39 resultados para hypertensive crises

em BORIS: Bern Open Repository and Information System - Berna - Suiça


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Background Current knowledge about risk factors promoting hypertensive crisis originates from retrospective data. Therefore, potential risk factors of hypertensive crisis were assessed in a prospective longitudinal study. Methods Eighty-nine patients of the medical outpatient unit at the University Hospital of Bern (Bern, Switzerland) with previously diagnosed hypertension participated in this study. At baseline, 33 potential risk factors were assessed. All patients were followed-up for the outcome of hypertensive crisis. Cox regression models were used to detect relationships between risk factors and hypertensive crisis (defined as acute rise of systolic blood pressure (BP) ≥200mmHg and/or diastolic BP ≥120mmHg). Results The mean duration of follow-up was 1.6 ± 0.3 years (range 1.0–2.4 years). Four patients (4.5%) were lost to follow-up. Thirteen patients (15.3%) experienced hypertensive crisis during follow-up. Several potential risk factors were significantly associated with hypertensive crisis: female sex, higher grades of obesity, the presence of a hypertensive or coronary heart disease, the presence of a somatoform disorder, a higher number of antihypertensive drugs, and nonadherence to medication. As measured by the hazard ratio, nonadherence was the most important factor associated with hypertensive crisis (hazard ratio 5.88, 95% confidence interval 1.59–21.77, P < 0.01). Conclusions This study identified several potential risk factors of hypertensive crisis. Results of this study are consistent with the hypothesis that improvement of medical adherence in antihypertensive therapy would help to prevent hypertensive crises. However, larger studies are needed to assess potential confounding, other risk factors and the possibility of interaction between predictors.

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OBJECTIVE: To determine the prevalence and independent predictors of significant atherosclerotic renal artery stenosis (RAS) in unselected hypertensive patients undergoing coronary angiography and to assess the 6-month outcome of those patients with a significant RAS. METHODS: One thousand, four hundred and three consecutive hypertensive patients undergoing drive-by renal arteriography were analyzed retrospectively. Univariate and multivariate logistic regression analyses were performed to identify independent predictors of RAS. In patients with significant RAS (>or=50% luminal narrowing), 6-month follow-up was assessed and outcome was compared between patients with or without renal revascularization. RESULTS: The prevalence of significant RAS was 8%. After multivariate analysis, coronary [odds ratio 5.3; 95% confidence interval (CI) 2.7-10.3; P < 0.0001], peripheral (odds ratio 3.3; 95% CI 2.0-5.5; P < 0.0001), and cerebral artery (odds ratio 2.8; 95% CI 1.5-5.3; P = 0.001) diseases, and impaired renal function (odds ratio 2.9; 95% CI 1.8-4.5; P < 0.0001) were found as independent predictors. At least one of these predictors was present in 96% of patients with RAS. In 74 patients (66%) with significant RAS, an ad hoc revascularization was performed. At follow-up, creatinine clearance was significantly higher in revascularized than in nonrevascularized patients (69.2 vs. 55.5 ml/min per 1.73 m, P = 0.029). By contrast, blood pressure was comparable between both groups, but nonrevascularized patients were taking significantly more antihypertensive drugs as compared with baseline (2.7 vs. 2.1, follow-up vs. baseline; P = 0.0066). CONCLUSION: The prevalence of atherosclerotic RAS in unselected hypertensive patients undergoing coronary angiography was low. Coronary, peripheral, and cerebral artery diseases, and impaired renal function were independent predictors of RAS. Ad hoc renal revascularization was associated with better renal function and fewer intake of antihypertensive drugs at follow-up.

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Amyloid precursor protein (APP) and amyloid-beta (Abeta) appear to participate in the pathophysiology of retinal ganglion cell (RGC) death in glaucoma. We, therefore, determined the distribution of APP and Abeta in the retinas of C57BL/6 mice after induction of chronic ocular hypertension.

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Potassium-enriched diets exert renal and cardiovascular protective effects, but the underlying mechanisms are largely unknown.

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Esophageal motility abnormalities include a series of manometric findings that differ to a significant degree from findings in normal, asymptomatic volunteers.

