Parkia speciosa empty pod extract exerts anti-inflammatory properties by modulating NFκB and MAPK pathways in cardiomyocytes exposed to tumor necrosis factor-α.

Parkia speciosa Hassk is a plant found abundantly in the Southeast Asia region. Its seeds, with or without pods, have been used in traditional medicine locally to treat cardiovascular problems. The pathogenesis of cardiovascular diseases involves inflammation and oxidative stress. Based on this information, we sought to investigate the potential protective effects of Parkia speciosa empty pod extract (PSE) on inflammation in cardiomyocytes exposed to tumor necrosis factor-α (TNF-α). H9c2 cardiomyocytes were divided into four groups; negative control, TNF-α, PSE + TNF-α and quercetin + TNF-α. Groups 3 and 4 were pretreated with PSE ethyl acetate fraction of ethanol extract (500 µg/mL) or quercetin (1000 µM, positive control) for 1 h before inflammatory induction with TNF-α (12 ng/mL) for 24 h. TNF-α increased protein expression of nuclear factor kappa B cell (NFκB) p65, p38 mitogen-activated protein kinase (p38 MAPK), inducible nitric oxide synthase, cyclooxygenase-2 and vascular cell adhesion molecule-1 when compared to the negative control (p < 0.05). It also elevated iNOS activity, nitric oxide and reactive oxygen species levels. These increases were significantly reduced with PSE and quercetin pretreatments. The effects of PSE were comparable to that of quercetin. PSE exhibited anti-inflammatory properties against TNF-α-induced inflammation in H9c2 cardiomyocytes by modulating the NFκB and p38 MAPK pathways.

Inhibitory effect of compounds from Zingiberaceae species on human platelet aggregation.

Twelve compounds isolated from Alpinia mutica Roxb., Kaempferia rotunda Linn., Curcuma xanthorhiza Roxb., Curcuma aromatica Valeton and Zingiber zerumbet Smith (Family: Zingiberaceae) and three synthesized derivatives of xanthorrhizol were evaluated for their ability to inhibit arachidonic acid- (AA), collagen- and ADP-induced platelet aggregation in human whole blood. Antiplatelet activity of the compounds was measured in vitro by the Chrono Log whole blood aggregometer using an electrical impedance method. Among the compounds tested, curcumin from C. aromatica, cardamonin, pinocembrine and 5,6-dehydrokawain from A. mutica and 3-deacetylcrotepoxide from K. rotunda showed strong inhibition on platelet aggregation induced by AA with IC(50) values of less than 84 microM. Curcumin was the most effective antiplatelet compound as it inhibited AA-, collagen- and ADP-induced platelet aggregation with IC(50) values of 37.5, 60.9 and 45.7 microM, respectively.

Platelet-activating factor (PAF) receptor-binding antagonist activity of Malaysian medicinal plants.

Forty-nine methanol extracts of 37 species of Malaysian medicinal plants were investigated for their inhibitory effects on platelet-activating factor (PAF) binding to rabbit platelets, using 3H-PAF as a ligand. Among them, the extracts of six Zingiberaceae species (Alpinia galanga Swartz., Boesenbergia pandurata Roxb., Curcuma ochorrhiza Val., C. aeruginosa Roxb., Zingiber officinale Rosc. and Z. zerumbet Koenig.), two Cinnamomum species (C. altissimum Kosterm. and C. pubescens Kochummen.), Goniothalamus malayanus Hook. f. Momordica charantia Linn. and Piper aduncum L. are potential sources of new PAF antagonists, as they showed significant inhibitory effects with IC50 values ranging from 1.2 to 18.4 microg ml(-1).

Neutral endopeptidase and angiotensin I converting enzyme insertion/deletion gene polymorphism in humans.

