UMLS:C0020538 - FACTA Search

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

Cardiovascular manifestations develop in the majority of SLE patients at some time during the course of their illness, the most common being acute fibrinous pericarditis and pericardial effusion. Echocardiography has demonstrated an increased incidence of pericardial effusion, even in those who have minimal symptoms. Chronic adhesive pericarditis, pericardial tamponade, and constrictive pericarditis occur rarely. While myocarditis is commonly noted at autopsy, it is often silent clinically. Diagnosis during life can be confirmed only by endomyocardial biopsy. Electrocardiographic changes are often nonspecific. Endocarditis with superimposed nonbacterial verrucous vegetations (Libman-Sacks) is noted in more than 40% of hearts at autopsy, but is rarely diagnosed during life. Valve dysfunctions, such as aortic stenosis, aortic insufficiency, mitral stenosis, and mitral insufficiency, occasionally manifest during life and rarely may necessitate surgery. Atrial and ventricular arrhythmias, first degree AV block, and acquired CHB occur in association with pericarditis, myocarditis, vasculitis, and myocardial fibrosis, respectively. CCHB developing in newborns of mothers with SLE, particularly those who have an antibody to soluble tissue ribonuclear protein RO(SS-A), is increasingly being appreciated by both pediatric cardiologists and rheumatologists. Recently, severe coronary atherosclerosis resulting in angina pectoris and/or myocardial infarction in young adults has been noted, particularly in those who had developed risk factors such as hypertension and hyperlipidemia while receiving prolonged corticosteroid therapy. Rarely, coronary arteritis may produce similar symptoms. Congestive heart failure of either single or multiple etiologies carries an ominous prognosis. It remains a cause of high morbidity and mortality unless recognized early and treated properly. Extracardiac vascular manifestations of SLE include telangiectasia, vasculitis, livedo reticularis, Raynaud's phenomena, and thrombophlebitis, all of which may occur either alone or in different combinations. Evidence is now slowly accumulating that substantiates that immune complex deposition, complement activation and subsequent inflammatory reaction is responsible for the majority of the cardiovascular manifestations of SLE, for example, pericarditis, myocarditis, endocarditis, coronary arteritis, coronary atherosclerosis, and systemic and pulmonary vasculitis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiovascular manifestations of systemic lupus erythematosus: current perspective. 286 Jun 99

Experimental renovascular hypertension or supravalvular aortic constriction results in left ventricular hypertrophy and impaired minimum coronary vascular resistance. However, these experimental models expose the coronary arteries to increased intra-arterial pressure, so that hypertensive vascular changes might be responsible for the impaired minimum coronary resistance. This study was performed to test the hypothesis that left ventricular hypertrophy in the absence of increased coronary pressure results in abnormalities of myocardial perfusion. Aortic valve stenosis was produced by plication of the noncoronary aortic cusp of 11 dogs at 6-8 weeks of age. Studies were carried out when the animals reached adulthood; mean left ventricular:body weight ratio was 7.1 +/- 0.4 as compared to 4.4 +/- 0.3 g/kg in 11 normal dogs (P less than 0.01). Under quiet resting conditions, myocardial blood flow measured with microspheres was significantly greater than normal in dogs with aortic stenosis. However, during maximum coronary vasodilation with adenosine, mean left ventricular blood flow in dogs with hypertrophy (3.29 +/- 0.39) was substantially less than in normal dogs (6.19 +/- 0.54 ml/min per g; P less than 0.01), whereas minimum coronary resistance was increased from 14.1 +/- 1.7 in normal dogs to 23.7 +/- 5.4 mmHg. min X g/ml (P less than 0.01). To examine the response of myocardial perfusion to cardiac stress, blood flow was measured during pacing at 200 and 250 beats/min. Compared with normal dogs, animals with hypertrophy had a subnormal increase in myocardial blood flow during tachycardia; this perfusion deficit was most marked in the subendocardium. These data demonstrate that left ventricular hypertrophy alone, without increased coronary artery pressure, is associated with impaired minimum coronary vascular resistance and with abnormalities of myocardial blood flow during pacing stress.
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PMID:Alterations of myocardial blood flow associated with experimental canine left ventricular hypertrophy secondary to valvular aortic stenosis. 293 24

