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

Although there are controversies in the role of calcium as an antihypertensive agent, the use of "health food" supplements, such as dolomite and bone meal, is on the rise especially among the older population. One brand of commercial dolomite tablets were investigated for metallic contents such as aluminum (Al), arsenic (As), cadmium (Cd), chromium (Cr), copper (Cu), lead (Pb), manganese (Mn), sclemium (Se), and zinc (Zn). Ten randomly selected tablets were weighted, dried, pulverized and low-temperature plasma ashed. An ash aliquot of each tablet was dissolved in 35% Ultrex nitric acid, and after dilution analyzed using a Perkin-Elmer Model 5000 atomic absorption spectrophotometer equipped with an HGA-500 graphite furnace, As-1 autosampler, and PRS-10 printer sequencer. The results (presented as mean wt/g of powder +/- 95% confidence limits) are: Al 900 +/- 300 micrograms/g; As 1.3 +/- 0.3 micrograms/g; Cd 0.16 +/- 0.04 micrograms/g; Cr 5.9 +/- 1.4 micrograms/g; Cu 3.0 +/- 0.6 micrograms/g; Pb 1.9 +/- 0.5 micrograms/g; Mn 66 +/- 7.0 micrograms/g; Se 1.6 +/- 0.4 micrograms/g; and Zn 147 +/- 88 micrograms/g. These trace metals could pose health hazards to the public such as lead poisoning, dementia, and hypertension due to cadmium. Also, zinc can potentiate cadmium-hypertensive effects. The need exists to initiate some regulations to limit maximal content of trace metals in "health food" supplements to protect high-risk groups and that sector of the population who use megadoses of such products.
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PMID:Alert to users of calcium supplements as antihypertensive agents due to trace metal contaminants. 341 87

According to echocardiographic observations, the hypertrophic left ventricle in hypertension and in aortic stenosis is inclined to asymmetric septal hypertrophy. The heart surgeon, after removal of the stenosed aortic valve, is not so rarely forced to resect an additional muscular hump of the basal ventricular septum. These findings contrast with our experiences from autopsy examinations; we see asymmetric septal hypertrophy only in hypertrophic cardiomyopathy (or coronary heart disease). The aim of this study was to demonstrate or refute this impression by measurements of the relevant parameters. In ten hearts with aortic stenosis and in 12 hearts of hypertensive patients there was no evidence of accentuated septal hypertrophy. In some hearts we found a prominent crista supraventricularis, which could explain the echocardiographic feature of a thickened ventricular septum. The muscular hump stenosing the left ventricular outflow tract can easily be explained by concentric hypertrophy. The thickness of the septum corresponded to that of the free wall, but only below the aortic valve did the hypertrophy become functionally relevant. There is no doubt that in certain cases this muscular hump has to be removed. The term asymmetric septal hypertrophy, however, is inadequate.
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PMID:[Asymmetric septum hypertrophy in the pressure-overloaded heart]. 342 9

Three cases of hypertrophic cardiomyopathy (HCM) which presented with different modes of appearance of left ventricular hypertrophy are reported. Case 1: A 24-year-old man had three relatives with HCM. At 13 years of age, he showed no electrocardiographic or echocardiographic abnormalities characteristic of HCM. During the ensuing 11 years, he developed asymmetric septal hypertrophy (ASH) and systolic anterior motion of the mitral valve (SAM), with right bundle branch block and T-wave inversion. Cardiac catheterization confirmed the diagnosis of hypertrophic obstructive cardiomyopathy by demonstrating an intraventricular pressure gradient of 25 mmHg. These observations indicate that this case developed abnormal hypertrophy during adolescence on the basis of genetic predisposition of an autosomal dominant trait. Case 2: A 51-year-old woman had three proven and three possibly affected relatives. At 35 years of age, she had a normal electrocardiogram, although the echocardiogram was not available. Now, 16 years later, she had developed ASH with abnormal Q-waves and was diagnosed as having non-obstructive HCM. These suggest that ASH can be manifested as late as during middle-age, even in those with genetic predisposition. Case 3: A 47-year-old woman was diagnosed as having hypertension and her blood pressure was 190/100 mmHg at 40 years of age, though she had no abnormal electrocardiographic findings and heart murmurs. Now, at 47 years of age, she had developed T-wave inversion, ASH, SAM, and an intraventricular pressure gradient of 50 mmHg. Thus, her ASH appeared during middle-age, and was probably provoked by hypertension, though a complete family survey could not be conducted. These three patients' findings indicate that there may be various modes of appearance of left ventricular hypertrophy in HCM. In the majority of patients with genetic predisposition, abnormal hypertrophy may develop during adolescence as in Case 1. In others, it may develop in middle-age, as it did in Case 2. The disease spectrum of HCM may additionally include those who develop abnormal hypertrophy during middle-age, following provocation by hypertension, as in Case 3.
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PMID:[Hypertrophic cardiomyopathy manifesting different modes of illness: report of three cases]. 342 21

