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

The pathological changes in blood vessels observed in primary (essential hypertension) are similar to those seen in secondary hypertension due to renal disease or other causes. In benign hypertension, the major changes are in the small arteries and arterioles especially in the kidney. Interlobular arteries exhibit intimal thickening and duplication of the elastic lamina (elastosis) and there is hyaline change in the media of many arterioles. In some respects these changes are an accentuation of vessel ageing. Malignant hypertension usually presents in a younger age group (35--50 years) and is characterized pathologically by fibrous endarteritis in the interlobular arteries of the kidney and fibrinoid necrosis in the walls of a proportion of the efferent glomerular arterioles. Similar vessel changes are seen in other organs but many of the pathological changes in the heart and brain of patients with benign hypertension are related to the accentuation of arterosclerosis. There is an increased mortality from cardiac failure, myocardial infarction, cerebral haemorrhage and subarachnoid haemorrhage due to ruptured berry aneurysms in patients with benign hypertension. Although there is ischaemic damage to the kidneys in benign hypertension, death from renal failure is uncommon. Severe ischaemic damage to renal glomeruli and renal failure does, however, occur in malignant hypertension.
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PMID:Vascular pathology in hypertension. 46 85

To assess the hemodynamic characteristics in malignant hypertension, echocardiography was performed in 18 patients with malignant essential hypertension (MH-I, n = 9) and secondary hypertension (MH-II, n = 9). Patients with benign hypertension with or without left ventricular hypertrophy (n = 8 and 7, respectively), patients with hypertensive heart failure (n = 7) and normotensive volunteers (n = 10) were subjected to controls. Plasma noradrenaline (NA) and renin activity (PRA) were also measured prior to the antihypertensive therapy. There were no significant differences in the durations of hypertension before the malignant phase, and the mean arterial pressure between MH-I and MH-II. Although posterior wall thickness (PWTd) in MH-II was similar to that in MH-I, interventricular septal thickness (IVSTd) was less marked in MH-II. The plasma NA and PRA were markedly increased in both MH-I and MH-II. End-diastolic dimension (Dd) of the left ventricle was within normal range, but end-systolic dimension (Ds) was significantly increased in MH-I, MH-II and hypertensive heart failure. The moderate decreases in ejection fraction (EF) and mean velocity of circumferential fiber shortening (mVcf) were observed in both MH-I and MH-II. Marked decreases in EF and mVcf were also observed in patients with hypertensive heart failure. The relationship between systolic blood pressure and Dd/PWTd was shifted toward the right and upper portion of the normal relation in MH-I and MH-II. The present study demonstrated that the hemodynamic characteristics in malignant hypertension are an inappropriate left ventricular hypertrophy due to a marked increase in systolic stress; dilatation of the left ventricle in systole; and a moderate decrease in ventricular systolic function. It is suggested that a decrease in left ventricular systolic function in malignant hypertension might be due in part to a marked increase in the influence of neurohumoral factors on hemodynamics.
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PMID:[Echocardiographic features of left ventricular hypertrophy and contractility in malignant hypertension]. 253 Mar 33

Isolated calcium-tolerant rat ventricular cardiomyocytes were used to characterize the effects of atrial natriuretic peptide (ANP), Angiotensin II (AII) and their interaction on the myocardial contraction-/relaxation pattern free of interference from other types of cardiac cells. Binding of 125I-ANP showed a KD of 12 pM and approximately 600 binding sites per cell. At 37 degrees C (rate 140 bpm) ANP decreased the contraction maximum with an EC50 of about 70 pM, maximal decrease was 35%. ANP (10(-7) M) raised cellular cyclic-GMP from 0.76+/-0.12 to 1.32+/-0.13 pmole/10(6) cells (73%, p less than 0.05). Angiotensin II increased contractility by a maximum of 32% at 10(-7) M; the EC50 was 8 x 10(-10) M. AII markedly delayed relaxation (reduction of maximum relaxation velocity from 0.092 to 0.063 mm/s; p less than 0.05). ANP (10(-7) M) increased the effect of AII (10(-8) M) on contractility by 66% without changing relaxation parameters significantly. This unexpected interaction may be relevant in pathological conditions where both AII and ANP are stimulated, such as heart failure or secondary hypertension.
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PMID:Action of atrial natriuretic peptide and angiotensin II on the myocardium: studies in isolated rat ventricular cardiomyocytes. 255 Dec 88

