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)

In 103 hearts with various forms of cardiac muscle hypertrophy the following parameters were estimated: diameter, length, volume, density and number of myocytes, as well as the density of nuclei of myocytes. The values of all histometric parameters correlated well with the LV weight up to 350 g. In heavier hearts these parameters were approximately at the same magnitude. The number of myocytes was significantly higher in hearts with LV weight above 250 g than in hearts below 250 g: 5.53 x 10(9) vs 4.31 x 10(9), p less than 0.001. The influence of coronary artery diameters, degree of atherosclerosis, weight and percent of fibrous tissue and age on LV weight were evaluated as well. Only coronary artery diameters significantly influenced on LV weight. On the basis of linear discriminant function, three classes of hearts were separated: 1) LV weight 250 g - absence of hyperplasia, only hypertrophy 2) LV weight 251-350 g - hypertrophy + signs of hyperplasia 3) LV weight 350 g - marked signs of hyperplasia Among 18 patients with the LV weight above 350 g (all patients with congestive heart failure), 11 suffered from valvular disease, 3 were postinfarction patients, 2 suffered from primary hypertension and 2 from primary congestive cardiomyopathy. It indicates that, irrespective to the etiologic factor, hyperplasia is a simple result of the cardiac muscle mass increase.
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PMID:[Myocardial structure in various forms of hypertrophy. II. Myocyte hypertrophy or hyperplasia? Results of the study]. 215 Jun 80

To investigate the clinical roles of mechanical and non-mechanical factors in hypertensive hypertrophy, 125 patients with essential hypertension, 20 with hypertrophic cardiomyopathy (HCM) and 20 with dilated cardiomyopathy (DCM), were studied using echocardiography. The hypertensive patients were separated into 3 groups: those with left ventricular (LV) hypertrophy (H), those without hypertrophy (H(-)) and those with dilatation (D). Group H patients were separated into 3 subgroups: those with subnormal LV end-systolic wall stress (ESS) (HI), those with normal ESS and mild hypertrophy (HIIA), and those with normal ESS and severe hypertrophy (HIIB). The inotropic response to isoproterenol infusion (0.02 microgram/kg/min for 5 min) was measured by the increase of fractional shortening (FS) corrected for the decrease of ESS (delta FS/delta ESS). After antihypertensive treatment for 4.4 +/- 1.7 years, echocardiography was repeated. delta FS/delta ESS was significantly larger in HI and HCM than in HIIA, was significantly larger in HIIA than in HIIB in which it was significantly larger than in D and DCM. After the treatment, LV mass decreased significantly except in HI. In conclusion, hypertensive hearts are regulated by mechanical and non-mechanical factors. Non-mechanical factors, for example the function of beta-adrenergic receptors in myocardium, have a variety of influences on myocardium, causing a broad spectrum of clinical features and courses.
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PMID:Mechanical and non-mechanical factors in hypertensive hypertrophy, their clinical roles. 217 81

Tissue typing applied to the Russian population was used to study distribution of HLA antigens, classes I and II, in patients with essential hypertension (EH), coronary heart disease (CHD), hypertrophic cardiomyopathy (HCMP), dilated cardiomyopathy (DCMP) and virus myocarditis (VM). As control use was made of the data on HLA antigen distribution in 267 healthy persons (donors) of the Russian nationality. The genetic markers of the predisposition to the indicated diseases were revealed: in EH, DR 1 (RR-3.56), DR 4 (RR-2.17); in CHD, B 12 (RR-2.91), DR 1 (RR-3.41), DR 4 (RR-3.14); in HCMP, DR 1 (RR-2.25), DR 4 (RR-3.29); in DCMP, DR 4 (RR-3.90); in VM, DR 3 (RR-5.26), DR 4 (RR-3.51). DR 4 turned out to be the common marker of the predisposition to cardiac diseases. Besides, DR 1 was discovered to be the marker of the predisposition to EH and DR 3 to VM. The data obtained may be of importance for the clinical practice in forming risk groups.
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PMID:[The HLA system antigens in patients with cardiovascular diseases]. 227 76