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AIMS: The adaptation of the myocardial microcirculation in humans to pathologic and physiologic stress has not been examined in vivo so far. We sought to test whether the relative blood volume (rBV) measured by myocardial contrast echocardiography (MCE) can differentiate between left ventricular (LV) hypertrophy (LVH) in hypertensive heart disease and athlete's heart. METHODS AND RESULTS: Four groups were investigated: hypertensive patients with LVH (n = 15), semi-professional triathletes with LVH (n = 15), professional football players (n = 15), and sedentary control individuals without cardiovascular disease (n = 15). MCE was performed at rest and during adenosine-induced hyperaemia. The rBV (mL mL(-1)), its exchange frequency (beta, min(-1)), and myocardial blood flow (mL min(-1) g(-1)) were derived from steady state and refill sequences of ultrasound contrast agent. Hypertensive patients had lower rBV (0.093 +/- 0.013 mL mL(-1)) than triathletes (0.141 +/- 0.012 mL mL(-1), P < 0.001), football players (0.129 +/- 0.014 mL mL(-1), P < 0.001), and sedentary individuals (0.126 +/- 0.018 mL mL(-1), P < 0.001). Conversely, the exchange frequency (beta) was significantly higher in hypertensive patients (11.3 +/- 3.8 min(-1)) than in triathletes (7.4 +/- 1.8 min(-1)), football players (7.7 +/- 2.3 min(-1)), and sedentary individuals (9.0+/-2.5 min(-1)). An rBV below 0.114 mL mL(-1) distinguished hypertensive patients and triathletes with a sensitivity of 93% and a specificity of 100%. CONCLUSION: Pathologic and physiologic LVH were differentiated non-invasively and accurately by rBV, a measure of vascularisation assessed by MCE.

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The presence of irreversible pulmonary hypertension in patients with atrial septal defect (ASD) is thought to preclude shunt closure. We report the case of a woman with plexiform pulmonary arteriopathy secondary to an ostium secundum ASD who was able to successfully undergo percutaneous shunt closure following therapy with chronic intravenous prostacyclin (Flolan). One year after closure, the patient was weaned off Flolan over a period of 7 months following the institution of oral Bosentan therapy. Our case illustrates how aggressive vasodilator therapy with prostaglandins may be capable of reducing pulmonary artery pressure and permitting shunt closure in a patient once considered to have "inoperable" pulmonary arteriopathy.

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Approximate entropy (ApEn) of blood pressure (BP) can be easily measured based on software analysing 24-h ambulatory BP monitoring (ABPM), but the clinical value of this measure is unknown. In a prospective study we investigated whether ApEn of BP predicts, in addition to average and variability of BP, the risk of hypertensive crisis. In 57 patients with known hypertension we measured ApEn, average and variability of systolic and diastolic BP based on 24-h ABPM. Eight of these fifty-seven patients developed hypertensive crisis during follow-up (mean follow-up duration 726 days). In bivariate regression analysis, ApEn of systolic BP (P<0.01), average of systolic BP (P=0.02) and average of diastolic BP (P=0.03) were significant predictors of hypertensive crisis. The incidence rate ratio of hypertensive crisis was 14.0 (95% confidence interval (CI) 1.8, 631.5; P<0.01) for high ApEn of systolic BP as compared to low values. In multivariable regression analysis, ApEn of systolic (P=0.01) and average of diastolic BP (P<0.01) were independent predictors of hypertensive crisis. A combination of these two measures had a positive predictive value of 75%, and a negative predictive value of 91%, respectively. ApEn, combined with other measures of 24-h ABPM, is a potentially powerful predictor of hypertensive crisis. If confirmed in independent samples, these findings have major clinical implications since measures predicting the risk of hypertensive crisis define patients requiring intensive follow-up and intensified therapy.

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AIMS: In pressure overload left ventricular (LV) hypertrophy, gender-related differences in global LV systolic function have been previously reported. The goal of this study was to determine regional systolic function of the left ventricle in male and female patients with hypertensive heart disease. METHODS AND RESULTS: Regional LV function was analyzed from multiplane transesophageal echocardiography with three-dimensional (3D) reconstruction of the left ventricle. In 24 patients (13 males and 11 females), four parallel (2 basal and 2 apical) equidistant short axis cross-sections from base to apex were obtained from the reconstructed LV. In each short axis 24 wall-thickness measurements were carried out at 15 degrees intervals at end-diastole and end-systole. Thus, a total of 192 measurements were obtained in each patient. Wall thickening was calculated as difference of end-diastolic and end-systolic wall thickness, and fractional thickening as thickening divided by end-diastolic thickness. Fractional thickening and wall stress were inversely related to end-diastolic wall thickness in both, males and females. Females showed less LV systolic function when compared to males (p<0.001). However, when corrected for wall stress, which was higher in females, there was no gender difference in systolic function. CONCLUSION: There are regional differences in LV systolic function in females and males which are directly related to differences in wall stress. Thus, gender-related differences in LV regional function are load-dependent and not due to structural differences.

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Pituitary apoplexy, diabetes insipidus, thyroid storm, myxedema coma, parathyrotoxic crisis, hypocalcemia tetany, pheochromocytoma and Addison crisis, diabetic ketoacidosis, diabetic hyperosmolar nonketotic coma, hypoglycemia and carcinoid crisis are the most important endocrine crises. Some of them are common, others very rare. All physicians nevertheless need to have at least a basic knowledge of all of them, since symptoms and signs of endocrine crises overlap with those of other severe disease states, and the failure to recognise endocrine crises as such and to begin rapidly the specific therapy can have fatal consequences.