Biomedical subjects

Yasuhide Nakashima

Publications and source records attributed to Yasuhide Nakashima.

At least 19 recordsLinked to original sources

PubMed2006

Comparison of HERG channel blocking effects of various beta-blockers-- implication for clinical strategy.

beta-Blockers are widely used in the treatment of cardiovascular diseases. However, their effects on HERG channels at comparable conditions remain to be defined. We investigated the direct acute effects of beta-blockers on HERG current and the molecular basis of drug binding to HERG channels with mutations of putative common binding site (Y652A and F656C). beta-Blockers were selected based on the receptor subtype. Wild-type, Y652A and F656C mutants of HERG channel were stably expressed in HEK293 cells, and the current was recorded by using whole-cell patch-clamp technique (23 degrees C). Carvedilol (nonselective), propranolol (nonselective) and ICI 118551 (beta(2)-selective) inhibited HERG current in a concentration-dependent manner (IC(50) 0.51, 3.9 and 9.2 microM, respectively). The IC(50) value for carvedilol was a clinically relevant concentration. High metoprolol (beta(1)-selective) concentrations were required for blockade (IC(50) 145 microM), and atenolol (beta(1)-selective) did not inhibit the HERG current. Inhibition of HERG current by carvedilol, propranolol and ICI 118551 was partially but significantly attenuated in Y652A and F656C mutant channels. Affinities of metoprolol to Y652A and F656C mutant channels were not different compared with the wild-type. HERG current block by all beta-blockers was not frequency-dependent. Drug affinities to HERG channels were different in beta-blockers. Our results provide additional strategies for clinical usage of beta-blockers. Atenolol and metoprolol may be preferable for patients with type 1 and 2 long QT syndrome. Carvedilol has a class III antiarrhythmic effect, which may provide the rationale for a favourable clinical outcome compared with other beta-blockers as suggested in the recent COMET (Carvedilol Or Metoprolol European Trial) substudy.

Adrenergic beta-Antagonists↗

PubMed2005

Vascular neuronal NO synthase is selectively upregulated by platelet-derived growth factor: involvement of the MEK/ERK pathway.

OBJECTIVE: We demonstrated recently that neuronal NO synthase (NOS) is expressed in arteriosclerotic lesions and exerts important vasculoprotective effects in vivo. In this study, we examined the molecular mechanism(s) for vascular neuronal NOS (nNOS) expression. METHODS AND RESULTS: In cultured rat aortic smooth muscle cells, treatment with platelet-derived growth factor (PDGF) selectively upregulated nNOS expression but not inducible NOS (iNOS) or endothelial NOS (eNOS) expression. Treatment with PDGF also significantly caused activation of mitogen-activated protein kinase (MAPK) family, including extracellular signal-regulated kinase (ERK), p38MAPK, and c-Jun N-terminal kinase (JNK). ERK kinase (MAPK kinase [MEK]) inhibitors inhibited PDGF-induced nNOS expression, whereas a p38MAPK inhibitor or JNK inhibitor was without effects. Importantly, gene transfer of MEK per se elicited nNOS induction, and gene transfer of dominant-negative MEK abolished PDGF-induced nNOS expression. In isolated aortas of wild-type, eNOS(-/-), and iNOS(-/-) mice, but not in those of nNOS(-/-) mice, treatment with PDGF significantly enhanced nNOS expression and nitrite plus nitrate production, both of which were again attenuated by a MEK inhibitor. CONCLUSIONS: These results provide the first evidence that vascular nNOS expression is upregulated selectively in response to PDGF through the MEK/ERK pathway. Upregulated nNOS may play an important compensatory role under arteriosclerotic/inflammatory conditions associated with eNOS dysfunction to maintain vascular homeostasis.

Angiotensin II↗

PubMed2005

Experimental hyperhomocysteinemia impairs coronary flow velocity reserve.

