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Biomedical subjects

M Fujishima

Publications and source records attributed to M Fujishima.

At least 253 records · Page 14Linked to original sources
PubMed1997

Role of eicosanoids in alteration of membrane electrical properties in isolated mesenteric arteries of salt-loaded, Dahl salt-sensitive rats.

1. The role of eicosanoids in altered membrane electrical properties of Dahl salt-sensitive (DS) rats was investigated, by use of conventional microelectrodes technique, in isolated superior mesenteric arteries of DS rats and Dahl salt-resistant (DR) rats fed either a high or low salt diet. 2. The membrane was significantly depolarized in salt-loaded DS rats compared with the other three groups. In addition, the arteries of salt-loaded DS rats exhibited spontaneous electrical activity. 3. Spontaneous electrical activity in salt-loaded DS rats was inhibited by the following: indomethacin, a cyclo-oxygenase inhibitor; ONO-3708, a prostaglandin H2/thromboxane A2 receptor antagonist; OKY-046, a thromboxane A2 synthase inhibitor; nicardipine, a Ca(2+)-channel antagonist and by Ca(2+)-free solution. In addition, spontaneous electrical activity was enhanced by a thromboxane A2 analogue and by prostaglandin H2. Spontaneous electrical activity was unaffected by phentolamine, atropine and tetrodotoxin. 4. Membrane potential in arteries of salt-loaded DS rats was not affected by either indomethacin or ONO-3708. 5. Spontaneous contraction, sensitive to indomethacin, was present, and contractile sensitivity to high potassium solution was enhanced in arteries of salt-loaded DS rats. 6. These findings suggest that eicosanoid action, together with membrane depolarization, may lead to the activation of voltage-dependent Ca(2+)-channels, thereby causing spontaneous electrical activity in mesenteric arteries of salt-loaded DS rats. In addition, tension data suggest that these changes in membrane properties are related to enhanced contractile activities in salt-loaded DS rats. Mechanisms of depolarization remain to be determined.

Animals↗
PubMed1997

The mechanisms of the relaxation induced by vasoactive intestinal peptide in the porcine coronary artery.

1. This study was designed to investigate the mechanism of the relaxation induced by vasoactive intestinal peptide (VIP) in medial strips of the porcine coronary artery, by determining the effect on the cytosolic Ca2+ concentration ([Ca2+]i), the [Ca2+]i-force relation and the involvement of G-protein. 2. Front-surface fluorometry of fura-2 revealed that U46619, a thromboxane A2 analogue, and the high K(+)-depolarization induced increases in both the [Ca2+]i and force of the medial strips. At a steady state of contraction, the extent of an increase in [Ca2+]i induced by 100 nM U46619 was similar to that induced by 30 mM K(+)-depolarization. VIP concentration-dependently (1 nM-1 microM) induced transient decreases in both the [Ca2+]i and force of the medial strips precontracted with 100 nM U46619. The decreases in the [Ca2+]i and force induced by VIP during the contraction with U46619 were much greater than those with 30 mM K(+)-depolarization. 3. The VIP-induced decreases in the [Ca2+]i and force were attenuated by K+ channel blockers such as tetrabutylammonium (TBA: non-selective K+ channel blocker), charybdotoxin (large conductance Ca(2+)-activated K+ channel blocker), and 4-aminopyridine (4-AP: voltage-dependent K+ channel blocker). However, neither glibenclamide (ATP-sensitive K+ channel blocker) nor apamin (small conductance Ca(2+)-activated K+ channel blocker) had any significant inhibitory effect. 4. In the 30 mM K(+)-depolarized strips, pretreatment with thapsigargin, a specific Ca(2+)-ATPase inhibitor of the Ca2+ store sites, completely abolished the VIP-induced decrease in [Ca2+]i, but partially attenuated the VIP-induced decrease in force. 5. VIP shifted the [Ca2+]i-force relation of the U46619-induced contractions to the right in a concentration-dependent manner. In the alpha-toxin-permeabilized strips, VIP decreased the force development at a constant [Ca2+]i level (pCa = 6.5) in a GTP-dependent manner, which was antagonized by guanosine-5'-O-(beta-thiodiphosphate) (GDP beta S). 6. We thus conclude that VIP relaxes the coronary artery via three mechanisms: (1) a decrease in [Ca2+]i by inhibiting the Ca2+ influx presumably through the membrane hyperpolarization mediated by the activation of the large conductance Ca(2+)-activated (charybdotoxin-sensitive) K+ channels and voltage-dependent (4-AP-sensitive) K+ channels; (2) a decrease in [Ca2+]i by sequestrating cytosolic Ca2+ into thapsigargin-sensitive Ca2+ store sites; and (3) a decrease in the Ca(2+)-sensitivity of the contractile apparatus through the activation of G-protein.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1997

Enhancement by exogenous and locally generated angiotensin II of purinergic neurotransmission via angiotensin type 1 receptor in the guinea-pig isolated mesenteric artery.

