significantly with LVDd (r = 0.83, p less than 0.005), and correlated inversely with the normalized rapid filling rate (r = -0.80, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of this study is to investigate mitral valve prolapse (MVP) in patients with suggested endomyocardial disorder. The study population consisted of 24 patients (group M) aged 41 +/- 17 years old, who were suspected or confirmed to have the history of myocarditis and 45 patients (group C) with collagen disease aged 42 +/- 14 years old. All patients had no left ventricular (LV) hypertrophy, no LV dilatation, and normal systolic function of the LV. Thirty normal subjects (group N) aged 43 +/- 17 years old were used for the control study. In both groups M and C, cardiac symptoms were observed in 54 and 53%, ECG abnormalities in 58 and 38%, and ventricular premature contractions of 3 or 4 degree by Lown's classification in 46%, respectively. M-mode measurements (LVDd, LVDs, %FS, LAD, IVST+PWT) were not different among three groups. MVP were detected in 54% of group M and in 49% of group C. Left ventricular peak filling velocity in the atrial contraction phase (A) divided by the peak filling velocity in the rapid filling phase (R) was significantly higher in groups M and C than in group N. There was no difference in clinical features and echo findings except for the frequency of mitral regurgitation between patients with and without MVP. Thus, MVP was frequently observed in patients with myocarditis and patients with collagen diseases, who were both suspected to have endomyocardial damages. It is suggested that in these patients, MVP might be caused by post-endomyocarditis lesion of the mitral apparatus.
Although the prognosis of dilated cardiomyopathy (DCM) is poor, some patients occasionally follow favorable clinical courses and have significant improvement in cardiac function. To elucidate the mechanism of such improvement, we compared the clinical and pathological findings of 54 cases with DCM, including 12 cases with significant improvement (Dd less than 55 mm, %FS greater than 22%) during two years' follow-up (improved group), 26 without significant improvement (unimproved group), and 16 who died within two years (decreased group). Percent fractional shortening (%FS) in the deceased group was less than that in the unimproved group (12.4 +/- 3.9 vs 17.2 +/- 6.2, p less than 0.01). Pulmonary capillary pressure (PC) and % fibrosis in the deceased group were greater than those in the unimproved group [(22.7 +/- 9.5 vs 11.4 +/- 4.2 mmHg, p less than 0.001), (21.7 +/- 9.9 vs 13.4 +/- 3.6, p less than 0.01)], respectively. Although Dd, Ds, %FS, end-diastolic wall thickness (Thd), and PC in the improved group were not different from those in the unimproved group. End-systolic wall stress (WSes) in the improved group was greater than that in the unimproved group (376 +/- 73 vs 319 +/- 60 g/cm2, p less than 0.02), but % fibrosis was less in the improved group (7.6 +/- 3.4 vs 13.4 +/- 3.6, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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In cultured rabbit aortic smooth muscle cells (SMC), 12-O-tetradecanoylphorbol-13-acetate (TPA) induced DNA synthesis in the presence of plasma-derived serum to a small extent, but inhibited markedly the rabbit whole blood serum (WBS)-, platelet-derived growth factor (PDGF)- and epidermal growth factor-induced DNA synthesis. Phorbol-12,13-dibutyrate (PDBu) mimicked this antiproliferative action of TPA, but 4 alpha-phorbol-12,13-didecanoate was inactive in this capacity. Prolonged treatment of the cells with PDBu caused the partial down-regulation of protein kinase C. In these protein kinase C-reduced cells, WBS still induced DNA synthesis, but TPA did not inhibit the WBS-induced DNA synthesis. We have previously shown that protein kinase C is involved at least partially in the PDGF-induced DNA synthesis in rabbit aortic SMC. The present results together with this earlier observation suggest that protein kinase C has not only a proliferative but also an antiproliferative action in rabbit aortic SMC.
Dipyridamole test, isoproterenol test, and treadmill exercise test were performed in two groups of patients with vasospastic angina (Group 1: 10 patients with 70% or greater coronary narrowings, Group 2: 8 patients with narrowings less than 70%. The results were correlated with coronary anatomy. In Group 1, vasodilation of resistance vessels by dipyridamole elicited ischemic episodes in 9 patients and an increase in myocardial oxygen consumption by isoproterenol caused anginal attacks in 7 patients. None of patients of Group 2 showed positive responses to either drug. All patients of Group 1, and 3 patients of Group 2 gave positive responses to treadmill test. These observations show that several different mechanisms are involved in the pathogenesis of myocardial ischemia in patients with vasospastic angina. Pharmacological interventions have higher specificity than exercise tests in predicting coronary anatomy and are useful for the choice of therapy in the patients.
