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Biomedical subjects

K Miyatake

Publications and source records attributed to K Miyatake.

At least 127 records · Page 7Linked to original sources

Choice of replacement valve in the elderly.

BACKGROUND AND AIMS OF THE STUDY: Little comparative information exists on the outcome of the valve replacement with bioprostheses or mechanical valves in the elderly. This study was carried out to make such a comparison. METHODS: Follow up data were examined from 219 patients aged > or = 65 years who underwent aortic and/or mitral valve replacement using bioprosthetic (n = 67) or mechanical valve (n = 152) between April 1979 and December 1993. The mean follow up periods were 6.3 +/- 2.8 years after bioprosthesis and 4.9 +/- 2.1 years after mechanical valve implantation. RESULTS: Although the actuarial rate of structural deterioration was higher in patients with bioprosthetic valves than in those with mechanical valves (58% versus 100% freedom at 10 years after surgery, p < 0.01), no such prosthesis-related difference was seen in the subgroup of patients aged > or = 70 (100% versus 100% at nine years, p = N.S.). The actuarial rate of major bleeding was higher after mechanical valve implantation than after bioprosthetic valve placement (90% versus 100% freedom at 10 years, p < 0.05); this lower rate with bioprosthetic valves was maintained in patients aged > or = 70 (78% versus 100% at nine years, p < 0.05). There were no significant differences in the incidences of thromboembolism and bacterial endocarditis between the two valve types. CONCLUSIONS: Structural degeneration of bioprosthetic devices was a major problem in patients aged 65-70 years, but it was essentially negligible in those aged > or = 70 years. Anticoagulant-related bleeding was a major problem with mechanical valves in both age groups. Therefore, for patients older than 70 years, valve replacement with a bioprosthesis appears to be the method of choice.

Age Factors↗

[Non-invasive determination of the quantity of pleural effusion and evaluation of the beneficial effect of pleuracentesis in patients with acute exacerbation of chronic congestive heart failure].

A non-invasive method to determine the quantity of pleural effusion and to evaluate the beneficial effect of pleuracentesis in patients with acute exacerbation of chronic congestive heart failure was evaluated. Twenty-three patients with pleural effusion due to acute exacerbation of chronic congestive heart failure were studied. The angle (x) formed by the diaphragm and lung (right side) or pericardium (left side) was measured by ultrasonography in the sitting position using the subscapular approach. Pleuracentesis was then performed in 15 patients, and the quantity of aspirated pleural effusion (y) was measured and compared with the angle x. There was significant relationship between y and x: y = 0.125 x 10(0.017x) (r = 0.77, p < 0.01). The 18 patients with more than 500 ml of estimated one-sided pleural effusion were divided into two groups; the nonpleuracentesis group (n = 8) and the pleuracentesis group (n = 10). The intravenous furosemide dose per increased body weight, and the term of oxygen supply and time to disappearance of edema were compared between the two groups. Intravenous furosemide dose was lower (p < 0.05) and the term of oxygen supply was shorter in the pleuracentesis group than in the nonpleuracentesis group (p < 0.05), whereas time to disappearance of edema was not significantly different. This non-invasive method can estimate the quantity of pleural effusion, and pleuracentesis had beneficial effect on patients with pleural effusion of greater than 500 ml (the angle x > 35 degrees ) in patients with acute exacerbation of chronic congestive heart failure.

Aged↗

[Evaluation of intramyocardial coronary flow velocity pattern before and after surgical repair of Bland-White-Garland syndrome by pulsed Doppler echocardiography].