BACKGROUND: Hyperhomocysteinemia has been identified as an independent risk factor for coronary artery disease. One mechanism is considered to be deteriorated endothelial function that is recovered by vitamin C. However, its direct action on coronary circulation has yet to be examined. This study was designed to test the hypothesis that experimental acute hyperhomocysteinemia would impair coronary flow velocity reserve (CFR) by increasing oxidative stress. METHODS: Eleven healthy male volunteers (aged 23.3+/-0.9 years) were enrolled. CFR induced by intravenous 5'-adenosine triphosphate infusion was measured by transthoracic-Doppler echocardiography. Measurements were taken before and 4 h after administration of a placebo, oral methionine (L-methionine 0.1 g/kg) or oral methionine plus vitamin C (2 g) on 3 separate days. RESULTS: The baseline average diastolic peak velocity (APV) was similar in all 3 groups. In the methionine group, plasma homocysteine increased (12.9+/-7.0 to 32.1+/-9.4 nmol/ml, p<0.0001), while APV under hyperemic conditions (APV-hyp) and CFR significantly decreased (87.2+/-11.4 cm/sec and 4.02+/-0.70 to 73.2+/-10.2 cm/sec and 3.35+/-0.52, p=0.0022 and 0.0030, respectively). Moreover, there was a significant inverse correlation between the plasma homocysteine and CFR (r=-0.620, p=0.0021). However, upon simultaneous administration of vitamin C, APV-hyp and CVR did not decrease despite an elevation in plasma homocysteine. CONCLUSIONS: Experimentally induced acute hyperhomocysteinemia significantly decreased CFR, and this decrease was significantly reversed by vitamin C administration. Oxidative stress is suggested to play a major role in the deleterious effects of homocysteine on the coronary microcirculation.

Adenosine Triphosphate↗

PubMed2005

Heparin-released extracellular superoxide dismutase is reduced in patients with coronary artery atherosclerosis.

OBJECTIVES: We studied whether the amount of heparin-released extracellular superoxide dismutase (EC-SOD), which is an antioxidative enzyme, is associated with coronary artery disease (CAD). METHODS AND RESULTS: EC-SOD was measured in plasma at basal and at post-heparin injection in 315 patients. Heparin-released EC-SOD was calculated as the difference between the two values. After exclusion of a mutant EC-SOD group (n = 27:8.6%), 288 patients were divided into three groups by angiographic findings; those with normal coronary (the normal group; n = 63), those with atherosclerosis without significant stenosis (the mild atherosclerosis group; n = 36), and those with significant stenosis (the atherosclerosis group; n = 189). Although the basal values were similar among the three groups, heparin-released EC-SOD levels were significantly lower in the atherosclerosis group (131.0 +/- 42.8 ng/ml, p = 0.0003) than in the normal group (156.9 +/- 66.2 ng/ml). Moreover, logistic analysis revealed that heparin-released EC-SOD independently contributed to CAD. The coronary score showed a significant correlation with heparin-released EC-SOD. As for factors affecting the level of heparin-released EC-SOD, the level of high-density lipoprotein cholesterol and age showed a positive correlation. CONCLUSIONS: The results suggest that heparin-released EC-SOD is significantly reduced in CAD and that the tissue-bound location of this enzyme might be important for antioxidative function.

Adult↗

PubMed2005

Synergistic induction of monocyte chemoattractant protein-1 by integrins and platelet-derived growth factor via focal adhesion kinase in mesangial cells.

BACKGROUND: Growth factors, extracellular matrix and its receptor integrins are upregulated in various glomerular diseases. We investigated the mechanism of collaboration between integrins and platelet-derived growth factor (PDGF) in focal adhesion kinase (FAK)- and extracellular signal-related kinase (ERK)1/2-mediated signal pathways that lead to monocyte chemoattractant protein (MCP)-1 expression in cultured rat mesangial cells (MCs). METHODS: Serum-starved MCs were plated on fibronectin- or polylysine-coated plates with or without PDGF, and examined for phosphorylation of ERK1/2, mitogen-activated protein or ERK kinase (MEK)1/2 and FAK by western blotting, and for expression of MCP-1 mRNA and protein by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. The effects of dominant-negative FAK on MCP-1 expression were examined. RESULTS: Cell adhesion to fibronectin increased phosphorylation of FAK, MEK1/2 and ERK1/2, and induced MCP-1 mRNA and protein expression. PDGF increased phosphorylation of FAK, MEK1/2 and ERK1/2 even without cell adhesion to fibronectin, and induced MCP-1 mRNA and protein expression. PDGF with integrin activation by fibronectin synergistically increased phosphorylation of FAK, MEK1/2 and ERK1/2, and expression of MCP-1 mRNA and protein. Dominant-negative FAK attenuated fibronectin enhancement of PDGF-induced ERK1/2 phosphorylation and MCP-1 expression, indicating involvement of FAK in this signalling. CONCLUSIONS: Our results suggest the cooperative role of integrin and PDGF receptor in activation of the ERK pathway possibly via FAK in MCs. The synergistic activation of integrin and PDGF signalling may play an important role in the progression of glomerular diseases through the induction of MCP-1.

