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Biomedical subjects

A A Lopes

Publications and source records attributed to A A Lopes.

At least 55 records · Page 3Linked to original sources
PubMed1995

The low birth weight hypothesis as a plausible explanation for the black/white differences in hypertension, non-insulin-dependent diabetes, and end-stage renal disease.

It is well known that black Americans have a higher risk for low birth weight (LBW) than white Americans. In addition, blacks are at a higher risk for hypertension (HT), non-insulin dependent diabetes mellitus (NIDDM), and end-stage renal disease (ESRD), particularly ESRD attributed to HT (ESRD-HT) and NIDDM (ESRD-NIDDM). It has been shown that LBW is associated with postpartum anatomic and functional alterations in the kidney and pancreas as well as with progressive renal damage in animals and increased risk for HT and NIDDM during adulthood in humans. Based on these empirical findings, it is here proposed that a greater risk of HT, NIDDM, and ESRD, particularly ESRD-HT and ESRD-NIDDM, in black Americans during adulthood may be partly related to their higher risk of LBW. However, LBW is proposed here as a component factor rather than a sufficient cause or a necessary factor for the development of these diseases. The ultimate contribution of LBW to the black/white disparities regarding HT, NIDDM, and ESRD may depend not only on the black/white differences in LBW but also on the race-specific prevalences of other component factors, both environmental/behavioral and genetic, that may or may not require the presence of LBW to cause each of these diseases.

Birth Weight↗
PubMed1995

Differences in the patterns of age-specific black/white comparisons between end-stage renal disease attributed and not attributed to diabetes.

To assess differences in the patterns of age-specific black/white comparisons between end-stage renal disease (ESRD) attributed to diabetes (ESRD-DM) and not attributed to diabetes (ESRD-NON-DM), data for subjects 20 to 79 years of age reported by the US Renal Data System as incident cases of ESRD during 1988 to 1991 were analyzed. While the black to white incidence rate ratio (B/W RR) for ESRD-NON-DM peaked in patients before the age of 40 years, the most striking B/W RRs for ESRD-DM were observed in patients older than 40 years. This study also explored evidence supporting the hypothesis that an increased risk of premature death attributed to cardiovascular disease (CVD death) in black patients, alone or in combination with black/white differences in prevalence of diabetes, influences the pattern of age-specific black/white ESRD-DM comparisons. By using estimates of the diabetic population as denominators for the rates, the incidence or ESRD-DM remained much higher in black patients than in white patients for those aged 45 years or above. However, the incidence of ESRD-DM for patients aged below 45 years was found to be significantly (P < 0.05) lower (B/W RR = 0.6) for black male diabetic patients and slightly, yet significantly, higher (P < 0.05; B/W RR = 1.1) for black female diabetic patients than for their white counterparts. Therefore, prevalence of diabetes could not fully explain the pattern of age-specific B/W RR for ESRD-DM.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Abnormal degradation of von Willebrand factor main subunit in pulmonary hypertension.

We wished to investigate whether the abnormalities in multimeric structure and biological function of von Willebrand factor (vWF) observed in pulmonary hypertensive patients could be related to increased proteolytic degradation. We therefore analysed plasma vWF subunit composition in 24 pulmonary hypertensive patients, aged 1.2-45 yrs. After immunoisolation, vWF was subjected to 5.5% sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE) followed by Western immunoblotting, vWF intact subunit (225 kDa) and four proteolytic fragments (189, 176, 150 and 140 kDa) were visualized by peroxidase staining and analysed in a laser densitometer. In pulmonary hypertensive patients, the relative density of the intact subunit was decreased, and this was associated with an increase in the 176 kDa proteolytic fragment. The mean densities of the other fragments were not significantly changed, but in some patients the 150 and 140 kDa polypeptides were markedly increased. Abnormalities in multimeric structure of vWF (loss of high molecular weight multimers and increase in low molecular weight forms in comparison with controls), were associated with a significant decrease in biological activity (62-92% activity, 95% confidence interval (CI) for the mean). Total proteolytic fragment density correlated positively with multimeric abnormalities (rs = 0.45), and negatively with biological activity of vWF (rs = -0.49). Thus, in pulmonary hypertension, multimeric abnormalities and decreased biological activity are related to proteolytic degradation of vWF main subunit, possibly reflecting extensive endothelial dysfunction.

Adolescent↗
PubMed1995

[Pulmonary valve agenesis. Clinico-surgical evaluation of 32 patients].