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.
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PMID:Assessment of diastolic function in normal and hypertrophied hearts: comparison of Doppler echocardiography and M-mode echocardiography. 295 50

The influence of isoenzyme pattern of myosin on cardiac energetics was investigated in a modified in situ heart-lung preparation in the rat. Chronic pressure load (spontaneous hypertension, aortic stenosis, Goldblatt hypertension), intermittent feeding, and swim-training elicited redistribution in the concentration of alpha chains of myosin ranging from 18 to 94%. The influence of isoenzyme pattern of myosin on cardiac energetics could be quantitatively assessed by extrapolation of the regression line of oxygen and substrate consumption related to tension time index. Fast myocardium with 100% alpha chains had an ATP and oxygen consumption which exceeded that of slow myocardium with 0% alpha chains by about 60%. This corresponds well to the state of activity of myofibrillar ATPase of fast myocardium which also exceeds that of slow myocardium by about 50%. Furthermore it could be shown that acute increase in the ATPase activity depends on the isoenzyme pattern of myosin. Under the influence of catecholamines the oxygen consumption related to tension time index increased by 30-40% in fast myocardium, whereby in a myocardium with 40% alpha chains no increase in oxygen consumption per unit tension time index was observed, when catecholamines were applied.
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PMID:Implications of myocardial transformation for cardiac energetics. 295 58

The surface electrocardiogram remains an insensitive method for detection of ventricular hypertrophy. Technical problems related to body size and habitus and distance from the heart cannot be overcome. Coronary arterty disease and amyloidosis, although frequently associated with hypertrophy, tend to obscure the electrocardiographic changes because of the attendant loss of voltage. The progress made in the last 20 years is due primarily to re-evaluation of traditional criteria in terms of careful anatomic correlation. The studies cited have the advantage of using specific clinical diagnoses in a defined population, specific chamber weights, and a 97.5 percentile confidence level for distinguishing normal pathologic and electrocardiographic data from abnormal. They are limited because the results may not apply to females or patients with mitral stenosis and congenital heart disease. In general, the electrocardiogram can be expected to detect left ventricular hypertrophy in six out of ten patients with the disease, and will misdiagnose the problem in about one out of every ten without the disease. Methodology using multiple criteria will achieve the best sensitivity and specificity. Several methods are available and of comparable accuracy. Simplicity of these methods varies widely and will be a factor in the choice of the method selected. The electrocardiogram will perform best in the population of patients with hypertension and aortic stenosis or regurgitation and have its greatest limitation in patients with coronary artery disease and myocardial infarctions. Echocardiography is proven to be more sensitive than the electrocardiogram for detection of left ventricular hypertrophy. Sensitivity is around 90 per cent with 95 per cent specificity. Its major limitations lie in the expense as compared to the electrocardiogram and in inadequate image resolution in a small proportion of patients. In order to achieve the results reported by centers proficient in this technique, careful attention must be paid to precise standardization of measurements and selection of images to be measured. When this is done the echocardiogram certainly offers a distinct advantage over the electrocardiogram in detecting left ventricular hypertrophy. We recommend the use of left atrial abnormality as a criterion to diagnose left ventricular hypertrophy when there is right bundle branch block. When left bundle branch block is present on the electrocardiogram, traditional criteria are probably no more accurate than the bundle branch block itself.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Recent progress in the electrocardiographic diagnosis of ventricular hypertrophy. 296 47

We have previously shown that swim conditioning corrects the depressed mechanical function and myosin adenosinetriphosphatase (ATPase) activities associated with renovascular hypertension (HTN) in the rat. The present study was designed to assess the effects of swim conditioning on another form of systolic overload, subdiaphragmatic suprarenal aortic stenosis. Cardiac mechanics in an isolated working heart apparatus and myosin enzymology were studied in four groups of rats: controls (C), animals with chronic systolic overload secondary to aortic constriction (St), swim-conditioning animals (Sw), and animals exposed to a combined load (St-Sw). Heart weight was increased by 23% in St, 27% in Sw, and 36% in St-Sw. In contrast to HTN, cardiac pump and muscle function were not depressed in St. Sw was associated with improved cardiac output, stroke work, and velocity of circumferential fiber shortening. St-Sw showed improved mechanical cardiac performance relative to both C and St. The percent of ventricular myosin of the V1 type and Ca2+-activated myosin ATPase activity relative to C was unchanged in Sw but was depressed in St and St-Sw. These data demonstrate that the salutory mechanical effects of Sw can be superimposed on the systolic overload of St. However, the dissociation between mechanics and myosin enzymology suggests that factors in excitation-contraction coupling other than myosin isoenzyme shifts are responsible for this finding.
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PMID:Effects of systolic overload and swim training on cardiac mechanics and biochemistry in rats. 296 13

