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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibromuscular dysplasia of renal arteries was the cause of hypertension in four consecutive children with renal artery stenosis. Two were asymptomatic, the third had had hypertension for seven years but had not been treated, and the fourth, a 9-month-old infant, presented with cardiac failure. Heart enlargement and left ventricular hypertrophy were present in all. Rapid sequence urograms demonstrated a smaller kidney and delayed appearance and disappearance of the contrast medium on the affected side in all. Angiograms showed left RAS in all. Peripheral plasma renin activity was elevated in only three of the four patients. Antihypertensive and diuretic drugs were not very effective therapeutically. Ischemia of the ipsilateral kidney probably prevented normal growth and led to shrinkage of the kidney in one patient. Following nephrectomy the BP has remained normal without any therapy for 24 to 64 months. With normalization of BP, accelerated growth ensued, the cardiomegaly regressed and the hypertensive retinopathy resolved. These patients demonstrate that: (1) FMD is an important cause of RAS. (2) the well-known radiologic feature of FMD, the beaded appearance, is usually not seen in children. (3) control of BP leads to normalization of linear growth, usually impaired in severe hypertension, and (4) target organ complications such as cardiomegaly, LVH, and hypertensive retinopathy are reversible in one to 10 months.
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PMID:Fibromuscular dysplasia of renal arteries: an important cause of renovascular hypertension in children. 15 54

Isolated hearts from adult spontaneously hypertensive rats (SHR; Okamoto 1969), with established hypertension, were investigated in an antegrade perfusion apparatus where preload and afterload could be varied independently. Frank-Starling curves were constructed at constant afterloads ranging from 50 mmHg to 150 mmHg. As earlier reported, the SHR hearts exhibited a rightward shift of their Frank-Startling relationships compared to those from the normotensive control hearts, though visible only at afterloads up to about 100 mmHg. At higher afterloads the SHR hearts performed significantly better then the NCR ones as their maximal stroke volume was significantly greater compared to that of controls. Thus, left ventricular hypertrophy obviously increases the work capacity of the heart, though at the cost of an altered Frank-Startling relation dependent on the reduced diastolic compliance. For such reasons the myocardial hypertrophy in established SHR hypertension must be considered a physiologic adaptation and not a degenerative phenomenon, though naturally degenerative processes may later become superimposed.
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PMID:Performance of the hypertrophied left ventricle in spontaneously hypertensive rat. Effects of changes in preload and afterload. 16 Jul 44

The electrocardiogram of 100 normal subjects and 216 patients with arterial hypertension in different stages have been analysed. P wave especially has been taken into consideration: it is often abnormal in the presence of left ventricular hypertrophy (LVI). The point-score system elaborated by Romhilt and Estes allows, if only QRS-T is considered, to diagnose LVI in 32 of the hypertensive patients (15%) and in 41 cases (19%) if the increase of P wave terminal forces is emphasized. Nevertheless this P wave characteristic does not appear more useful than others (axis less than or equal to 40 degrees; duration greater than or equal to 0.12 sec; presence of notch). The best results are achieved by considering the coexistence of two or more abnormalities of the P wave. Thus LVI is diagnosed in 52 (24%) of our cases, without false positive.
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PMID:[P wave analysis for the electrocardiographic diagnosis of left ventricular hypertrophy. A study of a population with arterial hypertension (author's transl)]. 16 32

In a 16-member black kindred with Fabry's disease, four hemizygous males had plasma alpha-galactosidase levels less than 6% and seven heterozygous females had plasma alpha-galactosidase levels between 10% and 50% of normal. A 16-year-old index male had hypertension with left ventricular hypertrophy, abnormal renal function, tortuous retinal veins, "myelin" inclusions in bone marrow macrophages, and intraepithelial inclusion bodies in the kidney. Scrotal angiectasia developed a year after diagnosis. The three other affected males had left ventricular hypertrophy and retinal vein tortuosity. Of the seven carrier females, five had frequent headaches, four had retinal vessel changes, three had proteinuria with normal renal function, and two had bundle-branch blocks on ECGs. There was no deuteranomalopia in this family, although the inheritance pattern of the Fabry gene is X-linked recessive.
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PMID:Fabry's disease in a black kindred. 22 50

Left ventricular stiffness is defined by the relationship between pressure and volume and can be altered by a variety of disorders. In disorders with high VLVED, such as mitral regurgitation, protection of pulmonary capillaries from high pressure is provided by a PV shift. In contrast, increased stiffness is produced by ventricular hypertrophy or ischemic heart disease, which puts the patient at increased risk for pulmonary capillary hypertension. Changing the ventricular PV relationship by therapy is an exciting prospect.
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PMID:Left ventricular stiffness. 34 43

Little is known of the clinical significance of myocardial bridges, which may be recognized angiographically as systolic coronary artery narrowing (SCAN). A retrospective review of a 1 year's experience (313 consecutive coronary arteriograms) revealed 5 patients with SCAN, an incidence of 1.6%. SCAN involved the proximal and/or middle segments of the left anterior descending coronary artery in all patients. It is of particular note that the administration of nitroglycerin noticeably accentuated the SCAN phenomenon in each of 3 patients to whom it was administered. Four of the 5 patients had left ventricular hypertrophy due to hypertrophic cardiomyopathy (2), aortic stenosis (1), and hypertension (1). All 5 patients with the SCAN phenomenon had anginal chest pains, and critical obstructive coronary atherosclerosis was observed in only 2 cases. The other 3 patients showed, otherwise normal coronary arteriograms. Thus, myocardial bridges appear to be angiographically manifest predominantly in patients with cardiac hypertrophy. Nitroglycerin, which accentuates SCAN, might be useful as a provocative test to enhance the angiographic recognition of this phenomenon. The possible role of myocardial bridges in the production of myocardial ischemia warrants further investigation.
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PMID:Myocardial bridges in man: clinical correlations and angiographic accentuation with nitroglycerin. 40 19

