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

The concept of clinical application of the vasodilator therapy for the treatment of cardiac failure is based on the experimental findings that defined the inverse relationship between force and velocity or extent of muscle shortening at constant muscle lengths. In the intact heart, a new construct has recently been proposed in hopes of better understanding the behavior of the normal or depressed human ventricle in which the shortening during ejection is considered to reflect the appropriateness of the matching between the existing afterload and the level of inotropic state, as modulated by the preload (or Frank-Starling) reserve. In the normal left ventricle, if the preload is not allowed to compensate for an acute increase in afterload, or if the limit of preload reserve is reached, shortening of the ventricular wall will diminish; that is, afterload mismatch will ensue. The view that an afterload mismatch can exist in the basal state provides an explanation for the fact that cardiac output and ventricular function can be improved when afterload is reduced in patients with severe left ventricular failure complicated with acute myocardial infarction or with mitral or aortic regurgitation. However, in the ischemic myocardium, the effect of interventions which alter the afterload on the left ventricular ejection is also determined by the pre-existing ischemic status. Thus, depending on the magnitude of coronary flow reduction, a potentially beneficial drug can be detrimental to an ischemic myocardium.
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PMID:[Afterload reduction and vasodilator therapy (author's transl)]. 703 10

The results of haemodynamic, echocardiographic and bicycle exercise investigations in a 72-year-old man with a permanent complete atrioventricular block and heart failure following infarction are presented. Comparative measurements were obtained under the conditions of a ventricular and an av-sequential pacemaker (PM). The ventricular demand pacemaker (VVI) was implanted three years ago and because of further impairment of cardiac performance an av-sequential pacemaker (DDD) was used to restore atrio-ventricular synchronisation. The treatment with bifocal PM improved dramatically cardiac output and exercise capacity. The echocardiographic findings demonstrate the significance of Frank-Starling mechanism in this case due to better filling of the ventricles. As noninvasive methods, echocardiography and bicycle-exercise test allow long-term analysis of cardiac function.
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PMID:[Hemodynamic and exercise capacity in a 72 years old patient under a ventricular and bifocal pacemaker (author's transl)]. 725 4

Systolic time intervals were measured from simultaneous high speed recordings of the electrocardiogram, phonocardiogram, and carotid artery pulse in 15 men with chronic severe anaemia not in heart failure and with a normal heart size, and in 15 normal men. Heart rates, electromechanical systole (QS2), pre-ejection period index (PEPI), left ventricular ejection time index (LVETI), and the ratio of pre-ejection period to left ventricular ejection time (PEP/LVET) did not differ significantly in the two groups. After the intravenous administration of frusemide in 10 of the anaemic patients, the pre-ejection period index was prolonged, the PEP/LVET ratio increased, heart rate increased, and the left ventricular ejection time index shortened. Intravenous digoxin did not alter the QS2 interval and heart rate significantly in the anaemic subjects. Left ventricular function in chronic severe anaemia as measured by systolic time intervals does not differ from that of normal controls. The effect of frusemide on the systolic time intervals is explained as an effect of the fall in preload, bringing cardiac function further down on the ascending limb of the Frank-Starling curve. Other related studies are discussed.
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PMID:Systolic time intervals in chronic severe anaemia and effect of diuretic and digitalis. 727 17

Adaptation to exercise was studied by post-exercise Doppler echocardiography in patients with chronic cardiac failure and an apparently healthy control population matched for age. This post-exercise Doppler echocardiographic method initially introduced for the detection of myocardial ischaemia has already been validated in normal subjects for the analysis of haemodynamic changes caused by exercise providing the data is recorded in the first 5 minutes following recovery in the recumbent position. Eleven patients with chronic cardiac failure in NYHA classes II or III with a mean age of 54 +/- 11 years and 6 controls (mean age: 46 +/- 9 years) were investigated. The patients had been stabilised for at least 3 months with a vasodilator and diuretic therapy: the control subjects had no medication. After bicycle ergometry performed to 70% of maximum capacity, the subjects were positioned in the left lateral recumbent position. Doppler echocardiography was then performed in the immediate recovery phase. When compared to the control population, the patients with cardiac failure had a reduced chronotropic reserve, a smaller increase in the parameters of myocardial contractility (maximal aortic velocity, maximal aortic acceleration and left ventricular fractional shortening) without an increase in left ventricular end diastolic dimensions in subjects with severe dilatation under basal conditions (left ventricular end diastolic dimension 69 +/- 3 mm). This result suggests the absence of a Frank-Starling effect. The lack of adaptation of the peripheral vascular system was demonstrated by the lack of reduction of left ventricular end systolic stress, already greatly increased at rest (176 vs 77 +/- 10 g/cm2 for patients, compared with controls; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Adaptation to effort in patients with chronic cardiac insufficiency; study by post-exercise Doppler echocardiography, comparative results with a control population]. 764 61