Neutral endopeptidase (NEP) hydrolyses angiotensins (Ang) I and II and generates angiotensin-(1-7) [Ang-(1-7)]. In humans, the insertion/deletion (I/D) angiotensin-I converting enzyme (ACE) gene polymorphism determined plasma ACE levels by 40%. In rats, a similar polymorphism determines ACE levels which are inversely associated to NEP activity. The objective of this study is to evaluate the relationship between ACE expression and plasma NEP activity in normotensive subjects and in hypertensive patients. In total, 58 consecutive patients with hypertension, evaluated in our Hypertension Clinic, were compared according to their ACE I/D genotypes with 54 control subjects in terms of both plasma ACE activity and NEP activities. Plasma ACE activity was elevated 51 and 70% in both DD ACE groups (normotensives and hypertensives) compared with their respective ID and II ACE groups (P<0.001). A significant effect of the ACE polymorphism and of the hypertensive status on ACE activity was observed (P<0.001). In normotensive DD ACE subjects, NEP activity was 0.30+/-0.02 U/ml, whereas in the normotensive II ACE and in the normotensive ID ACE subjects NEP activity was increased 65 and 48%, respectively (P<0.001). In the hypertensive DD ACE patients, NEP activity was 0.47+/-0.03 U/mg. An effect of the I/D ACE genotypes on NEP activity (P<0.04) and an interaction effect between the I/D ACE genotype and the hypertensive status were also observed (P<0.001). These results are consistent with a normal and inverse relationship between the ACE polymorphism and NEP activity in normotensive humans (as is also observed in rats). This normal relationship is not observed in hypertensive patients.

[Early prevention of experimental left ventricular hypertrophy in experimental hypertension and angiotensin II levels]. / Prevención precoz de hipertrofia ventricular izquierda en la hipertensión experimental y concentraciones de angiotensina II.

INTRODUCTION: Angiotensin II levels can be partially inhibited during chronic administration of angiotensin converting enzyme (ACE) inhibitors, limiting from a clinical point of view its efficacy in the treatment of hypertension. There are few studies relating ACE activity directly with early prevention of left ventricular hypertrophy (LVH) in systemic hypertension during the administration of an ACE inhibitor (ACEI). AIM: To evaluate the effects of early ACE inhibition with perindopril on the development of hypertension, LVH and levels of angiotensin II (Ang II) in plasma as well as in LV in the rat Goldblatt model (Gb; 2 kidneys-1 clip), 2 weeks after surgery. RESULTS: Systolic blood pressure and relative LV mass increased by 42% and 20% respectively, in the Gb group (p < 0.001). Plasma and LV ACE activities were significantly higher in the Gb rats compared with the control rats. Plasma and LV Ang II levels also increased by 129% and 800%, respectively. Perindorpil prevented hypertension and LVH development by inhibiting plasma ACE (and also LV ACE), and also circulation Ang II in plasma and in the LV. CONCLUSIONS: In this experimental model of hypertensive LVH, there is an early activation of plasma and cardiac ACE. Early administration of an ACE inhibitor prevents the development of hypertension and LVH by inhibiting the increases of plasma and LV Ang II.

Genetic study of patients with dexamethasone-suppressible aldosteronism without the chimeric CYP11B1/CYP11B2 gene.

Glucocorticoid-remediable aldosteronism is an inherited disorder caused by a chimeric gene duplication between the CYP11B1 (11beta-hydroxylase) and CYP11B2 (aldosterone synthase) genes. The disorder is characterized by hyperaldosteronism and high levels of 18-hydroxycortisol and 18-oxocortisol, which are under ACTH control. The diagnosis of glucocorticoid-remediable aldosteronism had been traditionally made using the dexamethasone suppression test; however, recent studies have shown that several patients with primary aldosteronism and a positive dexamethasone suppression test do not have the chimeric CYP11B1/CYP11B2 gene. The aim of this work was to evaluate whether other genetic alterations exist in CYP11B genes (gene conversion in the coding region of CYP11B1 or in the promoter of CYP11B2) that could explain a positive dexamethasone suppression test and to determine another genetic cause of glucocorticoid-remediable aldosteronism. We also evaluated the role of 18-hydroxycortisol as a specific biochemical marker of glucocorticoid-remediable aldosteronism. We studied eight patients with idiopathic hyperaldosteronism, a positive dexamethasone suppression test, and a negative genetic test for the chimeric gene. In all patients we amplified the CYP11B1 gene by PCR and sequenced exons 3-9 of CYP11B1 and a specific region (-138 to -284) of CYP11B2 promoter. We also measured the levels of 18-hydroxycortisol, and we compared the results with those found in four subjects with the chimeric gene. None of eight cases showed abnormalities in exons 3-9 of CYP11B1, disproving a gene conversion phenomenon. In all patients a fragment of 393 bp corresponding to a specific region of the promoter of CYP11B2 gene was amplified. The sequence of the fragment did not differ from that of the wild-type promoter of the CYP11B2 gene. The 18-hydroxycortisol levels in the eight idiopathic hyperaldosteronism patients and four controls with chimeric gene were 3.9 +/- 2.3 and 21.9 +/- 3.5 nmol/liter, respectively (P < 0.01). In summary, we did not find other genetic alterations or high levels of 18-hydroxycortisol that could explain a positive dexamethasone suppression test in idiopathic hyperaldosteronism. We suggest that the dexamethasone suppression test could lead to an incorrect diagnosis of glucocorticoid-remediable aldosteronism.