Left ventricular hypertrophy in left ventricular pressure overload occurs in response to excessive work load imposed on the left ventricle by increased impedance to ejection. Right ventricular hypertrophy may occur in patients with these findings, but has been considered to be secondary to pulmonary hypertension. To determine the frequency of right ventricular hypertrophy and its relation to increased left ventricular wall thickness in patients with left ventricular pressure overload, right ventricular wall thickness was measured using M-mode echocardiography with two-dimensional echocardiographic guidance in 65 patients with left ventricular pressure overload; 49 patients had essential hypertension and 16 had aortic valve stenosis. These measurements were compared with data from 13 patients with "thin-walled" dilated cardiomyopathy and 20 normal subjects. Average right ventricular wall thickness in hypertensive patients (7 +/- 2 mm) and patients with aortic stenosis (6 +/- 2 mm) was significantly greater than that in normal subjects (4 +/- 1 mm) and patients with dilated cardiomyopathy (4 +/- 1 mm) who had normal left ventricular wall thickness, even though left ventricular mass was increased in all patient groups. Increased right ventricular wall thickness was present in 40 (80%) of 49 patients with hypertension and 10 (63%) of 16 patients with aortic stenosis. The magnitude of increase in right ventricular wall thickness was linearly correlated (r = 0.76, p less than 0.005) with left ventricular wall thickness, but was not associated with pulmonary hypertension. It is concluded that increased right ventricular wall thickness is common in patients with left ventricular pressure overload, is directly related to increases in left ventricular wall thickness, and is independent of right ventricular hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased right ventricular wall thickness in left ventricular pressure overload: echocardiographic determination of hypertrophic response of the "nonstressed" ventricle. 316 25

The relationship between V1P-terminal force (V1-PT) and the characteristics of left ventricular (LV) diastolic filling and atrial contraction were evaluated using LV inflow velocity patterns obtained by pulsed Doppler echocardiography. Subjects consisted of 54 patients with old myocardial infarction, 56 with essential hypertension, 48 with angina pectoris, 19 with dilated cardiomyopathy, and 16 with miscellaneous disease other than of mitral valve lesions. The patients were classified as the positive group: V1-PT less than or equal to -0.04 mmsec, intermediate group: 0 greater than V1-PT greater than -0.04 mmsec, and negative group: V1-PT greater than or equal to 0 mmsec. The following were the results obtained: 1. In the positive group, the rapid filling wave (R) had reduced velocity, the prolonged deceleration time and the decreased acceleration and deceleration ratios. 2. In the positive group, velocity of the atrial contraction wave (A) was increased and the atrial contraction time was prolonged compared to the other groups. 3. In the positive group, the A/R was greater than in the other groups. 4. In the positive and intermediate groups, V1-PT correlated significantly with the A/R (r = 0.83, p less than 0.01), R (r = -0.58, p less than 0.01) and A (r = 0.48, p less than 0.01). In the positive group, LV inflow volume was decreased in the rapid filling phase. In the atrial contraction phase, the inflow volume was increased to compensate for loss of inflow volume in the rapid filling phase. These findings suggested that LV diastolic filling was disturbed in the positive group. In conclusion, the value of V1-PT is influenced by any disturbance of LV diastolic filling.
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PMID:[V1P-terminal force evaluated by left ventricular inflow velocity patterns in pulsed Doppler echocardiography]. 344 72

The interrelationship between myocardial hypertrophy and myocardial function is a complex one. In patients with essential hypertension, the appearance of left ventricular hypertrophy may be an ominous sign, often presaging the evolution of congestive heart failure. In other settings, such as valvular heart disease, congestive cardiomyopathy, and ischemic heart disease, myocardial hypertrophy serves as a compensatory mechanism in response to excessive loading conditions. This article reviews experimental and clinical data concerning the evolution of hypertrophy and its relationship to myocardial function.
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PMID:Myocardial hypertrophy and cardiac failure: a complex interrelationship. 622 98