Anomalous origin of the left main coronary artery from the pulmonary artery (Bland-White-Garland syndrome) is a rare congenital anomaly. Intramyocardial coronary flow dynamics by pulsed Doppler echocardiography were studied in three patients with this syndrome who underwent surgical repair by Hamilton's method. Before surgery, the intramyocardial flow at the ventricular septum showed a retrograde velocity pattern which had two peaks in systole and diastole in all patients. After surgery, two patients with successful repair showed a biphasic intramyocardial flow pattern which consisted of retrograde and antegrade flows in systole and diastole, respectively. In contrast, one patient who had a residual shunt between the left coronary artery and the pulmonary artery showed a biphasic pattern which had antegrade flow in systole and retrograde flow in diastole. These results may suggest that the evaluation of postoperative intramyocardial coronary flow velocity pattern by pulsed Doppler echocardiography is useful for detecting a residual shunt after surgical repair of Bland-White-Garland syndrome.

Adult↗

Intravascular ultrasound evidence for importance of plaque distribution in the determination of regional vessel wall compliance.

Regional vessel wall distensibility was determined by measuring luminal area and pressure, using intravascular ultrasound (Sonicath; Boston-Scientific, Watertown, MA, USA; 3.5 Fr, 30 MHz) in 45 left coronary sites from 40 patients. Luminal area in diastole (A) and in systole was measured at the diseased sites. With the ratio of luminal area changes (dA) to coronary pressure changes (dP) during a cardiac cycle, the total distensibility index was calculated by the formula: [(dA/A)/dP] x 10(3). At sites with non-circumferential disease, perimeters in diastole (L) and in systole were measured at the normal and diseased portions, and the changes in perimeters (dL) during a cardiac cycle were calculated. The regional distensibility index was obtained by the formula: [(dL/L)/dP] x 10(3). In 22 sites with circumferential disease, the total distensibility index was 1.03 +/- 0.61/mmHg, significantly lower than that for 23 sites with non-circumferential disease (1.45 +/- 0.89/mmHg; P < 0.05). In non-circumferential disease, the regional distensibility index at the diseased portion was significantly lower (0.33 +/- 0.47/mmHg) than that at the normal portion (1.11 +/- 0.75/mmHg; P < 0.01). Coronary sites with residual non-circumferential disease after angioplasty also exhibited heterogeneity of regional distensibility (0.73 +/- 0.76 at disease sites versus 1.58 +/- 0.95/mmHg at normal sites, n = 10, P < 0.05). These results indicate that heterogeneous regional wall distensibility exists at sites with non-circumferential disease where the total vessel distensibility is preserved by the presence of compliant normal portion. This heterogeneity of regional wall distensibility may represent a biomechanical factor that explains the mechanism of plaque rupture that occurs mainly at the shoulder of the non-circumferential disease.

Biomechanical Phenomena↗

Mitral valve dysfunction resulting from thickening and stiffening of artificial mitral valve chordae.

BACKGROUND: There is little information about changes in mitral valve function caused by thickening and stiffening of artificial chordae during follow-up. Using serial echocardiographic examination, we evaluated thickening and stiffening of artificial chordae and the effect of those changes on mitral valve function. METHODS AND RESULTS: Between November 1986 and November 1993, 40 patients underwent mitral valve repair with artificial chordae using glutaraldehyde-tanned xenograft pericardium (GTXP) or polytetrafluoroethylene suture (PTFE). Seven GTXP patients and 20 PTFE patients underwent serial echocardiographic examination after surgery and were included in the final analysis. Thickening and stiffening of the artificial chonlae were classified according to echocardiographic changes after surgery: grade 1, no change; grade 2, thickening and/or stiffening without impairment of the motion of the mitral valve leaflet; and grade 3, thickening and stiffening that impaired motion of the mitral valve leaflet. The mean follow-ups in patients with GTXP and PTFE were 6.0 and 3.6 years, respectively. During follow-up, there were 2 GTXP patients with grade 2 thickening and stiffening and 4 patients with grade 3. There were 6 PTFE patients with grade 2 thickening and stiffening and 2 patients with grade 3. Grade 3 occurred earlier in GTXP than in PTFE patients (P < .05). Mitral valve area in GTXP patients decreased from 2.5 +/- 0.4 to 2.1 +/- 0.3 cm2 (P < .05); however, mitral valve area in PTFE patients showed no significant change during follow-up (2.1 +/- 0.4 to 2.0 +/- 0.4 cm2, P = NS). CONCLUSIONS: Although mitral valve repair with artificial chordae is useful, more attention should be paid to mitral valve function resulting from thickening and stiffening of artificial chordae.