Animals↗

PubMed2005

Nephrogenic diabetes insipidus in mice lacking all nitric oxide synthase isoforms.

Nitric oxide (NO) is produced in almost all tissues and organs, exerting a variety of biological actions under physiological and pathological conditions. NO is synthesized by three different isoforms of NO synthase (NOS), including neuronal, inducible, and endothelial NOSs. Because there are substantial compensatory interactions among the NOS isoforms, the ultimate roles of endogenous NO in our body still remain to be fully elucidated. Here, we have successfully developed mice in which all three NOS genes are completely deleted by crossbreeding singly NOS-/- mice. NOS expression and activities were totally absent in the triply NOS-/- mice before and after treatment with lipopolysaccharide. Although the triply NOS-/- mice were viable and appeared normal, their survival and fertility rates were markedly reduced as compared with the wild-type mice. Furthermore, these mice exhibited marked hypotonic polyuria, polydipsia, and renal unresponsiveness to an antidiuretic hormone, vasopressin, all of which are characteristics consistent with nephrogenic diabetes insipidus. In the kidney of the triply NOS-/- mice, vasopressin-induced cAMP production and membranous aquaporin-2 water channel expression were reduced associated with tubuloglomerular lesion formation. These results provide evidence that the NOS system plays a critical role in maintaining homeostasis, especially in the kidney.

Analysis of Variance↗

PubMed2005

Prolonged survival in a female with untreated tetralogy of Fallot.

It has been reported that most patients with untreated tetralogy of Fallot (TOF) die by the time they reach adulthood. We report the case of a 72-year-old female diagnosed by echocardiography and cardiac cathetherization as having TOF and diagnosed at birth with a ventricular septal defect (VSD). During childhood, she was very thin and lacking in physical strength. On first consultation at our hospital, she was suffering from mild dyspnea, classified as NYHA functional class III, and her fingers were clubbed and cyanotic. Her PaO2 was 48.0 mmHg under room air, and hypoxia was recognized. An echocardiography and cardiac cathetherization showed a VSD, hypertrophy of the right ventricle, over-riding of the aorta and stenosis of the right ventricular outflow tract with a pressure gradient of 84 mmHg. There was a bidirectional shunt with 24% flow from the left to right and 43% from the right to left ventricle. Her Qp/Qs was 0.75. Surgical treatment was recommended. However, the patient refused, because her symptoms were alleviated with home oxygen therapy. This report shows the prolonged survival of this 72-year-old female with untreated TOF.

Aged↗

PubMed2005

Extracellular superoxide dismutase overexpression reduces cuff-induced arterial neointimal formation.

The mechanisms of neointimal formation in cuff-injury models are still uncertain. To examine whether extracellular superoxide dismutase (EC-SOD) can reduce neointimal formation in a cuff-injury model, adenoviruses expressing EC-SOD (AxCAEC-SOD) or Escherichia coli beta-galactosidase (AxCALacZ) was injected between the cuff and the adventitia of rat femoral arteries. As a result, EC-SOD protein was effectively produced in the adventitia, as assessed by immunohistochemical staining. In comparison with cuff-treated control arteries and AxCALacZ-transfected arteries, neointimal formation was significantly reduced in AxCAEC-SOD-transfected arteries. Furthermore, proliferating smooth muscle cells in neointima and media were reduced by EC-SOD treatment. Similarly, augmented iNOS expression, apoptosis and collagen content in the vascular wall were also reduced by EC-SOD treatment. Reactive oxygen species (ROS) generation in tissue was reduced by EC-SOD expression, as assessed by dihydroethidium staining and coelenterazine chemiluminescence. These results suggest that ROS, especially superoxide anions at an adventitia, are responsible for neointimal formation in a cuff-injury model.

Animals↗

PubMed2005

Autonomic cardiovascular responses to hypercapnia in conscious rats: the roles of the chemo- and baroreceptors.

