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

In a survey of 3 California communities by the Stanford Heart Disease Prevention Program, we obtained data on blood pressure, medications, age, height and weight, blood for measurement of plasma renin activity (PRA), plasma renin concentration (PRC), plasma renin reactivity (RR), and plasma renin substate concentration (PRS), and urine for measurement of urinary sodium and creatinine. No effect of conjugated estrogens (Premarin) on blood pressure could be discerned when the blood pressure, corrected for age and relative weight, of 575 women on no medication was compared to that of 82 women taking only Premarin. Premarin increased PRA, PRS, and RR, but had no effect on PRC. We also found in both Premarin-treated woman and controls 1) that RR was positively correlated with PRS, and 2) that PRA is dependent on PRC and PRS. These data indicate that the reninrenin substrate reaction of plasma, even at normal substrate concentration, is strongly deprendent on PRS.
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PMID:The effect of conjugated estrogens on the renin-angiotensin system. 19 9

Intrarenal distribution of blood flow was measured by the 133xenon washout curve in 33 patients with heart disease. Plasma renin activity and sodium concentration were also measured on the day when the xenon study was performed. The patients were divided into three groups according to cardiac index: Group I whose cardiac index showed higher than 3.50 1/min/M2, BSA, group II whose index ranged from 2.50 to 3.50, and group III who had lower than 2.50. Total renal blood flow was significantly decreased in group II (p less than 0.001), as compared with normal controls. The percents of the total renal blood flow supplied to component I decreased significantly in group I, II (p less than 0.05) and group III (p less than 0.01). The flow rate in component I decreased significantly only in group II (p less than 0.05) and group III (p less than 0.01). There was a significant increase in the percent distribution of component II in group II (p less than 0.05) and in group III (p less than 0.01). The flow rate of component II showed a slight increase in group I and III. The study of autoradiographs done in dogs with heart failure demonstrated that component I corresponded to a cortical area having a relatively faster flow rate, whereas component II corresponded to the cortical area which was perfused more slowly. Accordingly, component III indicated outer medulla. There was no apparent relation between intrarenal distribution of blood flow and plasma renin activity although the latter tended to be elevated in patients treated with diuretics. In view of the data available it was concluded that outer cortical as well as outer medullary blood flow are decreased in chronic congestive heart failure and that there is no apparent correlation between outer cortical flow and plasma renin activity.
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PMID:Intrarenal distribution of blood flow and renin in chronic congestive heart failure. 111 37

1. Nine paatients with clinically unimportant heart disease or benign essential hypertension were given frusemide intravenously during right-heart catheterization. 2. Pressures in both atria decreased rapidly and in parallel. The magnitude of the pressure decrease was clearly related to decrease in plasma volume loss. 3. Plasma renin activity increased significantly after 5 min (P less than 0-01), but did not correlate with plasma volume loss. 4. Venous tone in the forearm was unchanged. 5. It is concluded that the pressure reduction was secondary to plasma volume depletion through diuresis and that increased plasma renin activity was mainly caused by intrarenal changes.
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PMID:The early effects of intravenous frusemide on central haemodynamics, venous tone and plasma renin activity. 120 85

The effect on plasma renin activity of intravenous furosemide combined with saline replacement of the volume depletion was studied in twelve patients with insignificant heart disease. In ten of the patients the investigation was repeated without saline replacement. It was found that saline infusion, reducing or eliminating hemoconcentration, had no significant influence on the marked plasma renin increase. In eight of the patients the combined furosemide-saline study was performed during right-hear catheterization. Decrease in atrial pressures, known to occur within 15 min after furosemide intravenously, was virtually absent with the saline replacement. It is concluded that plasma volume reduction after intravenous furosemide is responsible for decreased filling pressures of the ventricles but not for plasma renin increase.
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PMID:Unimpeded plasma renin increase after intravenous furosemide during saline replacement. 125 93

The renin-angiotensin system (RAS) plays a major role in the control of blood pressure and cardiovascular homeostasis and is involved in the pathogenesis of a number of cardiovascular disorders. The efficacy of angiotensin-converting enzyme (ACE) inhibitors in the treatment of hypertension and congestive heart failure has led to the widespread clinical use of ACE inhibitors in primary or secondary prevention of heart disease. The demonstration of the expression of the components of the RAS in several extrarenal tissues, as well as local generation of angiotensin II, has confirmed the existence of a tissue RAS that may serve organ-specific functions and act independently from the plasma RAS. The concept of paracrine/autocrine functions of the local RAS has changed our understanding of the functions of the RAS and suggests that tissue ACE inhibition may be of greater importance than inhibition of circulating ACE in the treatment of congestive heart failure and other cardiovascular disorders. Whereas the circulating endocrine RAS appears to be responsible for mediation of acute effects, the tissue RAS seems to be involved in more chronic situations, such as secondary structural changes of the cardiovascular system, and therefore could contribute to the pathogenesis of hypertension as well as other cardiovascular disorders, such as cardiac hypertrophy, coronary artery disease, and atherosclerosis. Several experimental and clinical findings suggest that reversal of cardiovascular structural changes secondary to cardiovascular disease and enhancement of renal sodium excretion by ACE inhibitors are important long-term antihypertensive actions possibly mediated by inhibition of the tissue RAS.
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PMID:Effects of angiotensin-converting enzyme inhibitors on tissue renin-angiotensin systems. 141 88

