Factors associated with the knowledge, treatment, and control of arterial hypertension in an adult population of the community of Valencia

OBJECTIVE: To identify the level of hypertension awareness, treatment and control in the adult population (14 years and older) at the Valencian Region. Type of treatment and associated factors to the hypertension awareness will be also explored. DESIGN: Cross-sectional study (population survey). SETTING: Valencian Region, Spain. PARTICIPANTS AND MEASUREMENTS: Data from this study are based on a representative sample of the adult population collected for the Nutrition and Health Examination Survey carried out in the Valencian Region in 1994. Blood pressure measurement was based in two readings on each person at a single sitting. RESULTS: Awareness of hypertension among subjects classified as hypertensive was 50%. The frequency of treated patients among all those subjects who knew as hypertensive, was 85%. The proportion of well controlled among treated hypertensive people was lightly higher than 50%. 14.6% of people aware of being hypertensive were not under treatment. CONCLUSIONS: The rule of halves still applies to the Valencian Region, though the proportion of diagnosed hypertensive under treatment is much better (> 85%).     

Prevalence of arterial hypertension in Cushing''s syndrome

Subacute cerebral infarcts may appear normal on T2-weighted MRI as an area isointense with surrounding normal tissue. This MRI "fogging effect" has been described in only a few cases. We present a further case of fogging observed during the evolution of a cerebellar infarct.     

Risk factors for myocardial infarct: a case-control study in Oporto, Portugal

A case-control study of coronary heart disease (CHD) was conducted in Oporto, Portugal. The cases series consisted of 100 consecutive patients with first time acute myocardial infarction who were admitted to the Coronary and Intermediate Care Units of a major teaching hospital. The community controls were 198 individuals without evidence of CHD by the Rose questionnaire and electrocardiography, selected by random digit dialing, with a participation rate of 70%. Data was collected by trained interviewers using a structured questionnaire and blood samples were obtained for selected laboratory data. The main analysis was made through unconditional logistic regression with calculations of odds ratios (OR). Age, OR: 1.5 (95% CI: 0.8-2.9), male gender, OR: 6.7 (3.6-12.3), family history of premature CHD, OR: 2.4 (1.4-4.3), diabetes, OR: 3.4 (1.6-7.4), antecedents of hypertension, OR:1.9 (1.1-3.1), history of high cholesterol levels, OR: 2.3 (1.4-3.9), high levels of physical activity, OR: 2.0 (0.9-4.1) and tobacco smoking, OR: 8.3 (3.8-18.5) were significant risk factors of acute myocardial infarction. After controlling for demographic variables and for the mutual confounding effects of the risk factors, the investigated factors that remained significantly associated with the risk of developing acute myocardial infarction were male gender, OR: 17.3 (4.8-62.3), family history of CHD, OR: 3.6 (1.4-9.6), diabetes, OR: 4.2 (1.0-18.1), high cholesterol levels OR: 2.7 (1.2-6.1) and smoking habits, OR: 7.7 (1.8-32.4). A negative association with high education levels was significant after controlling for all the variables, OR: 0.01 (0.01-0.5).     

Angiotensin-converting enzyme inhibitors in the treatment of arterial hypertension

An outbreak of infectious bursal disease (IBD) occurred concurrently with acute septicaemic colibacillosis in 15 week old prelayer hens. The septicaemia was preceded by a subclinical IBD. Mortality in the outbreak began with lesions of septicaemia and Escherichia coli was isolated from the heart blood of the birds. After antibiotic treatment of the bacteraemia, mortality continued, spiked, declined and then ceased. IBD was confirmed by bursal lesions characterized by severe lymphocytolysis and cystic degeneration of the lymphoid follicles. Out of 253 birds, 42 (16.60%) died within eight days. The circumstances of the outbreak suggested that lack of IBD booster vaccination favoured the establishment of subclinical IBD, which suppressed immunity to predispose the birds to colisepticaemia.     