Adult↗

Brain capillary endothelial cells express two forms of erythropoietin receptor mRNA.

To study the existence of the erythropoietin receptor (Epo-R) mRNA in brain capillary endothelial cells, the reverse transcription (RT) PCR was performed using total RNAs from rat brain capillary endothelial cells (RBECs) and MBEC4, which is one of the established mouse brain capillary endothelial cell lines. Southern analysis of the RT-PCR products indicated that both RBECs and MBEC4 expressed an authentic form of Epo-R mRNA as a minor form and an intron-5-inserted form of Epo-R mRNA, thus a soluble form of Epo-R mRNA, as a major form. Furthermore, the effect of recombinant human erythropoietin (rHuEpo) on the DNA synthesis in RBECs was analyzed. rHuEpo showed a dose-dependent mitogenic action on RBECs as a competence factor. Radioiodinated rHuEpo was bound specifically to RBECs with time, cell number and dose dependencies. Binding studies with 125I-rHuEpo showed that RBECs had a single class of receptors with low-affinity (Kd = 860 pM) and that the number of sites/cell (10300) was abundant. These results suggest that brain capillary endothelial cells express not only an authentic form of Epo-R but also a soluble form of Epo-R and that erythropoietin acts directly on brain capillary endothelial cells as a competence factor.

Animals↗

Wall composition in intravascular ultrasound layered appearance of human coronary artery.

To evaluate the impact of histological factors on the appearance of the wall of the coronary artery by intravascular ultrasound (IVUS), we performed an in vitro study of 34 coronary artery segments from eight autopsied patients. We assumed the coronary cross section to be divided into four equal parts, and assessed the quadrants with maximal and minimal wall thickness by IVUS (30 MHz; 4.3 Fr; 1800 rpm) and by a histological study. The histological layer thickness and composition were also evaluated in terms of their contribution to the appearance of the ultrasound layer. Fifty-eight quadrants were clearly visible on ultrasound. A three-layered appearance, with inner echogenic, subjacent sonolucent, and outer echogenic layers, was observed in 32 quadrants, while 26 quadrants showed a two-layered appearance with inner and outer echogenic layers. The thickness of the inner echogenic layer (0.77 +/- 0.38 mm) was moderately correlated with the intimal thickness (0.51 +/- 0.45 mm; r = 0.85, standard error of estimate [SEE] = 0.24 mm); however, the correlation was significantly improved when the thickness of the inner echogenic plus sonolucent layers (0.89 +/- 0.47 mm) was compared with that of the intima plus media (0.69 +/- 0.47 mm; r = 0.94, SEE = 0.15 mm; P = 0.012 between the coefficients). Discriminant analysis showed that intimal hyalinization, associated with intimal thickening, was strongly related to the presence of the three-layered appearance on IVUS (F to enter 40.0, P < 0.0001). These results indicate that the ultrasound layered appearance of human coronary arteries varies with histological alterations. We suggest that the thickness of the inner echogenic plus sonolucent layers on IVUS represents the intimal plus medial thickness observed by histology, and that the use of this value may be appropriate in the assessment of coronary wall thickening associated with atherosclerosis.

Aged↗

Intravascular ultrasound evidence of angiographically undetected left main coronary artery disease and associated trauma during interventional procedures.