Cardiac hypertrophy in heart disease is associated with a deterioration of the patient's prognosis. From experimental work it is known that hypertrophy can recede, sometimes it is, however, associated with an undesirable increase of fibrous tissue in the heart muscle. In clinical practice we can reduce cardiac hypertrophy (assessed mainly by echocardiography), at least in some patients, by reducing or eliminating the evoking cause (e.g. in sportsmen terminate training, in aortic valve disease by replacement of the valve, in hypertonic patients we reduce the pressure by drugs). After regression of hypertrophy later also the amount of fibrous tissue recedes and as a rule the function does not deteriorate. Lately we are trying to influence factors which directly participate in the hypertrophy of the myocytes, in particular in hypertonic subjects by preferential action on the adrenergic system and the renin angiotensin system.
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PMID:[Is it possible to treat cardiac hypertrophy?]. 214 May 23

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

It seems established that hypertension, to some degree, is a frequent consequence of cardiac transplantation. The hypertension occurs de novo and is not related to whether hypertension was present in association with the heart disease that led to the need for transplantation. The etiology of this hypertension is multifactorial and varies depending on the time that has ensued after transplantation. Acutely, it is primarily a problem related to intravascular volume expansion and persistently increased systemic vascular resistance. Although it may be modest in severity, it seems to be particularly resistant to therapy with most antihypertensive drugs. Moreover, the total "hyperbaric impact" of the hypertension is rendered greater because the blood pressure and heart rate in these patients with denervated hearts fails to show the usual 10 to 15 percent fall when recumbent/asleep at night, which occurs in normotensive individuals and in most with hypertension of other etiologies. The major factor in the persistence of the hypertension through the later stages post-transplantation appears to be the cyclosporine that is used as an immunosuppressive. Although cyclosporine has been the major contributor to reduced rejection in these individuals, and to their increasingly prolonged survival, it inevitably produces slowly progressive impairment of renal function. The damage to the kidney is reflected both in tubular as well as glomerular and vascular damage, with a steady fall in glomerular filtration and a rise in creatinine. From our studies it appears that the renal alterations are associated with a gradual rise in plasma renin activity and angiotensin II, which perhaps further damages the kidney and causes persistence of the increased systemic vascular resistance. The use of lower doses of cyclosporine during the ischemic phase in the kidney that immediately follows surgery and of reduced doses over time, often with azathioprine added, seems to minimize the renal damage, or at least to stabilize it and to slow progression of the renal dysfunction and hypertension. Treatment of the hypertension with conventional drugs has definite but limited value. Diuretics and vasodilators have been the mainstay of our approach during the early phases of the hypertension but our recent data indicate that ACE inhibitors may become relatively specific in management during the later phases of the post-transplantation period as PRA levels rise in response to vascular damage by cyclosporine. ACE inhibitors have inherent dangers that require careful monitoring.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypertension following orthotopic cardiac transplantation. 240 98

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

Exercise testing has assumed a position of growing importance in the assessment of patients with chronic congestive heart failure. The hemodynamic and neurohumoral adjustments that occur during dynamic exercise are very complex, but are basically designed to ensure that oxygen delivery is commensurate with oxygen demand. These responses are clearly altered in the presence of certain types of heart disease. Patients with chronic congestive heart failure have an attenuated heart rate and blood pressure response throughout exercise, but this is most clearly evident when the data are expressed as a percent of peak oxygen consumption (VO2) rather than as a function of absolute VO2. Likewise, the sympathetic response to exercise is altered in patients with heart failure. Plasma norepinephrine is normally augmented as a function of VO2 during exercise, but this augmentation occurs during the later stages (beyond 50% of peak VO2). Patients with congestive heart failure show a greater than normal augmentation of plasma norepinephrine during exercise when the data are expressed in terms of absolute VO2. However, when the data are expressed as a percent of peak VO2, there appears to be a relative attenuation of the sympathetic response to exercise. Current information suggests that increased plasma norepinephrine and renin activity during exercise in patients with heart failure are not directly related to a decrement in nutritive blood flow to skeletal muscles. The mechanisms responsible for exercise intolerance in patients with heart failure are not known, but do not seem directly related to a decrement in cardiac output or an increase in left ventricular filling pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic and neurohumoral responses to dynamic exercise: normal subjects versus patients with heart disease. 289 Apr 48


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