The heart may play an active, passive, or incidental role in the pathogenesis of hypertension. Echocardiography probably contributes little to understanding of active mechanisms, although it may provide important information relative to structural and functional adaptive changes associated with development of left ventricular hypertrophy. Moreover, because other clinical conditions frequently coexist with hypertensive heart disease, echocardiography may provide another dimension in the assessment of obesity, coronary heart disease, mitral valve prolapse, idiopathic hypertrophic subaortic stenosis, and asymmetric septal hypertrophy in the overall problem. Critical in this understanding are the subtle changes that occur in the individual patient, reflecting the natural history of the disease or response to its treatment. Since technical problems preclude echocardiographic evaluation in all patients with hypertension, particular care must be exercised in making epidemiologic generalizations.
Hypertension 1987 Feb
PMID:Future directions in the use of echocardiography. 380 1

Wall thickness, the extent of disarray, the number and the size of myocytes and the amount of interstitial space were measured in the ventricular septum (VS) and left ventricular (LV) free wall in hearts of 6 patients with chronic systemic hypertension and asymmetric septal hypertrophy (ASH). Twenty-five subjects (15 with no cardiac disease, and 10 with systemic hypertension) without ASH served as the controls. In the six patients with ASH, the degree of ASH ranged from 1.3 to 1.6. The extent of disarray in VS was 20% in one heart and within normal limits (mean +/- SD = 3 +/- 3%) in the other 5. The size of myocytes increased both in the VS and LV free wall and the VS/LV ratio ranged from 0.9 to 1.0. There was no significant difference in the % area of interstitial space between hearts with ASH and controls, and the VS/LV ratio ranged from 0.9 to 1.1. The number of transmural muscle layers (number of myocytes) was 680 +/- 90 in the VS and 440 +/- 40 in the LV free wall of these with ASH, and 500 +/- 60 in the VS and 490 +/- 60 in the LV free wall of control subjects. The VS/LV ratio of the number of myocytes ranged from 1.3 to 1.7 and was correlated with the VS/LV ratio of wall thickness. Although the sample is small, our findings suggest that most hearts from patients with chronic systemic hypertension and ASH have no diffuse disarray in the VS and that ASH probably occurs secondary to pressure overload.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Number and size of myocytes, amount of interstitial space and extent of disarray of the hearts in patients with systemic hypertension and asymmetric septal hypertrophy. 404 Jan 82

Electrocardiograms and M-mode echocardiograms were obtained prospectively from 72 patients with hemoglobin SS (n = 55) or SC (n = 17) disease to assess the prevalence of abnormal Q waves in sickle cell disease and to determine if such Q waves could be explained by, or related to, echocardiographically determined anatomic or functional abnormalities. The mean age (+/- SD) of the population under study was 28 +/- 9 years, and the mean hematocrit reading was 28 +/- 5 percent; 43 male and 29 female patients were evaluated. No patient had a history of systemic arterial hypertension, valvular heart disease, or congestive heart failure. Abnormal septal Q waves (amplitude greater than or equal to 0.30 mV; duration less than or equal to 29 msec) were noted in leads V4, V5, or V6 in 15 of 72 patients, and 50 percent (36) of the population under study demonstrated electrocardiographic voltage changes consistent with left ventricular hypertrophy. M-mode echocardiography showed that 29 of 72 patients had a thickened interventricular septum (greater than or equal to 1.2 cm), 16 of 72 had an abnormally thickened left ventricular posterior wall (greater than or equal to 1.2 cm), and 31 of 72 had increased left ventricular mass (greater than 215 g). The prevalence of electrocardiographic and echocardiographic abnormalities was not significantly different between patients with hemoglobin SS and SC disease. Septal excursion was decreased in 11 of the patients, and global left ventricular function (percent fractional shortening) was slightly decreased in three patients. Regional wall motion was normal in all 72 patients. Six percent (four) of the patients met echocardiographic criteria for asymmetric septal hypertrophy. Linear regression analysis yielded significant positive correlations between septal dimension (r = 0.38; p less than 0.001) and left ventricular mass (r = 0.37; p less than 0.005) when each was compared with Q-wave amplitude. A significant negative correlation (r = 0.40; p less than 0.001) was noted between hematocrit reading and Q-wave amplitude. We conclude that abnormal septal Q waves are common in sickle cell disease and are related, in part, to septal thickness, as well as left ventricular mass and degree of anemia.
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PMID:Abnormal septal Q waves in sickle cell disease. Prevalence and causative factors. 404 4

