Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Plasma renin activity was estimated in 11 infants with severe congestive heart failure. The infants had congenital heart disease with left to right shunts and were receiving diuretic treatment. Plasma renin activity was measured by radioimmunoassay of generated concentrations of angiotensin I. The mean (SD) plasma renin activity was 84 (21) ng angiotensin I/ml/hour, which is considerably above normal infant values. A hyperactive renin-angiotensin system may be detrimental in these patients. Angiotensin converting enzyme inhibitors may be of value in treating infants with severe congestive heart failure.
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PMID:Plasma renin activity in infants with congenital heart disease. 331 12

To determine the hemodynamic and clinical effects of long-term positive inotropic stimulation on the myocardium, we treated 31 patients with severe chronic heart failure with oral amrinone (600 mg daily) and performed invasive hemodynamic studies during short- and long-term treatment with the drug. Stroke volume and stroke work indexes increased markedly during the first 48 hr of therapy (p less than .01) but returned to pretreatment values after 2 to 10 weeks; upon drug withdrawal, both variables deteriorated rapidly to values significantly lower than those observed before treatment with amrinone (p less than .01), despite similar values for left ventricular filling pressure, mean arterial pressure, and systemic vascular resistance. This pattern of response indicated that progression of the underlying heart disease had occurred during treatment with amrinone and contributed importantly to its failure to produce long-term benefits. Progression of left ventricular dysfunction was associated with a progressive increase in heart rate and plasma renin activity and a decline in serum sodium concentration. Clinically, amrinone therapy was complicated by sustained symptomatic ventricular tachycardia in four patients, worsening myocardial ischemia in four patients, and worsening congestive heart failure in eight patients, all of whom had been stable before entry into the study; only three of the 31 patients improved clinically. Ten patients died during the first 2 weeks of treatment, and 16 (52%) were dead within 3 months, a mortality rate twice as great as that seen during comparable trials with vasodilating drugs. Although noncardiac adverse effects were frequent, they were not the primary reason for drug failure. In conclusion, long-term therapy with amrinone may accelerate progression of left ventricular dysfunction, exacerbate myocardial ischemia, and provoke life-threatening ventricular tachyarrhythmias, thereby shortening survival in patients with severe chronic heart failure. Prolonged administration of inotropic drugs may achieve short-term gains at the expense of long-term detrimental effects on the myocardium.
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PMID:Hemodynamic and clinical limitations of long-term inotropic therapy with amrinone in patients with severe chronic heart failure. 638 99

The aim of the study was to compare the changes in plasma renin activity induced by a vasodilator in normal dogs and in dogs with an impaired cardiac reserve. In normal conscious dogs, a 60-min nitroprusside infusion increased plasma renin activity from 1.05 +/- 0.26 to 8.35 +/- 1.20 ng, angiotensin I ml-1 h-1 (P less than 0.002) and heart rate from 83 +/- 6 to 149 +/- 15 beats/min (P less than 0.002). In five dogs in which a aortocaval fistula had been created 4 weeks earlier, the same infusion still increased plasma renin activity but significantly less than in normal dogs (0.90 +/- 0.29 to 4.44 +/- 0.64 ng ml-1 h-1; P less than 0.01) and the heart rate was unchanged (134 +/- 4 to 139 +/- 7 beats/min; NS). Similarly, in five dogs with a previous myocardial infarction, the heart rats response to nitroprusside was blunted (108 to 107 beats/min;NS) and plasma renin activity increased less than in normal dogs. Plasma renin activity also increased acutely after hydralazine administration in dogs which myocardial infarction (1.05 +/- 0.26 to 8.99 +/- 0.79 ng ml-1 h-1; P less than 0.05); after 1 week of hydralazine, plasma volume had increased from 54.9 +/- 0.9 ml kg-1 to 74.5 +/- 4.9 ml kg-1 (P less than 0.05) and plasma renin activity remained higher than control (4.66 +/- 0.66 ng ml-1 h-1; P less than 0.01). In conclusion, vasodilator therapy rapidly activates vasoconstrictor forces and fluid retention even in dogs with limited cardiac reserve. Although the regulation of plasma renin secretion appears altered in these models of heart disease, the renin response remains sufficient to seriously limit the beneficial effects of vasodilator therapy.
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PMID:Changes in plasma renin activity and haemodynamics during vasodilator therapy in conscious dogs with myocardial infarction or chronic volume overload. 641 20

