Blood pressure influences the occurrence of complex ventricular arrhythmia in hemodialysis patients.

We investigated the relationship between blood pressure and the occurrence of complex ventricular arrhythmias (multiform, couplets, or runs) as assessed by 48-hour Holter monitoring in 74 stable long-term hemodialysis patients (44.5 +/- 12 years old; 54% men; 74% whites; dialysis duration, 51.3 +/- 36.1 months; systolic pressure, 146.6 +/- 19.3 mm Hg; diastolic pressure, 89.2 +/- 12.1 mm Hg; prevalence of arterial hypertension, 33.8%). Systolic and diastolic pressures represented the average of all predialysis determinations during the 3 months preceding the tests. Hemodialysis was performed midway through the Holter monitoring period. M-mode and bidimensional echocardiograms and myocardial perfusion tests were also obtained from all patients. Complex arrhythmias were observed in 37 individuals (50%). Univariate analysis showed that systolic pressure (P < .001), diastolic pressure (P < .05), age (P < .001), left ventricular posterior wall thickness (P < .01), left ventricular mass index (P < .05), and ischemic alterations on myocardial perfusion tests (P < .005) were significantly associated with complex arrhythmias. With the use of a multivariate model (stepwise logistic regression analysis) only systolic pressure (P < .01) and age (P < .05) were independently associated with complex arrhythmias. Sex; angina; dialysis duration; New York Heart Association functional class; use of digitalis; plasma levels of creatinine, sodium, potassium, calcium, and phosphate; hematocrit; left ventricular fractional shortening; left ventricular diastolic diameter; and ST segment deviation were not correlated with complex arrhythmias. The severity and frequency of complex arrhythmias were not influenced by hemodialysis. At follow-up (5 to 80 months) 5 patients had died of sudden death, 4 of whom were hypertensive and older than 45 years.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Lack of effect of a single oral dose of cyclosporine on systemic blood pressure and on forearm blood flow and vascular resistance in humans.

The acute hemodynamic effect of cyclosporine in man is controversial. A randomized, double blind, placebo-controlled, cross-over study was undertaken to evaluate the effect of a single oral dose of cyclosporine (20 mg/kg body weight) on mean blood pressure (MBP), heart rate (HR), forearm blood flow (FBF), and vascular resistance (FVR) in 16 healthy adult subjects. Subjects were studied twice, with an intervening period of 2 weeks, before and after the administration of either cyclosporine or the vehicle olive oil. Blood pressure was measured on brachial and digital arteries. After 30 min of rest, basal measurements were obtained and individuals were randomly assigned to receive either cyclosporine or the vehicle, and the same measurements were repeated 2 h later. Mean whole blood levels of cyclosporine were 1542+/-387 ng/mL (range 1000 to 2550) 2 h after the administration of a single oral dose of cyclosporine. Cyclosporine did not cause any significant change in the hemodynamic parameters when compared with vehicle. Pre- and post-cyclosporine data were as follows (means +/-/SD): MBP (determined by Finapres on the digital artery), 92+/-10 v 95+/-11 mm Hg; HR, 66+/-10 v 68+/-11 beats/min; FBF, 3.90+/-1.3 v 3.8+/-1.8 mL/ 100 mL/min; and FVR, 28+/-9 v 33 +/-18 units, respectively. For the vehicle the results were: MBP, 94+/-9 v 94+/-9; HR, 67+/-9v 67 /-11; FBF, 3.3+/-1.6 v 3.2+/-2.0; FVR, 35+/-14 v 37+/-15, respectively. These figures did not differ from those obtained with the auscultatory method applied to the brachial artery among 10 selected subjects studied with Finapres. In conclusion, we found no evidence that at supratherapeutic doses cyclosporine causes acute increase in blood pressure or peripheral vasoconstriction in humans.

The pressor response to acute hyperlipidemia is enhanced in lean normotensive offspring of hypertensive parents.

