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)

BACKGROUND AND METHODS. To determine the effects of hypertension on brain function, positron emission tomography (PET) studies using (18F)-2-fluoro-2-deoxy-D-glucose (FDG) were performed on a group of 17 otherwise healthy older hypertensive men (mean age +/- SD = 69 +/- 8 yr) and 25 age- and gender-matched controls. Subjects had medically treated essential hypertension for a minimum of 10 years (range = 10 to 24 yr) with no evidence of end-organ impairment from hypertension by routine clinical screening and by history. All hypertensive and control subjects were determined to be cognitively normal by extensive neuropsychological testing. The hypertensive subjects previously had been reported to have lateral ventricle enlargement and left hemisphere brain atrophy by quantitative MRI. PET data were analyzed using t-tests to look at group differences.
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PMID:Brain metabolic function in older men with chronic essential hypertension. 774

We have compared prospectively the sensitivity, specificity and accuracy of CT and MRI in a series of 27 consecutive patients (age 23-76 yrs, 17 females, 10 males) with clinically suspected primary aldosteronism. We found 13 patients with a unilateral aldosterone-producing adenoma (11 on the left and 2 on the right side), 6 with idiopathic hyper-aldosteronism and 8 with primary hypertension, which in two cases was associated with a nonfunctioning adrenal adenoma. The diagnosis of aldosterone-producing adenoma was confirmed at surgery and pathology in all cases. Idiopathic hyper-aldosteronism was diagnosed on the basis of the results of dexamethasone-suppressed adrenal scintigraphy and/or selective adrenal vein sampling. MRI correctly identified all cases of aldosterone-producing adenoma, but gave false positive results in five cases: one had idiopathic hyper-aldosteronism with bilateral nodular hyperplasia and four primary hypertension, which in two patients was associated with a nonfunctioning adrenal adenoma. Therefore, the sensitivity of MRI was 100%, its specificity 64% and overall diagnostic accuracy 81%. In comparison, CT correctly recognized only eight of the 13 patients with aldosterone-producing adenoma and gave false positive results in three primary hypertensives, including the two patients with a nonfunctioning adrenal adenoma. Therefore, its sensitivity, specificity and accuracy were 62, 77 and 69%, respectively. Based on these results, it could be anticipated that about four of every ten patients with aldosterone-producing adenoma would not be correctly diagnosed by CT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Imaging of aldosterone-secreting adenomas: a prospective comparison of computed tomography and magnetic resonance imaging in 27 patients with suspected primary aldosteronism. 841 Sep 26

Neurovascular compression (NVC) of the left ventrolateral medulla (VLM) has been implicated as a cause of essential hypertension. We investigated whether high-resolution MRI of the posterior cranial fossa could identify patients with essential hypertension who may benefit from surgery. A retrospective analysis of imaging and clinical records from 162 patients was performed. There were 38 patients with essential hypertension and 124 who were normotensive. Contact or compression of the VLM was present in 42.1 % (16/38) of the hypertensive group on the left and 47.3 % (18/38) on the right. In the normotensive group it was seen in 32.2 % (40/124) on the left and 26.6 % (33/124) on the right. There was no significant difference between the hypertensive and control groups with regard to contact or compression of the left VLM. The results support the contention that neurovascular compression (NVC) of the left or right VLM is a common finding on MRI in normotensive individuals. We therefore believe that high-resolution MRI cannot be used as a screening tool to identify patients who may benefit from surgery.
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PMID:The role of MRI in screening for neurogenic hypertension. 1066 83

-Neurovascular contact of the left rostral ventrolateral medulla has been implicated in the pathogenesis of "essential" hypertension, and recent intervention studies suggest that surgical decompression of the ventrolateral medulla lowers blood pressure in these patients. We assessed the prevalence of this vascular anomaly in patients with essential hypertension by using an advanced MRI technique. We performed MRI of the brain stem in 125 hypertensive patients and in 105 age-matched, sex-matched, and body mass index-matched normotensive control subjects. Imaging of the root-entry zone of cranial nerves IX and X was performed by combining a high-resolution 3D constructive interference in steady-state sequence with a flow-sensitive time-of-flight technique, and images were independently assessed by 4 readers using predefined criteria. Left-sided neurovascular contact was found in 23% of the hypertensive patients and in 16% of the normotensive individuals (P:=0.12). Blood pressure level, heart rate, and number of antihypertensive medications in treated hypertensive patients were similar among patients with positive, borderline, and negative brain stem findings. Our findings cast doubt on the importance of left-sided neurovascular contact as a frequent cause of essential hypertension or as a major factor determining the severity of hypertension in patients with this anomaly.
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PMID:Neurovascular Contact of Cranial Nerve IX and X Root-Entry Zone in Hypertensive Patients. 1120 74

