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

Nineteen patients with LBBB were studied by clinical, electrocardiographic (ECG), echocardiographic, electrophysiological and coronary angiographic examination. The commonest etiology of LBBB observed was idiopathic/degenerative in 10 (52.6%), followed by atherosclerotic coronary artery disease in 6 (31.5%) and hypertrophic cardiomyopathy, dilated cardiomyopathy and systemic hypertension in 1 case each (15.7%). In all patients with coronary artery disease (CAD), significant lesion of the left anterior descending artery was observed. On ECG, presence of Q in I, aVL, V5 or V6 was most helpful in predicting the presence of CAD while primary T-wave changes were least helpful. The degree of QRS axis was not helpful in predicting the presence as well as severity of CAD. Altered septal/regional wall motion abnormalities were commonly encountered on echocardiography and left ventriculography. Although infrahisian conduction delay was frequently observed and 11 (61.1%) had prolonged HV interval, in 2 of these there was additional suprahisian conduction delay. All patients with prolonged PR interval (more than or equal to 200 msec) or wide QRS duration (more than 140 msec) had infrahisian block with or without associated suprahisian block. Hence, hemodynamic evaluation, coronary angiographic studies and electrophysiological evaluation is essential in patients with LBBB.
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PMID:Noninvasive and invasive evaluation of left bundle branch block (LBBB). 233 87

The clinical pharmacokinetics and pharmacodynamics of enalapril and its de-esterified active metabolite, MK 422, were determined in eight patients with congestive cardiomyopathy and five patients with hypertension. After administration of single doses of 2.5, 5, and 10 mg enalapril in the congestive heart failure patients and 20 or 40 mg in the hypertensive patients, serum levels and urine elimination of enalapril and MK 422 were determined. Standing and supine heart rate and blood pressure were measured as was ejection fraction in the congestive heart failure group and renin activity, aldosterone levels, and converting enzyme activity in the hypertensive group. Apparent oral clearance after administration of 5 and 10 mg enalapril was lower in the congestive heart failure patients (0.6 +/- 0.2 and 0.7 +/- 0.4 L/min) than after 20 and 40 mg given to hypertensive patients (2.5 +/- 1.3 and 2.7 +/- 2.7 L/min). The elimination of MK 422 was also slower in the congestive heart failure patients (7.8 +/- 5.0 and 6.8 +/- 2.5 h after 5 and 10 mg enalapril, respectively, vs. 4.6 +/- 2.0 and 5.3 +/- 1.1 h after 20 and 40 mg, respectively, in the hypertension group). The enalapril area under the concentration-time curve increased disproportionately to dose increments in both groups, but was more pronounced in congestive heart failure. Twenty and 40 mg enalapril lowered the blood pressure by 2 h after dosing in the hypertension group, and peak effects were seen 4-5 h after dosing. Peak effects correlated with peak serum MK 422 concentrations but not with enalapril (MK 421) levels. Supine heart rates were unchanged after 20 mg, but increased after 40 mg; standing heart rates were transiently increased after 20 and 40 mg enalapril. Blood pressure was not significantly changed in the congestive heart failure group, and cardiac ejection fraction was unchanged. In the hypertension group, renin stimulation and converting enzyme activity inhibition were seen at 4 h and persisted for at least 24 h after administration of 40 mg enalapril. In summary, the clearance of enalapril and elimination of MK 422 was slower in congestive heart failure patients versus hypertensive patients. Therefore, slower onset and longer duration of drug effect might be anticipated in patients with congestive heart failure versus patients with hypertension during enalapril administration.
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PMID:Pharmacokinetics and pharmacodynamics of enalapril in patients with congestive heart failure and patients with hypertension. 241 Jul 20

The authors report 66 cases of peri- and postpartum cardiomyopathy. The patients' age ranged from 16 to 42 years (mean +/- SD 30 +/- 7 years). All were black women native of the western part of the Republic of Niger, Sahelian in the north, Sudanese in the south. At first examination, all had signs of congestive cardiac failure. In 67 p. 100 of the cases these signs appeared during the first six postpartum weeks. Clinical, radioscopic and echocardiographic features were always those of dilated cardiomyopathy, even when arterial pressure was high. Hypertension was present at first examination in 50.8 p. 100 of the cases, but it remained stable under treatment in 13 p. 100. These data suggest an acute postpartum hypertension. The following risk factors of the disease were identified: rural living, absence of school attendance, low family income, multiparity, identical pathology after a previous pregnancy, postpartum "quarantine" period, ritual ablutions with very hot water, large amounts of sodium in the diet, hypertension, breast-feeding and postpartum oestrogen secretion decrease. Seasonal variations were noted, with doubling of new cases during the hot and humid season. The hypothesis of a latent gravidic myocarditis is discussed: the accumulation of risk factors during the postpartum period might trigger off the clinical disease. Forty seven patients were followed up for a mean period of 15 months. Seven died, 21 (31.8 p. 100) were in complete remission and 19 in partial remission. In case of relapse, complete remission was less frequent and appeared more slowly under treatment. Persistent cardiomegaly under treatment was of poor prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Postpartum cardiomyopathy in the Sudanese-Sahelian area. Clinical and epidemiologic studies of 66 cases]. 250 Sep 9

