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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three measurements of diastolic filling were compared in 29 patients with essential hypertension and 27 age matched normotensive controls. Systolic function was normal in all but one of the patients. The mean (1SD) first one third filling fraction (a measurement of early diastolic filling) was significantly lower in the hypertensive groups (0.27 (0.24] than in the control group (0.45 (0.16)). The hypertensive group was subdivided into those with electrocardiographic abnormalities and those without. In the subgroup with a normal electrocardiogram the mean (1SD) first one third filling fraction measurement (0.28 (0.16)) was significantly lower than in the control group. In the subgroup with an abnormal electrocardiogram, the first one third filling fraction was even lower (0.24 (0.9)). In addition, the time to peak filling rate (213 (56) ms) was significantly longer in the subgroup with the abnormal electrocardiogram than in the control group (164 (45) ms). However, the interobserver reproducibility of the time to peak filling measurement was poor. The peak filling rate was low in the subgroup with an abnormal electrocardiogram, but not significantly different from the normal controls. The discriminatory value of the three diastolic measurements did not improve with exercise. These results showed an early diastolic filling abnormality in essential hypertension that did not appear to be caused by disease of the large coronary vessels as it was present in patients with normal wall motion and a normal exercise electrocardiogram. The occurrence of diastolic abnormalities when systolic function is still normal may mark an early stage in the development of hypertensive heart failure, at a time when the process is still potentially reversible.
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PMID:Radionuclide measurements of diastolic function for assessing early left ventricular abnormalities in the hypertensive patient. 278 18

The results of clinicoinstrumental investigations in 33 patients with coronary heart disease and coronary heart disease combined with essential hypertension complicated by stage I-II cardiac insufficiency showed that therapy with captopril at a daily dose of 25-75 mg resulted in the correction of cardiac insufficiency in 84% of the patients, with a hypotensive effect in 80%. Captopril improved myocardial contractility, decreased pressure in the pulmonary artery and total peripheral vascular resistance and produced no major side-effects.
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PMID:[Captopril in the treatment of mild cardiac insufficiency in combination with arterial hypertension]. 329 82

Total body elemental composition was measured in 40 patients with well documented heart failure who were oedema-free on digoxin and diuretics. The results were compared with values for 20 patients with untreated essential hypertension matched for height, weight, age, and sex. Total body potassium alone was also measured in 20 normal subjects also matched for anthropomorphic measurements. Patients with hypertension had a very similar total body potassium content to that of normal subjects, but patients with heart failure had significantly reduced total body potassium. This could not be explained by muscle wasting because total body nitrogen, largely present in muscle tissue, was well maintained. When total body potassium was expressed as a ratio of potassium to nitrogen mass a consistent depletion of potassium was revealed in the group with heart failure. Potassium depletion was poorly related to diuretic dose, severity of heart failure, age, or renal function. Activation of the renin-angiotensin-aldosterone system was, however, related to hypokalaemia and potassium depletion. Such patients also had significantly lower concentrations of serum sodium and blood pressure. Serum potassium was related directly to total body potassium. Despite the absence of clinically apparent oedema total body chlorine was not consistently increased in heart failure, but the calculated extracellular fluid volume remained expanded in the heart failure group. Total body sodium was significantly increased in patients with heart failure, but less than half of this increase could be accounted for by extracellular fluid volume expansion. Potassium depletion in heart failure may account in part for the high frequency of arrhythmias and sudden death in this condition.
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PMID:Total body electrolyte composition in patients with heart failure: a comparison with normal subjects and patients with untreated hypertension. 331 Oct 97

