Hélio Bernardes Silva

Lipid Metabolism Alterations in Normotensive Subjects With Positive Family History of Hypertension

Metabolic abnormalities are usually reported in hypertensive patients. These metabolic alterations seem to begin in childhood. The young offspring of hypertensive parents have not been studied thoroughly for metabolic alterations. The aim of this study was to examine the level of total cholesterol, LDL cholesterol, VLDL cholesterol, HDL cholesterol, uric acid, glycemia, aldosterone, and plasma renin activity in a population of 42 young, slender normotensive subjects with positive family history of hypertension (FH+) or negative family history of hypertension (FH-). Measurements were made in 20 young normotensive subjects (age 21.1+/-2.2 years, 11 males, 15 white, 5 oriental, body mass index of 22.1+/-2.3 kg/m2) with FH+ and 22 young normotensive subjects (age 19.9+/-1.4 years, 17 males, 17 white, 5 oriental, body mass index of 22.1+/-2.3 kg/m2) with FH-. The total cholesterol (4.47+/-0.8 versus 3.95+/-0.6 mmol/L), LDL cholesterol (2.74+/-0.63 versus 2.36+/-0.61 mmol/L), VLDL cholesterol (0.5+/-0.25 versus 0.35+/-0.09 mmol/L), and triglycerides (2.52+/-1.26 versus 1.76+/-0.5 mmol/L) were significantly elevated (P<.05) in the FH+ group compared with the FH- group. The total cholesterol/HDL cholesterol ratio was significantly higher in the group with a positive family history of hypertension (3.75+/-0.02 versus 3.11+/-0.02, P<.05). Glycemia was slightly elevated in the FH+ group (2.16+/-0.29 mmol/L) but was not significantly different from that of the FH- group (2+/-0.2 mmol/L). Uric acid, plasma renin activity, and aldosterone were similar in both groups. We conclude that young, slender normotensive subjects with a positive history of hypertension show alterations in lipid metabolism, suggesting a positive correlation between lipid metabolism and hypertension heredity.

Essential hypertension and histocompatibility antigens. An association study.

Data from a previous study concerning the distribution of human leukocyte antigen (HLA) haplotypes in siblings with essential hypertension suggested that at least one of the genes responsible for the genetic susceptibility to this disease is located in or near the HLA complex. The objective of the present study was to investigate if a given HLA-A, B, or DR gene could represent a marker for susceptibility to essential hypertension at the population level. Thus, the frequencies of HLA antigens were determined in Caucasian patients with essential hypertension (HLA-A and B antigens were determined in 89 cases, 85 of which were also typed for HLA-DR antigens). The results showed an increased frequency (p = 0.00064) of HLA-DR4, which was present in 34% of the patients and in 16% of local ethnically matched control subjects. We conclude that HLA-DR4 may represent a marker for susceptibility to essential hypertension in the Brazilian Caucasian population.

Essential hypertension and histocompatibility antigens. A linkage study.

&NA; It is well established that genetic and environmental factors are involved in the etiology of essential hypertension. The presence of genes predisposing to essential hypertension in the human leukocyte antigen (HLA) complex is controversial because studies of an association between HLA antigens and essential hypertension have failed to yield consistent results. Our aim in the present study was to further investigate this issue through the method of linkage analysis. Analysis of 96 hypertensive siblings distributed in 31 families indicated a significant distortion (p=0.0009) of the normal segregation pattern of inheritance of HLA haplotypes. Thus, our data indicate that at least one of the genes responsible for genetic predisposition to essential hypertension is located very near or within the HLA complex. (Hypertension 1989;14:604‐609)

Malignant hypertension and hypertensive encephalopathy in primary aldosteronism caused by adrenal adenoma

Two cases are reported as follows: 1) 1 female patient with accelerated-malignant hypertension secondary to an aldosterone-producing adrenal adenoma; and 2) 1 female patient with adrenal adenoma, severe hypertension, and hypertensive encephalopathy. This association is a rare clinical finding, and malignant hypertension may modify the hormonal characteristic of primary aldosteronism, making its diagnosis more difficult. The diagnosis of primary aldosteronism should be considered in patients with malignant hypertension or hypertensive encephalopathy if persistent hypokalemia occurs. Identification of primary aldosteronism is of paramount importance for the patients evolution, because the surgical treatment makes the prognosis more favorable.

Long-Lasting Inhibition of Angiotensin Response in Rats by Depot Administration of Octanoyl-[Leu8]-Angiotensin II

Depot administration of a lipophilic angiotensin II (AII) antagonist was tested for obtaining prolonged inhibition of the pressor response to AII in rats. Intramuscular injections of 1.5 or 5.0 mg of octanoyl‐[Leu8]AII (oct‐LAII), in oil solution produced the same degree of AII inhibition either 6 h or 24 h after the injection. The inhibition was comparable to that expected from the continuous intravenous infusion of oct‐LAII at the rate of 1.2 μg kg−1 min−1. The prolonged effect of intramuscular injections of oct‐LAII in oil solution may be useful for chronic studies of physiopathological states involving the renin‐angiotensin‐aldosterone system.