Primary aldosteronism (PA) is a disorder typically characterized by resistant hypertension, hypokalemia, alkalosis and suppressed plasma renin activity, and excessive aldosterone production. A true estimate of the prevalence of the disorder is difficult to estimate because its detection is dependent on the awareness of the healthcare provider to the disorder, but it has generally been felt to be a rare occurrence. Its frequency of detection began to change when Hiramatsu suggested calculating the ratio of plasma aldosterone/plasma renin activity as a screening tool for the disorder. He found a ratio greater than 75 as a sensitive indicator for aldosterone-producing adenomas. Using the ratio, several investigators have found prevalence ranging from 3 to 9%. Two major classifications of PA exist: aldosterone-producing adrenal adenoma (APA) and zona glomerulosa hyperplasia (IHA). Distinguishing between these 2 entities is important clinically, because removal of a unilateral aldosterone-producing adenoma may result in correction of elevated blood pressure and hypokalemia. Thus, when evaluating hypertensive patients, PA should be suspected in those with moderate to severe hypertension or with hypertension refractory to standard treatment or in hypertensive patients with disease onset at an early age. The aldosterone-to-renin ratio is an easy, inexpensive, and rapid means of screening for the disorder. The ratio is the screening test of choice, but further confirmatory testing is required to clinch the diagnosis. Frequently employed confirmatory tests include urinary aldosterone excretion on a high-salt diet, aldosterone suppression after a saline infusion, and the fludrocortisone suppression test, which is considered the most sensitive confirmatory maneuver. Both high-resolution CT and MRI scans appear to have similar ability to differentiate between APA and IHA. As with essential hypertension, the goal of treatment is to prevent the long-term sequela of hypertension. The underlying pathology resulting in PA dictates the treatment strategy. The drug of choice is spironolactone. Surgical intervention should be entertained in those patients with PA in whom imaging studies suggest an adenoma.
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PMID:Hyperaldosteronism: the internist's hypertensive disease. 1238 96

The most common causes of the heart failure syndrome are coronary heart disease, dilated cardiomyopathy, secondary decompensated hypertension and cardiac defects. Apart from the establishment of the diagnosis, essential diagnostic aims are the clarification of the etiology, the identification of reversible causes, the clarification of specific therapeutic options, assessment of severity and evaluation of the prognosis. A standardized diagnostic work-up based on current consensus recommendations, makes good sense. Symptoms and clinical findings have limited sensitivity and specificity. The leading diagnostic procedure is (Doppler) echocardiography. In the case of ischemic cardiomyopathy, the angiographic coronary status and myocardial vitality evaluation are necessary to clarify the revascularisation option. Further diagnostic examinations (invasive hemodynamics, myocardial biopsy, CT/MRI, ergospirometry, markers of neurohormonal activation) should be carried out as dictated by the individual situation. In patients with an increased risk of developing heart failure (e.g. post-myocardial infarction status, essential hypertension, diabetes mellitus) the aim should be the early detection of an asymptomatic ventricular dysfunction by means of echocardiography.
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PMID:[Diagnostic procedures in chronic heart failure. What is necessary, significant, contraindicated?]. 1253 41

We have observed dot-like low intensity spots (a dot-like hemosiderin spot: dotHS) on T2*-weighted (T2*-w) MRI, subsequently diagnosed histologically as previous microbleeds associated with lipohyalinosis, amyloid angiopathy and cerebral small vessel disease (SVD) including an intracerebral hematoma (ICH) and a lacunar infarction. According to the literature, primary aldosteronism (PA), characterized by hypertension, is related to SVD. A 49-year-old female with a long history of untreated hypertension secondary to PA was admitted to our hospital for medical examinations on July 18th, 2000. She had the stepwise development of dementia, dysarthria and gait disturbance (right hemiparesis). CT and MRI demonstrated multiple lacunar infarctions. She was readmitted to our hospital on Jan 23rd, 2002. A neurological examination revealed right hemiparesis, dysarthria and consciousness disturbance. CT on admission demonstrated ICH in the left midbrain. Six days after the hemorrhage, T2*-w MRI showed thirty-two dotHSs in the basal ganglias and the cortical-subcortical regions. The incidence of ICH in patients with hypertension secondary to PA is reported to be higher than in patients with essential hypertension. Multiple dotHS may be associated with ICH, lacunar infarction, and severe microangiopathy related to hypertension secondary to PA.
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PMID:[Multiple intracerebral microhemorrhages associated with primary aldosteronism: a case report]. 1465 95