Methods of clinico-instrumental investigation and biochemical monitoring (CPK and its membranous fraction) were employed for examination of 432 patients with acute myocardial infarction (AMI). Among them there were patients with an uncomplicated course of disease (19.4%), recurrences (13.7%) and AMI spreading (9%). Lung edema, a cardiogenic shock, ventricular fibrillation and complicated cardiac rhythm disorders were not detected on the 1st day of disease. Clinico-anamnestic data provided no opportunity for defining factors promoting AMI recurrences whereas AMI spreading frequently developed in patients with repeated AMI, suffering from essential hypertension, obesity and heart failure. Higher diastolic pressure in the pulmonary artery, an increase in the cardiac volume, a decrease in the ejection fraction and left ventricular stroke work--changes which were most pronounced in AMI spreading, were noted in patients with AMI lingering forms. Signs of disseminated intravascular blood coagulation were noted in the venous and arterial blood of patients with lingering AMI forms. A high blood enzyme level was shown to be accompanied by a low level of antibodies to LDH and CPK.
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PMID:[Clinico-pathogenetic variants of protracted forms of acute myocardial infarct]. 361 39

Indenolol hydrochloride is a recently introduced antihypertensive substance. Although it has beta-adrenoceptor blocking activity, its action is due to total peripheral resistance reduction. We investigated the effects of indenolol therapy on left ventricular performance in 15 patients with essential hypertension. Assessments were made using systolic time intervals and computerized echocardiography. The echocardiographic and mechanocardiographic tracings were recorded three times: at the beginning of the trial, after seven days of placebo, and after three weeks of indenolol treatment. The indenolol therapy significantly decreased (P less than 0.001) systolic and diastolic blood pressures and heart rate in all patients, both in supine and standing positions. After three weeks of treatment, systolic time intervals and echocardiographic determinants of left ventricular function were substantially unchanged in comparison with the basal and placebo evaluations. We conclude that indenolol exerted a marked effect on chronotropism but no demonstrable negative effect on inotropism in patients with essential hypertension. No clinical signs of heart failure were recorded. Side effects were absent, and patient compliance was good in all cases.
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PMID:Computerized echocardiographic study of left ventricular function and cardiodynamic investigation with a new antihypertensive agent (indenolol). 399 29

Measurements of total body potassium (T.B.K.) were made by whole-body counting in four groups of patients receiving oral frusemide for one year. Patients in group 1 had essential hypertension and normal renal function and received 40 mg frusemide daily without potassium supplements. Patients in group 2 were similar but received oral potassium supplements for the first four months of treatment. Patients in group 3 had hypertension associated with renal disease and received 120 mg frusemide daily without potassium supplements. Patients in group 4 also had hypertension and renal impairment and in addition to 120 mg frusemide daily they received oral potassium supplements for four months. No evidence of depletion of T.B.K. was found in any of the groups after continuous treatment with frusemide for one year. It is questioned whether potassium supplementation in long term diuretic therapy with frusemide is necessary unless there is evidence of pre-existing potassium depletion or of some other factor such as cardiac failure, cirrhosis of the liver, or the nephrotic syndrome.
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PMID:Total body potassium in long-term frusemide therapy: is potassium supplementation necessary? 421 34

Ten years of experience with three different converting enzyme inhibitors (CEI; teprotide, captopril and enalapril) in over 300 hypertensive patients reveals that CEI act largely to block renin-angiotensin mediated vasoconstriction. Thus, their effectiveness or lack of it is predicted by the baseline plasma renin measurement. Accordingly, responses to these pharmacological agents can be used to identify and quantify renin-mediated vasoconstriction in the spectrum of hypertensive diseases. The converse is also generally true. Patients failing to respond to CEI exhibit low renin values and their increased peripheral resistance appears related to other mechanisms, possibly involving a subtle increase in total body sodium. Thus, low renin states such as low-renin essential hypertension, primary aldosteronism, and anephric man exhibit little or no response to CEI. The relationship between the renin system activity and effectiveness of CEI reflects a specific interference with a particular pathogenic mechanism which is further supported by the fact that two other types of renin system inhibitors (beta-blockers and saralasin) are similarly effective or ineffective according to the operant renin profile also by studies in patients with congestive heart failure without hypertension in whom the same relationships can be demonstrated. Like hypertensives, heart failure patients exhibit a broad spectrum of renin activity values, and their pretreatment renin levels predict the responses to CEI. We have also found that plasma renin values in heart failure are dependent on sodium intake. When salt is administered, renin falls and patients then become unresponsive to CEI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Converting enzyme inhibition to identify and treat renin-mediated or sodium-volume related forms of increased peripheral resistance in hypertension and in congestive heart failure. 608 35