Family history is an important predictor of the cardiovascular risk factor cluster associated with insulin resistance. The dyslipidemia associated with insulin resistance may contribute to elevated blood pressure (BP). This study was undertaken to further explore the link between family history, dyslipidemia, and BP regulation. Twenty-three lean normal volunteers with a negative family history (FH-, n = 11) or positive family history (FH+, n = 12) of hypertension were evaluated under baseline conditions and during a 4-h infusion of intralipid and heparin (acute hyperlipidemia). Fasting blood was drawn for lipids including nonesterified fatty acids (NEFA). After 2 and 4 h of intralipid and heparin, blood was drawn for NEFA. The BP was measured at baseline and every 30 min after starting the intralipid and heparin infusion. Baseline triglycerides and very low density lipoprotein cholesterol concentrations were higher in FH+ than FH- subjects (P < .05). However, NEFA increased similarly in both groups during the infusion of intralipid and heparin. The BP and heart rate increased with acute hyperlipidemia in all subjects combined (P < .05). Despite the similar increase of NEFA, mean BP, pulse pressure, and pressure-rate product increased significantly in FH+ subjects but not in FH- volunteers with acute hyperlipidemia. Although systolic BP increased in both groups, the increase was greater in FH+ than in FH- volunteers during acute hyperlipidemia (14 +/- 2 v 10 +/- 2 mm Hg, P < .05). These results suggest that higher plasma lipids combined with a greater pressor response to hyperlipidemia may contribute to the development of high BP in subjects with a family history of hypertension.

Blood pressure and the risk of complex arrhythmia in renal insufficiency, hemodialysis, and renal transplant patients.

Complex arrhythmia is frequent in hemodialysis patients but it is not clear if this is a consequence of dialysis or uremia or is secondary to the hemodynamic and cardiovascular alterations often associated with chronic renal failure. The incidence of complex ventricular arrhythmia (frequent multiform premature beats, couplets, and runs) in 31 subjects who had their uremic status recently corrected by renal transplant (Group 1) and in 23 predialysis (Group 2) and 73 hemodialysis (Group 3) chronic renal failure patients were studied with 24-h Holter monitoring. Patients were not receiving antiarrhythmic drugs or digitalis and significant coronary artery disease was excluded by clinical and noninvasive methods. Complex arrhythmia was two times more frequent in dialysis patients but the difference did not reach statistical significance (Group 1: 16%; Group 2: 17%; Group 3: 34%; chi2 4.9, P = .086). The stepwise model of logistic regression analysis identified systolic blood pressure (odds ratio 1.015, 95% confidence interval [CI] 1.001-1.027, P = .03) and left ventricular systolic dysfunction (odds ratio 7.04, 95% CI 1.3-36.7, P = .02) as the only factors that independently influenced the probability of complex arrhythmia. Age, gender, race, diabetes, smoking status, body mass index, diastolic blood pressure, serum creatinine, hematocrit, left ventricular mass index, and use of diuretics, beta-blockers, angiotensin converting enzyme (ACE) inhibitors, sympatolytics, and calcium channel blockers did not influence the occurrence of complex arrhythmia. The data indicate that blood pressure and myocardial dysfunction are more important determinants of complex arrhythmia than dialysis or uremia in chronic renal disease patients.

Autonomic abnormalities demonstrable in young normotensive subjects who are children of hypertensive parents.

Although a slightly elevated office blood pressure (BP) has been reported in several studies, little is known about the prolonged resting blood pressure, heart rate (HR) and baroreflex sensitivity (BRS) of prehypertensive subjects with a family history of hypertension. Office blood pressure, prolonged resting (1 h) BP and HR were measured in 25 young normotensives with a positive family history of hypertension (FH+) and 25 young normotensives with a negative family history of hypertension (FH-), matched for age, sex, and body mass index. After BP and HR measurements, blood samples were collected for the determination of norepinephrine, plasma renin activity and aldosterone levels, and baroreflex sensitivity was then tested. Casual BP, prolonged resting BP and heart rate were significantly higher in the FH+ group (119.9 +/- 11.7/78.5 +/- 8.6 mmHg, 137.3 +/- 12.3/74.4 +/- 7.9 mmHg, 68.5 +/- 8.4 bpm) compared to the FH- group (112.9 +/- 11.4/71.2 +/- 8.3 mmHg, 128.0 +/- 11. 8/66.5 +/- 7.4 mmHg, 62.1 +/- 6.0 bpm). Plasma norepinephrine level was significantly higher in the FH+ group (220.1 +/- 104.5 pg/ml) than in the FH- group (169.1 +/- 63.3 pg/ml). Baroreflex sensitivity to tachycardia (0.7 +/- 0.3 vs 1.0 +/- 0.5 bpm/mmHg) was depressed in the FH+ group (P<0.05). The FH+ group exhibited higher casual blood pressure, prolonged resting blood pressure, heart rate and plasma norepinephrine levels than the FH- group (P<0.05), suggesting an increased sympathetic tone in these subjects. The reflex tachycardia was depressed in the FH+ group.