Angiotensin I-converting enzyme modulates neutral endopeptidase activity in the rat.

Angiotensin I is a substrate for both ACE and for neutral endopeptidase 24.11 (NEP). We hypothesized that high ACE expression is related to low NEP activity. Accordingly, circulating and tissue NEP and ACE activities were measured by fluorometry in homozygous rats (F(0) and F(2)) for the Lewis microsatellite allele (LL, low ACE) and for the Brown Norway microsatellite allele (BB, high ACE). Plasma, lung, and aortic ACE activities in F(0) and F(2) were higher in BB rats than in LL rats (P<0.01), whereas left ventricular ACE activity was similar in both genotypes. In contrast, NEP activity in the LL group was higher in the serum, aorta, and lungs in F(0) and F(2) homozygous (P<0.05). Plasma ACE activity was inversely correlated with serum (r=-0.6 and -0.598 in F(0) and F(2), respectively; P<0.03) and lung NEP activities (r=-0.77 in F(0) and r=-0.59 in F(2), P<0.01). Aortic ACE and NEP activities were also correlated (r=-0.696 and -0.584 in F(0) and F(2), respectively; P<0.03). In conclusion, genetically determined high ACE expression in rats is inversely related to tissue NEP activity, which could determine lower angiotensin-(1-7) tissue levels.

Inhibition of platelet-activating factor receptor binding by aporphine and phenanthrenoid alkaloids from Aromadendron elegans.

Six aporphine and one phenanthrenoid alkaloids isolated from Aromadendron elegans Blume were investigated for their inhibitory effect on platelet-activating factor (PAF) binding to rabbit platelets using 3H-PAF as a ligand. Of the compounds tested, (-)-N-acetylanonaine, 1-(N-acetyl-N-methylamino)ethyl-3,4,6-trimethoxy-7-hydroxy-phenanthrene, and predicentrine showed strong inhibition of

[Hyperuricemia as a marker for anaerobic threshold in chronic cardiac failure]. / La hiperuricemia es un marcador del umbral anaeróbico en la insuficiencia cardíaca crónica.

BACKGROUND: Patients with chronic cardiac failure often have elevated plasma uric acid levels, that are associated to a dismal prognosis. AIM: To investigate possible metabolic mechanisms to explain elevated uric acid levels in these patients. PATIENTS AND METHODS: Eighteen patients with chronic cardiac failure aged 61 +/- 10 years old, without gout or renal failure and not using high doses of diuretics (equal or less than 80 mg/day furosemide or 50 mg/day hydrochlorothiazide) were studied. Plasma uric acid levels were correlated with anaerobic threshold, maximal oxygen uptake, plasma noradrenaline and creatinine and left ventricular ejection fraction, measured radioisotopically. RESULTS: Mean maximal oxygen uptake was 16.6 +/- 4.2 ml/kg/min. There was a negative correlation between uric acid levels and maximal oxygen uptake or maximal oxygen uptake/body surface area (r = 0.521 and -0.533 respectively, p < 0.05). Patients with uric acid levels over 7 mg/dl had a lower anaerobic threshold than patients with lower levels (9.81 +/- 2.41 and 13.08 +/- 3.28 ml/kg/min respectively, p < 0.05). No significant differences in maximal oxygen uptake were observed in these two groups of patients (15.5 +/- 4.24 and 18.08 +/- 3.86 ml/kg/min respectively). Uric acid levels did not correlate with plasma noradrenaline, creatinine or left ventricular ejection fraction. CONCLUSIONS: These results suggest that a defect in cellular oxygenation contributes to the elevation of plasma uric acid levels in patients with chronic cardiac failure.