In this review, hypotheses are discussed with regard to the role of local, tissue renin-angiotensin systems in the progression of cardiovascular dysfunction. After local renin-angiotensin systems had been described as functionally distinct systems, recent experimental studies have suggested an association between hyperactivity of these local renin-angiotensin systems, and cardiovascular dysfunction. Moreover, the existence of these local renin- angiotensin systems has been confirmed in humans, and early data indicate that the human cardiac renin-angiotensin system may be activated in heart disease. Furthermore, polymorphisms in genes coding for the renin-angiotensin system seem associated with hypertension and left ventricular hypertrophy. These observations may be clinically relevant as inhibition of local renin-angiotensin systems may be an important prerequisite to obtain an optimal clinical effect.
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PMID:Hyperactive tissue renin-angiotensin systems in cardiovascular dysfunction: experimental evidence and clinical hypotheses. 761 22

Antihypertensive drug therapy can lower blood pressure and prolong life, but many hypertensive patients continue to develop further risk factors and to die prematurely of heart disease. Antihypertensive drugs can also interfere with the patient's quality of life, and many are not compatible with the concomitant medical conditions of the patient and the medications taken to treat them. For these reasons, the antihypertensive therapy selected should meet the specific and complete needs of each patient, not just treat the high blood pressure. An analysis of the drugs that inhibit the renin-angiotensin system suggests that several of these drugs have a more favorable therapeutic profile than other classes of hypotensive agents. The newly developed receptor-site-specific blockers are expected to be tolerated better by hypertensive patients and, consequently, to enhance their quality of life. The first of the new class of nonpeptide blockers of the AT1 receptor, losartan--which has no partial agonist activity--is likely to have the advantages of the angiotensin-converting enzyme inhibitors without their adverse effects, notably cough. In selected patients, the AT1-receptor blockers could become the drugs of first choice for the management of hypertension.
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PMID:Antihypertensive therapy targeted to the needs of the patient: focus on the renin-angiotensin system; older and newer agents. 763 60

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

The effect of the angiotensin I-converting enzyme (ACE) inhibitor benazepril (55 mg/kg orally) on the preservation of cardiac performance in diabetic-hypertensive Dahl S rats was investigated. Diabetes mellitus was produced by streptozotocin. Fasting (4-h) blood glucose levels were 279 +/- 50 mg/dL in diabetic Dahl salt-sensitive v 79 +/- 5 mg/dL in nondiabetic Dahl salt-sensitive rats. Cardiac performance was determined at the end of 8 weeks in an isolated perfused working heart apparatus. Peak left ventricular pressure (LVPmax), left ventricular peak negative dP/dt, and coronary flow were depressed in diabetic Dahl S rats (P < or = .05 v control). These deficits in cardiac function were not observed in diabetic Dahl S rats chronically treated with benazepril. The beneficial effects of benazepril apparently were independent of systolic blood pressure reduction. Although plasma ACE activity was increased in diabetic Dahl S rats, plasma renin activity was reduced. This suggests that the beneficial effects of ACE inhibition may be due to an effect upon the kinin system rather than the renin-angiotensin system. The benazepril-associated preservation of cardiac function in this study suggests that ACE inhibitors may be beneficial in the treatment of diabetic heart disease.
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PMID:Preservation of left ventricular function and coronary flow by angiotensin I-converting enzyme inhibition in the hypertensive-diabetic Dahl rat. 782 56

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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