The enzyme renin splits a single peptide bond in the plasma glycoprotein angiotensinogen liberating the biologically inactive decapeptide angiotensin I (ANG I). A second enzyme, angiotensin converting enzyme (CE), releases the strong vasoconstricting octapeptide ANG II via degradation of a C-terminal dipeptide. The effect of this compound on blood pressure can be attenuated by interference with the enzyme-controlled peptide cascade of the renin-angiotensin system (RAS). This is accomplished by inhibition of renin and CE, respectively. Orally active CE inhibitors are valuable drugs in the treatment of renal and essential hypertension and of heart failure. Strong inhibitors of renin have also been synthesized, however, peptide moieties which have still to be present in these compounds impede oral absorption. Finally, antagonistic analogues of ANG II are able to block its effect on the receptor level. Their application is limited by the still existing partial agonistic activity.
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PMID:Chemistry of the inhibitors of the renin-angiotensin system. 609 62

For the past 7 years we have treated 30 patients with malignant hypertension with hemodialysis. The diagnosis of the disease was made according to the criteria recommended by the Ministry of Public Welfare, Japan, as described below. These patients were divided into three groups according to the therapies. Group A (15 patients) were medicated with large doses of beta-blockers for the control of hypertension. Characteristic features of this group were abnormally high reninemia, hyponatremia, and severe hypertension which were not controlled by large doses of beta-blockers in combination with dialysis. Their body weights were quite subnormal. Twelve patients out of 15 had essential hypertension (EH) as an underlying disease, and the remaining 3 had chronic glomerulonephritis (CN). Ten patients out of 15 died of hypertensive heart failure or hypertensive cerebrovascular accidents. Group B (6 patients) were treated by beta-blockers intermittently. They showed good results responding well to the treatment; high reninemia was brought down to normal level by the administration of beta-blockers and dialysis. Their underlying diseases were EH (3 patients) and CN (3 patients). Group C (9 patients) did not receive beta-blockers, because hypertension was easily controlled by dialysis alone. In the Group C patients, normoreninemia, normonatremia, and a favorable clinical course were characteristic. Their underlying disease was CN in all. From these results, it is concluded that the factors influencing the prognosis of te disease may be the existence of EH as an underlying disease, high reninemia, and hyponatremia which are not correctable either by administration of beta-blockers or by hemodialysis.
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PMID:Analysis of 30 patients with malignant hypertension treated with hemodialysis. 611 66

Heart rate (HR), blood pressure and systolic time intervals (STI), including total electromechanical systole (QS2), left ventricular ejection time (LVETc), pre-ejection period (PEPc), the PEP/LVET index and the time to the peak of carotid upstroke (Ut), were measured in 24 patients with moderate essential hypertension after 15 days of treatment with oral furosemide (F), hydrochlorothiazide (H), propranolol (P), atenolol (A), furosemide + propranolol (F + P) and hydrochlorothiazide + propranolol (H + P). Except F, all treatments significantly reduced blood pressure; maximal reductions were brought about by A and H + P. The heart rate was most reduced by A. THe QS2c interval was reduced only after F and H, LVETc was significantly reduced by H, A and H + P. Drug combinations prolonged PEPc, while the PEP/LVET index was increased only by H + P. Beta-blockers significantly prolonged the Ut. It is concluded that diuretics shorten QS2c mainly through reduction in blood volume. The H + P combination diminishes contractility and cardiac output and should not be employed in heart failure.
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PMID:Modification of blood pressure and systolic time intervals by diuretics and beta-blockers in essential hypertension. 613 68


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