Beta blockers in the treatment of arterial hypertension]

The authors present a detailed review on beta-blockers (BB) in the treatment of hypertension. In the introduction they deal with the organ distribution and effects of stimulation of adrenergic receptors, followed by a detailed classification of beta-blockers by selectivity and the presence of internal sympathetic activity (ISA or PAA). The mechanisms of the antihypertensive action of beta-blockers are due mainly to a reduction of the minute volume. However, other possible effects of BB are also mentioned. The authors discuss in detail the use of BB in hypertension and associated diseases, side-effects of BB, contraindications for their administration, possible interaction with other groups of drugs and the strategy of their use in patients with high blood pressure.     

Endothelin and arterial hypertension

Endothelins (ETs) are peptides of 21 amino acids synthesized and released by variety of cells. Endothelin (now this peptide is called endothelin-1 (ET-1)) was isolated and identified in 1988 by Yanagisawa et al. Following studies revealed two other isoforms of endothelin': Endothelin-2 (ET-2) and endothelin-3 (ET-3). All of them bind to two types of receptors (A and B (ET-A r, ET-Br). ET-A r are responsible for concentration mediating. Two subtypes of ET-B r are known. ET-B1 r mediates vasorelaxation; ET-B2 vasoconstriction. ETs (especially ET-1) have variety of biological actions but the most important are vasoconstrictor and mitogenic action. Through these two mechanism ETs may participate in the pathogenesis and/or in the maintenance of hypertension in both experimental animal models and human essential hypertension. The intravenous infusion of synthetic ET induces a long-lasting elevation of blood pressure in experimental animals and in healthy humans. Number of studies have shown enhanced responses to ET in hypertensive subjects but decreased responses have also been reported. Similarly, plasma levels of ET-1 are either normal or elevated in experimental and human essential hypertension. Numerous investigators have suggested an interaction between ET and angiotensin-converting enzyme inhibitors through the renin-angiotensin system or through the accumulation of endogenous bradykinin. Also calcium antagonists of different classes prevent endothelin-induced contractions. Endothelin- converting enzyme inhibitor (phosphoramidon) and ET-A/B r antagonists (bosentan, BQ-123, FR139317) may have potential role as vasodilators in the treatment of hypertension.     

Microalbuminuria in arterial hypertension

Microalbuminuria is a considerable good indicator of atherogenic disease and cardiovascular risk. In the arterial hypertension, the main centre organ is the kidney. Structural and functional changes that happen in the hypertensive nephropathy are going to cause alterations m the albumin urinary excretion. The authors have done a revision of the main factors which can origin the existence of microalbuminuria in patients with arterial hypertension, and they conclude that this is an useful biochemist indicator in order to evaluate the degree of renal disease in these patients.     

Microalbuminuria, arterial hypertension and the cardiovascular risk

Both the Entamoeba histolytica lectin, a virulence factor for the causative agent of amebiasis, and the mammalian hepatic lectin bind to N-acetylgalactosamine (GalNAc) and galactose (Gal) nonreducing termini on oligosaccharides, with preference for GalNAc. Polyvalent GalNAc-derivatized neoglycoproteins have >1000-fold enhanced binding affinity for both lectins (Adler,P., Wood,S.J., Lee,Y.C., Lee,R.T., Petri,W.A.,Jr. and Schnaar,R.L.,1995, J. Biol. Chem ., 270, 5164-5171). Substructural specificity studies revealed that the 3-OH and 4-OH groups of GalNAc were required for binding to both lectins, whereas only the E.histolytica lectin required the 6-OH group. Whereas GalNAc binds with 4-fold lower affinity to the E.histolytica lectin than to the mammalian hepatic lectin, galactosamine and N-benzoyl galactosamine bind with higher affinity to the E. histolytica lectin. Therefore, a synthetic scheme for converting polyamine carriers to poly-N-acyl galactosamine derivatives (linked through the galactosamine primary amino group) was developed to test whether such ligands would bind the E.histolytica lectin with high specificity and high affinity. Contrary to expectations, polyvalent derivatives including GalN6lys5, GalN4desmosine, GalN4StarburstTMdendrimer, and GalN8StarburstTMdendrimer demonstrated highly enhanced binding to the mammalian hepatic lectin but little or no enhancement of binding to the E.histolytica lectin. We propose that the mammalian hepatic lectin binds with greatest affinity to GalNAc "miniclusters," which mimic branched termini of N-linked oligosaccharides, whereas the E.histolytica lectin binds most effectively to "maxiclusters," which may mimic more widely spaced GalNAc residues on intestinal mucins.     

