Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Regression of ventricular hypertrophy has been studied in cases of valvular disease after valve replacement, as well as in hypertension under drug treatment. All studies have focussed on the left ventricle. The right heart chamber has not been quantitatively assessed. Regression has been found in both conditions in the range of 15-40% of initial left ventricular muscle mass. In hypertrophic cardiomyopathy consistent results have not been obtained. The ECG, correlating with muscle mass only loosely, is but a semiquantitative, albeit reliable indicator of regression. Vectorcardiography seems to be useful and deserves further study and application. Echocardiography has been validated for both TM- and 3D-mode and allows quantitative estimation of LV-mass during regression. Further improvement can be achieved through the subcostal approach. Left ventriculography remains standard of comparison, but can be considered valid only if angulated biplane technique is used. Repeated application of this technique is limited, unless digital subtraction angiography is used. This technique, however, has not been applied for serial studies of LV-mass during the process of regression. Computed tomography and nuclear magnetic resonance have been used for estimation of muscle mass. The capability of NMR seems particularly high. First results are presented and show excellent quantitation of LV-mass.
 ...
PMID:[Regression of heart hypertrophy. Criteria of regression from the viewpoint of the clinician]. 293 14

Verapamil and nifedipine are the most frequently used calcium channel blocking agents in Sweden at present time. The pharmacokinetics of verapamil has been described both in healthy volunteers as well as in patients with supraventricular arrhythmias, angina pectoris, liver cirrhosis, hypertrophic cardiomyopathy or hypertension. Intravenous pharmacokinetics of nifedipine has been investigated in healthy volunteers and oral pharmacokinetics in healthy volunteers as well as in patients with hypertension. The pharmacokinetics of verapamil and of one of its metabolites, norverapamil, is changed after multiple oral dosing as has been described in patients with supraventricular tachyarrhythmias, angina pectoris or in patients with essential hypertension. Plasma concentration-effect relationships have been established for verapamil in different clinical situations and in a few cases also for nifedipine. An update of the pharmacokinetics of these two important calcium channel blocking agents is presented.
 ...
PMID:Pharmacokinetics of calcium channel blocking agents. 294 Jul 99

Left ventricular (LV) filling was examined by Doppler and M-mode echocardiography in 24 patients with LV hypertrophy (five with aortic stenosis, six with hypertrophic cardiomyopathy, and 13 with LV hypertrophy secondary to systemic hypertension) and in 18 normal subjects. Patients with LV hypertrophy had significantly lower Doppler-determined peak filling rates (218 +/- 17 vs 288 +/- 66 cc/sec, p less than 0.01), but M-mode determined peak rate of chamber enlargement and normalized peak rate of chamber enlargement did not differ significantly between groups. Doppler measures of the ratio between early and late filling were significantly depressed in patients with LV hypertrophy and correlated inversely with age in the normal subjects. The M-mode derived normalized peak rate of chamber enlargement and the Doppler-derived normalized peak filling rate correlated weakly, but significantly, when both groups were combined (r = 0.56, p less than 0.01). Thus Doppler measurements can detect abnormalities of LV filling in patients with LV hypertrophy. These abnormalities are present when M-mode filling indices and systolic function are still normal.
 ...
PMID:Assessment of diastolic function in normal and hypertrophied hearts: comparison of Doppler echocardiography and M-mode echocardiography. 295 50

We report a case of idiopathic giant cell myocarditis accompanied by asymmetric septal hypertrophy. A 64-year-old woman was admitted because of dyspnea. There was no past history of hypertension or heart disease and no family history of hypertrophic cardiomyopathy. Laboratory examinations revealed general inflammatory changes and mild elevation of serum CK and GOT. The clinical course was fulminant and the patient died of heart failure one day after admission. On autopsy, asymmetric septal hypertrophy was revealed and the pathohistological examination revealed panmyocarditis with mononuclear cell infiltration, interstitial edema, necrosis of myocytes, and giant cells. The inflammatory changes were most severe in the ventricular septum with asymmetric septal hypertrophy. The extent of myocardial fibers with disarray was within normal limits. Thus, the asymmetric septal hypertrophy appeared to be due to marked interstitial edema and inflammatory cell infiltration in the septum. This case suggests that myocardial inflammation and edema may cause thickening of the ventricular wall during the course of acute myocarditis.
 ...
PMID:Idiopathic giant cell myocarditis accompanied by asymmetric septal hypertrophy. 295 39