PURPOSE: To study the surgical and clinical evolution of 32 cases with absent pulmonary valve to propose the ideal period of time for surgical correction. METHODS: Clinical and laboratorial analysis were performed in 32 infants, under 12 months of age, between 1980 an 1993, in an evolutive character. From the clinical viewpoint, hypoxic and/or congestive features were considered in previous and late periods related to surgical repair. Laboratorial studies as ECG (cavities overload), chest X-ray (cardiac size and pulmonary vascular markings) and echocardiogram (associated defects, pressure gradients and anatomical aspects of pulmonary arteries) were also analyzed. Cardiac catheterization was performed in 15 patients. RESULTS: Early cyanosis in 84% of cases and "to and for "murmur in 90% of them facilitate clinical diagnosis in whom tetralogy of Fallot was associated in 30 patients. Refractory respiratory and cardiac insufficiency were responsible for operative indication in 12 patients, half of them, operated on under 12 months of age, died. Survival patients were repaired between two to 11 years old. Four deaths occurred early in life, before any surgical consideration and the 16 remaining patients will electively be considered for an opportune repair. CONCLUSION: Conservative clinical treatment is indicated, waiting for a more rigid bronchial wall can support the pressure of the dilated pulmonary arteries. This way, surgical repair is postponed for at least two years of age.

Electrocardiography↗
PubMed1995

Decreased biological activity is related to abnormal multimeric structure of von Willebrand factor in pulmonary hypertension.

We evaluated the correlation between decreased biological activity and abnormalities in the multimeric structure of plasma von Willebrand factor (vWF) in 27 pulmonary hypertensive patients (median age, 21 years). The biological activity of vWF was measured by the ristocetin cofactor assay and its multimeric structure was assessed by Western immunoblotting after SDS-agarose gel electrophoresis. In spite of high antigenic activity of vWF in plasma (139 +/- 65 vs 91 +/- 27% in controls, P = 0.003), the biological activity expressed as a percent of the control value was decreased in pulmonary hypertensive patients (60-88% activity, 95% CI for the mean). High molecular weight multimers (biologically active forms) were absent in patients and there was a significant increase in the concentration of low molecular weight polymers in comparison with normals (56 +/- 12 and 35 +/- 12% of total multimer density, respectively, P < 0.001). Multimeric abnormalities were positively correlated with plasma vWF levels (r = 0.51, P = 0.007) and negatively correlated with vWF biological activity (r = -0.54, P = 0.004). Thus, decreased biological function is related to abnormalities in the multimeric structure of vWF, possibly reflecting extensive endothelial dysfunction in pulmonary hypertension.

Adult↗
PubMed1994

The joint effects of race and age on the risk of end-stage renal disease attributed to hypertension.

To describe the joint effects of race and age on the risk of end-stage renal disease (ESRD) attributed to hypertension (ESRD-HT), we analyzed data for white and black adults, 20 to 84 years of age, reported by the United States Renal Data System during the period 1987 to 1990. The risk of ESRD-HT increased substantially with age for both blacks and whites; however, at each age, the risk was greater for blacks. A more in-depth description of the combination of effects involving race and age on ESRD-HT incidence was provided by two models of joint effects, one additive and the other multiplicative. Both models used the 20- to 24-year age group as the referent. Under the additive model the risk of ESRD-HT in blacks attributable to the joint effects between race and age increased continuously from younger to older groups. This indicates that although ESRD-HT risk increases with age for both blacks and whites, the increase for blacks is greater than expected if the effects of race were independent of the effects of age. However, the multiplicative model indicated that the proportional increase with age in ESRD-HT risk among blacks, as compared with whites, was more striking for younger ages (< or = 50 years among women and < or = 40 years among men), and especially so for men. This suggests a more accelerated course of hypertension toward ESRD for blacks (especially younger men) than for whites. A conceptual model to explain these patterns of race-age joint effects is proposed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Circulating platelet aggregates indicative of in vivo platelet activation in pulmonary hypertension.

The authors investigated the existence of circulating cellular aggregates in 12 patients with moderate to severe pulmonary hypertension, using scanning electron microscopy. Peripheral venous blood was collected in the presence of 11.5 mM buffered ethylenediaminetetraacetic acid, in order to disperse freshly formed disaggregable aggregates. Irreversible aggregates represented by platelet clusters and/or platelet attachment to either leukocytes or red cells were identified in 7 patients with pulmonary hypertension. Endogenous platelet activation was further confirmed by a significant increase in plasma levels of beta-thromboglobulin in comparison with controls (33.8 +/- 14.1 vs 22.7 +/- 11.5 ng/mL respectively, p < 0.025). The presence of irreversible aggregates in the blood stream strongly suggests that cell-cell interactions actually occur in vivo in these patients. If so, therapeutic measures aimed at preventing in situ thrombosis and its consequences may be beneficial in this disorder.

