Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A frequency distribution curve and interval percentages of variations in right versus left renal vein renin (RVR) were calculated from 227 sets of renin data from patients with mild and moderate essential hypertension (EH). A renal vein renin ratio (RVRR), large/small, of approximately 2.0 or more falls beyond the 95 per cent confidence interval, and may therefore by considered to be abnormal. Although assay variability and sampling errors may contribute to artifactually large RVRR's in EH, they usually indicate true disparity, probably secondary to asymmetrical nephrosclerosis. Recent hypotheses regarding diagnostic value of RVR in hypertension are evaluated in light of data yielded by this investigation. Simultaneous and/or replicate sampling should reduced within-patient variability and improve clinical interpretation of test results.
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PMID:Renal vein renin in essential hypertension. 119 55

In order to develop the tentative criteria of the differential diagnosis, 18 patients with obstructive hypertrophic cardiomyopathy (OHCMP), 3 with nonobstructive hypertrophic cardiomyopathy (NOHCMP), 8 with essential hypertension (EH) with inadequate left ventricular hypertrophy (LVH) and 10 normal persons were subjected to clinical examination and to ultracardiosonography. The patients with OHCMP mainly complained of dizziness and syncopes. Since childhood they had systolic murmur and ECG abnormalities. Ultracardiosonography showed asymmetrical LVH, a considerable decrease of the ventricular cavity as well as abnormalities of the localization and function of the papillary muscles. NOHCMP was marked by the combination of the good well-being of the patients with gross abnormalities on the ECG. Ultracardiosonography demonstrated moderately pronounced and asymmetrical LVH. The group suffering from EH with inadequate LVH was characterized by the early development of severe circulatory failure with arterial hypertension of moderate intensity. The changes in the architectonics of the left ventricle and its subvalvular structures turned out to be similar to those in OHCMP but were less remarkable.
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PMID:[The differential diagnosis of various forms of hypertrophic cardiomyopathy and hypertension with inadequate left ventricular hypertrophy]. 253 35

This study was designed to ascertain the contribution of hypertension to the early diastolic time intervals in asymmetrical apical hypertrophy (AAH). Eighteen patients with untreated AAH were categorized as those with (n = 13) and without (n = 5) hypertension. Isovolumic relaxation time and early diastolic filling were determined in four groups: normotensive subjects (n = 20), patients with essential hypertension (n = 20), AAH with hypertension, and AAH without hypertension. Early diastolic function was measured by the interval from the aortic closure sound (IIA, phonocardiography) to the opening of the mitral valve (MVO, echocardiography) and the interval from MVO to the O point of the apexcardiogram. The IIA-O interval was also calculated. Peak velocities in the rapid filling phase (R) and atrial contraction phase (A) were measured using two-dimensional Doppler echocardiography in the center of the mitral orifice in diastole. The MVO-O/IIA-MVO and A/R ratios were also calculated. 1. In the AAH with and without hypertension groups, the IIA-O, IIA-MVO, and MVO-O intervals were significantly prolonged. The IIA-O and MVO-O intervals in the AAH without hypertension group were more prolonged than were those in the AAH with hypertension group. In patients with essential hypertension, the IIA-O and the IIA-MVO intervals were prolonged, but there was no prolongation of the MVO-O interval. 2. The MVO-O/IIA-MVO ratio was lower in essential hypertension and in the AAH with hypertension groups, and significantly higher in the AAH without hypertension group. 3. There was no significant change of the R, A, and A/R in each group. These results indicated that prolonged left ventricular relaxation was distinguished in essential hypertension. In AAH with hypertension, the same prolongation was observed, but the disturbance of early diastolic filling was mild. It is suggested that apical hypertrophy has a possible association with hypertension, though it may more properly belong to cardiomyopathy.
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PMID:[Contribution of hypertension to left ventricular diastolic function in patients with asymmetrical apical hypertrophy]. 281 33

A study of 20 patients with essential hypertension, stage IIB, asymmetrical myocardial hypertrophy and chest pains has suggested that the pain syndrome, presenting as "possible angina", positive functional tests and reduced label accumulation around the ventricular septum may be indicative of coronary insufficiency.
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PMID:[Origin of the pain syndrome in asymmetric myocardial hypertrophy in patients with stable hypertension]. 296 72