Evolução a longo prazo e complicaçöes da hipertensão arterial após transplante cardíaco

PURPOSE: To evaluate the progression of arterial hypertension (AH) and its consequences , in patients submitted to cardiac transplantation (CT) in use of cyclosporine (CY). METHODS: In 65 patients submitted to orthotopic CT, we evaluated blood pressure, serum creatinine and blood levels of CY before, 15 and 30 days, and 6, 12, 24, 48 and 60 months after CT; in 20 patients we analyzed cardiac index and systemic vascular resistance pre-CT, 15 and 30 days, 6 and 12 months after CT; in 33 patients, we studied anatomic and functional modifications by echocardiography, 24±13 months after CT. RESULTS: Thirty days after CT, AH was present in 58.5% (50% mild), and after one year, 93% of patients were hypertensives (85% moderate-to-severe), remaining unchanged during the rest of follow-up. The serum creatinine progressively increased, reaching values significantly higher than those pre-CT after one year, persisting with a mild increment until 60 months. Echocardiography showed left ventricle hypertrophy in 54% of patients, all of which had normal function. Two patients died as a direct consequence of hypertensive complications. CONCLUSION: AH in patients submitted to CT on CY use occurs early, increases in prevalence and severity during the follow-up and is mediated by an increase in vascular resistance. Also, the AH does not correlate to CY blood levels or nefrotoxicity, but it can impair renal function and compromise longevity of transplantation by inducing ventricular hypertrophy.PURPOSE To evaluate the progression of arterial hypertension (AH) and its consequences, in patients submitted to cardiac transplantation (CT) in use of cyclosporine (CY). METHODS In 65 patients submitted to orthotopic CT, we evaluated blood pressure, serum creatinine and blood levels of CY before, 15 and 30 days, and 6, 12, 24, 48 and 60 months after CT; in 20 patients we analyzed cardiac index and systemic vascular resistance pre-CT, 15 and 30 days, 6 and 12 months after CT; in 33 patients, we studied anatomic and functional modifications by echocardiography, 24 +/- 13 months after CT. RESULTS Thirty days after CT, AH was present in 58.5% (50% mild), and after one year, 93% of patients were hypertensives (85% moderate-to-severe), remaining unchanged during the rest of follow-up. The serum creatinine progressively increased, reaching values significantly higher than those pre-CT after one year, persisting with a mild increment until 60 months. Echocardiography showed left ventricle hypertrophy in 54% of patients, all of which had normal function. Two patients died as a direct consequence of hypertensive complications. CONCLUSION AH in patients submitted to CT on CY use occurs early, increases in prevalence and severity during the follow-up and is mediated by an increase in vascular resistance. Also, the AH does not correlate to CY blood levels or nefrotoxicity, but it can impair renal function and compromise longevity of transplantation by inducing ventricular hypertrophy.

Hormonal and cardiovascular reflex assessment in a female patient with pure autonomic failure

We report the case of a 72-year-old female with pure autonomic failure, a rare entity, whose diagnosis of autonomic dysfunction was determined with a series of complementary tests. For approximately 2 years, the patient has been experiencing dizziness and a tendency to fall, a significant weight loss, generalized weakness, dysphagia, intestinal constipation, blurred vision, dry mouth, and changes in her voice. She underwent clinical assessment and laboratory tests (biochemical tests, chest X-ray, digestive endoscopy, colonoscopy, chest computed tomography, abdomen and pelvis computed tomography, abdominal ultrasound, and ambulatory blood pressure monitoring). Measurements of catecholamine and plasmatic renin activity were performed at rest and after physical exercise. Finally the patient underwent physiological and pharmacological autonomic tests that better diagnosed dysautonomia.

Cardiac and neurologic complications in malignant hypertension due to oral contraceptive use.

Malignant hypertension is a rare consequence of contraceptive use. We report here on two young women with malignant hypertension secondary to contraceptive use whose main symptomatology was neurological. Both patients had renal failure, severe left ventricle hypertrophy, and hemorrhagic stroke, all reversible after control of blood pressure and discontinuation of the contraceptive pill.

Increased arterial distensibility and renovascular hypertension in Goldenhar syndrome

This is a report of the successful angioplastic treatment of an association of renovascular hypertension with renal artery stenosis and the Goldenhar syndrome (a variant of oculoauriculovertebral dysplasia). For the first time to date, this association, which occurred in a 13-year-old girl, is reported. Additionally, increased arterial distensibility in spite of arterial hypertension was detected by noninvasive methods. The similarity of this finding and in those for other genetic diseases, suggests that the vascular lesions could be linked to the Goldenhar syndrome.