Biomedical subjects

H Kasuya

Publications and source records attributed to H Kasuya.

At least 55 records · Page 3Linked to original sources

PubMed1995

Diagnosis of vascular compression in facial spasm by stereoscopic short-range magnetic resonance angiography. Technical note.

The authors describe the use of stereoscopic short-range magnetic resonance (MR) angiography to diagnose whether and by what means the brainstem is compressed in a case of facial spasm. The MR images were obtained on a 1.5-tesla imaging system with three-dimensional time-of-flight pulse sequence (repetition time 39 msec, echo time 9 msec). Six-source MR images, in which the internal acoustic meatuses were described, were processed using a maximum-intensity projection technique to reconstruct the MR angiograms. The internal acoustic meatuses, the posterior fossa, and the nearby arteries are shown on a single MR angiogram. When two MR angiograms with projection angles 10 degrees apart are placed side by side and observed through polarized glasses, a stereoscopic view of the compressing artery can easily be seen.

Brain Stem↗

PubMed1995

Vasoreactivity and restenosis after coronary angioplasty in the atherosclerotic pig model.

BACKGROUND: The effect of coronary angioplasty on coronary spasm remains unknown. We examined the effects of balloon angioplasty, using an oversized balloon, on coronary hypercontraction and eventual restenosis in a pig model of coronary spasm. METHODS: We performed balloon angioplasty, using an oversized balloon at the site of coronary spasm superimposed on atherosclerosis with 6 (group A, n = 14) or 1 (group B, n = 14) atmospheres of inflation pressure in miniature pigs. Using coronary angiography we assessed the coronary basal diameter and diameter change in response to histamine and serotonin before, immediately after, and 4 weeks after angioplasty. Histological examinations were performed immediately after and 4 weeks after the angioplasty. RESULTS: Before angioplasty, histamine- and serotonin-induced hypercontraction was reproducibly noted at the atherosclerotic site. Immediately after angioplasty, the coronary diameter became larger (P < 0.01) than before angioplasty in group A, but there was no significant difference in group B. The hypercontraction in group A was abolished immediately after and 4 weeks after angioplasty, whereas the hypercontraction in group B was unchanged. Histological examination revealed medial necrosis immediately after and medial fibrosis 4 weeks after angioplasty, which were more prominent in group A. Four weeks after angioplasty, the magnitude of restenosis was greater in group A than in group B. CONCLUSIONS: Angioplasty using an oversized balloon with the higher atmosphere of inflation pressure abolished coronary hypercontraction immediately after and 4 weeks after angioplasty, which probably resulted from the irreversible damage to medial smooth muscles; however, this did not prevent restenosis.

Angioplasty, Balloon, Coronary↗

PubMed1995

Endothelin-1 is not involved in serotonin-induced coronary spasm in a swine model.

OBJECTIVES: The role of endothelin-1 (ET-1) in the pathogenesis of coronary artery spasm is not well understood. We aimed to determine if ET-1 is involved in serotonin-induced coronary spasm in the swine model. METHODS: In 10 miniature pigs, a segment of the left anterior descending coronary artery was denuded and irradiated with X-ray. Three months after endothelial denudation, coronary vasomotion was assessed in vivo by quantitative arteriography. RESULTS: Intracoronary serotonin at 10 micrograms/kg provoked coronary spasm (augmented narrowing of the luminal diameter) at the denuded site (diameter reduction 93 +/- 4%) but not at the non-denuded control site (19 +/- 4%, P < 0.01) associated with ST segment elevation in the region perfused by the denuded artery. Intracoronary administration of ET-1 at 25 ng/kg caused mild vasoconstriction of the denuded (26 +/- 4) and non-denuded site (16 +/- 3%, n.s.), but provoked ST segment elevation in the regions perfused by both the denuded and non-denuded arteries. The treatment with an endothelin antagonist (BQ123 0.1 mg/kg) significantly attenuated coronary vasoconstriction and ST segment elevation evoked with ET-1, but did not alter serotonin-induced vasoconstriction either at the denuded or control site. CONCLUSIONS: The results of this study suggest that endogenous ET-1 may not be involved in the pathogenesis of serotonin-induced coronary spasm in our swine model.

Animals↗

PubMed1994

Glibenclamide prevents coronary vasodilation induced by beta 1-adrenoceptor stimulation in dogs.