Adolescent↗
PubMed1993

Abnormal multimeric and oligomeric composition is associated with enhanced endothelial expression of von Willebrand factor in pulmonary hypertension.

Abnormalities in endothelial von Willebrand factor (vWF) structure have been reported in pulmonary hypertension. These include loss of high molecular weight plasma multimers, resulting in decreased biologic activity. If endothelial processing of vWF is altered in this disorder, abnormalities in oligomeric composition may also be expected. We examined this possibility in ten adult patients with primary pulmonary hypertension. Enhanced endothelial vWF expression in these patients was indicated by increased plasma levels of vWF antigen (vWF:Ag) (214 +/- 91 vs 99 +/- 51 percent activity in controls, p < 0.001) and intense immunoperoxidase stain of pulmonary arterial endothelium for vWF (autopsy, 1 patient). Plasma from these patients also had a decreased capacity of inducing platelet aggregation in the presence of ristocetin, relative to vWF:Ag levels (57 +/- 20 percent activity). In addition to mild loss of the largest multimers, changes in oligomeric composition of plasma vWF were observed in most patients using both agarose and polyacrylamide gel electrophoresis. These included decreased concentration of dimeric (470 kDa) vWF in most patients, variable concentration of the 860-kDa fraction, and a relative decrease in subunit (223 kDa) density in subjects with elevated vWF:Ag. These findings provide additional information on the mechanisms responsible for endothelial production of dysfunctional vWF in patients with pulmonary hypertension.

Adult↗
PubMed1993

The excess risk of treated end-stage renal disease in blacks in the United States.

Analysis of national data from the United States Renal Data System for 1988 revealed an important joint effect of age and race in determining the higher risk of ESRD for blacks as compared with whites. For adults, both hypertension and diabetes made important contributions to the combined effect of age and race. In contrast, glomerulonephritis was not considered to be an important contributor to this joint effect. The combined effect of gender and race was weaker than that of age and race; however, among blacks, differences in the proportions of ESRD attributed to hypertension and diabetes across gender were observed. The age-race joint effect is consistent with the hypothesis that a combined effect of lack of treatment and aging on the process that leads to ESRD may play an important role in the excess risk for ESRD among blacks.

Adolescent↗
PubMed1991

Lung beta-adrenoceptors in pulmonary hypertension. A study of biopsy specimens in children with congenital heart disease.

Characteristics of beta-adrenoceptors were analyzed using radioligand-binding techniques with 3H-dihydroalprenolol in lung specimens from 11 children with pulmonary hypertension (median age, three years) undergoing surgical repair of congenital heart defects and four pediatric control subjects (median age, five years) undergoing thoracotomy for removal of neoplasms or cysts. Scatchard analysis of 3H-DHA binding to lung membranes showed similar values of the dissociation constant in both groups (Kd = 0.72 +/- 0.22 nM in patients vs 1.22 +/- 0.22 nM in controls; p = NS). The receptor density was significantly increased in patients in comparison with controls, with respective values of 164 +/- 19 and 95 +/- 13 fmol/mg of protein (p less than 0.025), and correlated directly with mean pulmonary arterial pressure (r = 0.82; p less than 0.0005). No significant relationship was observed between receptor number and pulmonary arterial medial thickness. Thus, the increase in receptor density in these patients may be related to adaptative changes in cells other than vascular smooth muscle.

Adolescent↗
PubMed1990

Aggregation of platelets in whole blood from children with pulmonary hypertension.

The response of aggregation of platelets to adenosine diphosphate (7.5-120 microM) and collagen (1.25 micrograms/ml) was assessed in whole blood (impedance method) in 10 children with pulmonary hypertension (hematocrit range, 42 to 71%). The response to collagen was normal (9.08 +/- 3.47 vs. 10.36 +/- 1.86 ohms in controls, P = NS) while there was a decreased response to adenosine diphosphate (6.98 +/- 3.83 vs. 11.21 +/- 2.02 ohms, P less than 0.01), in spite of high concentrations of the inducer. Lowering the hematocrit in vitro to 40% with autologous platelet-rich plasma resulted in a rise in the platelet count from 171 +/- 63 to 225 +/- 84 x 10(9) platelets/1 (P less than 0.001) and a significant increase in the response to adenosine diphosphate from 6.98 +/- 3.83 to 9.89 +/- 3.66 ohms (P less than 0.02). As in the baseline condition, high concentrations of adenosine diphosphate were required. The response to collagen did not change significantly. The results indicate that aggregatory response of platelets is relatively preserved in these children. The decreased response to adenosine diphosphate may be a result of a low count and interference of red cells on the accretion of platelets on the electrodes. Because high concentrations of adenosine diphosphate were still required after hemodilution to achieve an aggregatory response close to normal, we speculate that leakage of endogenous adenosine diphosphate from red cells may have accounted for partial activation of the platelets, resulting in a relative refractory state to in vitro stimulation.