An excess of thyroid hormone is known to produce cardiac dysfunction and failure, i.e., thyrotoxic heart. We studied the protective effect of coenzyme Q10 (CoQ10) on the thyrotoxic heart in 29 rabbits. A group treated with 1-thyroxine sodium salt (T4; 167 micrograms/kg) for 3 weeks showed marked decreases in the myocardial content of norepinephrine (NE) and ATP (0.5 +/- 0.2 microgram/g wet weight, P less than 0.05 and 31.1 +/- 2.6 nmol/mg protein, P less than 0.05, respectively) as compared with a group treated with CoQ10 solvent (2 ml/kg) for 3 weeks (1.1 +/- 0.1 microgram/g wet weight and 45.7 +/- 4.7 nmol/mg protein). The mitochondrial Ca2+ content of the T4 group showed significant increases (21.3 +/- 0.6 nmol/mg protein, P less than 0.05) compared with the solvent group (18.2 +/- 0.8 nmol/mg protein), while the total tissue Ca2+ content of the T4 group was unchanged compared with the solvent group. These biochemical derangements suggest that T4-treated rabbits were in a state of cardiac dysfunction. In contrast, a group which was assigned to concomitant treatment of T4 and CoQ10 (5 mg/kg) for 3 weeks showed no reductions in NE and ATP (0.9 +/- 0.2 micrograms/g wet weight and 44.6 +/- 1.9 nmol/mg protein, respectively) and protected an increase in the mitochondrial Ca2+ content (18.2 +/- 1.2 nmol/mg protein). A group treated with CoQ10 (5 mg/kg) for 3 weeks showed no changes in myocardial NE, ATP, and Ca2+ content in the mitochondria. These results suggest that exogenously administered CoQ10 may protect against biochemical derangements in the thyrotoxic heart.
In rabbit aortic smooth muscle cells (SMC), protein kinase C-activating 12-O-tetradecanoylphorbol-13-acetate (TPA) inhibited the whole blood serum (WBS)-induced DNA synthesis. The inhibitory action of TPA was mimicked by another protein kinase C-activating phorbol ester, phorbol-12,13-dibutyrate (PDBu), but not by 4 alpha-phorbol-12,13- didecanoate known to be inactive for this enzyme. Prolonged treatment of the cells with PDBu caused the down-regulation of protein kinase C. In these cells, WBS still induced DNA synthesis but the inhibitory action of TPA was abolished. DNA synthesis started at 18 h and reached a maximal level 24 h after the addition of WBS. TPA inhibited the WBS-induced DNA synthesis even when added 12 h after the addition of WBS. These results suggest that protein kinase C has an antiproliferative action in rabbit aortic SMC and that this action is attributed to the inhibition of the progression from the late G1 into S phase of the cell cycle. TPA also inhibited the phospholipase C-mediated hydrolysis of phosphoinositides which was induced by WBS within several minutes, but the relevance of this effect on the antiproliferative action of TPA is uncertain.
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In cultured rabbit aortic vascular smooth muscle cells (VSMC), protein kinase C-activating phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and phorbol-12,13-dibutyrate (PDBu) stimulated DNA synthesis in the presence of 10% cell-free plasma-derived serum. This stimulation was half that shown by PDGF. 4 alpha-Phorbol-12,13-didecanoate, known to be inactive for protein kinase C, was without effect in stimulating DNA synthesis. Prolonged treatment of the cells with PDBu led to a marked decrease in protein kinase C. In the pDBu-treated cells, the TPA-stimulated DNA synthesis was completely abolished whereas the PDGF-stimulated DNA synthesis was decreased to about half that in the control cells. These results suggest that protein kinase C is involved in PDGF-stimulated proliferation of VSMC.
The effects of intracoronary injection of nitroglycerin, adenosine, nifedipine and prostacyclin on restoring coronary perfusion during flow-reducing partial coronary obstruction in anesthetized dogs were studied. Coronary obstruction was obtained by inflation of an intraluminal balloon to decrease coronary blood flow and rate of rise in left ventricular pressure (dP/dt) by approximately 30 to 40 and 10%, respectively. Nitroglycerin (0.01 to 10 micrograms/kg per min) increased coronary blood flow and distal coronary pressure and decreased stenosis resistance associated with improved left ventricular dP/dt depending on its dose. In contrast, adenosine (0.3 to 1.0 micrograms/kg per min) decreased coronary blood flow and distal coronary pressure and intensified stenosis resistance associated with depression of left ventricular dP/dt. Nifedipine and prostacyclin caused divergent effects on the coronary circulation related to each dose. Nifedipine (0.01 and 0.1 micrograms/kg per min) and prostacyclin (0.01 micrograms/kg per min) increased coronary blood flow and distal coronary pressure and reduced stenosis resistance. Nifedipine (1.0 micrograms/kg per min) and prostacyclin (0.3 micrograms/kg per min) did not increase coronary blood flow, but reduced distal coronary pressure and intensified stenosis resistance. Thus, the vasodilators produced different effects on restoration of coronary perfusion during pliable severe coronary stenosis. Nitroglycerin and lower doses of nifedipine and prostacyclin improved coronary perfusion due to selective or preferential dilation of large coronary arteries. Adenosine and higher doses of nifedipine and prostacyclin had deleterious effects on the coronary circulation due to potent arteriolar vasodilation.