This study aimed to determine whether a putative ATP-sensitive K(+)-channel blocker, glibenclamide (Glb), prevents metabolic coronary vasodilation associated with increased myocardial oxygen consumption (MVO2) caused by beta 1-adrenoceptor stimulation in anesthetized open-chest dogs. Isoproterenol (Iso) was infused selectively into the left circumflex coronary artery before and after Glb. Coronary blood flow (CBF) by an electromagnetic flowmeter, regional myocardial function by sonomicrometers, and left ventricular and arterial pressures were continuously measured. An intracoronary infusion of Iso (10 ng.kg-1 x min-1) resulted in the sustained increase in CBF as well as in the myocardial inotropic and chronotropic state. Glb (10, 30, and 100 micrograms/min ic) attenuated the Iso-induced increase in CBF in a dose-dependent manner, whereas inotropic and chronotropic responses to Iso were not affected by Glb. After beta 1-blockade with bisoprolol (0.3 mg/kg), which completely inhibited inotropic and chronotropic responses to Iso, the Iso-induced increase in CBF, presumably mediated by vascular beta 2-receptor stimulation, was not affected by Glb. Intracoronary denopamine (0.1 microgram.kg-1 x min-1), a beta 1-selective agonist, increased CBF, which was almost completely abolished by Glb. The increases in MVO2 induced by Iso or denopamine were similar before and after Glb, indicating that attenuation of the Iso- or denopamine-induced increase in CBF by Glb did not result from the decrease in MVO2. These results indicate that Glb prevented the increase in CBF associated with increased MVO2 caused by beta 1-adrenoceptor stimulation. It is suggested that ATP-sensitive K+ channels may play an important role in metabolic coronary vasodilation in dogs.

Adenosine Triphosphate↗

PubMed1994

Insulin-like growth factor-1 in the arterial wall after exposure to periarterial blood.

Intimal proliferation is thought to be initiated by the migration and proliferation of smooth muscle cells after endothelial damage. These changes may be induced, in part, by mitogenic growth factors such as insulin-like growth factor-1 (IGF-1). This study was designed to investigate the role of locally synthesized IGF-1 and its receptor in the arterial wall in response to the exposure to periarterial blood. Rat femoral arteries were exposed to periarterial blood for various time periods (control, 1, 3, 7, 14, and 21 d). Total ribonucleic acid was extracted from the arteries of 10 to 15 animals, and the expression of IGF-1 messenger ribonucleic acid in treated and untreated arteries was analyzed using dot blot analysis. To identify and localize IGF-1 receptors on the arterial walls, an in situ ligand binding of IGF-1 to the arterial sections was utilized using [125I]IGF-1 as a tracer. Our results revealed that luminal narrowing was maximum at 7 days posttreatment. Intimal proliferation occurred at 14 and 21 days. The results of dot blot analysis showed that the expression of IGF-1 messenger ribonucleic acid was increased four-fold by Day 3 and remained elevated up to 7 days, then gradually decreased. In situ [125I]IGF-1 binding to the normal rat femoral artery localized IGF-1 receptors to the arterial wall. There was a marked increase in the number of receptors at 3 and 7 days after treatment with periarterial blood. These results suggest that locally synthesized IGF-1 and its receptor may function in an autocrine and/or paracrine loop as part of the response of the arterial wall to periarterial blood, resulting in intimal proliferation.

Animals↗

PubMed1994

Effects of N-nitro-L-arginine on coronary artery tone and reactive hyperemia after brief coronary occlusion in conscious dogs.

AIM: To determine the role of an endothelium-derived relaxing factor (nitric oxide) in controlling basal coronary tone and coronary vasomotion after brief coronary occlusion (reactive hyperemia). METHODS: In 10 chronically instrumented conscious dogs, we studied the diameter changes of the large epicardial coronary artery and coronary blood flow in response to intracoronary administration of acetylcholine (0.1 and 1 microgram) and brief coronary occlusion for 5 and 20 s before and after intracoronary infusion of N-nitro-L-arginine (LNNA). RESULTS: Intracoronary infusion of LNNA (1, 3, and 10 mg) decreased the diameter of the large epicardial coronary artery and coronary blood flow in a dose-dependent manner without altering arterial pressure and heart rate. LNNA (10 mg) significantly attenuated the increase in artery diameter and coronary blood flow by acetylcholine. The ratio of artery dilation to the blood flow response after acetylcholine was not affected by LNNA. LNNA (10 mg) significantly decreased the ratio of repayment to debt flow volume of reactive hyperemia, but did not affect the ratio of peak to resting flow; it also significantly attenuated the reactive dilation of the large epicardial coronary artery after reactive hyperemia. The ratio of artery dilation to repayment flow volume (micron/ml) during reactive hyperemia was attenuated significantly by LNNA. CONCLUSION: These findings suggest that endothelium-derived nitric oxide may contribute to basal coronary tone and that reactive dilation of the large epicardial coronary artery during reactive hyperemia was caused by flow-mediated nitric oxide release, whereas coronary artery dilation after acetylcholine was caused largely by the direct receptor-mediated release of nitric oxide.