Moderate sodium restriction enhances the pressor response to hyperlipidemia in obese, hypertensive patients.

The effect of dietary sodium restriction on insulin, lipids, and blood pressure has been controversial. Evidence suggests that adverse short-term effects in response to very low-salt diets do not persist long-term with modest sodium restriction. In this study, the effects of modest dietary sodium restriction (60 and 120 mmol sodium) were measured for 3 weeks in 12 lean normotensives and 10 obese hypertensives. Blood pressure, plasma lipids, and the pressor response to an infusion of Intralipid and heparin were obtained. In contrast to previous reports concerning very low-salt diets, obese hypertensives did not manifest a pressor response or an adverse lipid effect with moderate salt restriction. Obese hypertensives were not more salt-sensitive than lean normotensives and did not manifest a different hemodynamic response to 4-hour infusion of Intralipid and heparin while on the 120-mmol/day salt diet. During the 60-mmol/day salt diet, however, plasma triglycerides increased more in obese than in lean volunteers during the Intralipid and heparin infusion (398+/-38 vs. 264+/-18 mg/dL; p<0.05), and there were greater increases in mean blood pressure (12+/-2 vs. 7+/-2 mm Hg; p<0.05) and systemic vascular resistance (111+/-38 vs. 225+/-44 dyne.sec.cm-5) as well as a larger decrease in small artery compliance (22.5+/-0.6 vs. 20.4+/-0.6 mL/mm Hg x 100; p<0.05). These data suggest that modest dietary sodium restriction in obese hypertensives does not adversely affect baseline blood pressure or lipids, but it does magnify their adverse lipid and hemodynamic response to fat loading.

Horner's syndrome and brachial paresis as a complication of lumbar sympathetic block: a case report.

An unusual case of Horner's syndrome secondary to a sympathetic block in a patient with chronic adhesive arachnoiditis (CAA) is described. The patient, a 40-year-old white woman, presented with spastic paraplegia, hyperreflexia, bilateral Babinski sign, superficial and deep sensitive hypoaesthesia at the T4 level, in addition to bladder and rectal dysfunction since she was 32. At age of 38 she complained of excessive daily sweating below the T4 level, mostly at night. A 4mL 0.5% bupivacaine lumbar sympathetic block was performed. Within 15 min a right brachial paresis and an ipsilateral Horner's syndrome were noted. Speculatively, an abnormal cephalic spread of the anaesthesic due to a putative erratic space secondary to the CAA may justify the clinical picture even using a relatively small amount of anaesthesic (4 mL).

[Efficacy and tolerance of a new calcium-channel blocking agent (nitrendipine) in the treatment of arterial hypertension]. / Eficácia e tolerabilidade de um novo bloqueador dos canais de cálcio (nitrendipina) no tratamento da hipertensão arterial.

PURPOSE: Assess the efficacy and tolerability of nitrendipine, 20 mg/day, in mild to moderate essential hypertension (diastolic blood pressure 95 to 114 mmHg). MATERIAL AND METHODS: Twenty patients in an open comparative trial (drug x placebo) during six weeks. Blood pressure and heart rate were measured in orthostatic and supine position and after hand-grip maneuver every two weeks. RESULTS: Systolic and diastolic blood pressure fell significatively in the treated group by the end of the study-supine (161 mmHg +/- 11 to 138 mmHg +/- 13 and 105 +/- 5 to 81 mmHg +/- 7 p less than 0.05) and orthostatic position (153 mmHg +/- 13 to 132 mmHg +/- 13 and 104 mmHg +/- 15 to 81 mmHg +/- 7, p less than 0.05) and after hand grip maneuver (170 mmHg +/- 21 to 148 mmHg +/- 22 and 108 mmHg +/- 5 to 85 mmHg +/- 7 p less than 0.05). Significant modifications were not observed in systolic and diastolic blood pressure in placebo group under the following conditions: supine (168 mmHg +/- 8 to 168 mmHg +/- 17 and 107 mmHg +/- 5 to 107 mmHg +/- 3) and orthostatic positions (167 mmHg +/- 9 to 163 mmHg +/- 14 and 107 mmHg +/- 5 to 107 mmHg +/- 4) and after hand grip maneuver (178 mmHg +/- 17 to 173 mmHg +/- 16 and 107 mmHg +/- 4 to 108 mmHg +/- 6). Significant changes in heart rate did not occur in both groups after treatment. Heart rate elevation observed after hand grip maneuver did not change. Adverse effects like headache, palpitation and dizziness occurred in both groups. Electrocardiogram, x-ray and blood chemistries were not modified during the trial.