The role of the autonomic nervous system, the central and peripheral chemoreceptors, and the arterial baroreceptors was examined in the cardiovascular response to hypercapnia in conscious rats chronically instrumented for the measurement of arterial blood pressure (ABP), heart rate (HR), and renal sympathetic nerve activity (RSNA). Rats were exposed to hypercapnia (6% CO2), and the cardiovascular and autonomic nervous responses in intact and carotid chemo- and/or aortic denervated rats were compared. In intact and carotid chemo-denervated rats, hypercapnia induced significant increases in mean ABP (MABP) and RSNA, and a significant decrease in HR. The HR decrease was reversed by atropine and eliminated by bilateral aortic denervation, which procedure, however, did not affect the MABP or RSNA response. Bilateral carotid chemo-denervation did not affect the baroreflex control of HR, although this control was attenuated by aortic denervation. Hypercapnia did not affect baroreflex sensitivity in intact rats. These results suggest that hypercapnia induces an increase in MABP due to an activation of sympathetic nervous system via central chemoreceptors and a decrease in HR due to a secondary reflex activation of the parasympathetic nervous system via arterial baroreceptors in response to the rise in ABP. In addition, carotid chemoreceptors do not play a major role in the overall cardiovascular response to hypercapnia in conscious rats. The mechanism responsible for the parasympatho-excitation may also involve CO2 induced aortic chemoreceptor simulation.

Animals↗

PubMed2005

Intrinsic mechanism of the enhanced rate-dependent QT shortening in the R1623Q mutant of the LQT3 syndrome.

OBJECTIVE: In the type 3 long QT syndrome (LQT3), arrhythmia events tend to occur at rest or during sleep. One of the mutations, R1623Q, is located in the voltage sensor of the cardiac sodium channel (hH1), and patients with R1623Q mutation have been also reported to show bradycardia-dependent cardiac events. Although the mutant channel has been characterized by inactivation gating defects, the intrinsic mechanism(s) that might explain why arrhythmia attack is most prevalent at slower heart rates has not been investigated. METHODS: cDNA encoding either the wild-type or the R1623Q mutant of hH1 was stably transfected into HEK293 cells. I(Na) was recorded using a whole-cell patch-clamp technique at 23 degrees C. RESULTS: A train of 50 depolarizing pulses from holding potentials (-120 and -80 mV) to -20 mV or a train of 50 action potential waveforms was applied at different frequencies. When using a rectangular waveform voltage clamp protocol, rate-dependent reduction of I(Na) was holding voltage-dependent but was not different between peak I(Na) and late I(Na). However, using the action potential clamp, preferential rate-dependent reduction of the phase 3 I(Na) was obvious as compared with peak I(Na). The discrepancy in the rate-dependent reduction between protocols was attributed to accelerated recovery from inactivation under non-equilibrium condition. CONCLUSION: The rate dependency of phase 3 I(Na) under non-equilibrium gating is a novel mechanism to explain the enhanced rate-dependent QT-shortening in LQT3 patients. Our findings are important for genotype-phenotype correlations in LQT3 mutants as well as for understanding the function of S4 segment of domain IV region in the cardiac Na(+) channel.

Action Potentials↗

PubMed2005

Blockade of HERG cardiac K+ current by antifungal drug miconazole.

1. Miconazole, an imidazole antifungal agent, is associated with acquired long QT syndrome and ventricular arrhythmias. Miconazole increases the plasma concentration of QT-prolonging drugs by inhibiting the hepatic cytochrome P450 metabolic pathway, but whether it has direct effects on cardiac ion channels has not been elucidated. 2. To determine the mechanism underlying these clinical findings, we investigated the effect of miconazole on human ether-a-go-go-related gene (HERG) K+ channels. 3. HERG channels were heterologously expressed in human embryonic kidney 293 (HEK293) cells and whole-cell currents were recorded using a patch-clamp technique (23 degrees C). 4. Miconazole inhibited HERG peak tail current in a concentration-dependent manner (0.4-40 microM) with an IC50 of 2.1 microM (n=3-5 cells at each concentration, Hill coefficient 1.2). HERG block was not frequency-dependent. It required channel activation, occurred rapidly, and had very slow dissociation properties. 5. The activation curve was shifted in a negative direction (V(1/2): -9.5+/-2.3 mV in controls and -15.3+/-2.4 mV after 4 microM miconazole, P<0.05, n=6). Miconazole did not change other channel kinetics (activation, deactivation, onset of inactivation, recovery from inactivation, steady-state inactivation). 6. The S6 domain mutation, F656C, abolished the inhibitory action of miconazole on HERG current indicating that miconazole preferentially binds to an aromatic amino-acid residue within the pore-S6 region. 7. Our findings indicate that miconazole causes HERG channel block by binding to a common drug receptor, and this involves preferential binding to activated channels. Thus, miconazole prolongs the QT interval by direct inhibition of HERG channels.

