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

Assessment and evaluation of cardiac function have become commonplace in the care of cardiac patients with acute or chronic disorders, since therapy of most cardiac diseases is designed specifically to improve ventricular function. Now, various techniques are available for quantitative measurements of the size, shape and motion of the ventricle. Ventricular dysfunction is defined with two components, systolic and diastolic dysfunction, and can be described hemodynamically in terms of the ventricular pressure-volume diagram. Pure systolic dysfunction is associated with a depression in the end-systolic pressure-volume relation, using the Frank-Starling relation to restore cardiac output toward normal. In contrast, pure diastolic dysfunction is associated with preservation of the end-systolic pressure-volume relation but distortion of the diastolic relation, showing higher diastolic pressure at any given volume. However, in patients presenting clinically with heart failure, both systolic and diastolic dysfunction are usually observed. In this context, factors and disorders that influence ventricular dysfunction are described, considering extrinsic or intrinsic to the ventricular chambers.
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PMID:[Assessment and evaluation of cardiac function]. 833 84

Invasive techniques have been important to assess the ventricular function. The approach for assessing function is based on measurement of cardiac output which depends on preload, afterload and contractility. Stroke work over a range of end-diastolic pressures was examined and termed the function curve. Clinical application of Frank-Starling principle is useful for characterizing heart failure. The isovolumic phase (positive dp/dt) and ejection phase index (ejection fraction) are responsive to acute change in contractility. The pressure-volume loop can be constructed by measurement of pressure and volume. The slope of end-systolic pressure-volume relation (ESPVR) is an expression of contractility. The linear relationship between stroke work and end-diastolic volume has been also proposed. The arterial system is characterized by the end-systolic pressure-stroke volume relationship and the slope is called as effective arterial elastance (Ea). One can evaluate stroke volume by coupling frame work between ESPVR and Ea. The isovolumic indices during diastole (negative dp/dt, time constant) can show impaired relaxation. The several factors influence the diastolic pressure-volume relation.
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PMID:[Invasive diagnostic technique for heart failure]. 833 93

Cardiac insufficiency is hemodynamically characterised by reduced cardiac output and increased diastolic filling pressure at rest and/or during physical activity. The increase in diastolic filling pressure compensates cardiac output and is either a result of increased initial tension of muscle fibers (Frank-Starling's Law) or a sign of decreased myocardial compliance. Increased initial tension of muscle fibers is a sign of systolic insufficiency, whereas reduced ventricular compliance indicates a disorder of diastolic ventricular function. In systolic insufficiency (= systolic dysfunction) a decrease in the ventricular ejection fraction is important, as is an increase in filling pressure. In diastolic congestive heart failure (= diastolic dysfunction) a reduced ventricular compliance with normal stroke function is typical.
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PMID:[Hemodynamics in heart failure: systolic and diastolic dysfunction]. 835 72

Myocardial cells are able to adapt the cardiac pump function rapidly and widely to the changing requirements of vital organs through intrinsic and extrinsic regulatory mechanisms. This regulation is achieved by alteration of [Ca2+]i mobilization, Ca2+ sensitivity of myofibrils or both. Frank-Starling's mechanism achieved by alteration of Ca2+ sensitivity and force-frequency relation, primarily due to modulation of [Ca2+]i mobilization, are important intrinsic mechanisms. As extrinsic mechanisms, catecholamines play a crucial role by activation of both beta- and alpha 1-adrenoceptors through cyclic AMP, and products of phosphoinositide hydrolysis, as messengers, respectively. Adenosine and ACh act via similar transduction processes, including Gi or Gk proteins coupled to inhibition of adenylate cyclase, or activation of K+ channels. Most of these regulations are modulated and constitute crucial pathophysiological mechanisms in chronic heart failure.
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PMID:[Signal transduction in regulation of myocardial contractility]. 839 32

The therapeutic efficacy of cardiac glycosides is not widely appreciated either in respect of their positive inotropic value or antiarrhythmic activity. Although cardiac glycosides do not prevent an increase in ventricular rates during exercise they do slow the heart rate at rest in patients with atrial fibrillation. The clinical importance of the potentially beneficial influence of the digitalis glycosides on the negative force-frequency relationship (Bowditch effect), preload-force relationship (Frank-Starling's Law) and baroreceptor dysfunction in heart failure await clarification. In patients with heart failure, the positive inotropic effects of the digitalis glycosides are mild, but show no tolerance during prolonged administration. Digitalis glycosides are the only group of positive inotropic drugs that persistently increase the ejection fraction during long-term administration in patients with heart failure. These haemodynamic benefits are translated into decreased symptoms and increased exercise capacity in patients with congestive heart failure. Although their clinical efficacy in the different stages of heart failure remains undefined, recent evidence indicates that their therapeutic benefit is on a par with diuretics and ACE inhibitors in symptomatic heart failure. Results of studies specifically directed to determining the impact of the cardiac glycosides on prognosis are awaited.
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PMID:Digitalis--friend or foe? 852 79

