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

Chronic myocardial ischemia is the leading cause of disturbances in myocardial contractility (myocardial infarction) or hemodynamic overload upon the left ventricle. The heart reactions consist in a series of adaptative mechanisms in order to maintain its pump function: Frank-Starling mechanism, myocardial hypertrophy and neurohumoral activation. In heart failure, the cardiac output is maintained by an increase of the preload which enhances the contractility (Frank-Starling law). Myocardial ischemia influences the systolic and diastolic function. The decrease of cardiac output leads to neurohumoral responses which, in the initial stages of cardiac failure are compensatory; along with the progression of the disease, they exert adverse effects. Increased activity of the sympathetic nervous system induces high cardiac rates, chronotropic incompetence. Activation of the renin-angiotensin system held to myocardial and vascular hypertrophy, vasoconstriction, fluid retention. Endothelin is the most powerful vasoconstrictor; its plasmatic concentrations correlate with the severity of the disease. Vasodilator mediators released in cardiac failure are the natriuretic peptide, nitric oxide, dopamine, prostacicline, bradikinin.
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PMID:[Heart failure due to ischemia--the adaptive mechanisms]. 1075 79

Complex paracrine interactions exist between endothelial cells and cardiac myocytes in the heart. Cardiac endothelial cells release (or metabolize) several diffusible agents (e.g., nitric oxide [NO], endothelin-1, angiotensin II, adenylpurines) that exert direct effects on myocyte function, independent of changes in coronary flow. Some of these mediators are also generated by cardiac myocytes, often under pathological conditions. This review focuses on the role of NO in this paracrine/autocrine pathway. NO modulates several aspects of "physiological" myocardial function (e.g., excitation-contraction coupling; myocardial relaxation; diastolic function; the Frank-Starling response; heart rate; beta-adrenergic inotropic response; and myocardial energetics and substrate metabolism). The effects of NO are influenced by its cellular and enzymatic source, the amount generated, the presence of reactive oxygen species, interactions with neurohumoral and other stimuli, and the relative activation of cyclic GMP-dependent and -independent signal transduction pathways. The relative physiological importance of endothelium- and myocyte-derived NO remains to be established. In pathological situations (e.g., ischemia-reperfusion, left ventricular hypertrophy, heart failure, transplant vasculopathy and rejection, myocarditis), NO can potentially exert beneficial or deleterious effects. Beneficial effects of NO can result from endothelial-type nitric oxide synthase-derived NO or from spatially and temporally restricted expression of the inducible isoform, inducible-type nitric oxide synthase. Deleterious effects may result from (1) deficiency of NO or (2) excessive production, often inducible-type nitric oxide synthase-derived and usually with concurrent reactive oxygen species production and peroxynitrite formation. The balance between beneficial and deleterious effects of NO is of key importance with respect to its pathophysiological role.
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PMID:Paracrine and autocrine effects of nitric oxide on myocardial function. 1076 May 46

The progression of heart failure is related to local and systemic neuroendocrine activation. On the level of the myocardium, neuroendocrine activation (angiotensin II, endothelin, aldosterone, norepinephrine) as well as mediators of inflammation and free oxygen radicals contribute to hypertrophy, dilation and remodeling of the ventricles. In addition, vascular endothelial dysfunction and alterations of skeletal muscle contribute to clinical symptoms of heart failure patients. Changes in ventricular geometry during the progression of cardiac disease 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+/Ca(2+)-exchanger. In consequence, alterations in force-frequency behavior were attributed to a decline in intracellular Ca2+ transients at higher stimulation rates. The reduced expression and desensitization of myocardial beta-adrenoceptors and alterations on the level of the G-proteins result in a reduced basal and catecholamine-stimulated activity of adenylate cyclase and a reduction in intracellular cAMP content. 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 isolated human myocardium from failing hearts. 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:[Pathophysiological basis of heart failure]. 1085 87

One of the most salient physiological characteristics of cardiac muscle is that a dilated heart pumps more vigorously, a phenomenon known as the Frank-Starling relationship (see Allen and Kentish, 1985). At least two cellular mechanisms participate in this phenomenon: the reduction of the interfilament lattice spacing which favors the formation of cross-bridges (Wang and Fuchs, 1995) and the increased affinity of troponin C (TnC) for calcium (Ca2+) (Babu et al., 1988). In the latter case, it has been established that TnC itself is not the length sensor (Moss et al., 1991). The intracellular structure(s) able to sense changes in cell length has always been challenged and is still not known. We previously observed on intact isolated cardiac cells that active tension is more closely related to passive tension than to sarcomere length per se (Cazorla et al., 1997). This might have some physiological implications in the working heart since we found that sub-epicardial cells are more supple than sub-endocardial cells. In the present work on skinned cells, we studied the relationship between different levels of passive tension (modulated by a mild trypsin digestion) and the shift in pCa50 of tension-pCa relations induced by a stretch of cells from 1.9 to 2.3 microns sarcomere length. A significant correlation was obtained between passive tension and the stretch-induced shift in pCa50, or stretch-sensitivity of the active force. These observations led us to assume that titin might play a role in sensing cell length to modulate the contractile activity. Besides, it is known that myocardial infarcted cells are less sensitive to stretch. We propose that, in such a rat model, alterations of titin might participate in heart failure.
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PMID:Is titin the length sensor in cardiac muscle? Physiological and physiopathological perspectives. 1098 82