[Primary hyperaldosteronism and adrenal tumors. Clinico-surgical experience with 9 patients]. / Hiperaldosteronismo primário e tumores adrenais. Experiência clínico-cirúrgica em nove pacientes.

PURPOSE: To report seven patients with diagnosis of primary aldosteronism, five of them due to aldosterone-producing adenoma (APA) and two due to idiopathic hyperaldosteronism (IHA), and two patients with adrenal non-producing tumors in order to discuss our experience on differential diagnosis and treatment of this hypertensive disease. METHODS: Hypokalemia and higher values of urinary potassium in the absence of diuretics were useful to the screening diagnosis of primary aldosteronism, reinforced by suppressed plasma renin activity either at rest and after deambulation and by higher values of plasma aldosterone. Computerized tomography in all patients and selenium-cholesterol scintigraphy were used to make the localization of tumors and differential diagnosis between APA and IHA. RESULTS: The patients with adrenal tumors were submitted to surgical treatment and the two patients with IHA were submitted to spironolacone therapy. After 1 to 5 years of follow-up, we observed cure of hypertension and hypokalemia in three patients after surgery and improvement of blood pressure control and normalization of serum potassium in the six others. CONCLUSION: The diagnosis of primary aldosteronism is important, besides its rarity, because surgical or appropriated clinical treatment provide cure of hypertension or improvement of blood pressure control in most of patients.

[Pheochromocytoma. Its diagnostic and therapeutic characteristics]. / Feocromocitoma. Peculiaridades diagnósticas e terapêuticas.

Pheochromocytoma is a cause of hypertension that frequently can be cured by surgery. The aim of this paper, based on 5 cases of pheochromocytoma, is to relate our experience in diagnosis and treatment in this pathology. In four of 5 patients with pheochromocytoma we observed unusual characteristics of the disease. Association with neurofibromatosis in one case, with rheumatic mitral regurgitation in another; and in a third case the tumor was malignant. One patient had catecholamine-mediated electrocardiographic changes which disappeared with treatment. Since symptoms of adrenergic hyperactivity were present in all cases, the rise in the levels of vanilmandelic acid and urinary metanephrines were useful in confirming the diagnosis. Computed tomography and I-131 meta-benzylguanidine for radioisotopic imaging, displayed not only all tumoral masses but also bone metastases in the malignant case. During the follow-up period, from the sixth month to the fourth year after surgery, four patients were asymptomatic, and have normal urinary catecholamine metabolite levels. The patient with a malignant form of pheochromocytoma continued to show elevated catecholamines release and remained hypertensive in spite of adrenal mass resection.

[A false diagnosis of hypertrophic myocardiopathy in pheochromocytoma]. / Falso diagnóstico de miocardiopatia hipertrófica em feocromocitoma.

A 24 year-old man was admitted with hypertensive crises and diagnosis hypothesis of neurofibromathosis and pheochromocytoma with blood pressure of 150 x 110mmHg and in use of anti-hypertensive drugs. The electrocardiogram (EKG) showed left ventricle hypertrophy. An echocardiogram showed interventricular septum (IVS) thickness of 16mm, posterior wall (PW) thickness of 11mm (ratio IVS/PW was 1.4). Diastolic ventricular diameter was 39mm with gradient of 52mmHg and mild mitral-valve murmur by pulsate Doppler. Increased vanillylmandelic acid and metanephrines in a 24-hour sample of urine has confirmed diagnosis of pheochromocytoma within was localized by 131I metaiodobenzyl-guanidine scan and computerized axial tomography. The patient was submitted to right adrenalectomy. Blood pressure was normalized. Evaluation an year later revealed a healthy man with normal laboratory exams, EKG and echocardiogram. It seems that the hypertrophy was consequence of the hypertension and pheochromocytoma, was not hypertrophic cardiomyopathy.