Diagnosis, course and prognosis of pulmonary arterial hypertension

Pulmonary arterial hypertension (PAHT) is defined by an increase in mean pulmonary artery pressure above 20 mmHg. Its diagnosis is often easy by cardiac echo-Doppler. Hemodynamic investigation is required in non-echogenic patients or in order to define the type of PAHT: pre- or post-capillary. It is important to determine, on the basis of non-invasive clinical and paraclinical (echocardiography) studies, those patients in whom catheterisation is indicated. PAHT may be due to chronic respiratory disease, left heart disorders, congenital heart disease or follow pulmonary embolism. It is sometimes apparently primary. The prognosis of PAHT depends upon its etiology: when PAHT is secondary to heart disease, it reflects worsening of the causative cardiac problem, which must be corrected. PAHT is a prognostic factor in chronic obstructive lung disease. The course is particularly grave in primary PAHT.     

Clinical hemorrheology and arterial hypertension

In order to have a good haemorheological approach to hypertensives, we have put together a review with haemorheological subjects and with the relationships between plasmatic and haematic viscosity and hypertension in relation to pathophysiology, diagnosis, prognosis and treatment. In this review we deal with: (1) Clinical haemorheology. (2) Haematic viscosity. (3) The relationship between haemorheology and hypertension and between antihypertensive drugs and haemorheology. The study of viscosity and erythrocytes deformability, and of erythrocytes and platelets stickiness could pharmacologically correct the haemorheological disorders which can be some of the causes of hypertension.     

Myocardial hypertrophy and arterial hypertension

Myocardial hypertrophy in different cardiac diseases is considered to be an adaptive mechanism to the increase of hemodynamic load which might restore to normal radius/wall thickness ratio and consequently to normalize wall stress. However, it has been widely demonstrated that beside the hemodynamic load, other factors contribute to the development of myocardial hypertrophy. It has been shown that in hypertensive patients, functional abnormalities (increased contribution of atrial systole to total diastolic filling, increased isovolumic relaxation period, prolonged diastolic duration, slowed ventricular filling and altered diastolic distensibility) precede the development of myocardial hypertrophy. Thus, in hypertensive patients, sign and symptoms of heart failure could be manifested in absence of myocardial hypertrophy, and might be exclusively due to diastolic dysfunction (with normal systolic function). Systolic function might be involved and compromised late when focal myocardial cell death and fibrosis occur and consequently ?adequate? hypertrophy is shifted to ?inadequate?. This evolution is accompanied by morphological and functional changes of the myocardium similar to those encountered in dilated cardiomyopathy. Impairment of systolic function in ?inadequate? hypertrophy is also due to structural changes; altered ratio between sarcomers and mitochondria, increased intercapillary distance, sarcoplasmatic reticulum dysfunction, increase of collagene component with a consequent increment of wall rigidity, hypertrophy of arterial tunica media, which alters coronary flow and coronary reserve. The progression of these morpho-functional abnormalities is a very slow process, in which adaptive mechanism mediated by several enzymes and contractile protein, contribute to maintain myocardial viability. However, over the long course, disseminated focal myocardial cell necrosis and fibrosis, which is an evolving process, is considered to be the main responsible factor for the irreversible myocardial damage and systolic dysfunction in advanced myocardial inadequate hypertrophy.