Adenosine Diphosphate↗
PubMed1990

Plasma anticoagulant system in patients with pulmonary hypertension.

Adults with pulmonary hypertension and polycythemia (N = 22) have low levels of plasma antithrombin III (84 +/- 18 vs 98 +/- 13% for controls, N = 35, P less than 0.005) and protein C (66 +/- 21 vs 125 +/- 30%, N = 8, P less than 0.0002) but normal levels of total protein S. Data are reported as means +/- SD and percent normal values obtained for pooled plasma from normal healthy adults. Children with the same disorder (N = 6) also had low protein C levels (66 +/- 16 vs 85 +/- 5%, P less than 0.025). Total protein S was normal for children, but free protein S was decreased (66 +/- 13 vs 91 +/- 23%, P less than 0.025). Since the levels observed in these patients are above those reported for congenital deficiencies, the reduction in plasma levels of anticoagulant proteins may be the result of chronic intravascular coagulation. Furthermore, normal levels of plasminogen and fibrin degradation products suggest a localized disorder or an acquired decrease in fibrinolytic activity.

Adolescent↗
PubMed1989

Effect of intentional hemodilution on platelet survival in secondary pulmonary hypertension.

Platelet regeneration time was assessed in 13 young adults with pulmonary hypertension and polycythemia secondary to congenital heart defects who underwent isovolemic hemodilution to improve clinical status and coagulation defects. The estimated platelet half-life in patients with Eisenmenger's complex was significantly shortened in comparison with normal subjects (3.8 +/- 1.9 vs 4.8 +/- 1.0 days, p less than 0.05). Hemodilution was carried out with no adverse effects, using low molecular weight dextran solutions. Lowering hematocrit from 61 to 50 percent resulted in a significant increase in platelet half-life from 3.8 +/- 1.9 to 5.7 +/- 1.8 days (p less than 0.02), which was followed by a marked rise in platelet count from 149 +/- 31 to 209 +/- 47 x 10(9) platelets/L (p less than 0.003). Arterial oxygen tension did not change significantly. These observations indicate that high hematocrit levels may have accounted for the shortened platelet survival and thrombocytopenia in these patients. Significant hemodilution may lead to a marked improvement in platelet abnormalities in patients with Eisenmenger's complex.

Adolescent↗
PubMed1989

[Treatment using balloon catheterization of pulmonary valve stenosis].

From October 84 to September 88 we performed pulmonary valvuloplasty with balloon catheter (PVBC) in 90 patients (pt) with pulmonary valve stenosis (PVS). The patients were divided in 3 groups (Gr) by their ages: group I (Gr. I) 7 pt (8%) aged 4 days to 11 months, Gr. II 66 pt (73%) aged 1 year to 12 years and Gr. III 17 pt aged 13 to 34 years. This study consists of clinical and echocardiographic evaluation adopting the following parameters of indication: a) transvalvar pulmonary gradient (G); b) absence of dysplasia or hypoplasia of the pulmonary annulus. There were associated lesions which were found in each group: Gr. I atrial septal defect (ASD) in 2 pt and tricuspid insufficiency (TI) in 1 pt, in Gr. II supra valvar stenosis (SVS) in 1 pt and patent arterial ductus (PAD) in 1 pt and in the Gr. III (ASD) in 1 pt. The results after pulmonary valvuloplasty with balloon catheter (PVBC) were: (Gr.I) in 5 pt the G were reduced below 50 mmHg and the average of right ventricular systolic pressure (RVSP) changed from 92 to 62 mmHg and the average of G from 76 to 44 mmHg. One of these pt was submitted to surgery 1 month after the procedure and 2 developed restenosis in 2 and 3 years respectively, being submitted to another dilatation with good results. The 2 pt in which the procedure was not effective were submitted to surgery. In the second group the PVBC was effective in 61 pt (92%) showing the RVSP changed from 118 to 64 mmHg and G changed from 86 to 23 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