Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment of severe hypertension is beneficial, but reversibility of target-organ damage has not been characterized. Serial studies were performed in 15 patients with severe essential hypertension (age of 56 +/- 3 years, mean +/- SEM) treated for 1 year with 60 to 150 mg/day of continuous-release nifedipine; 3 patients required 50 mg of chlorthalidone/day to lower diastolic blood pressure (BP) to less than 95 mm Hg. Left ventricular (LV) structure and function was evaluated with two-dimensional-directed M-mode echocardiography, digitized from videotape and analyzed blindly. BP was markedly reduced from 194 +/- 8/115 +/- 4 to 146 +/- 4/88 +/- 14 mm Hg (p less than 0.0001) and maintained at this level for 1 year. Posterior wall and septal LV thickness, elevated at entry (12.9 +/- 0.1 and 13.4 +/- 0.1 mm), dropped steadily over 1 year into the normal range (10.0 +/- 0.03 and 11.2 +/- 0.1 mm, p less than 0.001). LV mass index, above 95% for normals at entry, decreased by 19% at 6 months (129 +/- 10 to 104 +/- 7 g/m2, p less than 0.01), and remained at this level at 1 year. LV fractional shortening rose steadily over 1 year from 34 to 42% (p less than 0.02). Atrial natriuretic peptide, which reflects LV filling pressures, was markedly elevated at entry, but was significantly reduced by 6 months (76 +/- 22 vs. 45 +/- 14 pg/ml, p less than 0.05). Sustained reduction of arterial BP with continuous-release nifedipine for 1 year normalizes LV mass, improves LV systolic function, and reduces circulating levels of atrial natriuretic peptide.
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PMID:Effect of nifedipine GITS on left ventricular mass and diastolic function in severe hypertension. 171 75

Several factors have been implicated in the pathogenesis of myocardial hypertrophy, and the role of sodium has recently been suggested. In the present study, we assessed the influence of dietary sodium on the degree of left ventricular hypertrophy (LVH) and LV structure in 30 normotensive (NT) subjects aged 34 +/- 11 years (mean +/- SD) and 50 patients (39 +/- 10 years) with mild essential hypertension EH (canal blood pressure 154 +/- 16/96 +/- 11 mmHg), who had never received antihypertensive drugs. Posterior wall thickness (PWT) and left ventricular mass (LVM) were measured by M-mode echocardiography and urinary sodium excretion (UNa, mmol/24h) was taken as an index of sodium intake. In NT and EH, LVM was directly correlated with UNa (r = 0.48 and 0.49; p less than 0.006 and 0.002, respectively). A stepwise multiple regression analysis confirmed that UNa was a determinant of LVM independently of sex, age, and body weight in the two groups. In NT the correlation with UNaV was the result of an increase of the end-diastolic diameter without change in PWT whilst in EH it was the consequence of an increase in wall thickness (R = 0.49, p less than 0.0001) without a modification of LV diameter. These results suggest that salt intake may be an important determinant of cardiac structural adaptation in both NT and EH subjects; however, only EH have a salt sensitive LV wall hypertrophy.
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PMID:[Myocardial morphological changes related to sodium intake in normotensive and hypertensive patients never treated before]. 212 12

Many factors have been implicated in the pathogenesis of myocardial hypertrophy, and the role of sodium has recently been suggested. In the present study, we assessed the influence of dietary sodium on the degree of left ventricular hypertrophy (LVH) in 41 patients aged 38 +/- 10 (mean +/- SD) with mild essential hypertension (casual blood pressure 149 +/- 17/91 +/- 11 mmHg). Patients had never been given antihypertensive drugs before and ingested ad libitum sodium intake. Posterior wall thickness (PWT) and left ventricular mass (LVM) were measured by M-mode echocardiography and sodium intake was estimated from urinary sodium excretion rate (UNa, mmol/24h). Both PWT and LVM, and not telediastolic diameter or LV fractional shortening, were directly correlated with UNa (r = 0.47 and 0.46; p less than 0.02 and 0.002, respectively. A stepwise multiple regression analysis confirmed that UNa was a determinant of LVM independently of sex, age, body weight, blood pressure and duration of hypertension. No correlation was found between LVM and plasma renin activity, whilst a positive one existed between PWT and hematocrit (r = 0.42; p less than 0.007). These results suggest that dietary sodium may play a role in modulating left ventricular mass in untreated hypertensives, possibly in expanding volume or activating the adrenergic system.
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PMID:[Determinants of left ventricular hypertrophy in hypertensive subjects that have never been treated: role of the sodium intake]. 253 Sep 47

