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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In children with congenital heart disease duration and extent of hyperaldosteronism and the influence of spironolactone after surgery with a heart-lung-machine, were evaluated by direct measurement of plasma aldosterone levels. Secondary hyperaldosteronism as seen in 11 patients without spironolactone-therapy after surgery did not persist very long. 14 children receiving spironolactone immediately after surgery showed an onset of drug efficacy at a period when plasma aldosterone in the group without spironolactone had begun to fall. As a practical consequence, spironolactone treatment should be initiated a few days prior to surgery in order to achieve full efficacy on the day of surgery.
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PMID:[The effect of aldosterone antagonists in juvenile heart surgery]. 50 58

To assess the relation of hyperaldosteronism and potassium depletion to the intensity of diuretic therapy we have measured plasma aldosterone by radioimmunoassay and total exchangeable potassium by radioisotope dilution in 24 patients when they were stable at the end of their preparation for cardiac operation. Some patients required intensive frusemide therapy to reach an optimal state for operation and many showed hyperaldosteronism. Plasma aldosterone was significantly related to daily dose of frusemide (r=0.77). Depletion of total exchangeable potassium expressed in terms of predicted weight was significantly related to plasma aldosterone (r= -0.64). The reduction in total exchangeable potassium is interpreted as chiefly related to loss of lean tissue mass from the wasting that leads to cardiac cachexia, but evidence is presented on the basis of measurements of extracellular fluid volume as sulphate space (20 patients) of entry of sodium into the cells which may indicate a true cellular potassium loss. Although plasma potassium is usually easily maintained with oral potassium supplements or aldosterone antagonists, we postulate that intensive diuretic therapy in severe heart disease may provoke hyperaldosteronism which accentuates potassium loss and may contribute to wasting and to intracellular potassium depletion in critical tissue, such as myocardium.
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PMID:Relation of plasma aldosterone concentration to diuretic treatment in patients with severe heart disease. 50 54

The blood hydrocortisone and corticosterone content and the aldosterone level in the urine were determined for 24 hours in patients with congenital heart disease before and after operative treatment. In patients with symptoms of cardiac insufficiency both glucocorticoid and mineralocorticoid activity of the adrenal cortex was marked by deviations from the diurnal physiological rhythm. This is reflected in the continuous activation of the adrenal cortex during 24 hours; activation of mineralocorticoid function in the evening and during the night is a particularly characteristic phenomenon.
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PMID:[Diurnal rhythm of the adrenal cortex function in patients with circulatory disorders]. 56 52

The paper deals with causes of arterial hypertension in the early postperfusion and postoperative periods in treating congenital heart disease (CHD) under artificial circulation (AC). The hemodynamics and parameters of the renin-angiotensin-aldosterone system (RAAS) were examined clinically and biochemically in 100 patients. The findings showed that under hypothermic perfusion with nonpulsing blood flow, plasma renin activator and angiotensin converting enzyme became activated to affect the dynamics of mean arterial blood pressure. A method for RAAS blockage under AC has been developed, which includes administration of sodium thiopental and baralgin during AC. The method provides for reliable prevention of RAAS components activation and guarantees the normalization of the mean arterial pressure in the postperfusion and early postoperative periods.
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PMID:[Arterial hypertension of unclear etiology as a complication of anesthesia during heart surgery under conditions of artificial circulation]. 235 29

The aim of this paper was to study atrial natriuretic factor, plasma renin activity and antidiuretic hormone values during paroxysmal atrial arrhythmias with different ventricular rates before and after pharmacological cardioversion and during chronic atrial flutter-fibrillation. The study was carried out: 1) during acute arrhythmias (atrial flutter-fibrillation or supraventricular tachycardia) and after restoration of normal sinus rhythm in 2 patients without heart disease, in 13 with chronic heart disease and in 6 with acute myocardial infarction; 2) during chronic atrial flutter-fibrillation in 5 patients with chronic ischemic heart disease, without congestive heart failure. Atrial natriuretic factor, aldosterone, plasma renin activity and antidiuretic hormone values were measured by radio-immunoassay. During paroxysmal atrial arrhythmias atrial natriuretic factor levels were higher than normal in all patients, particularly in those with supraventricular tachycardia. Most of the aldosterone measurements were above the normal range. As far as plasma renin activity and antidiuretic hormone values are concerned, levels higher than the normal range were found in the patients with severe hemodynamic impairment. Central venous pressure was above normal in all patients except in the 2 without heart disease, and there was a positive correlation between atrial natriuretic factor and central venous pressure values. After restoration of normal sinus rhythm atrial natriuretic factor values returned to normal except in acute myocardial infarction patients, in 1 chronic ischemic heart disease patient with congestive heart failure and in 3 patients with mitral valve disease. In all patients with chronic atrial flutter-fibrillation and in 5 patients with acute atrial flutter-fibrillation and low rate, above normal atrial natriuretic factor values were found with normal central venous pressure values. Atrial distension due to high central venous pressure values, lack of atrial contraction and rhythmic detension of the atrial stretch receptors, may be considered the major stimuli responsible for atrial natriuretic factor release during acute paroxysmal atrial arrhythmias and atrial flutter-fibrillation with low ventricular rate, respectively.
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PMID:[Atrial natriuretic factor in acute atrial hyperkinetic arrhythmia and chronic atrial fibrillo-flutter]. 252 75