Acetylcholine↗

PubMed1993

Effects of a new calcium antagonist, CD-832, on experimental coronary artery spasm in miniature pigs.

The effects of a new calcium antagonist, CD-832, on experimental coronary artery spasms were studied in Göttingen miniature pigs. Pigs underwent endothelial denudation at the left anterior descending coronary artery using a balloon catheter. Changes in the diameter of the denuded and nondenuded site in response to an intracoronary administration of serotonin (10 micrograms/kg) or histamine (10 micrograms/kg) were assessed quantitatively by selective coronary arteriography 1 week after endothelial denudation. Percent reductions of the coronary artery diameter induced by serotonin or histamine in the denuded site were significantly greater than those in the nondenuded site (p < 0.01). Coronary artery spasm induced by serotonin or histamine in the denuded site was attenuated in a dose-dependent manner by intravenous infusion of CD-832 (10 and 30 micrograms/kg/min) or nifedipine (1 and 3 micrograms/kg/min). The degrees of inhibition of coronary artery spasm by CD-832 were similar to those produced by nifedipine. CD-832 and nifedipine at the high dose caused comparable increases in the basal coronary artery diameter. These results suggest that CD-832 may be a useful drug for the treatment of coronary artery spasm.

Animals↗

PubMed1993

The role of endothelium-derived nitric oxide in acetylcholine-induced coronary vasoconstriction in closed-chest pigs.

BACKGROUND: The effects of an inhibitor of endothelium-derived nitric oxide on acetylcholine (ACh)-induced coronary vasoconstriction were examined in 13 anesthetized closed-chest pigs. METHODS: Coronary blood flow was measured using a previously implanted ultrasonic transmit-time flow probe. The diameter of the large epicardial coronary arteries was assessed by coronary arteriography. RESULTS: Intracoronary infusions of ACh (0.1, 0.3, and 1.0 micrograms/kg/min) resulted in dose-dependent decreases in coronary blood flow. Arterial pressure and heart rate were minimally altered by ACh. The high dose of ACh decreased coronary blood flow by 67 +/- 11% and caused myocardial ischemia, demonstrated by ST-segment elevation. Coronary arteriograms revealed diffuse narrowing of peripheral coronary arteries and a filling delay of the contrast medium evoked with ACh. Vasospasm of the large epicardial coronary arteries was not observed. The decreases in coronary blood flow with ACh were inhibited by atropine (0.2 mg). Intracoronary administration of an inhibitor of endothelium-derived nitric oxide, NW-nitro-L-arginine (NNLA, 1.0 mg/kg), slightly increased arterial pressure but did not change baseline coronary blood flow. The percentage decreases in coronary blood flow induced by ACh were significantly augmented by NNLA administration, but those induced by prostaglandin F2 alpha (0.5 microgram/kg/min) were not affected by NNLA. The response of the large coronary arteries to ACh was not altered by NNLA. CONCLUSIONS: Our results suggest that, in pigs, ACh decreased coronary blood flow and caused myocardial ischemia as a result of the direct cholinergic vasoconstriction of peripheral small coronary arteries. The augmentation of ACh-induced coronary vasoconstriction by NNLA suggests that ACh facilitated the release of endothelium-derived nitric oxide, which attenuated the direct coronary vasoconstriction induced by ACh.

Acetylcholine↗

PubMed1993

Comparison of intrathecal administration of urokinase and tissue plasminogen activator on subarachnoid clot and chronic vasospasm in a primate model.