The atrial natriuretic factor (ANF) is a circulating peptide, consisting of 24 to 28 amino acids. Atrial natriuretic factor is synthetized in atrial cardiomyocytes and stored in specific cytoplasmatic granules. It possesses potent diuretic, natriuretic, and vasorelexant properties. The possible role of ANF in the pathogenesis of hypertension and heart failure was investigated in animal models and in men. We were able to show that the release of ANF from cardiac atria is positively correlated with atrial pressures in both men and rats. In experimental studies, plasma levels of ANF measured by radioimmunoassay, were increased by up to four-fold after acute blood volume expansion. Atrial natriuretic factor release in response to volume loading was markedly attenuated in four-week-old spontaneously hypertensive rats as compared to age-matched normotensive Wistar-Kyoto rats, but a similar responsiveness was found in 16-week-old rats of both strains. This finding can be reconciled with the hypothesis that ANF plays a pathophysiological role in initiating but not maintaining high blood pressure. Clinical studies demonstrate elevated plasma concentrations of ANF in patients with organic heart disease. Further increments in plasma levels of ANF were obtained during physical exercise and after acute volume loading. In patients with congestive cardiomyopathy, the elevated plasma concentrations of ANF reached almost normal levels following improvement of their hemodynamic disturbances after treatment with converting-enzyme inhibitors. These findings suggest that in patients with organic heart disease, plasma concentrations of ANF reflect the hemodynamic burden of the heart and may, therefore, be used as a noninvasive marker of the efficacy of the current cardiac therapy.
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PMID:Atrial natriuretic factor. Its possible role in hypertension and congestive heart failure. 252 5

A cohort of patients with peripartum cardiac failure (PPCF) was followed for 10 years after the initial illness. The follow up rate was 78%. Fifty two per cent of patients improved without further episodes of heart failure. PPCF recurred in 26 per cent. Heart failure unrelated to pregnancy was seen in 13%, and 9% of the patients progressed to dilated cardiomyopathy. Transient hypertension was seen in 87% of patients on admission, and later hypertension was found in 45%. Late hypertension influenced heart size more when recurrent PPCF or progressive heart failure was present. Anaemia on admission had no effect on subsequent heart size. The electrocardiogram may continue to be abnormal for up to 10 years in normotensive patients who had no heart failure. The abnormal electrocardiogram in patients with persistent cardiomegaly may represent progressive myocardial damage. Mortality rate was highest (11%) in the first year and declined thereafter. Cardiac deaths were common in patients with recurrent PPCF or progressive heart failure.
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PMID:Peripartum cardiac failure. A ten year follow-up study. 259 96

Ventricular arrhythmias (VA) are a major cause of sudden death. Life-threatening VA may be present in a variety of both acute and chronic conditions in which cardiac function is compromised: during acute myocardial infarction and subsequent reperfusion; some weeks after acute myocardial infarction, due to residual damage (scar formation with zones of heterogeneity); and as a consequence of congestive heart failure (CHF) resulting from myocardial infarction, dilated cardiomyopathy, hypertension or other causes. Symptomatic suppression of potentially life-threatening VA is unlikely to decrease mortality, since classical antiarrhythmic drugs have failed, so far, to improve life expectancy. Drugs that influence the underlying causes of CHF seem to have a better chance of reducing mortality. There is evidence that ACE inhibitors may exert beneficial effects on arrhythmogenicity by several mechanisms in these situations. Under acute ischaemic conditions both cellular damage and undue increases in circulating catecholamines and angiotensin II may be prevented. This has been demonstrated in various animal models and confirmatory clinical evidence is emerging. Two week after experimental myocardial infarction, the pig heart is less vulnerable to programmed electrical stimulation when ACE inhibitors are administered. Finally, in CHF a variety of proarrhythmic factors, such as left ventricular dysfunction, raised catecholamine levels and, in particular, decreased potassium concentrations, are influenced beneficially by ACE inhibitors.
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PMID:Cardiac arrhythmias--a new indication for angiotensin-converting enzyme inhibitors? 267 45

Alcohol, above certain levels in blood, becomes a depressor of myocardial fiber. Excessive intake of alcoholic drinks is responsible for disrhythmias, congestive heart failure, thromboembolic phenomena and, sometimes, sudden death. Dilated cardiomyopathy is the usual clinical presentation of these patients. More than 60 gr daily of ethanol may be an important factor in the etiology of high blood pressure. Yet, not everything is negative as far as alcohol and heart are concerned. Moderate consumption of ethanol decrease the risk of coronary heart disease, but, regarding the medical and social implications of alcoholic habits, they shall not be encouraged. Finally, it must be emphasized that in cases of disrhythmias, hypertension and deteriorated left ventricular function (ejection fraction below 35%) the use of alcoholic beverages must strongly discouraged. The same applies to patients taking anticoagulants or sedative drugs.
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PMID:[Alcohol and the heart]. 269 11