Action Potentials↗

PubMed2005

Oxidized low-density lipoprotein-induced apoptosis is attenuated by insulin-activated phosphatidylinositol 3-kinase/Akt through p38 mitogen-activated protein kinase.

1. The aim of the present study was to investigate whether p38 mitogen-activated protein kinase (p38 MAPK) is involved in oxidized low-density lipoprotein (oxLDL)-induced apoptosis of human umbilical vein endothelial cells (HUVECs). We also sought to determine whether this apoptosis is regulated by the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. 2. Low-density lipoprotein was oxidized with CuSO4 and used as oxLDL. Using HUVEC, we determined whether LDL/oxLDL induces apoptosis by DNA fragmentation and the cell cycle distribution (SubG1 method). The mechanism and activation of p38 MAPK and Akt were determined by western blot analysis. 3. The results showed that oxLDL induced DNA fragmentation, whereas cell cycle distribution showed that it also significantly increased the rate of cell death compared with the LDL group. SB203580 significantly inhibited cell death induced by oxLDL, as did the administration of insulin. Western blot analysis showed the activation of p38 MAPK by oxLDL, but not with LDL. It was found that Akt was activated in the presence of insulin. In the presence of either SB203580 or insulin, activation of p38 MAPK was significantly inhibited compared with stimulation by oxLDL alone. However, application of both insulin and wortmannin resulted in no significant difference compared with HUVEC stimulated by oxLDL only. 4. The results showed that apoptosis in HUVEC can be induced by oxLDL and involves p38 MAPK. It was also demonstrated that insulin inhibited oxLDL-induced apoptosis and may inhibit the activation of p38 MAPK through the PI3K/Akt pathway.

Apoptosis↗

PubMed2005

Home orthostatic self-training in neurocardiogenic syncope.

We assessed the efficacy of daily sessions of home orthostatic self-training (30 minutes per session standing against the wall without moving) in the prevention of neurocardiogenic syncope in 37 patients. Of these, 10 patients were instructed to perform two sessions per day, 14 were instructed to perform a single session per day, and the remaining 13 were instructed to perform one session every other day. The patients who performed one to two sessions of training per day continued to do so over a 6-month follow-up period, during that time none of them experienced spontaneous syncope. Only 5 of 13 patients who were instructed to train once every two days were able to continue doing so over the 6-month follow-up period; however, no spontaneous syncope was observed in these five patients. The remaining 8 of 13 patients could not continue their home training, and syncope or presyncope recurred in three of them during follow-up. We conclude that one session per day of home orthostatic self-training should be prescribed for the prevention of neurocardiogenic syncope.

Adult↗

PubMed2005

Prevalence of venous anatomic variants and occlusion among patients undergoing implantation of transvenous leads.

BACKGROUND: The implantation of transvenous leads may be prohibited by venous occlusion or anatomical variants. The prevalence of these conditions among patients undergoing transvenous pacing or implantable cardioverter defibrillator (ICD) leads implantation has not been systematically studied. This study examined the prevalence of venous anatomic variants and/or venous occlusion, and related risk factors, prior to lead implantation. METHOD: The study included 273 consecutive patients scheduled for implantation of transvenous pacing or ICD leads. Before the procedure, the venous network of arms, neck, and thorax was evaluated by bilateral intravenous digital subtraction angiography (DSA). RESULTS: Complete venous occlusion associated with developed collateral circulation was observed in 12 patients (4.4%); at the site of the left innominate vein in 9, left subclavian vein in 2, and right subclavian vein in 1 patient. Of 12 patients with venous occlusion, 7 patients had a history of prior surgical procedure. A persistent left superior vena cava was observed in 1 patient (0.4%). The presence of abnormal findings on DSA was significantly higher on the left than the right side (P < 0.001). The cardio-thoracic ratio (CTR) was significantly greater in patients with venous occlusions than patients with normal circulation (P = 0.012). CONCLUSIONS: Asymptomatic venous abnormalities are not rare among patients requiring transvenous pacing lead implantation. Careful attention should be paid when implanting pacing or ICD leads from the left side, especially in patients with an increased CTR or history of prior insertion for central venous catheter.

Aged↗

PubMed2005

Assessment of cardiac baroreflex function during fixed atrioventricular pacing using baroreceptor-stroke volume reflex sensitivity.