One third of 160 operatives working in a permanently noisy industrial environment, within the range of 63-8000 Hz and intensity of sound of about 100 db, were found to suffer from a syndrome of neurocirculatory asthenia and 8.1% from arterial hypertension. Study of the ECG according to the criteria of the Minnesota code showed an increased frequency of upward deflection of ST segment (index 9-2) in 20.6% of the cases, depression of the ST segment with an ascending orientation in 50.62% of the cases and left ventricular hypertrophy (index 3-1 and 3-3) in 20% of the cases. Audiometry revealed loss of hearing at frequencies of 4000 CS in 16.1% of the cases. The results obtained suggest that the detrimental effects are not restricted only to hearing, but also that the alterations detected might evolve towards organic cardiac disorders.
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PMID:Study of cardiovascular and auditory pathophysiological implications in a group of operatives working in noisy industrial surroundings. 40 53

Although electrocardiographic evidence of right ventricular hypertrophy is considered common in newborn infants with coarctation of the aorta, the reason for this finding is not well established. Investigations of the pulmonary vascular bed of these infants have resulted in variable findings, probably due to the differences in morphometric techniques, coexisting cardiac defects, and variable postnatal age at time of death. To study more carefully the pulmonary vascular bed, we produced coarctation of the aorta in fetal lambs at 103--126 days gestation. Twelve to 32 days later the fetuses were reoperated on and systemic and pulmonary arterial blood pressures, and arterial blood gas tensions were determined to be normal. At autopsy, juxtaductal coarctations extended a mean of 2.8 mm into the aortic lumen and occupied 9.5 mm of the aortic circumference. The fifth-generation pulmonary resistance vessels had increased medial width (p less than 0.01), decreased external diameter (p less than 0.001), and increased medial width/external diameter ratios (p less than 0.001) compared with vessels from control fetuses. The number of small muscular pulmonary vessels/cm2 lung tissue was significantly reduced (p less than 0.01) in the study animals compared with the control animals. These alterations of the pulmonary vascular bed were not due to fetal pulmonary arterial hypertension or fetal hypoxemia. These pulmonary vascular changes may explain the occurrence of pulmonary hypertension and right ventricular hypertrophy in newborn infants with coarctation of the aorta.
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PMID:Morphologic development of the pulmonary vascular bed in experimental coarctation of the aorta. 44 52

The Authors have verified in a group of 38 patients with chronic obstructive pulmonary disease (COPD) and suspected pulmonary arterial hypertension (PAH) of precapillary origin the possibility to forsee the pressure within the lesser circulation starting from some electrocardiographic and vectorcardiograhic criteria. The vectorcardiographic analysis has not been shown to be more reliable than the traditional ECG as far as the identification of an eventual PAH is concerned. The matching of both scalar and vectorial criteria has significantly increased the efficiency of the estimate, i.e. the possibility to foresee the right ventricular systolic pressure (RVSP) and the mean pulmonary arterial pressure (PAP), but the same efficiency has remained at unsatisfactory level (S = +/- 10,30 Torr as far as the PAP is concerned. With regard to the value of the various scalar and vectorial criteria or parameters, among the electrocardiographic criteria the most reliable has been the inversion of the T wave in the right precordial leads. This sign, however, did not often appear in the present series (18% of the cases). As to the VCG the analysis made by the Authors stresses as the most reliable criterion the direction of QRS loop rotation on the horizontal plane and the magnitude of the maximum rightward spatial vector. These two elements, among other things, escape detection on the traditional electrocardiographic investigation. The above mentioned conclusions, obviously, only apply to the PAH secondary to COPD, in which particular noncardiac (lung hyperinflation, lowering of the diaphgram, etc.) and cardiac (associated left ventricular hypertrophy) factors contribute to limit the diagnostic value of both the ECG and the VCG.
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PMID:[Predictability of electrocardiographic and vectorcardiographic criteria in pulmonary arterial hypertension caused by chronic bronchopneumopathies]. 45

In two experimental models of established hypertension in the rat (two kidney, one clip renal and genetic hypertension), the maximum by which stroke volume and cardiac output could be increased during an acute preload stress was significantly reduced despite the concomitant development of left ventricular hypertrophy. Reversal of cardiac hypertrophy by prolonged treatment with methyldopa (range 3 to 6 weeks) during the established phase of spontaneous hypertension normalized arterial blood pressure and improved ventricular pumping ability. The improved performance was in part due to reduced impedance to ventricular ejection because it did not persist when peripheral resistance was increased by an acute administration of phenylephrine hydrochloride. Thus, hemodynamic as well as structural factors contribute to alterations in cardiac function during the chronic established phase of arterial hypertension.
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PMID:Cardiac pumping ability in rats with experimental renal and genetic hypertension. 49 96


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