To determine the clinical significance of angiographically undetected left main coronary artery (LMCA) disease, we analyzed data from 47 patients, with a mean age of 58 years, who were examined with intravascular ultrasound (3.5 Fr, 30 MHz). For assessment of atherosclerosis, the lesion area was calculated from the ultrasound images of the formula, [(total vessel area--lumen area)/total vessel areas] x 100(%). In 37 LMCA segments of patients with significant distal coronary stenosis (> 50%), the percent intima-media area (the index) was 39 +/- 11% (mean +/- SD), significantly greater than that of 10 patients without distal disease (27 +/- 4%, P < 0.01). Among those with significant coronary stenosis, the index was markedly greater in patients with multi-vessel coronary stenosis (46 +/- 12%, n = 19) than in patients with single-vessel disease (33 +/- 9%, n = 18; P < 0.01). At three LMCA sites associated with multi-vessel disease, ultrasound analysis demonstrated disruption of the intima at the site where the guiding catheter for balloon angioplasty had been positioned. These results indicate that LMCA disease is more prominent in patients with multi-vessel distal coronary disease than in those with single vessel disease, even in the absence of angiographic stenosis. We suggest that LMCA trauma can occur where the guiding catheter for angioplasty is positioned, particularly in patients with multi-vessel distal disease.

Adult↗

Functional behavior and morphology of the coronary artery wall in patients with Kawasaki disease assessed by intravascular ultrasound.

OBJECTIVES: To examine the development of coronary artery lesions in Kawasaki disease, we assessed the functional behavior and morphology of coronary arteries by intravascular ultrasound. BACKGROUND: Long-term follow-up studies of patients with Kawasaki disease have demonstrated the development of localized coronary stenoses even after aneurysms have regressed. It is also possible that angiographically normal coronary segments in patients with this disease may retain histologic changes. METHODS: Twenty-three patients followed up by serial coronary angiography were examined at a mean age +/- SD of 14.9 +/- 2.9 years. The thickness of the intima-media complex was measured by intravascular ultrasound (30 MHz; 3.5 or 4.3 F; 1,800 rpm). Coronary reactivity to nitroglycerin was determined by measuring percent changes in cross-sectional coronary artery area after intracoronary injection (7 microgram/kg body weight) of this agent. RESULTS: A remarkably thickened intima-media complex was observed at the sites with persisting (0.54 +/- 0.20 mm, n = 19) and regressed (0.84 +/- 0.40 mm, n = 23) aneurysms. Mild thickening of the intima-media complex was often observed even in angiographically normal segments (0.22 +/- 0.05 mm, n = 31), in the left main coronary artery (0.47 +/- 0.15 mm, n = 20) and at normal branches (0.36 +/- 0.09 mm, n = 13). Coronary reactivity to nitroglycerin was significantly lower at the sites of regressed aneurysms (12.8 +/- 6.6%, n = 9) than in normal segments (32.8 +/- 10.9%, n = 13, p < 0.01), indicating the presence of functional impairment at the sites with regressed aneurysms. Decreased nitroglycerin reactivity was also observed in some segments without evidence of aneurysm. CONCLUSIONS: These results indicate that in patients with Kawasaki disease the coronary disease accompanying impaired reactivity to nitroglycerin is present at the sites of regressed aneurysms as well as in angiographically normal coronary segments. We suggest that these sites with morphologic and functional abnormalities are related to the development of significant stenosis.

Adolescent↗

Serial doppler echocardiographic evaluation of bioprosthetic valves in the tricuspid position.

OBJECTIVES: This study sought to evaluate bioprosthetic valve dysfunction in the tricuspid position by serial Doppler echocardiography. BACKGROUND: Few reports on the long-term results of tricuspid valve replacement with bioprosthetic valves are evaluated by serial Doppler echocardiography. METHODS: Between September 1979 and December 1993, 95 patients underwent tricuspid valve replacement with bioprosthetic valves at our facility. Sixty patients who underwent serial Doppler echocardiographic examination at intervals of at least 2 years after operation were included in the final analysis. These patients were followed up from 1.5 to 13.0 years (mean 5.8 +/- 2.5). RESULTS: The actuarial rates of freedom from bioprosthetic valve stenosis and regurgitation at 10 years were 46% and 51%, respectively. The prevalence of bioprosthetic valve stenosis and regurgitation increased progressively in a linear manner beginning 1 or 2 years after tricuspid valve replacement. Right heart failure developed during follow-up in 20 of the 25 patients with bioprosthetic valve dysfunction. CONCLUSIONS: The long-term durability of bioprosthetic valves in the tricuspid position was substantially lower in our study than that reported in previous studies. Tricuspid bioprosthetic valve dysfunction increased progressively in a linear manner beginning 1 to 2 years after tricuspid valve replacement.