Although a relationship has been suggested between abstinence from alcohol and improvement in left ventricular (LV) function, no long-term studies in large groups of patients have been done to confirm this impression or to demonstrate an effect on survival. To address these questions, the authors analyzed the outcome in 105 male patients with alcoholic cardiomyopathy and 64 control male patients with nonalcoholic dilated cardiomyopathy. Survival data were available for all patients. The correlates of survival were assessed via the Cox proportional hazards model. Variables considered were age, race, drinking pattern (current drinker versus former drinker), presence of coronary artery disease (CAD), hypertension, and diabetes, and these echo variables: left atrial (LA) size, posterior wall thickness, LV end diastolic dimension (LVDD), minimal E point septal separation, wall motion, presence of incomplete mitral leaflet closure (IMLC) or low cardiac output, and the ratio of relative wall thickness to LVDD. The two study groups were comparable with respect to all echocardiographic variables. At a mean follow-up of 17.2 months +/- 12.1 months, 42.85% of the alcoholics and 41% of the nonalcoholics had died. Nonsurvival in the alcoholic group was significantly associated with only two factors: an increased LVDD and the presence of IMLC. The drinking pattern was not significantly associated with survival. By contrast, in the nonalcoholics,the variables most closely related to survival were LVDD, low cardiac output, increasing age, and abnormal wall motion. Therefore: (1) the risk factors in alcoholic and nonalcoholic cardiomyopathy are similar although IMLC appears to be a relatively specific prognostic factor for alcoholic cardiomyopathy and (2) abstinence from alcohol does not appear to improve survival.
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PMID:Risk factors in alcoholic cardiomyopathy. 270 34

This study was undertaken to clarify the relationship between mild transient hypertension and dilated cardiomyopathy. Fifty-five patients were studied: group 1--controls (12 patients), group 2--hypertensives without clinical evidence of heart failure (14 patients), group 3--patients with hypertensive heart failure and diastolic blood pressure above 100 mmHg (10 patients), group 4--patients with possible dilated cardiomyopathy with mild hypertension, i.e. diastolic blood pressure of 90-100 mmHg (8 patients), group 5--patients with dilated cardiomyopathy and normal blood pressure (11 patients). The haemodynamic status and cardiac contractility indices were measured in each patient on admission, using M-mode echocardiography. Serum sodium and potassium as well as the urinary sodium, potassium and vanillyl mandelic acid excretions were also measured. The stroke volume, cardiac output and cardiac index fell with heart failure, but much more remarkably in group 4. The peripheral vascular resistance was higher in groups 2, 3 and 4 than in groups 1 and 5; so also were the aortic diameter, left posterior wall thickness and left ventricular mass. The plasma volume, aldosterone and cortisol levels were higher and the urinary sodium and potassium excretion lower in patients with heart failure (groups 3, 4 and 5). It is concluded that the raised blood pressure found in some patients suspected to have dilated cardiomyopathy is not due to the haemodynamic and biochemical changes that occur in heart failure. Such patients are 'chronic' hypertensives with hypertensive heart failure. Their presenting blood pressure is low because of their markedly reduced cardiac output.
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PMID:Mild hypertension in patients with suspected dilated cardiomyopathy: cause or consequence? 284 18

Idiopathic dilated cardiomyopathy can present in a number of different ways, with the majority of patients having heart failure. Natural history studies show a poor prognosis for most patients with this disease. However, a substantial number may stabilize or even improve, and have a survival curve similar to patients without the disease. Patients can be stratified for relative risk of mortality by age, cardiomegaly on chest roentgenograph, ventricular function, and quantitative assessment of ventricular arrhythmias. Therapy can be divided into three categories: alteration of factors associated or contributors to ventricular dysfunction, supportive therapy, and investigational therapy. The efficacy of therapy should be judged by its effect on functional capacity and survivorship. The first category includes controlling hypertension and abstaining from alcohol. This often leads to improved functional status, and may improve survival. The second category includes anticoagulant therapy and, most importantly, medications for heart failure (digoxin, diuretics, vasodilators, nonglycoside inotropes, etc.). These agents may improve functional status, but in general have had little impact on survival. Investigational medical therapy for future use depends upon identification of factors involved in the genesis of the disease and the pathophysiologic mechanisms responsible for morbidity and mortality. The inflammatory component in the genesis and/or maintenance of cardiomyopathy, the importance of frequent ventricular arrhythmias in prognosis and the influence of endogenous vasoconstrictors on heart failure and arrhythmias, have been mentioned as such areas of interest.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Natural history of idiopathic dilated cardiomyopathy. Implications for future therapy. 286 54


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