Numerous essential, physiological effects on the cardiovascular system are attributable to angiotensin II (Ang II). Because of this we can assume that genetic changes in the specific receptor of Ang II (Ang II type 1 receptor gene, AT1) play a decisive role in the occurrence of cardiovascular disease associated with blood pressure regulation, vascular tone, cardiac and vascular growth process. To test this hypothesis, we examined the presence of polymorphisms within the coding region of the AT1 gene using polymerase chain reaction (PCR) and subsequent non-radioactive sequencing of samples from a control group with no previous history of cardiovascular complaint in individuals or immediate family. Using the Taq-sequencing procedure we found polymorphic sites, especially in the 5' region of the gene (base pair positions 9, 16, 87, 133, 186), two of which led to an exchange of the amino acid (amino acid 6: Ser<==>Pro, amino acid 45: Gly<==>Arg). Together with the silent polymorphism at base pair position 573, which our group established previously, an additional polymorphism in the 3' region of the gene was discovered. This, however, did not confer any changes in amino acid sequence. In a preliminary study we found no association between the distribution of the C/T573 polymorphic site and cardiovascular disease, such as essential hypertension (n = 20) coronary artery disease (n = 16) hypertrophic cardiomyopathy (n = 12) or dilated cardiomyopathy (n = 21). Further studies will be needed to determine to what extent the polymorphisms described are associated with cardiovascular disease.
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PMID:Genetic polymorphisms of the angiotensin II type 1 (AT1) receptor gene. 771 99

Vasodilators (captopril or nifedipine) were administered to 85 patients with stage IIA-IIB circulatory insufficiency. Of them 36 had dilated cardiomyopathy (DC), 30 ischemic heart disease (IHD), 19 suffered from essential hypertension (EH). Morphofunctionally, myocardial lesion was of a dilated type in 50 patients (36 DC, 10 IHD and 4 EH cases), of a hypertrophic type in 18 patients (4 IHD, 14 EH cases), of a mixed type in 17 IHD patients. The response to acute tests with 25 mg captopril and 20 mg nifedipine along with clinicohemodynamic results of 3-5-week course treatment with the drugs point to noticeable advantage of captopril in the dilated lesion (18 responders of 26 patients), while nifedipine in the hypertrophic type (10 responders of 10 patients). In mixed-type IHD patients both drugs displayed high efficacy.
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PMID:[Differential use of vasodilators in various types of cardiac insufficiency]. 824 9

In the past 10 years, cardiomyopathy has been diagnosed in 16 athletes, out of them in 13 this abnormality has been ascertained for the first time when they were examined or they were in the outpatient department. The paper provides clinical and instrumental findings of 13 patients with hypertrophic cardiopathy and 3 with dilated cardiomyopathy whose diagnosis was established by making a differential diagnosis of congenital and acquired heart diseases, coronary heart disease, essential hypertension and athletic heart. Most athletes with hypertrophic cardiomyopathy has an asymptomatic or mild natural history.
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PMID:[Cardiomyopathies in the practice of sports medicine]. 830 77

The objectives of this study were, first, to compare stroke volume to brachial artery pulse pressure ratios (SV/PP) as noninvasive, indirect estimates of total arterial compliance, in young subjects with primary hypertension or dilated cardiomyopathy and age-matched normal subjects and, second, to determine the influence of prior submaximal exercise on this ratio, and on calf and total peripheral vascular conductance in these subjects. We studied young patients (< 40 years old) with primary hypertension (n = 12) or dilated cardiomyopathy (n = 12) and healthy normotensive subjects (n = 12) matched for age and body size. Doppler estimated stroke volume, brachial artery pulse pressure, and calf blood flow were determined during supine rest before and 60 min after exercise. Normotensive and hypertensive subjects returned 1 month later to determine the reproducibility of the SV/PP value. At rest, the SV/PP value was inversely related to left ventricular mass index (r = -0.55, p < 0.001) and was similar in normotensive and hypertensive subjects, but was significantly lower (p < 0.05) in cardiomyopathy. The SV/PP value was reduced 60 min after exercise in both normotensive (p < 0.05) and hypertensive (p < 0.05) subjects, but not in cardiomyopathy patients. In contrast, total and calf vascular conductance increased after exercise in all three groups. These aftereffects indicate that these estimates of compliance and conductance are dynamic, and can be modulated acutely and independently by exercise.
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PMID:Influence of prior exercise on stroke volume to pulse pressure ratio in young subjects with hypertension or dilated cardiomyopathy. 943 48


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