In youth, properties of the human arterial system are such that pulse pressure generated by ventricular ejection is low, and the major component of wave reflection returns to the heart after the aortic valve has shut, so making no contribution to ventricular load, but boosting pressure throughout diastole and so aiding coronary perfusion. That constitutes optimal arterial function and optimal vascular/ventricular interaction. With ageing, the aorta and elastic arteries stiffen, so that aortic pulse pressure is markedly increased. This is a consequence of a direct stiffening effect on the aorta itself, and of an indirect effect caused by early return of wave reflection consequent upon stiffening of the whole arterial system with an increase in its pulse wave velocity. There is a change in contour of the aorta pressure wave with wave generation of a late systolic peak and disappearance of the diastolic wave; the reflected wave moves from diastole and systole. Because the lowest diastolic pressure remains relatively constant [1,10], increased pulse pressure causes a substantial increase in aortic systolic pressure. Increased aortic systolic pressure is associated with increased left ventricular pressure and leads to left ventricular hypertrophy. Sustained elevation in systolic pressure and persistent left ventricular hypertrophy are associated with progressive degenerative changes in the hypertrophied myocytes such that these weaken, developing less force with each contraction. The weakened, hypertrophied fibres lengthen and the ventricle dilates, with force and cardiac output initally being maintained at greater muscle length and ventricular volume through the Frank-Starling mechanism. Ultimately compensation is lost. The hypertrophied ventricle normally functions as a flow source, which is capable of generating flow even against very high pressure. With the development of cardiac failure through muscle weakening, the ventricle comes to act as a pressure source, with ventricular output very sensitive to pressure and to changes in pressure. The normal ventricle functions in an intermediate position, even though it is closer in behaviour to a flow than to a pressure source. Wave reflection adds to pressure but subtracts from flow. In youth, wave reflection returns to the heart during diastole when the aortic valve is shut. Negative flow is not possible, so wave reflection is apparent only as a secondary pressure wave in the ascending aorta. In older subjects, when the left ventricle is beating powerfully, return of wave reflection during systole has less obvious an effect on the ascending aortic flow wave, but causes an obvious secondary boost to pressure in the ascending aorta and left ventricle. Hence, under normal circumstances, wave reflection at the heart is apparent as a positive secondary pressure wave, either because the aortic valve is shut when this wave returns, or because the ventricle possesses enough power that it virtually overcomes any negative influence on flow when reflection returns during systole. When the myocardium weakens and the heart fails, the heart starts to behave like a pressure source, and wave reflection starts to have a far greater effect on flow; wave reflection is manifested more as a negative influence on flow than as a positive influence on pressure. As heart failure develops, there is a progressive change in flow wave contour, with early deceleration of aortic flow and ultimately, abbreviation of systolic ejection duration with fall in stroke volume. Early wave reflection is the major factor in the genesis of systolic hypertension. Early wave reflection remains a major factor when heart failure develops, although its effect is apparent in reduction of late systolic flow rather than as a boost to late systolic pressure. Reduction in wave reflection through use of vasodilatory agents is a logical strategy in treatment of systolic hypertension. That type of therapy is equally logical in treatment
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PMID:Haemodynamic basis for the development of left ventricular failure in systolic hypertension and for its logical therapy. 872 7

In chronic heart failure, various regulatory systems including the Frank-Starling mechanism, the neuro-hormonal response, cardiac growth and peripheral oxygen delivery may be operative. Recently, the inter-relationship of the renin-angiotensin-aldosterone system (RAAS) and cardiac growth has drawn clinical interest. In the pressure-or volume-overloaded heart, the development of myocyte growth is primarily dependent on ventricular loading. Non-myocyte cell growth involving cardiac fibroblasts may also occur but this is not primarily regulated by the haemodynamic 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. In addition to relaxation abnormalities due to impairment of sarcoplasmic Ca(2+)-ATPase activity, this remodelling of the cardiac interstitium represents a major determinant of pathological hypertrophy in that it accounts for abnormal myocardial stiffness, leading to ventricular diastolic and systolic dysfunction and ultimately the progression of symptomatic heart failure. The effector hormones of the RAAS, angiotensin II (AngII) and aldosterone (Aldo), appear to be primarily involved in promoting the adverse structural remodelling of the myocardial collagen matrix. In cultured adult cardiac fibroblasts, AngII and Aldo have been shown to stimulate collagen synthesis while AngII additionally inhibits matrix metalloproteinase I activity, which is the key enzyme for degradation of fibrillar collagen in the cardiac interstitium, leading to excessive collagen accumulation. These findings may serve as rationale as to why angiotensin converting enzyme inhibition or blockade of the RAAS represents such remedial therapy beyond the effect of simply unloading the heart in patients with congestive heart failure.
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PMID:The renin-angiotensin-aldosterone system and myocardial collagen matrix remodelling in congestive heart failure. 868 74