Safety and efficacy of the thrombolytic agent urokinase (URO) in the elimination of subarachnoid clot and prevention of chronic vasospasm was compared with tissue-type plasminogen activator (rt-PA) in a blind, randomized placebo-controlled trial. Twenty monkeys were randomly assigned to one of five groups of four. Each group underwent baseline cerebral angiography followed by bilateral craniectomy and experimental subarachnoid hemorrhage. An Ommaya reservoir was inserted on the right side with its catheter placed into the ipsilateral subarachnoid space. Twenty-four hours later, depending upon group assignment, the animals received 100,000 IU URO, 200,000 IU URO, 1 mg rt-PA, 2 mg rt-PA, or the equivalent volume of normal saline (control group). On Day 7, angiography was repeated and the animals were killed. One animal died as a result of complications during the baseline angiography, presumably due to blood loss and prolonged anesthesia, and a replacement animal was obtained. No animals demonstrated any delayed neurological deficits. The study demonstrated that a single intracisternal bolus injection of rt-PA, 2.0 mg in 2 ml sterile water, or URO, 200,000 IU in 2 ml sterile water, 24 hours after induction of experimental subarachnoid hemorrhage in primates, was equally effective in thrombolysing ipsilateral clot, but neither dosage prevented angiographic vasospasm. Vasospasm occurred bilaterally in all groups. Whereas gross subarachnoid clot was found bilaterally in all animals in the placebo group and both smaller-dose URO and rt-PA groups, right-sided subarachnoid clot was virtually absent and left-sided clot reduced in both higher-dose URO and rt-PA groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Procollagen types I and III and transforming growth factor-beta gene expression in the arterial wall after exposure to periarterial blood.

The stiffening and thickening of the arterial wall after subarachnoid hemorrhage may reflect increased connective tissue. The purpose of this study was to examine the nature of collagen synthesis in response to periarterial blood. Rat femoral arteries were exposed to periarterial blood for varying lengths of time (control, 1, 3, 7, and 14 d). Dot-blot analysis of total ribonucleic acid extracted from the arteries (n = 10 to 15 animals each) demonstrated that the expression of procollagen Types I and III messenger ribonucleic acid increased at 7 (threefold) and 14 days. The expression of transforming growth factor-beta (TGF-beta), an important regulator of collagen synthesis, was markedly increased by 3 days (threefold), followed by a gradual decline. There were marked differences in procollagen Types I and III and TGF-beta gene expression between arteries exposed to blood and sham-operated arteries for a period of 7 days (n = 25 animals). Northern blot analysis of total ribonucleic acid extracted from cultured vascular smooth muscle cells showed that the treatment with a higher concentration of serum for 48 hours increased the expression of procollagen Types I and III and TGF-beta, whereas exposure to oxyhemoglobin did not. After exposure to periarterial blood, arterial walls show increased synthesis of procollagen Types I and III, perhaps a response to the increased secretion of TGF-beta, which in turn could be the result of exposure to serum factors.

Animals↗

PubMed1993

Mechanism of oxyhemoglobin-induced release of endothelin-1 from cultured vascular endothelial cells and smooth-muscle cells.

Release of endothelin-1 from cultured endothelial cells can be induced with oxyhemoglobin (oxyHb). The present study was conducted to explore whether oxyHb affects the release of endothelin-1 and the induction of endothelin-1 messenger ribonucleic acid (mRNA) and to examine the mechanism whereby oxyHb induces endothelin-1 production in cultured vascular smooth-muscle cells as well as in cultured endothelial cells. Oxyhemoglobin produces concentration-dependent (0.1 to 10 microM) and time-dependent (0 to 24 hours) increases in immunoreactive endothelin-1 in conditioned medium from bovine arterial endothelial cells. Oxyhemoglobin induces immunoreactive endothelin-1 in rat aortic smooth-muscle cells in the same fashion, although the rate is 30-fold less than that of endothelial cells. This promoting effect is much higher than that of other stimulators such as thrombin and phorbol 12-myristate 13-acetate. Northern blot analysis of total RNA from endothelial cells also showed endothelin-1 mRNA induction. Staurosporine, a protein kinase C (PKC) inhibitor, inhibited oxyHb-induced endothelin-1 production in both vascular endothelial and smooth-muscle cells, whereas an increase of intracellular cyclic adenosine monophosphate (cAMP) by forskolin or an addition of 8-bromo-cAMP only inhibited this effect in smooth-muscle cells. These findings suggest that oxyHb-induced endothelin-1 production in endothelial cells is regulated by PKC, and in smooth-muscle cells by both PKC and the cAMP-dependent pathway. The production of endothelin, the most potent vasoconstrictor, in both vascular endothelial and smooth-muscle cells by oxyHb may have significance in the pathogenesis of cerebral vasospasm.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1992

Relaxant effects on iloprost in canine cerebral artery.