Among the many factors that have been implicated in the pathogenesis of myocardial hypertrophy is a sodium effect. In the present study, the influence of dietary sodium, estimated by 24-h natriuresis, on left ventricular mass was assessed in 41 patients with mild essential hypertension who had never been treated. Posterior wall thickness and left ventricular mass, but not left ventricular internal diameter were directly correlated with 24-h natriuresis (r = 0.47 and 0.46; P less than 0.02 and 0.002, respectively). Stepwise multiple regression analysis confirmed that 24-h natriuresis was a determinant of left ventricular mass independently of sex, age, body weight, blood pressure and the duration of hypertension. These results suggest that dietary sodium may play a role in modulating left ventricular mass in untreated hypertensives.
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PMID:Influence of sodium intake on left ventricular structure in untreated essential hypertensives. 253 13

Regression of left ventricular hypertrophy occurs with a number of antihypertensive drugs, but the time course of this regression has not been defined clearly. We obtained echocardiograms at baseline and serially (on seven occasions) during a 1 year treatment period with the beta-adrenergic receptor inhibitor atenolol in 12 patients with previously untreated essential hypertension. To ensure control of blood pressure in all patients throughout the study, it was necessary to add a thiazide diuretic to the therapy of five patients. Baseline blood pressure was 155/100 mm Hg and fell to 136/84 mm Hg; there was a 20% reduction in heart rate. Posterior and septal wall thicknesses were reduced from 1.16 +/- 0.03 to 1.06 +/- 0.02 cm (p less than .05) and from 1.28 +/- 0.07 to 1.18 +/- 0.06 cm (p less than .05), respectively; this reduction became significant initially at 4 weeks. Left ventricular mass decreased from 144 +/- 9 to 127 +/- 7 g/m2 (p less than .05) and this fall first became statistically significant at 6 months. Significant reduction in electrocardiographic voltages was also seen at 6 months. Therefore, regression of left ventricular hypertrophy with atenolol-induced blood pressure control occurred as early as 4 weeks after starting therapy and was maintained thereafter without apparent compromise of left ventricular systolic function.
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PMID:Time course of regression of left ventricular hypertrophy in hypertensive patients treated with atenolol. 295 54

36 patients with previously untreated essential hypertension and left ventricular hypertrophy were treated with a fixed dose combination of atenolol 50 mg and sustained release nifedipine 20 mg once daily for a mean period of 12.1 months. Echocardiography showed a significant decrease after a mean period of 7.9 months in interventricular septal thickness (13.6%, p less than 0.01), posterior wall thickness (12.6%, p less than 0.001) and left ventricular mass index (18.3%). After 12.1 months the reductions were 20.7% (p less than 0.001), 22.5% (p less than 0.001) and 30.8% (p less than 0.001), respectively. Posterior wall thickness was significantly reduced, but left ventricular end-systolic and end-diastolic dimensions and fractional shortening remained unchanged. Treatment significantly reduced resting blood pressure from 153/105 mm Hg to 122/79 mm Hg (p less than 0.001), and exercise blood pressure at 100W from 189/109 to 157/93 mm Hg (p less than 0.001). Thus, nifedipine in combination with atenolol produces significant blood pressure reduction accompanied by regression of left ventricular hypertrophy without noticeable changes in left ventricular function.
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PMID:Regression of left ventricular hypertrophy during combined atenolol and nifedipine treatment. 296 52

To determine the impact of the renin-angiotensin-aldosterone system on left ventricular function and structure, 36 untreated patients with essential hypertension (WHO class I and II) were examined. Posterior wall thickness, relative wall thickness, and left ventricular mass were determined by M-mode echocardiography. Plasma renin activity, aldosterone, angiotensin I, and angiotensin II levels were measured by radioimmunoassay. Plasma renin activity was related to 24-hour urinary sodium excretion. Of all the endocrine parameters, only the angiotensin II level correlated with posterior wall thickness (r = 0.50, p less than 0.05) and relative wall thickness (r = 0.46, p less than 0.05). This relationship was confirmed by stepwise multiple regression analysis taking arterial pressure, obesity, and sodium excretion into account (p less than 0.05). Plasma renin activity but not the angiotensin II level correlated positively with the ejection fraction (r = 0.42, p less than 0.05) and velocity of circumferential fiber shortening (r = 0.57, p less than 0.01). Thus, angiotensin II emerged as a determinant of left ventricular structural adaptation in essential hypertension.
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PMID:Does the renin-angiotensin-aldosterone system modify cardiac structure and function in essential hypertension? 297 63