ANF is a newly discovered peptide hormone that has significant implications for critical care physicians. This hormone, released from the heart, is especially responsive to fluid challenges as well as to many of the drugs commonly used in the ICU, including pressor and anesthetic agents. It has potent arterial vasodilating effects in pharmacologic doses and may be an important natural vasodilating agent, especially in the renal vascular bed. In patients on dopamine, it may potentiate the renal vasodilating effect and may provide an effective therapy for developing acute renal failure. Children with congenital heart disease and patients with CHF have elevated levels that clearly alter the aldosterone-angiotensin II system and may help us to understand and treat these conditions more effectively. Additionally, ANF may be a marker for adequacy of treatment in these disease states. The potential uses for ANF include diuresis in patients with fluid overload and diuretic resistance, treatment of CHF, and as a short-acting vasodilator. In the ICU, many therapies affect cardiac pressures and volume regulation. Positive-pressure ventilation may decrease the release of ANF by decreasing venous return and thus contribute to water retention. Drugs used in the ICU may directly affect ANF levels and markedly affect the homeostasis of fluid and electrolyte balance. This hormone system interacts intimately with renin, angiotensin II, and aldosterone. These interactions may play a significant role in the development of essential hypertension. Although not addressed in this article, the treatment and understanding of essential hypertension may be significantly advanced by understanding these relationships. It is clear that ANF acts as a hormone with complex interactions between the heart, volume status, electrolyte balance, renin-angiotensin II-aldosterone, vasopressin, and vascular tone. Although currently no definitive picture exists for these complex interactions, this is an exciting new hormone with significant implications for patient management in the ICU. As research continues, the picture will become clearer and our understanding of this new hormone more precise.
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PMID:Atrial natriuretic factor in the pediatric intensive care unit. 297 48

Atrial natriuretic peptide (ANP) which is secreted from atrial muscle has been shown to produce relaxation of vascular smooth muscle, anti-hypertensive effects, and natriuresis, and to implicate renin-angiotensin-aldosterone network. In human, ANP (hANP) exists as three subtypes: alpha-, beta-, gamma-hANP which have molecular weight of 3,000, 6,000 and 13,000, respectively. In human tissue hANP has been shown to be present not only in heart atria, but also submandibular gland. In addition, it has been reported that in some conditions of heart disease hANP can be found in the ventricles. However, the exact distribution outside of the atrial system has not been definitely established. In our studies, we attempted by using immunohistochemical methods on human and dog hearts to answer this question. In addition, by using nucleic acid probes we have investigated possible areas where hANP may be synthesized. In the initial studies specific antibody to hANP was prepared in rabbits by immunization with synthetic alpha-hANP coupled to porcein thyroglobulin. The specificity of this antibody was confirmed by Western Immunoblotting. Immunoperoxidase staining demonstrated hANP in His-bundle and major branching bundles as well as atrial wall and AV-node of both human and dog hearts. Ventricular muscle cells outside of the conduction system did not contain hANP. The possibility of non-specific staining by antibody to thyroglobulin was muled out as antibody to thyroglobulin alone never showed positive staining. However, staining of the atrial muscles was always granular in the perinuclear areas, while that of the conduction system was usually diffuse.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Localization of atrial natriuretic peptide in the heart. Immunohistochemical and northern blot analyses]. 297 21

Digoxin has been reported to induce feminizing effects in man. It does not compete for estradiol cytosol receptors in human breast carcinoma cells, however, and has no uterotrophic effect. We therefore investigated whether feminization might be due to digoxin action on plasma concentrations of sex steroids. Six healthy men (31.5 +/- 4 yr old) received therapeutic doses of digoxin for 43 days. We measured plasma concentrations of testosterone, androstenedione, dehydroepiandrosterone, estrone, estradiol, progesterone, 17-hydroxyprogesterone, cortisol, and aldosterone. During 35 days on digoxin levels of these steroids remained in the normal range and there was no change from before-drug values. Digoxin was in the therapeutic range of 1.9 +/- 3 nmol/l throughout. After stimulation by adrenocorticotropic hormone or human choriongonadotropin, the rise in plasma steroids was in the same range as when digoxin was given, as well as 16 wk after it had been discontinued. A normal rise in luteinizing hormone after luteinizing hormone-releasing hormone showed that the hypothalamogonadal feedback was not altered by digoxin. Free testosterone, estradiol, and cortisol concentrations under basal conditions and after stimulation were also the same before and after drug. It is concluded that the estrogen-like activity of digoxin cannot be explained by altered steroid availability from plasma. Feminizing effects attributed to digoxin may be caused by other conditions known to influence sex steroid hormones that are common in patients with heart disease. Our data suggest that digoxin may be the preferred digitalis therapy to avoid feminizing effects.
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PMID:Digoxin does not alter plasma steroid levels in health men. 628 25