Inhibitors of the renin-angiotensin system, which are promising therapeutic agents with few side effects, have measurably improved the management of many patients with primary or secondary hypertension and those with heart failure. This paper briefly reviews the emerging evidence for the potential risk associated with long-term inhibition of the renin system. The current lack of methodology for quantification of renin-angiotensin inhibition in various tissues, however, precludes firm conclusions. Preliminary evidence suggests that in functional terms, a downregulation of the renin-angiotensin system, if therapeutically successful, is safer than aggressive and longer-lasting inhibition. It has been questioned whether antihypertensive therapy 'normalizes' the structural cardiovascular changes and whether interference with the initial adaptive phase may prove detrimental. However, no specific role for renin inhibition, apart from the antihypertensive effect, has yet been defined.
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PMID:Long-term benefit versus risk in therapeutic blockade of the renin-angiotensin system. 275 14

Chronic infusion of atrial natriuretic factor (ANF) decreased blood pressure in two-kidney, one clip (2-K, 1C), spontaneously hypertensive rat (SHR) and one-kidney, one clip (1-K, 1C) models of experimental hypertension in the rat, but produced increased sodium excretion only in the 1-K, 1C model. In ANF-infused 2-K, 1C animals plasma renin activity did not differ from normotensive controls. Atrial content of immunoreactive (ir) ANF was significantly lower in SHR and 1-K, 1C animals. At 40-50 days old, cardiomyopathic hamsters had a higher concentration of plasma irANF and a lower ANF content in the left but not in the right atrium, although the difference in plasma ANF was more obvious once heart failure was well established. At 110-130 and 200-300 days old, the hamster atrial ANF content was not only lower in the left but also in the right atrium. No differences were observed in plasma irANF between normal subjects and either untreated or treated essential hypertensive patients. However, a significantly higher plasma ANF was observed in two groups with secondary hypertension, primary hyperaldosteronism and renovascular hypertension. Bolus injection of ANF into healthy subjects produced a dose-related decrease in blood pressure and an increase in the heart rate and natriuresis.
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PMID:Some physiopathological aspects of atrial natriuretic factor. 294 34

Serum ANP levels were measured by radioreceptor assay in 40 patients with various forms of secondary hypertension and 6 patients with heart failure. In addition, serum ANP was determined in 4 patients with renal artery stenosis before and after dilatation, as well as in 5 anephric patients before and after haemodialysis. Our results showed elevated serum ANP level in most patients with various forms of secondary hypertension and chronic heart failure. A distinction between these two groups and a control group of healthy individuals was not possible due to the wide range and occasional normal levels in the first two groups. ANP levels in patients with renal stenosis decreased after dilatation but there was no correlation with the success of this procedure. A positive correlation between ANP and plasma renin level was detectable in patients with renal artery stenosis, but was also elevated in anephric patients with absent renin production. In summary, our results show that measurements of serum-ANP are of little significance in the diagnosis of hypertension and chronic cardiac failure.
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PMID:[Diagnostic value of atrial natriuretic peptide in hypertension and heart insufficiency]. 296 83

The available evidence suggests that angiotensin plays an important role in sodium homeostasis not only via aldosterone release but also through control of the renal circulation, and thereby renal sodium handling. Perhaps this intrarenal action is the renin-angiotensin system's original, primitive function. Through its vascular action, angiotensin has an important influence on glomerular filtration and tubular reabsorption. Angiotensin almost certainly also has an additional intraglomerular action. More circumstantial, but compelling, evidence suggests that angiotensin contributes to the renal response in a host of conditions characterized by renal vasoconstriction, a reduction in filtration rate, and sodium retention, including heart failure, cirrhosis of the liver, complications of pregnancy, the renal response to trauma and shock, and in selected patients with essential and secondary hypertension. Pharmacologic interruption of the renin-angiotensin system is proving useful not only for blood pressure control in patients with hypertension but also because of its influence on the kidney in some or all of these conditions--at least in part attributable to restoration of more normal renal sodium handling.
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PMID:The renin-angiotensin system and sodium homeostasis. 620 38