M-mode echocardiography was used in 12 patients with essential hypertension to study changes in cardiac anatomy during long-term therapy with hydrochlorothiazide (50 to 100 mg) and alpha-methyldopa (500 to 1,750 mg). Echocardiographic examination was performed after six weeks of treatment with hydrochlorothiazide alone and after four to six weeks, six months, and nine months of treatment with both hydrochlorothiazide and alpha-methyldopa. Hydrochlorothiazide alone induced a small, and not significant, change in blood pressure (from 157 +/- 16 (SD)/105 +/- 9 to 150 +/- 14/101 +/- 5 mm Hg). Changes in echocardiographic parameters of cardiac anatomy were not observed during short-term diuretic therapy. Addition of alpha-methyldopa further reduced blood pressure (to 133 +/- 11/90 +/- 6 mm Hg, p less than 0.001), which was maintained throughout the study. Gradual decreases in diastolic septal thickness (from 10.9 +/- 1.1 to 9.5 +/- 1.0 mm, p less than 0.01), relative wall thickness (from 0.40 +/- 0.06 to 0.36 +/- 0.06, p less than 0.05) and left ventricular cross-sectional area (from 18.9 +/- 2.9 to 17.3 +/- 2.6 cm2, p less than 0.05) were observed. Posterior wall thickness did not change significantly during the study. The results provide evidence for regression of echocardiographic parameters of cardiac muscle mass during long-term antihypertensive treatment with a diuretic and a centrally-acting sympatholytic drug. Regression of left ventricular mass was not clearly related to changes in casual blood pressure. However, patients who showed a decrease in septal thickness tended to have a greater decrease in systolic blood pressure than those in whom septal thickness did not change during therapy. Moreover, patients in whom a decrease in left ventricular transverse dimension was observed, had a greater decrease in both systolic and diastolic blood pressure than those in whom left ventricular diastolic dimension did not change.
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PMID:Effect of long-term antihypertensive therapy on cardiac anatomy in patients with essential hypertension. 622 88

AT1 receptor antagonists control blood pressure (BP) effectively and reduce left ventricular hypertrophy in patients with essential hypertension. Because left ventricular hypertrophy is very common in renal transplant recipients, we examined the cardiovascular effects and the safety profile of the AT1 receptor antagonist losartan in hypertensive renal transplant recipients. In 20 renal transplant recipients with stable renal graft function 50 mg of losartan was added to the preexisting antihypertensive treatment (no angiotensin-converting enzyme inhibitors) at least 6 months after renal transplantation. Twenty-four-hour ambulatory BP, two-dimensional-guided M-mode echocardiography, and duplex sonography, as well as renal function, red blood cell count, cyclosporine A and FK 506 levels, erythropoetin, and angiotensin II concentration were determined at baseline and after 6 months of therapy. With 24-h ambulatory BP measurement, systolic blood pressure (SBP) was reduced by 7.5 +/- 2.4 mm Hg and diastolic blood pressure (DBP) by 4.5 +/- 1.8 mm Hg (P < .01 and P < .05, respectively). Posterior, septal, and relative wall thickness decreased by 0.95 +/- 0.2 mm, 0.91 +/- 0.2 mm and 0.04 +/- 0.01 mm, respectively (all P < .001). Left ventricular mass index decreased by 18.1 +/- 4.7 g/m2 (P < .01). Ejection fraction and midwall fractional fiber shortening as systolic parameters and the relation of passive-to-active diastolic filling of the left ventricle were unaltered. Serum creatinine and cyclosporine A concentration remained stable in all patients. Hemoglobin and hematocrit decreased by 1.0 +/- 0.3 g/dL and 3.6% +/- 0.9%, respectively (P < .002 and P < .001) without a change in serum erythropoetin level. In renal transplant recipients the AT1 receptor antagonist losartan reduces left ventricular hypertrophy without altering systolic or diastolic function. It is safe with regard to renal function and immunosuppression, but slightly decreases hemoglobin level.
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PMID:Regression of left ventricular hypertrophy by AT1 receptor blockade in renal transplant recipients. 1113 Jul 74

Posterior reversible encephalopathy syndrome (PRES) has a distinctive clinical presentation and typical neuroimaging findings. However, data on its clinical course and recurrence are scarce. This study aims to investigate its clinical profile and factors that predict recurrence. We included patients diagnosed with PRES between 2005 and 2010 and collected data on demographics, presenting symptoms, co-morbidities, risk factors, clinical parameters, MRI findings, complications and recurrence. Patients were categorized into two groups: PRES due to primary hypertension and PRES due to secondary causes. Correlation with presenting symptoms, radiological features, and recurrence were analyzed. PRES was identified in 28 patients. Fourteen (50%) had primary hypertension. Secondary causes included immunosuppression-related (39%), preeclampsia/eclampsia (7%), and marijuana-intake-related (4%) causes. Patients presented with altered mental status (79%), headache (75%), seizure (68%), visual disturbance (39%) and hemiparesis (21%). On MRI 93% had the typical parietal-occipital involvement. The frontal lobe was affected in 64%, cerebellum in 29%, brainstem in 21%, and basal ganglia in 11%. About 36% had cortical involvement; 21% had diffusion-restricted lesions. Non-aneurysmal subarachnoid haemorrhage was found in 18% of patients and intracerebral hemorrhage in 14% of patients. No significant difference existed in presenting symptoms and the MRI distribution of vasogenic edema between the primary hypertension group and the secondary causes group. Recurrence occurred in four patients (14.3%, 95% confidence interval 4.2-33.7) and was significantly associated (p=0.05) with primary hypertension as the etiology. Intensive monitoring and treatment of hypertension is recommended for reducing morbidity.
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PMID:Is hypertension predictive of clinical recurrence in posterior reversible encephalopathy syndrome? 2321 27


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