Actuarial Analysis↗

Accumulation of methylmalonic acid caused by vitamin B12-deficiency disrupts normal cellular metabolism in rat liver.

To clarify the relationship between intracellular concentrations of methylmalonic acid and metabolic and growth inhibition in vitamin B12-deficient rats, hepatic methylmalonic acid levels were assayed and inhibition of glucose and glutamic acid metabolism by methylmalonic acid was studied in isolated hepatocytes. Vitamin B12-deficient rats (14 weeks old) excreted more urinary methylmalonic acid and had lower body weights than the control rats. Hepatic methylmalonic acid levels (3.6(SD 1.30)-5.3 (SD 0.51) mumol/g tissue; 7.9 (SD 2.90)-11.8 (SD 1.14) mM) were increased and correlated with the extent of the growth retardation during vitamin B12-deficiency. Isolated hepatocytes and mitochondria from normally fed rats were labelled with [14C(U)]glucose and [14C(U)]glutamic acid respectively, in the presence or absence of 5 mM-methylmalonic acid. Although methylmalonic acid did not affect the incorporation of 14C into protein and organic acid fractions in the hepatocytes, it inhibited 14CO2 formation (an index of glucose oxidation by the Krebs cycle) by 25% and incorporation of 14C into the amino acid fraction by 30%. In the mitochondria, methylmalonic acid inhibited 14CO2 formation (indicating glutamic acid oxidation by the Krebs cycle) by 70%, but not the incorporation of 14C into the protein fraction. The incorporation of 14C into the organic acid fraction was significantly stimulated by the addition of methylmalonic acid. These results indicate that the unusual accumulation of methylmalonic acid caused by vitamin B12-deficiency disrupts normal glucose and glutamic acid metabolism in rat liver, probably by inhibiting the Krebs cycle.

Animals↗

Mitochondrial NADH- or NADPH-linked aquacobalamin reductase activity is low in human skin fibroblasts with defects in synthesis of cobalamin coenzymes.

Mammalian livers have been reported to contain NADH- and NADPH-linked aquacobalamin reductases, which are distributed in both mitochondria and microsomes. The four aquacobalamin reductase isozymes have been purified and characterized from rat liver. It is unclear which aquacobalamin reductase among the four reductase isozymes participates in the synthesis of cobalamin coenzymes. To clarify the physiological roles of the aquacobalamin reductase isozymes, human mutant fibroblasts (cblC and cblA cells) with defects in cobalamin reductases involved in the coenzyme synthesis were used. In the cblC cells, the activity of the mitochondrial NADH-linked aquacobalamin reductase was reduced significantly, compared with normal human fibroblasts but the mitochondrial NADPH-linked enzyme was not. The reduced specific activity of the NADH-linked enzyme was not due to reduction in levels of the enzyme, but in its affinity for NADH. Although there was not a significant difference in the mitochondrial NADH-linked enzyme activity between normal and cblA cells, the activity of the mitochondrial NADPH-linked enzyme was not detectable in the mutant cells. These results indicate that the defects in the mitochondrial NADH- and NADPH-linked aquacobalamin reductases underlie cblC and cblA disorders, respectively.

Cells, Cultured↗

Hypoxia inhibits gastric emptying and gastric acid secretion in conscious rats.