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.

Critical analysis of autoregressive and fast Fourier transform markers of cardiovascular variability in rats and humans.

The autonomic nervous system plays an important role in physiological and pathological conditions, and has been extensively evaluated by parametric and non-parametric spectral analysis. To compare the results obtained with fast Fourier transform (FFT) and the autoregressive (AR) method, we performed a comprehensive comparative study using data from humans and rats during pharmacological blockade (in rats), a postural test (in humans), and in the hypertensive state (in both humans and rats). Although postural hypotension in humans induced an increase in normalized low-frequency (LFnu) of systolic blood pressure, the increase in the ratio was detected only by AR. In rats, AR and FFT analysis did not agree for LFnu and high frequency (HFnu) under basal conditions and after vagal blockade. The increase in the LF/HF ratio of the pulse interval, induced by methylatropine, was detected only by FFT. In hypertensive patients, changes in LF and HF for systolic blood pressure were observed only by AR; FFT was able to detect the reduction in both blood pressure variance and total power. In hypertensive rats, AR presented different values of variance and total power for systolic blood pressure. Moreover, AR and FFT presented discordant results for LF, LFnu, HF, LF/HF ratio, and total power for pulse interval. We provide evidence for disagreement in 23% of the indices of blood pressure and heart rate variability in humans and 67% discordance in rats when these variables are evaluated by AR and FFT under physiological and pathological conditions. The overall disagreement between AR and FFT in this study was 43%.

Increased sympathetic activity in normotensive offspring of malignant hypertensive parents compared to offspring of normotensive parents.

Malignant hypertension seems to be the consequence of very high blood pressure. Furthermore, an increase in sympathetic and renin-angiotensin system activity is considered to be the main mechanisms producing malignant hypertension. In the present study, 10 offspring of malignant hypertensive (OMH) parents (age 28 +/- 5 years, 7 males, 3 females, 2 white and 8 non-white) and 10 offspring of normotensive (ONT) parents (age 28 +/- 6 years, 2 males, 8 females, 3 white and 7 non-white) were evaluated. The OMH group had significantly higher (P < 0.05) casual blood pressure (125 +/- 10/81 +/- 5 mmHg) compared with ONT (99 +/- 13/67 +/- 5 mmHg). The increase in blood pressure was greater in OMH (Delta SBP = 17 +/- 2 vs Delta SBP = 9 +/- 1 mmHg in ONT) during cold pressor testing, but they had a lower increase in heart rate (Delta HR = 13 +/- 2 vs Delta HR = 20 +/- 3 bpm in ONT) during isometric exercise(handgrip test). Sympathetic activity, measured by microneurography, was significantly higher (P < 0.05) before exercise in OMH (17 +/- 6 vs 11 +/- 4 burst/min in ONT) and exhibited a greater increase (Delta = 18 +/- 10 vs Delta = 8 +/- 3 burst/min in ONT) during isometric exercise. This study showed increased sympathetic activity in OMH before exercise and a greater response during isometric exercise, suggesting an autonomic abnormality before exercise and a greater sympathetic response to physical stress in OMH compared to ONT.

Leptin levels in different forms of Chagas' disease.