1. Angiotensin II is known to enhance sympathetic neurotransmission in the vasculature by increasing the release of noradrenaline, but little is known about the effect on the co-released transmitter, adenosine 5'-triphosphate (ATP). In the present study we have examined the effect of angiotensin II on the excitatory junction potential (e.j.p.) elicited by repetitive field stimulation in the guinea-pig isolated mesenteric artery, to establish the angiotensin II receptor subtype involved in modulating the release of ATP and the role of the endothelium in converting angiotensin I to angiotensin II. 2. Suramin (300 microM), a P2 purinoceptor antagonist, abolished both the e.j.p.s and depolarizing response to alpha,beta-methylene-ATP, a stable analogue of ATP, without affecting the resting membrane potential and noradrenaline-induced depolarization. 3. Angiotensin II (0.1 microM) affected neither the resting membrane potential nor the amplitude of the first e.j.p., but increased the amplitudes of the subsequent e.j.p.s. This enhancing effect of angiotensin II was abolished by CV-11974 (0.1 microM), an angiotensin II type 1 (AT1) receptor antagonist, but unaffected by PD 123319 (1 microM), an angiotensin II type 2 (AT2) receptor antagonist, or CGP 42112A (1 microM), AT2 receptor ligand. 4. Angiotensin I (0.1 microM) exerted a similar effect on e.j.p.s to that of angiotensin II. CV-11974 (0.1 microM) or temocaprilat (10 microM), an angiotensin converting enzyme (ACE) inhibitor, abolished the effect of angiotensin I. Removal of the endothelium did not alter the action of angiotensin I. 5. The results of the present study indicate that the release of ATP from sympathetic nerves innervating the guinea-pig isolated mesenteric artery, as determined from the magnitude of the e.j.p., can be enhanced by angiotensin II via activation of prejunctional AT1 receptors. Qualitatively similar effects were observed with angiotensin I, which appears to be converted into angiotensin II by a subendothelial process.

Adenosine Triphosphate↗
PubMed1997

Carcinoid tumors of the duodenum: report of three cases treated by endoscopic resection.

Three patients with small (less than 1 cm) duodenal carcinoid tumors are described, two of whom underwent endoscopic resection using simple snare polypectomy. In the third patient, a small tumor (5 mm) could no longer be found after initial biopsies on subsequent repeated endoscopic-bioptic follow-up. All three patients are free of local recurrence or systemic symptoms 2-14 years after the procedure.

Adult↗
PubMed1997

Sudden death in chronic dialysis patients.

METHODS: Causes of sudden death were investigated in 113 chronic dialysis patients who died during the 10-year period from July 1979 to January 1989; postmortem examination was performed on 93 of the cases (autopsy rate; 82.3%). Sudden death was regarded as death 24 h after the onset of acute illness in patients without any restriction in their daily activities. There were 35 sudden death cases out of the 93 autopsied chronic dialysis patients. We analysed the causes of sudden death for all chronic dialysis patients and for those who died suddenly. RESULTS: The mean age of the 93 cases was 61.4 +/- 10.5 years (+/-SD). Stroke was the most frequent cause of death (24 cases, 25.8%) in the 93 autopsied cases. This was followed by cardiac disease in 18 (19.4%), infectious disease in 16 (17.2%), malignancy in 14 (15.1%), and dissecting aortic aneurysm in 5 (5.4%). The mean age of the 35 sudden death cases was 60.9 +/- 10.9 years. Of the 35 sudden death cases in chronic dialysis patients, dissecting aortic aneurysm was the most common cause of sudden death (5 cases, 14.3%), followed by cerebral haemorrhage in three (8.6%), acute subdural haematoma in three (8.6%), acute myocardial infarction in two (5.7%), cerebral infarction in two (5.7%), and subarachnoidal haemorrhage in one (2.9%). CONCLUSIONS: Dissecting aortic aneurysm, leading frequently to stroke as a cause of sudden death in chronic dialysis patients, at least in Japan, should be carefully differentiated from other cardiac diseases in chronic dialysis patients, such as severe atherosclerosis.