A 64-year-old man was hospitalized in March 1983 for recurrent episodes of dyspnea and palpitation despite medical treatment. At 48 years of age (1967), hypertension was diagnosed, but well controlled by propranolol. At the age of 59 years (1979), his first episode of dyspnea and palpitation was noted, with electrocardiographic (ECG) evidence of left ventricular hypertrophy (LVH), and abnormal Q waves in leads III and a VF. The echocardiogram, however, showed mild LVH with neither asymmetric septal hypertrophy (ASH) nor systolic anterior movement (SAM). On admission (1983), his blood pressure was 130/70 mmHg, and a grade III systolic murmur was heard along the left sternal border and over the apex. On ECG, the left precordial voltage (Sv1 + Rv5) was diminished and the depth of the Q wave in lead III increased compared with that of 1978. On echocardiography, we observed prominent septal hypertrophy (IVST: 20 mm) with ASH (IVST/PWT = 2.0), SAM, an enlarged left atrium, and a diminished left ventricular (LV) cavity. Left ventricular catheterization showed a pressure gradient of 90 mmHg between the LV apex and outflow tract and histological examination of the bi-ventricular endomyocardial biopsy material showed markedly hypertrophied and mildly disarranged myocardial fibers with bizarre nuclei. We considered that this was an interesting case in which ASH and SAM developed in the progression of LVH during the follow-up period.
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PMID:[Hypertrophic cardiomyopathy with progressive left ventricular hypertrophy: a case report]. 406 47

Whether giant negative T waves (GNT) of 1 mV or greater represent the electrocardiographic characteristics of idiopathic cardiomyopathy, particularly apical hypertrophic cardiomyopathy, is controversial. To clarify this point, a comparative study was conducted for 57 persons with GNT (GNT+ group) and 57 persons of hypertrophic cardiomyopathy with either asymmetric septal hypertrophy or diffuse hypertrophy of the ventricular wall in the absence of GNT (GNT- group). Patients with cerebral vascular accidents, myocardial infarctions, valvular heart disease, myopericarditis, and implanted pacemakers were excluded from the study because these patients' ECGs may show GNT. Left ventriculograms were investigated at end-diastole in the right anterior oblique projection. The GNT+ group showed a spade-like configuration indicating a marked reduction in the lumen of the apical cavity in 25 cases (43.9%); a kidney or banana-like configuration indicating the inferior wall bulging into the left ventricular cavity in its mid-zone in eight cases (14.0%), and an oval configuration which indicated no deformity of the left ventricular cavity in 24 (42.1%). The spade-like configuration was also seen in four cases (7.0%) of the GNT- group. A study of ventricular wall thicknesses based on left ventriculography showed that 25.5% of cases with GNT did not have concomitant apical hypertrophy. Generally, the GNT+ group cases had a significantly thicker anterior left ventricular wall and apical hypertrophy compared to the GNT- group. The hypertrophic states of the apical wall and anterior wall of the left ventricle correlated well. The GNT+ group included a significantly larger percentage of patients who were middle aged and older than did the GNT- group, and the frequency of accompanying hypertension was significantly higher in the former. The confirmed or suspected familial occurrence of cardiomyopathy (CM) was observed in 32 cases (56.1%) of the GNT- group, and in 18 cases (31.6%) of the GNT+ group, i.e., the incidence was significantly lower in the GNT+ group. In an endomyocardial biopsy study, 40 cases (70.1%) of HCM without GNT had bizarre myocardial hypertrophy with disorganization (BMHD). The incidence of BMHD in the GNT+ group was 21/57 (36.8%)-significantly lower than in the GNT- group. In the GNT- group, there was no significant difference in the incidence of BMHD between relatively young and old patients or between patients with and without accompanying hypertension; whereas, in the GNT+ group, it was significantly lower among those with accompanying hypertension and in older patients than in those without accompanying hypertension and in younger patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Do giant negative T waves represent apical hypertrophic cardiomyopathy? Left ventriculographic and cardiac biopsy studies]. 406 55