Leptin is produced primarily by adipocytes. Although originally associated with the central regulation of satiety and energy metabolism, increasing evidence indicates that leptin may be an important mediator in cardiovascular pathophysiology. The aim of the present study was to investigate plasma leptin levels in patient with Chagas' heart disease and their relation to different forms of the disease. We studied 52 chagasic patients and 30 controls matched for age and body mass index. All subjects underwent anthropometric, leptin and N-terminal pro-brain natriuretic peptide (NT-proBNP) measurements and were evaluated by echocardiography, 12-lead electrocardiogram (ECG), and chest X-ray. All patients had fasting blood samples taken between 8:00 and 9:00 am. Chagasic patients were divided into 3 groups: group I (indeterminate form, IF group) consisted of 24 subjects with 2 positive serologic reactions for Chagas' disease and no cardiac involvement as evaluated by chest X-rays, ECG and two-dimensional echocardiography; group II (showing ECG abnormalities and normal left ventricular systolic function, ECG group) consisted of 14 patients; group III consisted of 14 patients with congestive heart failure (CHF group) and left ventricular dysfunction. Serum leptin levels were significantly lower (P < 0.001) in the CHF group (1.4 +/- 0.8 ng/mL) when compared to the IF group (5.3 +/- 5.3 ng/mL), ECG group (9.7 +/- 10.7 ng/mL), and control group (8.1 +/- 7.8 ng/mL). NT-proBNP levels were significantly higher (P < 0.001) in the CHF group (831.8 +/- 800.1 pg/mL) when compared to the IF group (53.2 +/- 33.3 pg/mL), ECG group (83.3 +/- 57.4 pg/mL), and control group (32 +/- 22.7 pg/mL). Patients with Chagas' disease and an advanced stage of CHF have high levels of NT-ProBNP andlow plasma levels of leptin. One or more leptin-suppressing mechanisms may operate in chagasic patients.

Hemodynamic and metabolic profile in offspring of malignant hypertensive parents.

Malignant hypertension is a serious form of arterial hypertension in which the physiopathological mechanisms include increased activity of the sympathetic nervous system, renin angiotensin system, and endothelium dysfunction. Family history of hypertension is an important predictive factor for hypertension and is associated with metabolic and hemodynamic abnormalities. Studies of these abnormalities in malignant hypertensive offspring have not yet been published. Therefore, we studied 42 offspring of malignant hypertensive parents (OMH group: age, 22+/-7 years; 23 male subjects; 27 white) and 35 offspring of normotensive parents (ONT group: age, 21+/-4 years; 23 male subjects; 25 white). All subjects had blood pressure <140/90 mm Hg. We evaluated body mass index; office blood pressure; 24-hour ambulatory and continuous beat-to-beat blood pressure monitoring (Finapres); biochemical analysis, including total cholesterol and fractions, triglycerides, glucose, and insulin; and hormonal analysis, including plasma renin activity, aldosterone, and catecholamines. The subjects were also submitted to cold pressure test and handgrip measurements. The body mass index was significantly higher in the OMH group (24+/-5 kg/m(2)) than in the ONT group (22+/-4 kg/m(2)). The OMH group showed significantly higher blood pressure and heart rate in office and Finapres measurements (P<0.05). In 24-hour ambulatory monitoring, the OMH group presented higher 24-hour blood pressure and heart rate, higher blood pressure during the night, and higher heart rate variability during the day compared with those of the ONT group. They also presented lower HDL cholesterol, higher levels of plasma insulin and norepinephrine, and higher insulin-to-glucose ratio (P<0.05) than the ONT group. There were no differences in the other biochemical parameters measured. In conclusion, OMH subjects show early hemodynamic, neurohumoral, and metabolic alterations that are typical of hypertensive metabolic syndrome.

Hemodynamic effects of lipids in humans.

Evidence suggests lipid abnormalities may contribute to elevated blood pressure, increased vascular resistance, and reduced arterial compliance among insulin-resistant subjects. In a study of 11 normal volunteers undergoing 4-h-long infusions of Intralipid and heparin to raise plasma nonesterified fatty acids (NEFAs), we observed increases of blood pressure. In contrast, blood pressure did not change in these same volunteers during a 4-h infusion of saline and heparin. To better characterize the hemodynamic responses to Intralipid and heparin, another group of 21 individuals, including both lean and obese volunteers, was studied after 3 wk on a controlled diet with 180 mmol sodium/day. Two and four hours after starting the infusions, plasma NEFAs increased by 134 and 111% in those receiving Intralipid and heparin, P < 0.01, whereas plasma NEFAs did not change in the first group of normal volunteers who received saline and heparin. The hemodynamic changes in lean and obese subjects in the second study were similar, and the results were combined. The infusion of Intralipid and heparin induced a significant increase in systolic (13.5 +/- 2.1 mmHg) and diastolic (8.0 +/- 1.5 mmHg) blood pressure as well as heart rate (9.4 +/- 1.4 beats/min). Small and large artery compliance decreased, and systemic vascular resistance rose. These data raise the possibility that lipid abnormalities associated with insulin resistance contribute to the elevated blood pressure and heart rate as well as the reduced vascular compliance observed in subjects with the cardiovascular risk factor cluster.