Pregnancy causes substantial changes in the cardiovascular system: cardiac output (40%-50%) and blood volume (40%) increase whereas systemic peripheral resistance and arterial pressure decrease. The rise in progesterone and estrogen levels accompanying pregnancy stimulates the renin-angiotensin-aldosterone system. Increased prostaglandin production follows renin activation; simultaneously, the arterial vessels show diminished angiotensin sensitivity. The result is pronounced vasodilatation. Cardiovascular diseases remain the most important nonobstetric cause of maternal death. The physiological changes in the cardiovascular system during pregnancy influence cardiac diseases in different ways. Pregnancy, labor, and delivery appear to be well tolerated in gravidae with an atrial septal defect, ventricular septal defect, and patent ductus arteriosus. Sometimes congestive heart failure occurs and appropriate medical therapy is necessary. Pregnant women with uncorrected cyanotic congenital heart disease (Eisenmenger's syndrome, tetralogy of Fallot) constitute a high-risk group because of right ventricular insufficiency and hypoxic attacks. The consequences for anaesthesia in parturients with congenital heart disease are discussed. The symptoms of acquired mitral or aortic stenosis are aggravated by the physiological changes in the cardiovascular system during pregnancy; the clinical symptoms of valve insufficiency are ameliorated by vasodilatation. Peripartum cardiomyopathy clinically shows similar features to idiopathic dilated cardiomyopathy. The basis of treatment is the same as that of congestive heart failure, with the therapeutic spectrum ranging from diet to heart transplantation. Women with hypertrophic cardiomyopathy tolerate pregnancy, labor, and delivery surprisingly well. Vaginal delivery is possible, but epidural anaesthesia is contraindicated. Hypertensive disorders associated with pregnancy are classified into three groups: chronic, transient, and pre-eclamptic hypertension. Whereas chronic and transient hypertension do not affect the outcome of pregnancy appreciably, pre-eclampsia presents a potential danger to mother and fetus. Pre-eclamptic hypertension is accompanied by low cardiac output and plasma volume. An upregulation of angiotensin receptors enhances vascular reactivity, with the consequence of high peripheral resistance. For antihypertensive therapy hydralazine, alpha-methyldopa, and magnesium sulfate are the drugs of choice. A generalised recommendation of anaesthesia for the pre-eclamptic gravida cannot be made because both general and epidural anaesthesia have risks of severe side effects.
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PMID:[Cardiovascular diseases during pregnancy. Considerations for the anesthesiologist]. 765 90

Chagasic patients with advanced heart disease have fluid retention-dependent symptoms. Since fluid retention is mostly dependent on the renin-angiotensin-aldosterone system, chagasic patients with congestion related symptoms should have activation of the renin-angiotensin-aldosterone system. The purpose of this investigation was to determine the plasma renin activity baseline values of chagasic patients with and without congestive heart failure. Twenty-eight patients with positive serology for Chagas' disease were studied. Nineteen patients were asymptomatic (functional class I New York Heart Association) and nine were symptomatic (functional classes II-IV). Cardiac catheterization and ventricular cineangiography were performed on 20 patients. The symptomatic patients had significantly higher plasma renin activity levels (4.11 +/- 1.03 ng/ml/h) than the asymptomatic patients (1.08 +/- 0.11 ng/ml/h, P < 0.001) and the normal sedentary controls (1.65 +/- 0.22 ng/ml/h, P < 0.05, mean +/- S.E.). The plasma renin activity baseline values of the asymptomatic and symptomatic patients correlated directly with the baseline heart rate (r = 0.77, P < 0.0001). The symptomatic patients had larger ventricular volumes, moderately depressed ejection fractions and increased left ventricular end-diastolic pressures. The plasma renin activity baseline values also correlated directly with the left ventricular diastolic pressures (r = 0.70, P < 0.0006) and with the left ventricular diastolic (r = 0.66, P < 0.001) and systolic volumes (r = 0.67, P < 0.001). These results indicate that chagasic patients with fluid retention-dependent symptoms and hemodynamic evidence of left ventricular systolic dysfunction have activation of the renin-angiotensin-aldosterone system.
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PMID:Plasma renin activity in chagasic patients with and without congestive heart failure. 786 85


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