To define the pathogenetic role of myocardial fiber disarray in the progression of cardiac fibrosis, the percent area of fibrosis in tissue with disarray was compared with that in tissue without disarray. Thirty autopsied hearts, 10 from patients with hypertrophic cardiomyopathy, 10 from patients with hypertension and 10 from normal adults, were studied. The percent areas of fibrosis in tissues with and without disarray were significantly different (p less than 0.01) among hearts with hypertrophic cardiomyopathy (12.6 +/- 4.0 and 8.2 +/- 3.3%), hypertensive hearts (6.6 +/- 3.6 and 2.5 +/- 1.4%) and normal hearts (2.8 +/- 1.2 and 1.0 +/- 0.4%). The percent area of fibrosis in tissue with disarray was greater than in that without disarray in all 3 groups and the ratios of these percentages were similar in the 3 groups: 2.9 +/- 4.2 in hypertrophic cardiomyopathy 2.5 +/- 1.7 in hypertensive hearts and 2.5 +/- 1.8 in normal hearts. The conclusions are: 1) disarray promotes fibrosis to a similar degree, not only in hypertrophic cardiomyopathy, but also in hypertensive hearts and normal hearts; 2) the increased level of fibrosis in hearts with hypertrophic cardiomyopathy and in hypertensive hearts, together with widespread fibrosis in hearts with hypertrophic cardiomyopathy in particular cannot be explained by disarray alone.
 ...
PMID:Pathogenetic role of myocardial fiber disarray in the progression of cardiac fibrosis in normal hearts, hypertensive hearts and hearts with hypertrophic cardiomyopathy. 295 2

To determine the feasibility of detecting cardiovascular disease in a large group of young competitive athletes, a prospective screening evaluation of intercollegiate student athletes was undertaken at the University of Maryland. Initial clinical screening (including personal and family history, physical examination and 12 lead electrocardiogram) was performed in 501 athletes. Ninety of these subjects had positive findings on one or more of the three studies and agreed to further cardiologic evaluation. The vast majority (75 [84%] of 90) had no definitive evidence of cardiovascular disease, although 1 athlete had mild systemic hypertension and 14 (15%) had echocardiographic evidence of relatively mild mitral valve prolapse that had not been previously suspected. In three athletes with relatively mild ventricular septal hypertrophy (14 to 15 mm), it was not possible to discern with absolute certainty whether the wall thickening was a manifestation of hypertrophic cardiomyopathy or secondary to athletic conditioning ("athlete heart"). Therefore, this screening protocol identified no athletes with definite evidence of hypertrophic cardiomyopathy, Marfan's syndrome or other cardiovascular diseases that convey a significant potential risk for sudden death or disease progression during athletic activity. This failure to identify such diseases could have been due to a lack of sensitivity of the screening tests or to the low frequency with which these diseases occur in youthful healthy athletes. A systematic preparticipation screening program (such as the present one) does not appear to be an efficient means of detecting clinically important cardiovascular disease in young athletes.
 ...
PMID:Results of screening a large group of intercollegiate competitive athletes for cardiovascular disease. 296 Jul 27

During the last six years, there has been increased interest in the detection of abnormalities of left ventricular diastolic function in patients with heart disease. Before 1981, most studies on diastolic function were performed in the catheter laboratory using invasive techniques and complex methods. Recently, radionuclide angiograms and Doppler echocardiography have been employed to measure the dynamics of filling in normal individuals and in patients with heart disease. These methods are noninvasive, easy to perform, accurate, and reproducible. It is now clear that diastolic function may be altered globally and regionally, at rest and perhaps during exercise, in many patients with ischemic heart disease, hypertension, and hypertrophic cardiomyopathy. Interestingly, these diastolic abnormalities may even appear before systolic abnormalities are identified in these patients. Thus, diastolic abnormalities may permit assessment of presence of disease early in its evolution. Whether detection and quantitation of diastolic abnormalities will permit grading of disease severity or evaluation of therapeutic efficacy remains an important research question. At the present time, it appears that the decision to employ either radionuclide angiography or Doppler echocardiography for the assessment of diastolic abnormalities will depend on the local expertise to carry out the investigation. Both diagnostic modalities require standardization of accuracy and reproducibility with proper selection of control values from the appropriate populations of normal individuals. It is also important to remember that left ventricular diastolic abnormalities have to be identified after the elimination of the confounding influence of variables such as ejection fraction, heart rate, age, and preload (end-diastolic volume). Automation of the derivation of indexes of diastolic filling should provide an objective assessment of the dynamics of left ventricular filling. Although the value of measurement of diastolic filling in the individual patient remains controversial, we believe that the practice of cardiology is incomplete without consideration of the second half of cardiac function.
 ...
PMID:Diastolic function of the heart in clinical cardiology. 296 56