The Framingham heart study has shown that arterial hypertension is the major aetiological factor for the development of heart failure. In the presence of heart failure, various regulatory systems may be operative. These include the Frank-Starling mechanism, the neurohormonal system, regulation of cardiac growth and peripheral oxygen delivery. Recently, the interrelationship of the neuroendocrine system and cardiac growth has been examined. In the pressure or volume overloaded heart, growth of the myocardium involves the enlargement of cardiac myocytes, an adaptation governed by ventricular loading. Non-myocyte cell growth, including cardiac fibroblasts, may also occur. However, the haemodynamic load does not appear to be its major physiological stimulus. Cardiac fibroblast activation is responsible for the accumulation of type I and III collagens, the major fibrillar proteins of the myocardial collagen matrix, while vascular smooth muscle cell growth accounts for medial thickening of coronary resistance vessels. This structural remodelling of the cardiac interstitium represents a major determinant of pathological hypertrophy: it accounts for abnormal myocardial stiffness and impaired coronary reserve, thereby leading to ventricular diastolic and systolic dysfunction and ultimately the appearance of symptomatic heart failure. Several lines of evidence suggest that circulating and tissue renin-angiotensin-aldosterone systems are involved in the structural remodelling of the non-myocyte compartment, including the 'cardioprotective' effects of angiotensin converting enzyme (ACE) inhibition or the beneficial effects of anti-aldosterone treatment that were found to prevent myocardial fibrosis in renovascular hypertension due to unilateral renal ischaemia under experimental conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of the structural remodelling of the myocardium: from hypertrophy to heart failure. 771 13

According to the Framingham Study, arterial hypertension and coronary artery disease are the major etiologic factors in the development of heart failure. Regulatory systems that may affect heart failure include the Frank-Starling mechanism, neurohormonal responses, cardiac growth and peripheral oxygen delivery. Recently, the interrelationship between the neuroendocrine system and cardiac growth has aroused much interest. In the pressure- or volume-overloaded heart, hypertrophic growth of the myocardium includes the enlargement of cardiac myocytes, an adaptation governed by ventricular loading. Nonmyocyte cell growth involving cardiac fibroblasts may also occur but is not primarily regulated by the hemodynamic load. Cardiac fibroblast activation is responsible for the accumulation of fibrillar type I and type III collagens within the interstitium and adventitia of intramyocardial coronary arteries, while vascular smooth muscle cell growth accounts for the medial thickening of these vessels. This remodeling of the cardiac interstitium is a major determinant of pathological hypertrophy in that it accounts for abnormal myocardial stiffness and impaired coronary vasodilator reserve, leading to ventricular diastolic and systolic dysfunction and, ultimately, symptomatic heart failure. Several lines of evidence suggest that the renin-angiotensin-aldosterone system is involved in regulating the structural remodeling of the nonmyocyte compartment; this accounts for the cardioprotective effects of angiotensin converting enzyme (ACE) inhibition, which prevents myocardial fibrosis in rats with renovascular hypertension. In rats with genetic hypertension, established left ventricular hypertrophy, abnormal diastolic stiffness due to interstitial fibrosis and reduced coronary vasodilator reserve associated with medial wall thickening of intramyocardial resistance vessels, the ACE inhibitor lisinopril restored myocardial structure and function towards normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The cardiac structure-function relationship and the renin-angiotensin-aldosterone system in hypertension and heart failure. 782 69