This study examines the effects of hypoxia in the gastric function in conscious rats which adapted to a meal-feeding schedule, that allowed free access to a high protein (HP) diet (550 g casein/kg diet, Exp.1,2 and 4), a normal protein (NP) diet (200 g casein/kg diet, Exp.3) or a nonpurified rat (NPR) diet (Exp. 5 and 6) for 4 h every day for 2 wk. In Exp. 1, after 4 h of consuming the HP diet, rats were exposed to 7.6 or 10.5% O2 normobaric hypoxia. Hypoxia delayed the excretion of urinary urea for 12 h. In Exp.2 and 3, when rats were exposed to 7.6%O2 after 4 h of consuming the HP diet and exposed to 10.5% O2 after 4 h of consuming the NP diet, respectively, a significant delay in gastric emptying was found in the hypoxic rats. In Exp. 4, when rats were exposed to 7.6 O2 hypoxia after 4 hr of eating the HP diet, the plasma gastrin concentration in the 7.6% O2 hypoxic rats was 2.3-fold that of the normoxic rats after 6 h of hypoxia. Furthermore, when rats that did not consume any HP diet on the day of the experiment were exposed to 7.6 or 10.5% O2 hypoxia, the plasma gastrin concentration was higher in both hypoxic groups than in the normoxic group after 3 and 6 of hypoxia. In Exp. 5, rats that were not fed the NPR diet on the day of study were exposed to 7.6 or 10.5% O2 hypoxia for 3 h after pylorus ligation. Hypoxia inhibited the secretion of gastric acid and elevated the plasma gastrin concentration. In Exp. 6, unfed rats that had been consuming the NPR diet were exposed to 7.6% O2 hypoxia for 3 h after pylorus ligation and were orally administered HCl. The rise of the gastrin concentration due to hypoxia was completely inhibited by oral HCl. These results demonstrate that hypoxia inhibits gastric emptying and gastric acid secretion and that the inhibitory effect of hypoxia on gastric acid secretion stimulates gastrin release through positive feedback regulation.

Analysis of Variance↗

Purification and characterization of arginine:mono-ADP-ribosylhydrolase from Euglena gracilis Z.

Arginine:mono-ADP-ribosylhydrolase was purified from a protozoan, Euglena gracilis Z, using [32P]mono-ADP-ribosylated actin as a substrate. The enzyme showed molecular mass of 33 kDa both in SDS PAGE and gel filtration, indicating it to be a monomeric protein. It was strongly inhibited by ADP and ADP-ribose and activated by Mg2+, DTT, and 2-mercaptoethanol. These results suggest that it recognizes the ADP-ribose moiety of the modified protein. Since the enzyme activity increased in S phase and late G0 phase in a synchronous dividing culture, the enzyme may function in the regulation of the cell cycle.

Actins↗

Endothelins contract guinea-pig pulmonary artery and enhance its adrenergic response via ET(A) receptors.

1. This study has pharmacologically characterized endothelin (ET) receptor subtype(s) mediating contraction and enhancement of adrenergic contraction in guinea-pig pulmonary artery. Isometric tension of the isolated endothelium-denuded ring preparations was measured in the presence of indomethacin (10(-5) mol/L) and N(G)-nitro-L-arginine methyl ester (L-NAME; 3 x 10(4) mol/L) to exclude a mechanism via endothelium, cyclo-oxygenase-generated eicosanoids and nitric oxide. 2. In the additional presence of tetrodotoxin (TTX; 3 x 10(-7) mol/L), ET-1 (10(-11)-10(-7) mol/L) concentration-dependently contracted the preparations. The rank order of potency to contract the preparations among ET receptor agonists was ET-1, sarafotoxin (STX)6b > ET-3 > IRL 1620, STX 6c. BQ-123 (7 x 10(-7)-7 x 10(-6) mol/L) concentrations-dependently shifted the concentration-contraction curve for ET-1 to the right in a parallel manner. Pretreatment with STX 6c (3 x 10(-7) mol/L for 30 min) did not significantly desensitize contractions to ET-1, ET-3 or IRL 1620 (P > 0.05; t-test, 10 d.f). 3. ET-1 (10(-10)-10(-9) mol/L) and STX 6b (10(-9)-10(-8) mol/L) significantly enhanced the electrical field stimulation-induced contraction in a BQ-123-sensitive manner (P < 0.05: t-test, 24-38 d.f), while ET-3 (10(-11)-10(-8) mol/L) and STX 6c (10(-11)-10(-7) mol/L) did not affect contractions. ET-1 (10(-11) mol/L) significantly enhanced contractions to exogenous noradrenaline in the presence of TTX (3 x 10(-7) mol/L) (P < 0.05; t-test, 16 d.f.). 4. These data indicate that the BQ-123-sensitive ET(A) receptor mediates both contraction and enhancement of adrenergic contractions in the guinea-pig pulmonary artery.