[Selective training of respiratory muscles in patients with chronic heart failure]. / Entrenamiento selectivo de los músculos respiratorios en pacientes con insuficiencia cardíaca crónica.

BACKGROUND: Patients with chronic heart failure have a lower inspiratory muscle strength and fatigue endurance. AIM: To assess the effects of selective training of respiratory muscles in patients with heart failure. PATIENTS AND METHODS: Twenty patients with stable chronic heart failure, aged 58.3 +/- 3 years with an ejection fraction of 28 +/- 9%, were subjected to respiratory muscle training with threshold valves. The load was fixed in 30% of maximal inspiratory pressure (PImax) in 11 and in 10% of PImax in nine. Two sessions of 15 minutes, 6 days per week, during 6 weeks were done. Degree of dyspnea (Mahler score), maximal oxygen uptake, distance walked in 6 minutes, respiratory muscle function and left ventricular ejection fraction were measured before and after training. RESULTS: Both training loads were associated to an improvement in dyspnea (+2.7 +/- 1.8 and +2.8 +/- 1.8 score points with 30% PImax and 10% PImax respectively), maximal oxygen uptake (from 19 +/- 3 to 21.6 +/- 5 and from 16 +/- 5 to 18.6 +/- 7 ml/kg/min with 30% PImax and 10% PImax respectively, p < 0.05), PImax (from 78 +/- 22 to 99 +/- 22 and from 72 +/- 34 to 82.3 cm H20 with 30% PImax and 10% PImax respectively), sustained PImax (from 63 +/- 18 to 90 +/- 22 and from 58 +/- 3 to 69 +/- 3 cm H20 with 30% PImax and 10% PImax respectively), and maximal sustained load (from 120 +/- 67 to 195 +/- 47 and from 139 +/- 120 to 192 +/- 154 g with 30% PImax and 10% PImax respectively). The distance walked in 6 min only increased in subjects trained at 30% PImax (from 451 +/- 78 to 486 +/- 68 m). CONCLUSIONS: Selective training of respiratory muscles results in a functional improvement of patients with chronic heart failure.

[Treatment of advanced heart failure by heart transplantation]. / Tratamiento de la insuficiencia cardíaca avanzada mediante transplante de corazón.

BACKGROUND: Heart transplantation currently provides the most effective treatment for advanced heart failure. However, medical therapy for this condition has also improved, heart donors are scarce and the cost of the procedure is high. Therefore the indications and management of these patients need reevaluation. AIM: To analyze the results of 24 patients submitted to heart transplantation for end-stage heart failure needing repeated hospitalizations and i.v. inotropes for compensation. PATIENTS AND METHODS: The group was comprised by 21 men and 3 women with a mean age of 36.8 years, mean left ventricular ejection fraction 19 +/- 4.5%, mean systolic pulmonary artery pressure 48 +/- 13 mmHg (24-70) and mean pulmonary vascular resistance 2.6 Wood Units (1-5). Fourteen patients (58%) had a previous median sternotomy. Immunosuppression did not include induction therapy and steroids were discontinued early. RESULTS: Operative mortality was 4% at 30 days. Actuarial survival at one year was 90% and at 5 years 72%. Freedom from rejection at one year was 76% and at 5 years 50%. Freedom from infection was 70% at one year and 56.5% at five years. All patients with more than 3 months of follow-up were in functional class I. CONCLUSIONS: These results justify the proposed modifications for transplantation protocols.

[Prevalence of hypertension in Valparaíso. Results of the base survey of the CARMEN project (Set of measures for the multifactorial reduction of non-transmissible diseases)]. / Prevalencia de hipertensión arterial en Valparaíso. Resultados de la encuesta de base del programa CARMEN (conjunto de acciones para la reducción multifactorial de las enfermedades no transmisibles).