Echocardiographic investigation of 110 patients with different forms of stable arterial hypertension demonstrated a moderately close correlation between left-ventricular myocardial weight, and systolic and diastolic arterial blood pressure in patients with essential hypertension and chronic diffuse glomerulonephritis, and a weak correlation between left-ventricular myocardial weight and systolic pressure in patients with renovascular hypertension and chronic unilateral or predominantly unilateral pyelonephritis. Inadequate left-ventricular hypertrophy has similar incidence (15-20%) in patients with different forms of arterial hypertension, whereas excessive hypertrophy only occurs in patients with essential hypertension. The frequency of asymmetrical hypertrophy differs in the two groups.
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PMID:[Characteristics of left ventricular hypertrophy in patients with different forms of arterial hypertension based on echocardiographic data]. 315 74

For statistical analysis of 24-hour recordings of arterial pressure (AP) and heart rate (HR), it is necessary to establish a theoretical probability density function of the distributions. In the present study, 24-hour recordings of direct AP and HR were performed in 15 normotensives (NT) and 39 patients with essential hypertension (EH) by means of a new portable device with a digital memory for analyzing frequency histograms. In both NT and EH, frequency histograms of AP (systolic and diastolic AP) and HR during a 24-hour period showed bi-modal curves, whereas those made during sleep and waking produced asymmetrical patterns resembling Gamma distribution. From the AP and HR histograms made for each subject during sleep and waking, such parameters as mean (M), standard deviation, mode (Mo), skewness (Sk), kurtosis (K) and minimum values (Mi) were calculated. The Sk and M minus Mo were positive, and K was greater than 3 in both HR and AP histograms; the AP and HR histograms during sleep can be more correctly analyzed with Gamma distribution (mean parameter errors were less than 7.3%) than with Gaussian distribution (in this: S = O, M minus Mo = O, K = 3). The Mi would accord with the location parameter of the Gamma distribution.
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PMID:Non-Gaussian distribution of arterial pressure and heart rate during sleep and waking in hypertensive and normotensive subjects. 379 54

The authors report the clinical, ECG, PCG and echocardiography data obtained in mountaineers suffering from associated essential hypertension and high-altitude pulmonary hypertension. Demonstrate the advisability of distinguishing the high-altitude hypertrophic cardiomyopathy syndrome (HHCS) in part of mountaineers with essential hypertension living permanently at an altitude of 3600-4200 m over the sea level. The HHCS is marked by a lot of the clinical and echocardiographic signs which are regarded as characteristic of hypertrophic cardiomyopathy, particularly by appreciable asymmetrical hypertrophy of the interventricular septum. Criteria for the differential diagnosis between the HHCS and idiopathic hypertrophic subaortic stenosis are suggested. The possible mechanisms by which the HHCS develops in part of mountaineers are discussed.
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PMID:[Syndrome of high-altitude hypertrophic cardiomyopathy]. 404 Feb 72

To determine whether asymmetrical septal hypertrophy (ASH) in patients with essential hypertension (HT) is a type of hypertensive left ventricular (LV) hypertrophy or hypertrophic cardiomyopathy (HCM) combined with HT, we investigated a group of 7 hypertensive patients with ASH compared with 12 HCM patients and 10 healthy controls using radionuclide angiography and right ventricular endomyocardial biopsy. The LV time-volume curve and its first and second derivative curves were constructed from cardiac output and time-activity curves constructed by combined forward and reverse-gating from the R wave. The LV wall thickness and ejection fraction were significantly greater in both the HT and HCM groups than in the control group, whereas there were no differences in these indices between the HT and HCM groups. Rapid filling volume index and rapid filling fraction showed significantly lower values in the HCM group than in the control group (p < 0.005). In contrast to the HCM group, these indices in the HT group did not differ from those in the control group. The time to peak filling rate was prolonged in the control, hypertension, and HCM groups in increasing order. Histopathological study revealed a higher incidence of myocardial cell disarray in the HCM than in the HT group. The above results suggest that ASH in hypertensive patients is a type of hypertensive LV hypertrophy.
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PMID:Asymmetrical septal hypertrophy in patients with hypertension: a type of hypertensive left ventricular hypertrophy or hypertrophic cardiomyopathy combined with hypertension? 841 59