The Telmisartan Effectiveness on Left ventricular MAss Reduction (TELMAR) trial will assess the effect of the angiotensin II (Ang II) receptor blocker, telmisartan, on left ventricular hypertrophy (LVH) compared with the b-blocker, metoprolol, at similar antihypertensive doses. The rationale is that antihypertensives reduce LVH, a cardiac adaptation to pressure overload, principally by pressure-related effects. Ang II plays a key role in pressure-independent mechanisms causing LVH, and angiotensin-converting enzyme (ACE) inhibitors induce more pronounced LVH regression than some other antihypertensives. Blocking Ang II Type 1 receptors may be more effective than ACE inhibition in reducing LVH. TELMAR is a prospective, randomised, double-blind, double-dummy, parallel-group trial. A total of 140 patients (age 18 80 years) with uncontrolled essential hypertension (mean daytime systolic blood pressure [SBP] >140 mmHg or diastolic blood pressure [DBP] >90 mmHg and/or night-time SBP >120 mmHg or DBP >70 mmHg, measured by ambulatory blood pressure monitoring [ABPM]) and left ventricular mass index related to height (LVMI) >0.8 g/cm for females, >1.1 g/cm for males (defined by magnetic resonance imaging [MRI]) will be randomised to once-daily telmisartan or metoprolol. The telmisartan dose will be 40 mg for the first two weeks, 80 mg for 5.5 months and 40 mg for the last two weeks. Metoprolol will be given at a dose of 47.5 mg for two weeks, 95 mg for 5.5 months and 47.5 mg for two weeks. Concomitant add-on medication with hydrochlorothiazide and amlodipine will be allowed. The primary endpoint is the percentage change in LVMI at treatment end versus baseline, using MRI. Secondary variables include blood pressure changes and response rates assessed by ABPM and manual cuff sphygmomanometry, and end-systolic wall stress, systolic left ventricular function (LVF) and diastolic LVF determined by MRI. A separate study was performed prior to the main trial to define the normal range of MRI data in an age-matched population.
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PMID:Reduction (TELMAR) as assessed by magnetic resonance imaging in patients with mild-to-moderate hypertension--a prospective, randomised, double-blind comparison of telmisartan with metoprolol over a period of six months rationale and study design. 1468 71

Ischemic damage to the subcortical white matter of the brain, referred to as leukoaraiosis, is a frequent complication of hypertension-related microvascular disease and contributes to the risk of stroke and vascular dementia. A large genetic contribution to this late-life form of target organ damage was suggested by a study of elderly male twins. As part of the Genetic Epidemiology Network of Arteriopathy (GENOA), 483 non-Hispanic white subjects were recruited to undergo MRI for determination of the brain volume of leukoaraiosis (291 women and 192 men from 210 sibships providing 434 sibling pairs; mean age+/-SD=65.2+/-7.3 years). The GENOA-Rochester sibships contain 2 or more siblings with essential hypertension diagnosed before age 60. The frequency distribution of the volume of leukoaraiosis was positively skewed, with a median value of 6.61 cm3 (interquartile range: 4.77 to 9 0.83 cm3). Variance component models were used to estimate the heritability (ie, the proportion of phenotypic variation caused by additive genetic factors). After logarithm transformation of the volume of leukoaraiosis, the estimated heritability (+/-SE) was 0.802+/-0.102 (P<0.0001). Adjustments for sex, age, systolic blood pressure, and brain volume reduced the heritability estimate to 0.671+/-0.110 (P<0.0001). This evidence of strong genetic influence on the susceptibility to leukoaraiosis justifies efforts to localize the responsible genes and characterize the predisposing genetic polymorphisms.
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PMID:Heritability of leukoaraiosis in hypertensive sibships. 1471 59

Preferential visceral adipose tissue (VAT) deposition has been associated with the presence of insulin resistance in obese and diabetic subjects. The independent association of VAT accumulation with hypertension and its impact on insulin sensitivity and beta-cell function have not been assessed. We measured VAT and subcutaneous fat depots by multiscan MRI in 13 nondiabetic men with newly detected, untreated essential hypertension (blood pressure=151+/-2/94+/-2 mm Hg, age=47+/-2 years, body mass index [BMI]=28.4+/-0.7 kg x m(-2)) and 26 age-matched and BMI-matched normotensive men (blood pressure=123+/-1/69+/-2 mm Hg). Insulin secretion was measured by deconvolution of C-peptide data obtained during an oral glucose tolerance test, and dynamic indices of beta-cell function were calculated by mathematical modeling. For a similar fat mass in the scanned abdominal region (4.8+/-0.3 versus 3.9+/-0.3 kg, hypertensive subjects versus controls, P=0.06), hypertensive subjects had 60% more VAT than controls (1.6+/-0.2 versus 1.0+/-0.1 kg, P=0.003). Intrathoracic fat also was expanded in patients versus controls (45+/-5 versus 28+/-3 cm2, P=0.005). Insulin sensitivity was reduced (10.7+/-0.7 versus 12.9+/-0.4 mL x min(-1) x kg(ffm)(-1), P=0.006), and total insulin output was proportionally increased (64 [21] versus 45 [24] nmol x m(-2). h, median [interquartile range], P=0.01), but dynamic indices of beta-cell function (glucose sensitivity, rate sensitivity, and potentiation) were similar in the 2 groups. Abdominal VAT, insulin resistance, and blood pressure were quantitatively interrelated (rho's of 0.39 to 0.47, P<0.02 or less). In newly found, untreated men with essential hypertension, fat is preferentially accumulated intraabdominally and intrathoracically. Such visceral adiposity is quantitatively related to both height of blood pressure and severity of insulin resistance, but has no impact on the dynamics of beta-cell function.
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PMID:Visceral fat in hypertension: influence on insulin resistance and beta-cell function. 1524 49


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