Congestive heart failure is a major and growing public health problem. Because of improved survival of myocardial infarction patients produced by thrombolytic therapy or per-cutaneous revascularization it represents the only form of cardiovascular disease with significantly increased incidence and prevalence. Clinicians view this clinical syndrome as the final common pathway of diverse pathologies such as myocardial infarction and haemodynamic overload. Insights into mechanisms for heart failure historically derived from physiological and biochemical studies which identified compensatory adaptations for the haemodynamic burden associated with the pathological condition including utilization of the Frank Starling mechanism, augmentation of muscle mass, and neurohormonal activation to increase contractility. Therapy has largely been phenomenological and designed to prevent or limit the deleterious effects of these compensatory processes. More recently insights from molecular and cell biology have contributed to a more mechanistic understanding of potential causes of cardiac hypertrophy and failure. Many different analytical approaches have been employed for this purpose. These include the use of conventional animal models which permit serial observation of the onset and progression of heart failure and a sequential analysis of underlying biochemical and molecular events. Neonatal murine cardiomyocytes have been a powerful tool to examine in vitro subcellular mechanisms devoid of the confounding functional effects of multicellular preparations and heterogeneity of cell type. Finally, significant progress has been made by utilizing tissue from human cardiomyopathic hearts explanted at the time of orthotopic transplantation. Each of these methods has significant advantages and disadvantages. Arguably the greatest advance in our understanding of cardiac hypertrophy and failure over the past decade has been the exploitation of genetically engineered mice as biological reagents to study in vivo the effects of alterations in the murine genome. The power of this approach, in principle, derives from the ability to precisely overexpress or ablate a gene of interest and examine the phenotypic consequences in a cardiac specific post-natal manner. In contrast to conventional animal models of human disease which employ some form of environmental stress, genetic engineering involves a signal known molecular perturbation which produces the phenotype.
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PMID:Cardiac hypertrophy and failure: lessons learned from genetically engineered mice. 1167 32

A hundred and six clinically diagnosed cases of epidemic dropsy, admitted in June to August 1998 to the P-III unit of RML Hospital and the Department of Pediatrics, Safdarjang Hospital, were studied. All of them consumed mustard oil contaminated with Argemona mexicana, confirmed by ferric chloride and nitric acid tests. No specific sex predilection was seen. No child was affected below the age of 3 years. Pedal edema and reddish hyperpigmentation were the most consistent findings (100 per cent). Frank cardiac failure was seen in only 24 (22.64 per cent), yet persistent tachycardia was alarmingly high (104/106, i.e. 98.4 per cent). Notably ECG showed prolonged Q-T interval in 24 children (22.64 per cent), unrelated to serum Ca2+ level in patients with congestive cardiac failure (CCF). Color Doppler echocardiography showed biventricular dilatation in all the 24 patients with CCF. Wide pulse pressure was recorded in two patients only. Mortality occurred in only two patients (1.89 per cent). Eye involvement was a late finding. All those who survived (i.e. 104/106) recovered completely, except two patients who were left with sarcoid-like changes of skin telangiectasia.
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PMID:A two-centre collaborative study on clinico-epidemiological profile of a recent outbreak of epidemic dropsy in New Delhi (India) with special emphasis on its cardiac manifestations in pediatric patients. 1169 29

It is now clear that diastolic heart failure (DHF) is an important, perhaps even dominant form of heart failure in older Americans. However, our knowledge base regarding the epidemiology, pathophysiology, natural history, and therapy of this relatively recently recognized disorder is limited. A number of normal age related changes in the heart and vascular system may predispose to or lower the threshold for expression of DHF. Recent reports from large population-based observational studies indicate that over 50% of persons 65 years and older who have heart failure have normal LV systolic function (presumed DHF). Among these, 45% have no other confounding variables (coronary, valvular, or pulmonary disease) and meet the criteria for isolated DHF. DHF is substantially more common in older women than men. A history of systemic hypertension and left ventricular hypertrophy are almost invariably present. Mortality rates are about 50% lower in DHF than in systolic heart failure (SHF) when stable outpatients are considered. However, in hospitalized and very elderly patients, the mortality rate appears similar in DHF and SHF. Furthermore, due to its higher prevalence, the total mortality in the older population attributable to DHF exceeds that of SHF. Morbidity in DHF is substantial and approaches that of SHF. In the chronic setting, DHF patients can have severe exercise intolerance related to failure of the Frank-Starling mechanism with reduced peak cardiac output, heart rate, and stroke volume and increased LV filling pressure. DHF patients also appear to have increased vascular stiffness, accelerated systolic blood pressure response to exercise, neuroendocrine activation, and reduced quality of life. Acute exacerbations (pulmonary edema) frequently occur and are associated with severe hypertension, sodium indiscretion, and medication non-compliance. Surprisingly, overt myocardial ischemia appears to infrequently play a role in these acute exacerbations. Therapy is currently empiric and multicenter, randomized, controlled trials are urgently needed. Anecdotally, control of blood pressure appears to improve symptoms and reduce the frequency of acute exacerbations. In addition, non-pharmacologic intervention, including multi-disciplinary case management is useful.
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PMID:Diastolic heart failure in the elderly. 1179 Sep 20