In order to study the influence of various kinds of left ventricular hypertrophy on left ventricular filling pattern, 20 patients (five dilated cardiomyopathy, five hypertension, five end-stage renal disease, five hypertrophic cardiomyopathy), and five normals were studied by M-mode and pulsed 2D-Doppler echocardiography. Left ventricular dimensions, volumes and mass were derived from standard M-mode echocardiograms. Doppler velocity measurements of mitral inflow provided calculation of left ventricular diastolic filling parameters. While left ventricular diastolic function bore no relation to the impairment of left ventricular systolic function, there was a statistically significant correlation of left ventricular mass/volume ratio and impairment of left ventricular diastolic function. In patients with hypertrophic cardiomyopathy, the parameters varied widely, and additional factors seem to determine left ventricular diastolic function in this group.
 ...
PMID:Diastolic filling properties in different forms of left ventricular hypertrophy, assessed by 2-D echocardiography. 296 51

We investigated the relationship between parameters of left ventricular diastolic filling using pulsed Doppler echocardiography and the A wave ratio of apexcardiography (ACG), and then evaluate the characteristic features of diastolic behavior in hypertrophic hearts and in various cardiac diseases. The study population consisted of 68 patients and 25 normal subjects, and included 19 cases of chronic renal failure (CRF), 17 cases of ischemic heart disease (IHD), 16 cases of hypertension (HT), six cases of hypertrophic cardiomyopathy, two cases of aortic stenosis, two cases of arrhythmias, and six of other cardiac diseases. The A wave ratio of ACG was calculated as the ratio of A wave amplitude and total excursion [(A/E-O) x 100]. At the same time, the peak early filling velocity (R), the peak late filling velocity (A), the ratio of R to A (A/R), acceleration time (AT), and deceleration time (DT) were measured from the left ventricular inflow velocity pattern using pulsed Doppler echocardiography. The results were as follows: 1. There was a close positive correlation between the A wave ratio of ACG and the A/R of pulsed Doppler echocardiography. 2. In patients with left ventricular hypertrophy (LVH), both the A wave ratio and the A/R were significantly higher than those in normal subjects. And in LVH with asynergy, both the A wave ratio and the A/R were significantly higher than those in LVH without asynergy. 3. In CRF, IHD, and HT, both the A wave ration and the A/R were significantly higher than those in normal subjects, but there were no significant differences among these three disease entities.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Relationship between left ventricular diastolic behavior and the A wave ratio by the apexcardiogram: a study with echocardiography and pulsed Doppler echocardiography]. 296 12

721 cases of sudden coronary death (SCD) of men aged 30-59 were studied. It was found out that SCD happened in majority of cases in subjects with increased weight of heart: 44.2% of patients had heart weight of 500 g or more. A special histomorphometric study of kidneys (345 cases of SCD) revealed arterial hypertension (AH) in 41.2% of cases, which far exceeded AH incidence in the population of men of equal age. Nevertheless, not in all cases of SCD was myocardial hypertrophy caused by AH. In patients with no AH myocardial hypertrophy was usually caused by postinfarction cardiosclerosis. In certain cases of SCD without cardiosclerosis accompanied by manifest myocardial hypertrophy there were signs of dilatative or hypertrophic cardiomyopathy. The obtained results suggest that AH and increased weight of heart should be considered factors predisposing to SCD.
 ...
PMID:[Myocardial hypertrophy, arterial hypertension and sudden cardiac death]. 296 34


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>