Animals↗

Identification of pseudonormal transmitral flow pattern using color Doppler echocardiography.

The jet size of flow in color Doppler is dependent on both jet momentum and the compliance of the receiving chamber. Thus, the jet size of left ventricular (LV) late filling standardized by its jet momentum should reflect LV compliance. We investigated the feasibility of using color Doppler echocardiography to differentiate a pseudonormal from a normal transmitral flow pattern. We divided 37 patients with ischemic heart diseases who demonstrated a "normal" transmitral flow pattern into 2 groups according to their LV end diastolic pressure (LVEDP): a pseudonormalization group (LVEDP > or = 18 mmHg, 16 patients), and a normal group (LVEDP < 18 mmHg, 21 patients). We measured the maximum color Doppler jet length (L) and the peak velocity of transmitral flow during atrial contraction (Av). Filling volume (Q) was measured as the increase in LV volume during atrial contraction. A simplified jet momentum index (M) was obtained from Av x Q, and L/M was considered to reflect LV compliance. L/M was significantly lower in the pseudonormalization group that in the normal group (1.55 +/- 0.46 x 10(-3) vs 2.72 +/- 0.59 x 10(-3) p < 0.01). On the other hand, conventional Doppler variables such as isovolumic relaxation time and the deceleration time of early diastolic filling were not sufficient for discriminating between the 2 groups. In conclusion, color Doppler echocardiogram during atrial contraction was useful for differentiating a pseudonormal from a normal transmitral flow pattern.

Adult↗

Changes of plasma atrial and brain natriuretic peptide levels during hemodialysis.

OBJECTIVES: The purpose of this study was to evaluate the effect of hemodialysis on the plasma concentration of atrial and brain natriuretic peptides, and to determine the two-dimensional echocardiographic parameters affecting the changes of plasma atrial and brain natriuretic peptide levels in patients with chronic renal failure. BACKGROUND: Brain natriuretic peptide has been found in human cardiac tissue and increases in patients with congestive heart failure. However, the factors that stimulate the secretion of plasma brain natriuretic peptide have not yet been fully clarified. METHODS: In 15 patients with chronic renal failure, plasma atrial and brain natriuretic peptide levels and two-dimensional echocardiographic parameters were measured before and after each session of hemodialysis. RESULTS: Plasma atrial natriuretic peptide levels significantly decreased from 367 +/- 537 pg/mL to 138 +/- 167 pg/mL after hemodialysis (p < 0.01). However, plasma brain natriuretic peptide levels did not significantly change after hemodialysis. Left atrial dimension significantly decreased (41.1 +/- 6.6 vs. 36.3 +/- 6.2 mm, p < 0.01) and left ventricular end-diastolic dimension slightly decreased after hemodialysis (57.0 +/- 10.3 vs. 55.7 +/- 9.9 mm, p < 0.05). The decrease of left atrial dimension was greater than that of left ventricular end-diastolic dimension (4.9 +/- 1.6 vs. 1.3 +/- 0.6 mm, p < 0.05). Plasma brain natriuretic peptide levels significantly correlated with fractional shortening both before and after hemodialysis (r = 0.65, p < 0.05). CONCLUSION: Plasma atrial natriuretic peptide levels significantly decreased as the right and left atrial overloads decreased, and plasma brain natriuretic peptide levels did not significantly decrease after hemodialysis. Plasma brain natriuretic peptide levels were not significantly influenced by acute hemodynamic change, such as hemodialysis. However, plasma brain natriuretic peptide levels were significantly correlated with basic cardiac function.

Adult↗