Although echocardiography is a useful diagnostic tool in hypertrophic cardiomyopathy (HCM), it is sometimes difficult to differentiate it from hypertensive heart disease (HHD): some patients with HCM show symmetrical hypertrophy, whereas patients with HHD sometimes show asymmetrical septal hypertrophy. We used a radioiodinated long-chain fatty acid tracer to visualize the altered myocardial fatty acid metabolism of HCM and HHD. Carnitine is the essential substance for the beta-oxidation of long-chain fatty acids. We recently reported that serum free carnitine levels in HCM were elevated and that they were significantly correlated with the severity of myocardial fatty acid metabolic disorder. Therefore, we investigated serum carnitine levels in patients with HCM and HHD, which can contribute to the differentiation of each other. We studied 56 patients with HCM and 20 patients with essential hypertension. Serum free carnitine levels were significantly higher in patients with HCM than those with HHD (HCM 52.5+/-9.5 nmol/mL, HHD 46.6+/-6.4 nmol/mL, P<0.01), but they showed no statistical difference between patients with HHD and normal subjects. Serum acylcarnitine levels were significantly lower in patients with HCM than those with HHD (HCM 10.1+/-4.0 nmol/mL, HHD 14.5+/-4.9 nmol/mL, P<0.0005), although they did not differ between patients with HHD and normal subjects. Scintigraphic analyses with a long-chain fatty acid analog revealed that myocardial tracer uptake was much reduced in patients with HCM compared with that in patients with HHD (quantitative analysis: HCM 2.11+/-0.12, HHD 2.22+/-0.17, P<0.05; semiquantitative analysis: HCM 13.6+/-6.3, HHD 2.0+/-1.5, P<0.0001). In conclusion, the differences in serum carnitine levels between HCM and HHD reflect altered myocardial fatty acid metabolic impairment, and the levels can help to distinguish these 2 diseases.
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PMID:Can serum carnitine levels distinguish hypertrophic cardiomyopathy from hypertensive hearts? 1094 80

Genetics, oxidative stress: superoxide anion (O2*-) and hydrogen peroxide (H2O2), endothelial nitric oxide (eNO), lipid peroxides, anti-oxidants, endothelin, angiotensin converting enzyme (ACE) activity, angiotensinII, transforming growth factor-beta (TGF-beta), insulin, homocysteine, asymmetrical dimethyl arginine, proinflammatory cytokines: interleukin-6 (IL-6), tumor necrosis factor-a (TNF-alpha), C-reactive protein (hs-CRP), and long-chain polyunsaturated fatty acids (LCPUFAs), and activity of NAD(P)H oxidase have a role in human essential hypertension. There is a close interaction between endogenous molecules: eNO, endothelin, cytokines, and nutrients: folic acid, L-arginine, tetrahydrobiopterin (H4B), vitamin B6, vitamin B12, vitamin C, and LCPUFAs. Statins mediate some, if not all, of their actions through LCPUFAs, whereas these fatty acids (especially omega-3 fatty acids) suppress cyclo-oxygenase activity and the synthesis of pro-inflammatory cytokines, and activate parasympathetic nervous system, actions that reduce the risk of major vascular events. Some LCPUFAs form precursors to lipoxins and resolvins that have anti-inflammatory actions. Low-grade systemic inflammation seen in hypertension seems to have its origins in the perinatal period and availability of adequate amounts of LCPUFAs during the critical periods of brain growth prevents the development of hypertension. This indicates that preventive strategies aimed at decreasing the incidence of hypertension and its associated conditions such as atherosclerosis, type 2 diabetes, coronary heart disease (CHD), and cardiac failure in adulthood need to be instituted during the perinatal period if they are to be effective.
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PMID:Hypertension as a low-grade systemic inflammatory condition that has its origins in the perinatal period. 1671 19


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