BACKGROUND: There is little information about the real prevalence of hypertension in Chile. AIM: To assess the adjusted prevalence of hypertension and its main therapeutic measures among adults living in Valparaiso, Chile. MATERIALS AND METHODS: A random sample of dwellings in Valparaiso was chosen. Among these, an individual of 25 to 64 years old was randomly surveyed for risk factors for chronic diseases and sociodemographic parameters. Blood pressure, weight, height, oral glucose tolerance test, fasting cholesterol and triglycerides were also measured. Prevalence was pondered according to age, sex, and probability of selection in the dwelling interior. RESULTS: Three thousand one hundred twelve individuals were studied. The adjusted prevalence of hypertension was 11.4% (11.6% among females and 10.6% among men). The prevalence increased along with age from 3 and 1.9% in men and women of 25 to 34 years old respectively, to 18.2 and 27.4% among men and women of 55 to 64 years old (p < 0.01). People of low socioeconomic level had a higher prevalence of hypertension than those of high socioeconomic level (14.2 and 9.3% respectively, P < 0.05). Diabetes, obesity and hypercholesterolemia were significantly more frequent in subjects with hypertension than in the general population. Forty-four percent of diagnosed hypertensives were receiving medications (angiotensin converting enzyme inhibitors 40%, calcium antagonists 34%, beta blockers 22%). Twenty five percent of patients were treated with a combination of medications. Of those treated, only 22% had normal blood pressure levels at the moment of examination. CONCLUSIONS: High blood pressure is an important public health problem that requires more efficient detection and treatment programs.

[Selection and evaluation of candidate patients for heart transplant]. / Selección y evaluación de pacientes candidatos a trasplante cardíaco.

Cardiac transplantation is now a well-accepted therapy for patients with advanced heart failure. In appropriately selected recipients, it has shown to significantly improve the survival and quality of life. The shortage of appropriate cardiac donor hearts, the costs of cardiac transplantation and its associated long-term medical follow-up, and the potential morbidity and mortality associated with the procedure and with life after transplantation mandates the judicious application of cardiac transplantation to appropriate recipients. A review of current indications, contraindications and evaluation of patients for cardiac transplantation is presented.

[D/D genotype of the gene for angiotensin converting enzyme as a risk factor for post-stent coronary restenosis]. / El genotipo D/D del gen de la enzima conversiva de la angiotensina como factor de riesgo de reestenosis post-stent coronario.

INTRODUCTION: Although intracoronary stenting has decreased restenosis rate compared to percutaneous balloon angioplasty, still a high number of patients develop in-stent restenosis, which is an entity primarily due to tissue proliferation. Experimental studies have indicated that the renin-angiotensin system is involved in neointimal hyperplasia. Plasma and cellular levels of ACE are associated with an I/D polymorphism in the ACE gene. Indeed, DD subjects have the higher ACE levels. The purpose of this study was to explore the possibility that the I/D polymorphism might be related with in-stent restenosis. METHODS: We studied the ACE polymorphism in 48 consecutive patients who underwent successful implantation of an elective coronary stent in native coronary vessels and had a 6 month angiographic follow up. Restenosis (50% of the reference vessel) was observed in 23/48 patients. Patients with or without restenosis did not differ in demographic or clinical variables like diabetes, plasma cholesterol levels or in quantitative angiographic parameters such as vessel reference size or minimal lumen diameter after stent implantation. RESULTS: I/D polymorphism was distributed as follows: 22.9% of the patients were D/D; 14.5% were I/I and 62.5% of the patients were heterozygous I/D. The presence of restenosis was strongly related with the I/D polymorphism: 81.8% of the patients with D/D genotype had restenosis, compared with 40.0% of I/D patients and only 14.2% of the I/I patients (chi 2 p < 0.01). CONCLUSIONS: In this limited cohort, homocygous D/D of the ACE gene was significantly associated with in-stent restenosis, whereas restenosis was infrequent in patients with the I/I genotype.