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)
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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

Myocardial hypertrophy may influence coronary hemodynamics variably. Therefore, coronary sinus blood flow (gas chromatic argon technique) was determined in patients with left ventricular hypertrophy, with or without dilatation, associated with entirely normal coronary arteriographic results: 12 patients with hypertrophic obstructive cardiomyopathy (left ventricular mass-to-volume ratio, 3.66 +/- 0.52 g/ml), 22 patients with hypertensive heart disease due to essential hypertension (left ventricular mass-to-volume ratio, 2.12 +/- 0.26 g/ml), 18 patients with hypertensive dilatation (left ventricular mass-to-volume ratio, 1.6 +/- 0.48 g/ml), six patients with aortic stenosis (left ventricular mass-to-volume ratio, 1.99 +/- 0.41 g/ml), 12 patients with aortic incompetence, and 20 patients with normal heart function. Coronary sinus blood flow was determined as a control value and as the value following intravenous injection of dipyridamole (0.5 mg/kg of body weight). Coronary reserve was calculated as the ratio of coronary resistance before and after dipyridamole. Normal coronary reserve averaged 4.89 +/- 0.11. Similar values, despite marked left ventricular hypertrophy, were present for both hypertrophic obstructive cardiomyopathy (4.4 +/- 0.19) and aortic stenosis (4.66 +/- 0.12), whereas coronary reserve was considerably reduced in the concentrically hypertrophied hypertensive hearts (3.22 +/- 0.19) (p less than 0.001). Moderate decrease in coronary reserve was found in aortic incompetence and in dilated essential hypertension. These results indicate that patients with nonhypertensive hypertrophy, despite left ventricular mass augmentation, may have normal coronary reserve, whereas at a comparable degree of left ventricular hypertrophy, patients with hypertensive hypertrophy have a specific reduction in coronary reserve. Independent from vascular effects, ventricular dilatation may result in deterioration of coronary reserve because of an abnormal component of coronary vascular resistance. These results were also verified in experimental hypertension. Moreover, prevention and/or regression of the impaired coronary circulation in experimental hypertensive heart disease, most probably due to the reduction of smooth muscle layers of the media of coronary resistance vessels, could be achieved by long-term vasodilator therapy.
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PMID:Coronary hemodynamics in hypertensive heart disease. Basic concepts, clinical consequences, and experimental analysis of regression of hypertensive microangiopathy. 297 65

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

Left ventricular hypertrophy due to aortic stenosis, hypertension and other forms of heart disease is associated with abnormalities of diastolic function. It is uncertain whether these changes are an inherent consequence of the hypertrophic process or represent additional pathologic factors. To investigate this issue, echocardiographic indexes of left ventricular early diastolic function in highly trained athletes were compared with those in age-matched normal control subjects. Athletes were equally classified into two groups: 11 swimmers who had a pattern of myocardial hypertrophy with normal wall thickness to dimension ratio and 11 power lifters whose wall thickness to dimension ratio was increased. The peak rates of left ventricular dimension increase and wall thinning in swimmers and power lifters were greater than in control subjects despite significantly higher left ventricular wall thickness and left ventricular mass index in the athletes. This increase in diastolic function indexes was associated with greater ventricular size and systolic performance. Normalization of the peak rate of dimension increase for end-diastolic dimension and adjustment of the peak rate of wall thinning for the fractional systolic thickening resolved any differences between groups. Thus, after the effects of ventricular size and systolic function were taken into consideration, diastolic function was normal in these subjects with considerable physiologic hypertrophy. This is in contrast to the findings in patients with hypertrophy associated with left ventricular pressure or volume overload, and suggests that abnormalities of diastolic function seen in pathologic hypertrophy are due to factors other than cardiac hypertrophy itself.
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PMID:Left ventricular diastolic function in elite athletes with physiologic cardiac hypertrophy. 316 24

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