Iloprost caused relaxation of rings of canine cerebral arteries precontracted with prostaglandin F2 alpha or the thromboxane A2 analogue U46619, but it was without effect on arteries precontracted with potassium chloride. Pretreatment with iloprost did not significantly affect the concentration-response curve to any agent. Contractile responses to oxyhemoglobin were completed relaxed by iloprost. In arteries from animals with moderate cerebrovascular spasm, the response to prostaglandin F2 alpha was also reduced by iloprost. The observation that iloprost relaxes the response to oxyhemoglobin to prostaglandin F2 alpha in spastic arteries may be of interest in the management of cerebral vasospasm.

Animals↗

PubMed1992

Glibenclamide decreases basal coronary blood flow in anesthetized dogs.

The effects of ATP-sensitive K+ channel blockade on coronary blood flow were studied in 13 anesthetized open-chest dogs. A specific ATP-sensitive K+ channel blocker, glibenclamide, was infused into the left circumflex coronary artery (LCx). Coronary blood flow of LCx and systolic segment shortening at the LCx area were measured. Intracoronary infusion of glibenclamide (0.5, 5, and 50 micrograms.kg-1.min-1) decreased coronary blood flow dose dependently. Glibenclamide at the dose of 50 micrograms.kg-1.min-1 decreased LCx coronary blood flow by 55 +/- 4% (P less than 0.01), which was accompanied by a decrease in percentage segment shortening at the LCx area (P less than 0.01) and ST elevation. When coronary blood flow was maintained at the baseline level by simultaneous infusion of sodium nitroprusside (1-3 micrograms/min ic) or pinacidil (0.3-0.6 mg/min ic), glibenclamide did not alter percentage segment shortening or produced ST elevation. The latter results suggest that glibenclamide decreased coronary blood flow, which secondarily induced myocardial ischemia and dysfunction. Our results suggest that ATP-sensitive K+ channels of coronary arteries are involved in maintaining the level of resting coronary blood flow under physiological conditions in anesthetized dogs.

Animals↗

PubMed1992

Time course of changes in concentration of intracellular free calcium in cultured cerebrovascular smooth muscle cells exposed to oxyhemoglobin.

A culture of smooth muscle cells obtained from monkey middle cerebral arteries was developed to allow quantitative assessment of intracellular calcium and immunofluorescence analysis after various periods of exposure to oxyhemoglobin. Intracellular calcium concentration was examined for up to 7 days after a single exposure to oxyhemoglobin. Intracellular calcium concentrations were measured with the fluorescent dye fura-2 and were significantly elevated for 7 days after exposure to oxyhemoglobin (P less than 0.01). Less than 2 minutes after application of oxyhemoglobin, there was marked elevation of intracellular calcium from the control value of 75 +/- 2 nmol/L to 240 +/- 28 nmol/L (P less than 0.01 by analysis of variance). Intracellular calcium concentration of cells exposed for 24 hours to oxyhemoglobin and then grown in normal oxyhemoglobin-free medium fell close to normal levels on Days 3 and 7. On Day 3, the increase in intracellular calcium that followed repeated daily exposure to oxyhemoglobin was greater than that resulting from a single application of oxyhemoglobin (P less than 0.01 by Student's t test), but by Day 7 the elevation produced by these different approaches was similar. Smooth muscle cells exposed to oxyhemoglobin showed a reduction in immunoreactivity to alpha-actin. These data support the hypothesis that disruption of intracellular calcium regulation and calcium overloading may be important in the process of cell injury, which results in vasoconstriction and sometimes cell death, after exposure to oxyhemoglobin.

Actins↗

PubMed1992

[A long-term result of coronary artery bypass on left coronary ostial stenosis secondary to Takayasu's disease: a case report].