In the presence of a primary disorder in myocardial contractility and/or extraordinary hemodynamic pressure on the heart, ventricular performance depends on several compensating mechanisms. In the past, studies were mostly focused on the importance of the Frank-Starling mechanism and the hypertrophy and dilation of the heart in maintaining a circulation sufficient for metabolic intake during heart failure. Recently, however, the existence of neurohormonal systems has been demonstrated (the sympathetic nervous system, the renin-angiotensin system, atrial natriuretic peptide and several locally produced vasoactive substances), which change considerably according to the severity of the heart failure. While these compensatory mechanisms support the circulation in patients with acute heart failure, in whole or in part, neurohormonal activation over an extended period of time might be harmful to patients with chronic congestive heart failure since several neurohormonal factors might be inappropriately activated. This article will review the key neurohormonal systems and their importance in heart failure on the basis of the current literature.
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PMID:Neurohormonal systems during progression of heart failure: a review. 790 8

Blood flow across the atrioventricular valves and outflow tracts was measured in 55 normal fetuses and 32 fetuses with haemoglobin (Hb) Bart's disease between 18 and 26 weeks of gestation. The mean velocities remained unchanged in both normal and affected fetuses over the gestations studied. The volume flow across both atrioventricular valves and outflow tracts increased as the gestation advanced in both normal and affected fetuses, but was significantly higher in affected than in normal fetuses. The same magnitude of increased flow was found in both hydropic and non-hydropic fetuses with Hb Bart's disease. These findings suggest that fetuses with severe and long-standing anaemia have a remarkable cardiac compensatory mechanism for the maintenance of tissue oxygenation. In response to anaemia and circulatory loading, the cardiac chambers and outflow tracts enlarge proportionately up to twice the normal values. Because of this response and the operation of the Frank-Starling mechanism, the heart is able to maintain a normal mean velocity of propulsion and the net output is increased to two to three times that in normal fetuses. Hydropic changes in these anaemic fetuses appear unrelated to cardiac failure as cardiac failure is not observed at the time that hydropic changes develop.
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PMID:Cardiac blood flow studies in fetuses with haemoglobin Bart's disease. 797 64

Heart failure is a complex clinical syndrome in whose manifestations and prognosis compensatory mechanisms have a prominent role as a response of the organism to an elementary disturbance. There are five basic compensatory mechanisms: the Frank-Starling mechanism, structural changes of the heart, activation of neuroendocrine mechanism, adaptation to hypoxia and anaerobic metabolism. The interaction between the two main neurohumoral mechanisms, namely vasodilatation and vasoconstriction, has been drawing much of the attention recently. Vasoconstriction which evolved into maintaining cardiac output in hypovolemic state, leads to a number of deleterious hemodynamic and metabolic disturbances in heart failure. The organism tends to diminish this negative effects by changing beta adrenergic pathway and by activating vasodilative mechanisms. Once heart failure becomes severe, vasoconstriction predominates due to a loss of normal baroreceptor activity. It is considered that too marked activity of neurohumoral mechanisms is a significant cause of disease progression. By use of contemporary drugs (ACE inhibitors, beta blockers, digitalis), excessive vasoconstrictive mechanisms are tried to be diminished and prognosis of the disease improved.
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PMID:[Pathophysiologic mechanisms of cardiac decompensation]. 817

The maintenance of cardiac pumping ability in the presence of a primary disturbance of myocardial contractility and/or an excessive haemodynamic strain on the heart is dependent on several compensatory mechanisms. Particular attention has formerly been paid to the importance of the Frank-Starling mechanism and cardiac hypertrophy and dilatation in maintaining a blood supply sufficient to cover the metabolic needs of various tissues in heart failure. In recent years, however, it has been found that certain neurohormonal systems (the sympathetic nervous system, the renin-angiotensin-aldosterone system, atrial natriuretic peptide and several locally acting vaso-active substances) undergo considerable changes according to the degree of heart failure. These compensatory mechanisms support the circulation wholly or partially in acute heart failure, however sustained neurohormonal activation may be harmful in chronic heart failure, where several neurohormonal factors may be activated to ill-effect. The most significant neurohormonal systems and their importance in heart failure are reviewed on the basis of the available literature.
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PMID:[Neurohormonal activity in heart insufficiency]. 831 27


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