Although apical hypertrophy is characterized by a spade-like configuration of the left ventricle and giant negative T waves on electrocardiograms, the identity of apical hypertrophy in the disease spectrum of hypertrophic cardiomyopathy (HCM) is not fully established. The present study compared the demography, familial occurrence, and acquired factors of 43 patients who had apical hypertrophy with those of 104 patients who had asymmetric septal hypertrophy (ASH). Demographically, apical hypertrophy occurred predominantly in middle-aged males (86%). Family surveys showed that 13% of siblings of apical hypertrophy were affected, significantly less than in obstructive (31%) or non-obstructive (29%) HCM with ASH. Thirty-eight percent of siblings of ASH patients less than 35 years of age were affected, with a male/female ratio of 4/5, suggesting an autosomal dominant inheritance. The acquired factors associated with apical hypertrophy were assessed in a case-control study. Relative risk (odds ratio) of the condition was 3.46 (p less than 0.05) in those with histories of hypertension, and increased further to 8.09 (p less than 0.001) in those who were often hypertensive according to their physician's evaluations. Thus a strong association of hypertension with apical hypertrophy was suggested. However, hypertension in this condition was usually mild and labile, the blood pressure reverted to the normal range within several days of hospital admission, implying that transient hypertension during daily activity is associated with apical hypertrophy. Therefore, blood pressure response during exercise stress tests of 25 patients with apical hypertrophy was compared with that of age- and sex-matched controls. Slopes of linear regression between systolic blood pressure and heart rate and oxygen consumption during exercise, were used as indices of blood pressure response. They were significantly greater in apical hypertrophy than in the controls (1.2 +/- 0.4 vs 0.9 +/- 0.3, p less than 0.01 and 4.3 +/- 1.7 vs 2.8 +/- 0.8, p less than 0.001). This trend was observed even in patients without histories of hypertension. These findings suggested that apical hypertrophy has an inheritance pattern different from that of ASH, and has a possible association with acquired factors such as hypertension. Therefore, apical hypertrophy seemed to be a disease entity distinct from HCM with ASH, though it might be included in the disease spectrum of HCM.
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PMID:[Apical hypertrophy and its genetic and acquired factors]. 406 57

The mode of right ventricular hypertrophy was assessed by two-dimensional echocardiography (2DE) for 24 patients with hypertrophic cardiomyopathy (HCM), and the results were compared with those of 51 patients with hypertension (HT). The patients with HT were categorized in four groups depending on the thickness of the interventricular septum (IVST) and left ventricular posterior wall (PWT): HT-ASH with both left ventricular hypertrophy (LVH) (IVST greater than or equal to 13 mm) and asymmetric septal hypertrophy (ASH) (IVST/PWT greater than or equal to 1.3), severe HT with LVH and without ASH, and mild HT without LVH and ASH. Anterior wall thickness (AWT), posterior wall thickness (PWT), and diaphragmatic wall thickness (DWT) of the right ventricle were obtained from 2DE in the parasternal long-axis view, the short-axis view and subxiphoid view, respectively. These were recorded on video tape, and the measurements were made on the stop frames. Right ventricular hypertrophy (RVH) was estimated by the maximal right ventricular wall thickness (max RVWT), and the ratio of the maximal and minimal thickness (max RVWT/min RVWT) was calculated to evaluate asymmetrical hypertrophy (AH) of the right ventricle (RV). The incidence of RVH (Max RVWT greater than or equal to 5 mm) and asymmetrical hypertrophy (AH) (max RVWT/min RVWT greater than or equal to 1.3) of the RV in HCM, HT-ASH and mild HT were 67% and 41%, 57% and 45%, and 15% and 11%, respectively. The incidence of RVH with AH was more frequent in patients with HCM as well as HT with ASH than in patients with HT without ASH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Regional right ventricular hypertrophy in hypertrophic cardiomyopathy and hypertension]. 409 19


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