A 37-year-old woman was admitted to our hospital for post operative coronary angiography. At the age of 17, she was diagnosed as having Takayasu's disease and at that time prednisolone was administered. At the age of 22, she was operated on to receive a coronary artery bypass graft (CABG) because of a 95% isolated stenosis in the left coronary ostium. Pathological specimen obtained from the ascending aorta demonstrated a proliferative stage of Takayasu's aortitis. After the CABG, she married and delivered two children, with the inflammation being kept under control by prednisolone. Coronary angiography performed 13 years after the operation proved the saphenous vein graft to the left anterior descending artery to be still patent. To our knowledge, this case has the longest history of a patent CABG used in an operation to correct the ostial stenosis secondary to Takayasu's disease. According to the previous reports we collected, the long-term patency rate of CABG is 78%, whereas that of ostial endarterectomy is unknown. Whether CABG or endarterectomy is better as an operating method for ostial stenosis due to aortitis is still a controversial point. We hope that reports of further examples will be available in order to help make the final decision.

Adult↗

PubMed1991

The effect of continuous drainage of cerebrospinal fluid in patients with subarachnoid hemorrhage: a retrospective analysis of 108 patients.

The effects of continuous drainage of cerebrospinal fluid (CSF) on vasospasm and hydrocephalus were analyzed retrospectively in 108 patients with subarachnoid hemorrhage (SAH) who were operated on for ruptured aneurysms within 48 hours of their onset. Ninety-two of these patients underwent a procedure for CSF drainage (cisternal drainage, ventricular drainage, lumbar drainage, or a combination of these). The duration, the total volume, and the average daily volume of CSF drainage were 10.4 +/- 7.0 days (mean +/- SD). 2034 +/- 1566 ml, and 190 +/- 65.3 ml, respectively. Patients with a greater drainage volume at a lower height of drainage in the early period after SAH developed more cerebral infarctions later (P less than 0.025). The relationship between the total volume of CSF removed and shunt-dependent hydrocephalus was determined to be statistically significant (P less than 0.005). Cerebral infarction and hydrocephalus after SAH were also found to be statistically associated (P less than 0.001). Thus, continuous cerebrospinal fluid drainage should not be performed too readily in patients with SAH, because the removal of a large amount of CSF can induce cerebral vasospasm as well as hydrocephalus.

Adult↗

PubMed1991

Clinicopathological study of bacterial intracranial aneurysms.

The authors report the clinicopathological findings in six cases of bacterial intracranial aneurysms. All patients received appropriate high-dose antibiotics, and four were treated surgically. One patient with multiple aneurysms of the main trunks died of disseminated intravascular coagulation. Autopsy disclosed no apparent aneurysm or inflammatory cell infiltration, but a partially interrupted internal elastic lamina and thickened intima were disclosed at the angiographical aneurysm sites. These findings suggest that 1) appropriate high-dose antibiotics are effective against inoperable bacterial aneurysms in the main trunks, 2) new aneurysms may be formed in patients with cyanotic congenital heart disease, because bacterial emboli can directly reach the cerebral circulation and reimplant on the fragile arterial walls after vasculitis. Histological examination of aneurysmal walls revealed inflammatory cell infiltration after resolution of clinical endocarditis. This suggests that both appropriate high-dose antibiotic therapy and surgery should be considered in patients with distal bacterial aneurysms.

Adolescent↗

PubMed1991

[Evaluation of myocarditis using T1-201 myocardial scintigraphy with bull's eye functional map].

In order to evaluate myocardial damage in a patient with myocarditis, rest thallium-201 myocardial single photon emission computed tomography (SPECT) was performed in 15 patients with myocarditis. For qualitative and semiquantitative analysis, Bull's eye functional maps were made up with SPECT images. In the functional map, the abnormal area, where T1 uptake is less than mean-2SD of the T1 uptake of normal subjects, is generally distributed in the myocarditis group. But focal and sequential abnormal areas were recognized more often in the clinically severe cases. Abnormal area tended to be observed commonly at the antero-septal wall, but it was uncommon at the lateral wall. Extent score, i.e. degree of extension of abnormal area, and severity score, i.e. degree of abnormality, were in good negative correlation with left ventricular ejection fraction (r = 0.6, r = 0.7). Furthermore, existence of abnormal area was in good correlation with the left ventricular regional wall motion. Abnormal area existed 100% in the akinetic region, 71% in the region of severe hypokinesis, and 27% in the region of hypokinesis. Abnormal area occupied 30% of the normokinetic region in the myocarditis group, which was a higher rate than in the normal control group (p less than 0.05). It was suggested that latent myocardial damage existed in the normokinetic myocardium with myocarditis. Thus, rest T1-201 SPECT with Bull's eye map is useful for clinical diagnosis in patients with myocarditis.

Adolescent↗