To clarify the clinical significance of regional myocardial perfusion abnormality of the left ventricle in dilated cardiomyopathy (DCM), 20 patients with DCM underwent dipyridamole Tl-201 emission computed tomography (ECT). The subjects were divided into 2 groups: group 1 had (n = 9) reversible defects and group 2 (n = 11) had persistent defects only. Group 2 patients significantly advanced heart failure and significantly poorer prognoses than group 1 (55% vs 11% in 2 years survival rate, p less than 0.05). The echocardiographic left ventricular end-diastolic dimension was larger in group 2 than group 1 (68.3 +/- 8.2 mm vs 61.9 +/- 4.0 mm, p less than 0.05) and % fractional shortening was smaller in group 2 than group 1 (18.0 +/- 4.5% vs 24.5 +/- 6.9%, p less than 0.05). Moreover, 12 of the 13 segments with reversible defect showed fairly well preserved left ventricular wall motion, whereas 35 of 58 segments with persistent defect had severely impaired wall motion (1/13 vs 35/58, p less than 0.01). Dipyridamole Tl-201 ECT demonstrated conclusively that the two types of defects (reversible and persistent) are useful to evaluate not only the abnormal myocardial perfusion but also myocardial damage and the prognosis in DCM.
Selective sodium loading attenuated the development of hypertension in the deoxycorticosterone acetate (DOCA) treated rat. The DOCA treated rat fed a diet equimolar in sodium to a 7% sodium chloride diet and in chloride to a standard diet, differed in various parameters from the DOCA treated rat fed a 7% sodium chloride diet: it had higher sodium concentration in both erythrocytes and muscles, a higher erythrocyte ouabain sensitive 22Na efflux rate constant (Kos), and a lower norepinephrine turnover rate in the heart and the spleen. These results suggest that the suppressed sympathetic nervous system activity and the activated cell membrane sodium pump contribute in part to the mechanism for the suppression of the development of hypertension in the DOCA-selective sodium loaded rat.
Late potentials (LPs) recorded using the signal averaging technique were studied sequentially in 12 cases with acute myocardial infarction (AMI) in order to clarify how LPs develop in relation to ventricular arrhythmias (VA) in this disorder. Within 7 days after the onset of AMI there were no significant differences between LP durations with and without VA, and the overall mean value was relatively short (15.9 +/- 5.0 msec). On the 14th day, these cases were clearly divided into two groups according to LP duration. The group with LP duration over 20 msec (n = 5, average: 24.3 +/- 1.5 msec) exhibited a higher VA score and the other group with a shorter LP duration (n = 7, average: 15.0 +/- 2.1 msec) had a lower VA score (4.3 +/- 0.9 vs 0.6 +/- 0.5, p less than 0.001). This tendency was observed even in the late phase, and data such as peak CPK, cardiac index and mean pulmonary capillary pressure obtained in the acute phase could not predict this separation. In conclusion, LPs appear slightly later following the onset of AMI and correspond with the appearance of VA in the late phase; thus, LPs are useful for the prediction of VA in the course of AMI.
In 18 patients with dilated cardiomyopathy (DCM), the effects of a new cardiotonic agent, TA-064, given in both consecutive and intermittent (3 days on, 11 days off) oral doses were studied for 3 months by echocardiography and endomyocardial biopsy. After 3 months of consecutive administration, 11 patients (61%) had improved symptomatically and the %FS increased (p less than 0.001) and LVDd decreased (p less than 0.05), but the other 7 patients had not improved. At the pretreatment state these 7 patients in whom TA-064 was not effective had smaller %FS (p less than 0.01) and larger LVDd (p less than 0.05) than the 11 patients in whom the drug was effective. The non-effective group also had more severe myocardial fibrosis (p less than 0.05) and cellular hypertrophy (p less than 0.01) than the effective group. After 3 months of intermittent administration in 10 patients in whom consecutive administration had been proved effective, 7 patients sustained symptomatic improvement and increased %FS (p less than 0.01), but the other 3 patients did not sustain the improvement. The latter group had smaller %FS, larger LVDd and more severe myocardial fibrosis than the former group at the pretreatment state. These results indicate that the effects of TA-064 are dependent on the severity of basal cardiac function and myocardial damage, and that in patients with milder DCM, the effects can be sustained by intermittent administration.