Prevalence of the angiotensin I converting enzyme insertion/deletion polymorphism, plasma angiotensin converting enzyme activity, and left ventricular mass in a normotensive Chilean population.

The aim of this study was to estimate the prevalence of the different alleles of the angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and associated plasma ACE activity, as well as cardiac echocardiographic structure, in a healthy Chilean population. We selected 117 healthy normotensive subjects (aged 45 to 60 years, middle socioeconomic status, nonobese, and nondiabetic) from a population-based study concerning the prevalence of risk factors for chronic diseases (Conjunto de Acciones Para la Reducción Multifactorial de las Enfermedades no Transmisibles [CARMEN]). The frequencies of the I and D alleles were 0.57 and 0.43, respectively. Mean plasma ACE activity was 15.3 +/- 3.9 U/mL. Compared with subjects with the II genotype, plasma ACE activity was significantly higher in subjects with the ID and DD genotypes with no difference between them. No correlation was observed between blood pressure and plasma ACE activity. Among the three different genotypes there was no difference in left ventricular (LV) dimensions or in LV mass. No correlation between plasma ACE activity and LV mass was observed for either gender or different genotypes. Multivariate linear regression analysis using LV mass and LV mass index as dependent variables showed independent effects (P < .05) for gender (higher LV mass in men) and diastolic blood pressure, but not for the DD genotype. In conclusion, in this population, the presence of the D allele on the ACE gene determined higher circulating ACE activity. However, in this normotensive healthy population, male gender and diastolic blood pressure, but not the presence of the D allele, were associated with increased LV mass.

Reproducibility of plasma angiotensin-converting enzyme activity in human subjects determined by fluorimetry with Z-phenylalanine-histidyl-leucine as substrate.

Despite the major physiologic role of angiotensin-converting enzyme (ACE), few studies have evaluated the ideal conditions for measuring human plasma ACE activity, specifically when using Z-phenylalanine-histidyl-leucine as substrate. This study, performed in volunteer patients, assessed the reproducibility of human plasma ACE activity measured by fluorimetry with Z-phenyl-histidyl-leucine as the substrate. After blood centrifugation, plasma was stored under different conditions until processing. The following sources of variability were evaluated: (1) the interval to centrifugation of blood after collection, (2) the temperature and (3) safe time for storing the plasma after cold centrifugation, (4) the effect of fasting. Plasma ACE activity was 20.6+/-7.7 U/mL, 20.9+/-8 U/mL, and 20.5+/-7.9 U/mL (n = 25) when samples were centrifuged immediately, after 1 hour of blood sampling, and after 3 hours of blood sampling, respectively (not significant). In plasma kept at -20 degrees C, ACE activity was not different after 1 week (17.4+/-4.3 U/mL) nor after 1 month (17.9+/-4 U/mL), whereas baseline ACE was 16.7+/-4.3 U/mL (n = 10). In plasma stored at -80 degrees C, ACE activity was 15.5+/-5.7 U/mL after 1 month (baseline 15+/-5.3 U/mL; not significant; n = 12). No evidence for hydrolysis of the reaction product of ACE (his-leu dipeptide) was observed in plasma samples kept for 1 month at -20 degrees C or at -80 degrees C (by high-performance liquid chromatography analysis). In plasma obtained before breakfast, ACE activity was 12.8+/-7.1 U/mL, and it was 12.3+/-7.5 U/mL 2 hours afterwards (not significant; n = 12). Thus, to determine human plasma ACE activity by fluorimetry with reliability, with Z-phenylalanine-histidyl-leucine used as a substrate, there is a safe interval of at least 3 hours before blood centrifugation at -4 degrees C. Plasma may be kept at -20 degrees C or at -80 degrees C for at least 4 weeks before final processing. Fasting does not influence its enzymatic activity.

Effects of antihypertensive treatment on cardiac IGF-1 during prevention of ventricular hypertrophy in the rat.