Adult↗
PubMed1997

Effect of aging on regulation of brain stem circulation during hypotension.

This study was designed to determine age related changes in autoregulatory responses of the brain stem circulation in vivo. In anesthetized adult (4 to 6 months, n = 8) and aged (24 to 26 months, n = 7) Sprague-Dawley rats, local CBF to the brain stem was determined with laser-Doppler flowmetry and diameters of the basilar artery and its branches were measured through an open cranial window during stepwise hemorrhagic hypotension. In aged rats, the lower limit of CBF autoregulation shifted upward to 60 to 75 mm Hg from 30 to 45 mm Hg in adult rats. Dilator responses of the basilar artery (baseline diameter: 254 +/- 15 microns), large branch (109 +/- 23 microns), and small branch (44 +/- 10 microns) to hypotension were much smaller in aged rats than in adult rats. The maximum change in diameter of the basilar artery during profound hypotension was significantly smaller in aged rats (11 +/- 8%) than that in adult ones (23 +/- 12%, P < 0.05); that of the large branch was 12 +/- 8% versus 33 +/- 17% (P < 0.005); and that of the small branch was 17 +/- 7% versus 40 +/- 13% (P < 0.0005), suggesting greater attenuation of the responses in the smaller vessels. Thus, this study provides direct evidence that aging diminishes the compensatory dilatation of brain stem arterioles and arteries during hypotension and modifies the autoregulatory plateau of CBF, which seems to increase the risk of the brain stem ischemia during hypotensive conditions.

Acetylcholine↗
PubMed1997

Role of nitric oxide in regulation of brain stem circulation during hypotension.

We tested the hypothesis that nitric oxide (NO) plays a role in CBF autoregulation in the brain stem during hypotension. In anesthetized rats, local CBF to the brain stem was determined with laser-Doppler flowmetry, and diameters of the basilar artery and its branches were measured through an open cranial window during stepwise hemorrhagic hypotension. During topical application of 10(-5) mol/L and 10(-4) mol/L N(omega)-nitro-L-arginine (L-NNA), a nonselective inhibitor of nitric oxide synthase (NOS), CBF started to decrease at higher steps of mean arterial blood pressure in proportion to the concentration of L-NNA in stepwise hypotension (45 to 60 mm Hg in the 10(-5) mol/L and 60 to 75 mm Hg in the 10(-4) mol/L L-NNA group versus 30 to 45 mm Hg in the control group). Dilator response of the basilar artery to severe hypotension was significantly attenuated by topical application of L-NNA (maximum dilatation at 30 mm Hg: 16 +/- 8% in the 10(-5) mol/L and 12 +/- 5% in the 10(-4) mol/L L-NNA group versus 34 +/- 4% in the control group), but that of the branches was similar between the control and L-NNA groups. Topical application of 10(-5) mol/L 7-nitro indazole, a selective inhibitor of neuronal NOS, did not affect changes in CBF or vessel diameter through the entire pressure range. Thus, endothelial but not neuronal NO seems to take part in the regulation of CBF to the the brain stem during hypotension around the lower limits of CBF autoregulation. The role of NO in mediating dilatation in response to hypotension appears to be greater in large arteries than in small ones.

Animals↗
PubMed1997

Desmoid tumors in familial adenomatous polyposis/Gardner's syndrome.

To clarify the clinical risk of desmoid tumors developing in familial adenomatous polyposis, we reviewed the cases of 49 Japanese patients diagnosed with familial adenomatous polyposis at our institute. In six patients who manifested desmoid tumors at a mean age of 31 years, we reviewed the clinical features and compared various phenotypic manifestations with those in the 43 patients without desmoid tumors. During the observation periods (mean, 6.5 years), two of six patients with desmoid tumors died because of the tumors, which measured > 10 cm in diameter at the initial diagnosis, whereas the remaining four patients with desmoid tumors < 5 cm did not experience complications. The patients with desmoid tumors tended to be women (5 of 6 vs. 17 of 43; p = 0.05) and more frequently had gastric fundic gland polyposis (5 of 6 vs. 17 of 43; p = 0.05) than did the patients without desmoid tumors. There were no apparent differences in other clinical manifestations, including the incidences of colonic polyposis, gastroduodenal adenomas, and extraintestinal tumors. Desmoid tumors can be serious complication in patients with familial adenomatous polyposis. There may be some association in the genesis of desmoid tumors and gastric fundic gland polyposis.