The progression of heart failure is related to activation of neuroendocrine hormone systems. On the level of the myocardium, they contribute to hypertrophy, dilation and remodeling of the ventricles. In addition, vascular alterations with endothelial dysfunction and alterations of skeletal muscle contribute to clinical symptoms of heart failure patients. Changes in ventricular geometry during the progression of cardiac diseases are associated with specific subcellular alterations on the level of the myocytes. Especially, disturbed intracellular Ca2+ handling resulting in altered excitation contraction coupling may lead to impaired systolic and diastolic function. Disturbed Ca2+ homeostasis has been associated with reduced re-uptake capacity of the sarcoplasmic reticulum for Ca2+ and an enhanced activity of the sarcolemmal Na+/Ca2+ exchange. In consequence, alterations in force-frequency behavior were attributed to a decline in intracellular Ca2+ transients at higher stimulation rates. The reduced expression of myocardial beta-adrenoceptors and alterations on the level of the G-proteins result in a reduced activity of adenylate cyclase and reduction in intracellular cAMP content of the myocytes. In consequence, reduced phosphorylation of intracellular functional proteins in the failing human heart contributes to altered Ca2+ handling. The Frank-Starling-mechanism seems to be unaltered in failing isolated human myocardium. Endothelin and angiotensin may contribute to the regulation of myocardial contractility in the human heart, but their functional relevance in the regulation of myocardial contractility under clinical conditions remains to be evaluated.
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PMID:[New aspects of the pathophysiology of heart failure]. 965 96

We report a rare case of idiopathic thrombocytopenic purpura (ITP) associated with acute myocardial infarction (AMI). A 72-year-old woman with hypertension and hemorrhoids was admitted because of chest pain, severe anemia (RBC 340 x 10(4)/microliter, Hb 5.4 g/dl, Ht 21.7%) and thrombocytopenia (0.2 x 10(4)/microliter). AMI was diagnosed by electrocardiogram (ST elevation and negative T in V2-5), echocardiogram (hypokinesis in anteroseptal wall) and laboratory (CPK 470 U/l) findings and was treated with only blood transfusion. Chest pain disappeared the day after admission, and neither heart failure nor arrhythmia occurred. Based on bone marrow findings (hyperplasia of erythroblast and megakaryocyte), endoscopic (internal hemorrhoids) and laboratory (antiplatelet antibody positive, platelet associated IgG 257.8 ng/10(7) cells) findings, iron deficiency anemia and ITP were diagnosed. Anemia improved after blood transfusion, but thrombocytopenia (< 1.0 x 10(4)/microliter) without active bleeding continued after steroid and gamma-globulin therapy. At discharge, electrocardiogram showed a negative T in I, aVL and V2-5, and T1 and BMIPP myocardial scintigram showed defects in the anteroseptal and apical wall.
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PMID:[An elderly case of idiopathic thrombocytopenic purpura associated with acute myocardial infarction]. 1061 30

There are a number of misconceptions that first-year medical students have concerning the pathophysiology of heart failure. These stem from 1) a poor definition of heart failure, 2) a lack of care in distinguishing between similar but distinct concepts, and 3) the inability to recognize the relationship between the various stages of heart failure and the clinical manifestation of the disease. In this paper we provide a list of some of the misconceptions that we have encountered, some explanations of the distinctions to be made, and some of the rationale behind current surgical procedures and drug treatment. The misconceptions include failing to differentiate between the Frank-Starling mechanism and cardiac dilation as well as not grasping the significance that changes in cardiac beta-receptor function have in limiting the positive inotropic actions of circulating catecholamines. Finally, we review some of the altered neurohumoral mechanisms in heart failure and explain the basis for some common therapeutic approaches, including the use of angiotensin-converting enzyme inhibitors, in this disease.
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PMID:Common misconceptions that arise in the first-year medical physiology curriculum concerning heart failure. 1064 52


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