Coarctation of the aorta is an important and treatable cause of secondary hypertension. The prevalence of aortic coarctation varies from 5% to 8% of all congenital heart defects. Neonates and infants, especially when they have other associated cardiac defects, may present with signs and symptoms of heart failure. Children beyond infancy are usually asymptomatic and are most often diagnosed because of a murmur or hypertension on a routine examination. Palpation of the brachial and femoral pulses simultaneously will show decreased and delayed or absent femoral pulses. On measurement of blood pressure from arms and legs, a pressure difference of more than 20 mm Hg in favor of the arms may be considered as evidence for coarctation of the aorta. The coarctation can be demonstrated on suprasternal notch two-dimensional echocardiographic views along with increased Doppler flow velocity across the coarctation site. Cardiac catheterization shows significant peak-to-peak systolic pressure gradient across the coarcted segment, and aortography demonstrates the degree and nature of the aortic narrowing. Aortic coarctation may be relieved by surgery or by balloon angioplasty; in asymptomatic patients, therapy during the ages of 2 and 5 years is suggested. Surgical relief of coarctation may be achieved by resection and end-to-end anastomosis or by subclavian flap or prosthetic path angioplasty. Although results of surgery are generally good, there are some problems with the procedure, namely, mortality, morbidity and recoarctation, particularly in neonates and young infants and development of aneurysm, paraplegia, and paradoxical hypertension. Balloon angioplasty has been used by some cardiologists with resultant relief of obstruction, but concern for development of aneurysms and arterial complications remain. Although the immediate results for surgical or balloon therapy for isolated coarctation are good, long-term prognosis is largely undetermined. Limited long-term follow-up studies suggest significantly lower survival rates compared with normal population; age at intervention and the degree and duration of hypertension before intervention may affect long-term survival.
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PMID:Coarctation of the aorta. 777 27

The human heart secretes both atrial natriuretic peptide and brain natriuretic peptide. This study attempts to clarify the pathophysiological significance of the peptides in cardiovascular diseases. Using immunoradiometric assay, plasma brain natriuretic peptide and atrial natriuretic peptide levels in essential hypertension, various secondary hypertension, chronic renal failure, chronic heart failure during cardiac pacing, and acute myocardial infarction were determined. Mean plasma brain natriuretic peptide and atrial natriuretic peptide levels in healthy subjects were 3.7 +/- 0.3 and 5.7 +/- 0.3 pmol/L, respectively, and increased as a function of age. Plasma brain natriuretic peptide levels showed a larger increase than atrial natriuretic peptide levels in various cardiovascular diseases. In chronic renal failure, whereas plasma atrial natriuretic peptide levels decreased significantly after hemodialysis and were correlated with the changes in body weight, changes in plasma brain natriuretic peptide levels were less prominent and did not show such a correlation. In chronic heart failure, both basal plasma brain natriuretic peptide and atrial natriuretic peptide levels were also significantly elevated. However, in response to acute ventricular or atrial pacing, brain natriuretic peptide levels did not show any increase in contrast to the marked increase of atrial natriuretic peptide levels. In acute myocardial infarction, brain natriuretic peptide levels showed more prominent changes than atrial natriuretic peptide levels and were correlated with serum levels of creatine kinase and cardiac myosin light chain I in most patients. These results suggest that both brain and atrial natriuretic peptides play an important role in the regulation of cardiovascular homeostasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial and brain natriuretic peptides in cardiovascular diseases. 828 65

ACEI form a group of antihypertensives which inhibit the angiotensin II (A II) production and thus not only reduce the blood pressure but exert also a positive metabolic and antiproliferative effect (A II is a proliferative hormone). They are therefore indicated nowadays in the treatment of essential and secondary hypertension, left-ventricular hypertrophy, chronic heart failure, acute myocardial infarction, insulin resistance and other disorders. Despite intensive studies we still do not know many, in particular mediated effects, of ACEI but these drugs have become one of the key groups in therapy.
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PMID:[Pharmacodynamics of angiotensin-converting enzyme inhibitors]. 868 97


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