Adenomatous Polyposis Coli↗
PubMed1997

Diffuse cystic malformation and neoplasia-associated cystic formation in the stomach. Endosonographic features and diagnosis of tumor depth.

We have evaluated the endoscopic ultrasonography (EUS) features of cystic malformation of the stomach and the depth of associated neoplasia. We included 15 patients with multiple cystic components identified on EUS: 6 patients with multiple cysts restricted focally to gastric neoplasia and 9 patients with diffusely distributed cysts. We categorized the former findings as focal cystic malformation (FCM), and the latter as diffuse cystic malformation (DCM) of the stomach and reviewed the endosonographic features. Both FCM and DCM tended to show male preponderance and develop in older patients. Cystic changes in FCM extended from the neoplastic lesion to the submucosa regardless of the location in the stomach. Diffuse cystic malformation was located predominantly in the gastric body and mainly was shown as the thickened submucosa and/or deep mucosa with multiple cystic components. The boundary between the mucosal layer or the tumor echo and the submucosal layer was indistinct in eight patients, which led to a lower accuracy in EUS diagnosis of tumor depth. Diffuse cystic malformation has characteristic EUS features and occasionally is accompanied by gastric neoplasia. Endoscopic ultrasonography is inaccurate in determining tumor depth when multiple submucosal cysts are present.

Adult↗
PubMed1997

Association between hyperinsulinemia and intima-media thickness of the carotid artery in normotensive men.

OBJECTIVES: To determine whether hyperinsulinemia is associated with early atherosclerosis in normotensive men of a work site population. DESIGN AND METHODS: Six hundred and seventeen subjects were screened from 8678 male transport workers for the further examination of cardiovascular disease and diabetes. Subjects aged less than 40 years, those with hypertension or diabetes, or both, and those being administered medications for hyperlipidemia were excluded. Finally, 164 normotensive, nondiabetic subjects were enrolled. The intima-media thickness (IMT) was measured by B-mode ultrasonography with a 7.5 MHz probe. Electrocardiography, a 75 g oral glucose-tolerance test (OGTT) and blood chemistry measurements were also performed. The sum of insulin values (sigmaIRI) and the ratio of the sum of insulin values to blood glucose levels (sigmaIRI/sigmaBG) in the 75 g OGTT were used as markers of hyperinsulinemia. RESULTS: The mean age of the subjects was 52 +/- 5 years (mean +/- SD). In a univariate analysis, IMT was associated with age, systolic blood pressure, body mass index, sigmaIRI, and sigmaIRI/sigmaBG. Multivariate analysis showed that age, total cholesterol, and sigmaIRI (or sigmaIRI/sigmaBG) were independent risk factors for IMT. CONCLUSIONS: These results suggest that, in addition to age and total cholesterol, hyperinsulinemia as assessed by an OGTT is associated with early atherosclerosis in normotensive, nondiabetic men of a work site population.

Arteriosclerosis↗
PubMed1997

Photochemically induced colonic ischaemic lesions: a new model of ischaemic colitis in rats.

BACKGROUND: Recent clinical studies suggest that ischaemic colitis is caused by a microcirculatory disturbance that involves thrombosis of the colon. AIM: To establish a new model of photochemically induced ischaemic colitis in rats. METHODS: Thirty male Wistar rats were anaesthetised with amobarbital, the femoral veins were cannulated and laparotomies were performed. The serosal surface of the proximal colon was irradiated by using a krypton laser (wavelength 568 nm, 20 mW) for four minutes. An intravenous infusion of a photosensitising dye, rose bengal (20 mg/kg body weight), was administered over 90 seconds, beginning at the start of irradiation. Rats were killed immediately (n = 4), 12 hours (n = 2), 24 hours (n = 10), three days (n = 4), seven days (n = 4), 14 days (n = 2), or 28 days (n = 2) after irradiation. Two control rats received laser irradiation without dye infusion. Specimens of the irradiated sites were examined by using histopathology. RESULTS: Localised ulcers of the colon were present in rats killed at 12 hours, 24 hours, three days, and seven days after irradiation. Microscopy findings were consistent with the features of human ischaemic colitis. Reproducible ulcerative lesions were produced by photothrombosis of microvessels in the colon. CONCLUSION: This model may be useful for further investigation of the pathophysiology of ischaemic colitis.

Animals↗
PubMed1997

Juvenile polyposis of the stomach: clinicopathological features and its malignant potential.