A 77-year-old man who had undergone coronary artery bypass grafting (CABG) to segment 3, 7 and 12-14 with saphenous vein grafts (SVG) 15 years before, and ligation of coronary arteriovenous (AV) fistula 8 years before was admitted to our hospital, and diagnosed as acute heart failure and idiopathic thrombocytopenic purpura. Coronary angiography showed multiple stenosis of three vessels, and the grafts to segment 3 and 7 were occluded. The area of left anterior descending (LAD) had no viability, but the inferior wall had viability on dobutamine load echocardiography. The platelet count was about 5.0 x 10(4)/mm3. Minimally invasive direct coronary artery bypass (MIDCAB) for right coronary artery (RCA) using right internal thoracic artery (RITA) was performed through right parasternotomy. Operative and postoperative bleeding was slight, and postoperative course was uneventful. Reoperative MIDCAB can be safely performed in a patient with idiopathic thrombocytopenic purpura, and should be considered a viable alternative for highrisk patients.
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PMID:[Minimally invasive direct coronary artery bypass in a patient with idiopathic thrombocytopenic purpura; report of a reoperative case]. 1242 40

Endothelin-1 is involved in mechanical load-induced cardiac growth processes; it also has effects on contractility. The interaction of endothelin-1 and the Frank-Starling response is unknown. The present study aimed to characterize the role of endothelin-1 in the regulation of the Frank-Starling response, one of the major mechanisms regulating cardiac contractile force, in both normal and hypertrophied hearts. Nontransgenic rat hearts and hypertrophic hearts of hypertensive double transgenic rats harboring human angiotensinogen and renin genes were studied in a Langendorff isolated heart setup with a liquid-filled balloon inside the left ventricle used to measure contractile parameters. The rats were studied at compensated phase, before showing any signs of heart failure. Compensated hypertrophy in double transgenic rat hearts resulted in improved contractility at a given level of preload when compared with nontransgenic rat hearts. Hearts of both rat lines showed preserved Frank-Starling responses, that is, increased contractile function in response to increased end-diastolic pressure. The mixed endothelin A/B receptor antagonist bosentan attenuated the Frank-Starling response by 53% (P<0.01) in the double transgenic hearts but not in nontransgenic hearts. The diastolic parameters remained unaffected. The left ventricles of the double transgenic rat hearts showed an 82% higher level of endothelin type A receptor mRNA and a 25% higher level of immunoreactive endothelin-1 compared with nontransgenic rat hearts. The type 1 angiotensin II receptor antagonist CV-11974 had no significant effect on contractile function in response to load in either strain. These results show that endogenous endothelin-1 contributes to the Frank-Starling response in hypertrophied rat hearts by affecting systolic performance.
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PMID:Endothelin-1 contributes to the Frank-Starling response in hypertrophic rat hearts. 1251 36

A need exists for a mock circulation that behaves in a physiologic manner for testing cardiac devices in normal and pathologic states. To address this need, an integrated mock cardiovascular system consisting of an atrium, ventricle, and systemic and coronary vasculature was developed specifically for testing ventricular assist devices (VADs). This test configuration enables atrial or ventricular apex inflow and aortic outflow cannulation connections. The objective of this study was to assess the ability of the mock ventricle to mimic the Frank-Starling response of normal, heart failure, and cardiac recovery conditions. The pressure-volume relationship of the mock ventricle was evaluated by varying ventricular volume over a wide range via atrial (preload) and aortic (afterload) occlusions. The input impedance of the mock vasculature was calculated using aortic pressure and flow measurements and also was used to estimate resistance, compliance, and inertial mechanical properties of the circulatory system. Results demonstrated that the mock ventricle pressure-volume loops and the end diastolic and end systolic pressure-volume relationships are representative of the Starling characteristics of the natural heart for each of the test conditions. The mock vasculature can be configured to mimic the input impedance and mechanical properties of native vasculature in the normal state. Although mock circulation testing systems cannot replace in vivo models, this configuration should be well suited for developing experimental protocols, testing device feedback control algorithms, investigating flow profiles, and training surgical staff on the operational procedures of cardiovascular devices.
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PMID:Characterization of an adult mock circulation for testing cardiac support devices. 1476 90


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