There is some evidence that cardiac rather than circulating insulin-like growth factor-1 (IGF-1) levels contribute to the development of renovascular hypertensive left ventricular hypertrophy (LVH), remaining unknown the effects of antihypertensive drugs on IGF-1 levels. We have assessed here the preventive effects of enalapril, losartan, propanolol and alpha-methyldopa on left ventricle (LV) and circulating IGF-1 levels in a rat model of hypertension and LVH (Goldblatt, GB). Our results show that relative LV mass and the LV content of IGF-1 were significantly lower with all antihypertensive drugs in GB rats (p<0.001). Serum concentrations of IGF-1 were lower in GB rats treated with enalapril, alpha-methyldopa and propanolol (p<0.01), but not in those treated with losartan. These results support the hypothesis that local rather than seric IGF-1 contributes to the development of left ventricular hypertrophy induced by pressure overload in the rat.

[Recommendations for the use of ambulatory blood pressure monitoring. Consensus document of the Chilean Hypertension Society]. / Recomendaciones sobre el uso de la monitorización ambulatoria de presión arterial. Documento de consenso de la Sociedad Chilena de Hipertensión.

Continuous ambulatory blood pressure monitoring is a diagnostic technique devised as a consequence of the great variations in blood pressure measurements. It allows multiple daily measurements, nocturnal monitoring, avoids the stress of blood pressure measurements, gives a picture of pressure behavior during 24 hours and reduces observer related errors. The equipment used must be accurate and validated using international protocols. Accepted indications for continuous ambulatory blood pressure monitoring are white coat hypertension, episodic hypertension, resistance to medications and assessment of symptoms or autonomic dysfunction. Other indications with less clear cut usefulness, are high risk cardiac, renal or pregnant patients and an accurate blood pressure control. We describe equipment calibration, elements that must be considered in the reports, result interpretation and conclusions. Normal blood pressure ranges for children and pregnant women are also reported.

Enalapril restores depressed circulating insulin-like growth factor 1 in patients with chronic heart failure.

BACKGROUND: Congestive heart failure (CHF) is characterized by increased activity of the renin-angiotensin system. Recent experimental studies have shown that infusion of angiotensin II results in depressed plasma levels of insulin-like growth factor 1 (IGF-1) and weight loss. We have previously reported that stable patients with CHF have decreased activity of the growth hormone (GH)-IGF1 axis. We have hypothesized, therefore, that angiotensin-converting enzyme (ACE) inhibition therapy should restore GH-IGF1 activity in CHF patients. METHODS AND RESULTS: Nine patients with stable CHF who were taking digitalis and diuretics, New York Heart Association functional class III were studied before and after 8 weeks of therapy with Enalapril (10 mg twice daily). We measured IGF1 levels, radionuclide left ventricular ejection fraction (EF) and peak oxygen consumption (PVO2). We found that 7 of 9 patients had abnormally low levels of IGF1 (0.2-0.5 mU/ml). IGF1 levels reverted to normal after Enalapril therapy (0.36 +/- 0.03 to 0.8 +/- 0.14 mU/ml, P = .004). This was associated with a significant increase in EF (27.4 +/- 1.1 to 31.4 +/- 0.9%) and PVO2 (14.8 +/- 1.2 to 18.6 +/- 1.5 ml/kg/min) values (P < .05). CONCLUSION: Chronic ACE inhibition therapy restored previously reduced IGF1 plasma levels in patients with CHF, most likely by reducing angiotensin II activity.

Selective increase in cardiac IGF-1 in a rat model of ventricular hypertrophy.

There is evidence that insulin-like growth factor-1 (IGF-1) plays a role in the development of left ventricular hypertrophy, but it is uncertain whether cardiac IGF-1 changes before or after hypertension is established, and whether circulating IGF-1 are involved in cardiac hypertrophy. We have investigated changes in circulating and left ventricular IGF-1 and in the expression of the IGF-1 gene in the left ventricles of rats during the development of hypertensive left ventricular hypertrophy (Goldblatt model; 2 kidney-1 clamped). Our results show that the left ventricular contents of IGF-1 and its mRNA were increased at one and four weeks of hypertension and hypertrophy, and that both returned to control values after nine weeks. These changes were unrelated to the seric concentration of IGF-1 in the blood. These results show that local rather than circulating IGF-1 levels contributed to the development of renovascular hypertensive left ventricular hypertrophy.