AIMS: To clarify a clinical entity of juvenile polyposis of the stomach compared with generalised juvenile gastrointestinal polyposis. METHODS: The clinicopathological features of juvenile polyposis dominantly involving the stomach at initial presentation were reviewed in 12 patients (three new patients and nine from the literature). These were compared with 29 cases of generalised juvenile gastrointestinal polyposis. RESULTS: There were three men and nine women with juvenile polyposis of the stomach, aged 10-63 years. Hypoproteinaemia was present in nine patients, anaemia in seven, and a family history of intestinal polyposis in seven. No patient presented with a congenital abnormality. During the observation period, two patients developed colonic juvenile polyps. Gastric polyps invariably affected the antrum and extended to the fundus, eventually becoming more numerous, larger, and more pedunculated. Ten patients required gastrectomy for associated malignancy or uncontrolled protein losing gastropathy. Histological examinations of the resected specimens demonstrated neoplastic tissue arising from juvenile polyps in four of the 12 patients. Atypism in these mixed polyps varied from adenoma to well or moderately differentiated adenocarcinoma. CONCLUSIONS: Juvenile polyposis of the stomach has malignant potential, and may be a separate entity from generalised juvenile gastrointestinal polyposis.

Adenocarcinoma↗
PubMed1997

Membrane currents evoked by histamine in rabbit basilar artery.

The membrane current evoked by histamine in isolated smooth muscle cells from rabbit basilar artery was investigated using the perforated-patch technique. When 10 microM histamine was applied in the bath at a holding potential of -60 mV, an inward current (79.2 +/- 55.8 pA) was transiently activated. An outward current was additionally evoked by 10 microM histamine when the membrane was held at -40 mV or less negative potentials. The outward but not the inward current was completely blocked by 100 nM charybdotoxin. A higher concentration of histamine (30 microM) failed to produce the inward current (3.4 +/- 4.8 pA) when Cl- concentration in the pipette was reduced. The apparent reversal potential of the inward current induced by histamine in physiological salt solution, in high-tetraethylammonium (TEA+) solution (bath), or in low-Cl- solution (pipette) was -6.3 +/- 4.4, -7.5 +/- 4.9, or -45.8 +/- 8.5 mV, respectively. Niflumic acid (100 microM) reversibly blocked the inward current, which was also blocked by 10 microM pyrilamine but not by 10 microM cimetidine. When histamine was continuously applied in the bath, spontaneous transient inward currents were generated. Removal of external Ca2+ or addition of 1 microM nicardipine or 2 mM caffeine reduced the amplitude of the histamine-induced inward current. These results suggest that histamine induces an inward current via H1 receptors at the resting membrane potential, possibly due to activation of Cl- currents. The Cl- inward current might be generated by elevation of intracellular Ca2+ via histamine receptors. The inward current may also contribute to control of the Ca2+ influx via a change in the membrane potential.

Animals↗
PubMed1997

Role of ATP-sensitive potassium channels in brain stem circulation during hypotension.

The basilar artery and its branch arterioles dilate actively in response to a marked decrease in blood pressure and maintain cerebral blood flow (CBF) to the brain stem. We tested the hypothesis that ATP-sensitive potassium (KATP) channels play a role in the autoregulatory responses of the brain stem circulation in vivo. In anesthetized Sprague-Dawley rats, local CBF to the brain stem was determined with laser-Doppler flowmetry, and diameters of the basilar artery and branch arterioles were measured through a cranial window during stepwise hemorrhagic hypotension. During topical application of 10(-6) and 10(-5) mol/l of glibenclamide, a selective KATP-channel blocker, the lower limit of CBF autoregulation shifted upward to 60-75 from 30-45 mmHg in the vehicle group. Glibenclamide significantly impaired the dilator response of small arterioles (baseline diameter 45 +/- 2 microns) throughout hypotension (P < 0.03) but did not impair the dilatation of the basilar artery (247 +/- 3 microns) or large arterioles (99 +/- 4 microns). Thus KATP channels appear to play an important role in the regulation of CBF to the the brain stem during hypotension by mediating the compensatory dilatation of small arterioles. In contrast, these channels may not be a major regulator of the vascular tone of larger arteries during hypotension.

ATP-Binding Cassette Transporters↗
PubMed1997

An ATP-sensitive potassium channel activator reduces infarct volume in focal cerebral ischemia in rats.