UNLABELLED: Baroreflex sensitivity in paced patients. INTRODUCTION: The baroreceptor-heart rate (HR) reflex has prognostic value in cardiovascular medicine. However, it cannot be used in chronotropically incompetent or paced patients. In healthy subjects, the baroreceptor-stroke volume (SV) reflex, with power spectral analysis of SV and blood pressure (BP) variations in the low-frequency band, serves as an alternate measure of the baroreceptor-cardiac reflex. This study examined the baroreceptor-stroke volume (SV) reflex sensitivity in the supine and 60 degrees upright positions in paced patients. METHODS AND RESULTS: We studied 16 recipients of dual-chamber pacemakers paced at a fixed rate. The hemodynamics and baroreceptor-SV reflex sensitivity were measured during atrioventricular (AV) sequential pacing every 5 minute in the supine and 60 degrees upright positions. Mean SV decreased from 42.0+/-20.1 mL in the supine to 36.6+/-16.1 mL in the upright position (P<0.05), whereas BP and total peripheral resistance did not change. A significant fall in baroreceptor-SV reflex sensitivity from 29.2+/-18.0%/mmHg to 19.5+/-15.5%/mmHg was observed during upright tilt (P<0.005). CONCLUSION: Fixed-rate AV sequential pacing did not blunt the decrease in baroreceptor-SV reflex sensitivity consistent with the arterial baroreflex gain response to upright posture. The decreased baroreceptor-SV reflex sensitivity occurring with the upright posture may reflect a baroreflex-induced inotropic effect secondary to vagal withdrawal and sympathetic activation.

Aged↗

PubMed2005

Valvular and supravalvular aortic stenosis in heterozygous familial hypercholesterolemia, a case report.

Familial hypercholesterolemia (FH) is an autosomal dominant disorder characterized by a high level of LDL-cholesterol and frequent coronary atherosclerosis. We studied a 64 year old woman with heterozygous (hetero) FH, who showed symptoms of chest pain and dyspnea with no other coronary risk factors than post-menopause and hypercholesterolemia. Although her coronary symptoms didn't reveal significant stenosis on coronary angiography, she had severe aortic valvular and supravalvular stenosis at the ascending aorta, which qualified her for aortic valve replacement. Moreover, a coronary flow study revealed functional ischemia with a reduction of the coronary flow reserve. We report a case of valvular and supravalvular aortic stenosis corrected by aortic valve replacement, a rare complication of hetero FH.

Aortic Stenosis, Supravalvular↗

PubMed2004

Two cases of familial primary pulmonary hypertension.

Case 1, a 28-year-old woman (third daughter of Case 2) delivered her first child in September 2000, but leg edema and dyspnea on exertion appeared the following January. At the time of our first examination of the patient in May 2001, a chest X-ray showed cardiomegaly and pulmonary artery enlargement. Echocardiography demonstrated enlargement of the right ventricle and small left ventricular dimensions, and an electrocardiogram revealed right ventricle hypertrophy. After perfusion-ventilation lung scintigraphy and cardiac catheterization, she was diagnosed as having primary pulmonary hypertension (PPH). Although she was discharged with prescriptions for a diuretic, warfarin and beraprost sodium, she died of a pulmonary hypertensive crisis twenty days after readmission. Case 2, a 60-year-old woman(mother of Case 1) developed the same symptoms as those in Case 1, in May 2001, but recovered after medication. PPH is a rare disease and only a few familial cases are reported. In this family, the eldest daughter of Case 2 had also died of pulmonary hypertension ten years ago, several months after her first delivery. In contrast to the daughters, the mother's symptoms developed gradually.

Adult↗

PubMed2004

Infective tricuspid valve endocarditis due to abscess of an endogenous arteriovenous fistula in a chronic hemodialysis patient.

Patients on chronic hemodialysis are at high risk for endocarditis due to prosthetic access devices. Right-sided endocarditis without any predisposing factors is rare in dialysis patients. A 76-year-old female, who had chronic renal failure had been treated by hemodialysis and had a permanent pacemaker implanted, was admitted to our hospital with a high fever and lumbago after abscess formation at an autogenous arteriovenous fistula for hemodialysis. Methicillin Resistant Staphylococcus Aureus was identified by blood culture examination. Echocardiography revealed vegetation attached to the tricuspid valve. Chest X-ray and perfusion lung scintigraphy showed pulmonary infarction, perhaps due to vegetation-derived emboli. Computed tomography also showed pyogenic spondylitis in L4 and L5. Repeated vascular punctures even of autogenous grafts expose dialysis patients to bacteremia and imply a higher risk of infectious endocarditis.

Abscess↗