ATP-sensitive potassium channels are activated under hypoxic or ischemic conditions. The effects of ATP-sensitive potassium channel activators on cerebrovasculature and cerebral blood flow (CBF) are not well understood. We examined the effect of the ATP-sensitive potassium channel activator Y-26763 on focal cerebral ischemia in rats. In 24 spontaneously hypertensive rats, either Y-26763 (24 micrograms/kg) or vehicle was given by intracarotid infusion over 60 min, starting 30 min before photochemically induced thrombotic occlusion of the middle cerebral artery. CBF was measured by laser-Doppler flowmetry in the peri-ischemic penumbral cortex. Although Y-26763 lowered systemic blood pressure by 13 mmHg, the infarct volume assessed 3 days after the occlusion was significantly smaller in the Y-26763-treated group (n = 12, 71.2 +/- 22.0 mm3) than in the control group (n = 12, 94.7 +/- 20.4 mm3, P = 0.013). Y-26763 did not affect CBF before or after occlusion compared with CBF values of the control group. The results are consistent with the view that the activation of the ATP-sensitive potassium channel is neuroprotective in focal cerebral ischemia.

Adenosine Triphosphate↗
PubMed1997

Roles of TGF-beta and latent TGF-beta-binding protein in glomerulosclerosis induced by two consecutive injections of monoclonal antibody 1-22-3 in rats.

The present study demonstrated the elevated synthesis and gene expressions of transforming growth factor beta (TGF-beta) or latent TGF-beta binding protein (LTBP) in an irreversible glomerulosclerosis rat model induced by two consecutive injections of monoclonal antibody (MoAb) 1-22-3. The rats were intravenously injected with 500 microg of MoAb 1-22-3 either once or twice at an interval of 2 weeks. The rats were sacrificed at 24 h, 1 week, 2 weeks or 16 weeks after the last injection. At 24 h, the mesangiolytic changes in the rats with two injections of MoAb 1-22-3 were similar to those in the rats with one injection. The glomerular matrix score in the rats with two injections was significantly higher than that in the rats with one injection at weeks 1, 2 or 16. An increased LTBP localization in the glomeruli of the rats at week 1 after either one or two injections was detected in the segmentally expanded mesangial matrix. Moreover, LTBP in the glomeruli of rats at week 1 after two injections appeared to be more strongly stained in the enlarged mesangial matrix than that in the rats after one injection. A TGF-beta bioassay using mink lung epithelial cells revealed that the total TGF-beta in the glomerular culture conditioned medium in the rats at week 1 after two injections was significantly larger than that in the rats after one injection. A Northern blotting analysis of the glomeruli showed that both the expressions of TGF-beta and LTBP mRNA in the rats after two injections were higher than those in the rats after one injection. These findings suggested that the elevated TGF-beta or LTBP may thus be related to the irreversible glomerulosclerosis that was induced by two injections of MoAb 1-22-3 into rats.

Animals↗
PubMed1997

Intima-media thickness of the carotid artery in hypertensive subjects and hypertrophic cardiomyopathy patients.

While hypertension is known to cause left ventricular and vascular hypertrophy, the relationship between alterations of vascular and cardiac structures in patients with hypertrophic cardiomyopathy has not been fully clarified. We measured intima-media thickness of carotid arteries by ultrasonography in patients with hypertrophic cardiomyopathy (n = 16), normotensive subjects (n = 358), and hypertensive subjects (n = 386) in a cohort of 7940 male employees of a bus company. Our object was to determine whether vascular alteration occurs in hypertrophic cardiomyopathy similarly as in hypertension. Hypertrophic cardiomyopathy (wall thickness > or = 15 mm; asymmetrical hypertrophy without hypertension) was screened with family history and electrocardiography followed by echocardiography. The intima-media thickness in patients with hypertrophic cardiomyopathy (mean, 0.61 mm) did not differ from that of normotensive subjects (0.60 mm) but was significantly less than that of hypertensive subjects with left ventricular hypertrophy (wall thickness > or = 14 mm; n = 22; 0.73 mm). In a scatterplot of intima-media thickness versus interventricular septal thickness, these two parameters were significantly correlated in normotensives and hypertensives. The patients with hypertrophic cardiomyopathy distributed outside the 95% confidence range of the normotensive and hypertensive subjects. In summary, the increase in intima-media thickness of the carotid artery paralleled left ventricular hypertrophy in normotensive and hypertensive subjects. Patients with hypertrophic cardiomyopathy had a normal intima-media thickness regardless of the hypertrophied left ventricle. Thus, information on intima-media thickness may be useful in differentiating hypertensive left ventricular hypertrophy from hypertrophic cardiomyopathy.

Cardiomyopathy, Hypertrophic↗