Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To elucidate the physioanatomic roles of the pericardium, the alterations in gross anatomy and cardiac motion induced by posture were examined by two-dimensional echocardiography in seven patients with total absence of the left pericardium. Ten healthy subjects were served as controls. The heart was located deeper within the chest at end-diastole in patients with pericardial defect than in healthy subjects, especially in the left lateral decubitus position. With progression of systole, the cardiac apex swung anteriorly with the cardiac base as the fulcrum, and the heart approximated the normal position at end-systole. The deeper the position of the center of the cross-section of the left ventricular cavity at end-diastole, the more exaggerated the swinging motion in systole. The deep location of the heart in end-diastole is considered to result from release from pericardial support, and the systolic tonus of the cardiac muscle restores the apex to nearly normal position. The characteristic swinging motion of the heart and its alterations dependent of posture seemed the signs suggestive of total absence of the pericardium. The shape of the short-axis view of the left ventricular cavity was nearly circular throughout the cardiac cycle. Therefore, paradoxical motion of the ventricular septum observed on M-mode echocardiography in pericardial defect results from the anterior shift of the entire heart overcoming the proper motion of the interventricular septum. The left ventricular dimension become enlarged according to the postural change from the right to left lateral decubitus positions regardless of the presence or absence of the pericardium. The right ventricular cavity became enlarged in the left lateral decubitus position in patients with pericardial defect. The elevation of hydrostatic pressure due to postural change was considered excessive due to the absence of the pericardium. In the left lateral decubitus position, systolic excursions of the mitral and tricuspid rings became more prominent in healthy subjects, whereas these excursions, particularly of the tricuspid ring, were reduced in patients with pericardial defect. Depressed tricuspid ring motion was also observed in the right lateral position in cases with pericardial defects. The reduced excursion of the tricuspid, ring and the right ventricular dilatation may affect systemic venous return to the right atrium.
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PMID:[Pericardial defect: roles of the pericardium on kinetoanatomic changes of the heart influenced by patients' postures]. 378 82

Feline and canine cardiomyopathies (primary myocardial diseases) were reviewed and divided into three groups based on the clinical, hemodynamic, angiocardiographic, and pathologic findings: (1) feline and canine hypertrophic cardiomyopathy, (2) feline and canine congestive (dilated) cardiomyopathy, and (3) feline restrictive cardiomyopathy. All three groups consisted predominantly of mature adult male cats and dogs. Cardiomyopathy in the hamster and turkey was also reviewed. The most common presenting signs were dyspnea and/or thromboembolism in the cat, systolic murmurs with gallop rhythms on auscultation, cardiomegaly with (groups 1 and 3) or without (group 2) pulmonary edema, abnormal electrocardiograms, elevated left ventricular end-diastolic pressures, and angiocardiographic evidence of mitral regurgitation with left ventricular concentric hypertrophy (group 1), left ventricular dilatation (group 2), or midventricular stenosis (group 3). Some cats in groups 1 and 3 also had evidence of left ventricular outflow obstruction. The principal pathologic findings in all of the cats and dogs were left atrial dilation, hypertrophy, increased septal:left ventricular free wall thickness ratio with disorganization of cardiac muscle cells (group 1); dilatation of the four chambers with degeneration of cardiac muscle cells (group 2); and extensive endocardial fibrosis and adhesion of the left ventricle (group 3). Aortic thromboembolism was commonly observed in the cats of all three groups. These clinical and pathologic findings indicate that cardiomyopathy in the cat or dog is similar to the three forms of cardiomyopathy in humans (hypertrophic, congestive, and restrictive).
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PMID:Animal models of primary myocardial diseases. 644 12

A case of a HIV infected 61-year-old bisexual male with dilated cardiomyopathy (DCM) is reported. The death was originally recorded as from undetermined causes, but on autopsy, his heart showed left ventricular dilatation macroscopically, variety in size and vacuolation of cardiomyocyte, partial deciduation of cardiac muscle and diffuse perivascular fibrosis microscopically. These findings were compatible with DCM which was compounded by excessive weight loss. The further data indicated that the etiology of DCM in this case was directly related to the HIV infection.
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PMID:[An autopsy of an HIV infected patient with dilated cardiomyopathy (DCM)]. 774 97

The present study reports the development and characterization of a murine model of right ventricular dysfunction following graded constriction in the pulmonary artery via microsurgical approaches. To analyze in vivo ventricular function, a technique of x-ray contrast microangiography was developed to allow the quantitative analysis of ventricular volumes and of ejection fraction in normal and pressure-overloaded right ventricle. Severe, chronic pulmonary arterial banding for 14 days resulted in right ventricular dilatation and dysfunction, associated with right atrial enlargement, and angiographic evidence of tricuspid regurgitation. These effects were dependent on the extent of hemodynamic overload, since more moderate pulmonary arterial constriction resulted in hypertrophy with maintenance of right ventricular function. With severe pulmonary artery constriction, the murine right ventricle displays a failing heart phenotype including chamber dilation with reduced function that resembles right ventricular dysfunction in man during chronic pulmonary arterial hypertension. Northern and immunoblot analyses demonstrate a marked down-regulation of phospholamban mRNA and its corresponding protein with both levels of constriction, while a less pronounced but significant depression of sarcoplasmic reticulum Ca(2+)-ATPase protein was observed with severe overload, suggesting that this pattern is an early genetic marker of ventricular dysfunction. By coupling mouse genetics with this murine model and the ability to assess cardiac function in vivo, one should be able to test the role of the down-regulation of phospholamban and other defined alterations in the cardiac muscle gene program in the onset of the failing heart phenotype.
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PMID:Molecular and physiological alterations in murine ventricular dysfunction. 814 76

Stunned myocardium is a syndrome of reversible contractile failure that frequently complicates coronary artery disease. Cardiac excitation is uncoupled from contraction at the level of the myofilaments. Selective proteolysis of the thin filament protein troponin I has been correlated with stunned myocardium. Here, transgenic mice expressing the major degradation product of troponin I (TnI1-193) in the heart were found to develop ventricular dilatation, diminished contractility, and reduced myofilament calcium responsiveness, recapitulating the phenotype of stunned myocardium. Proteolysis of troponin I also occurs in ischemic human cardiac muscle. Thus, troponin I proteolysis underlies the pathogenesis of a common acquired form of heart failure.
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PMID:Transgenic mouse model of stunned myocardium. 1064 51

Although apoptosis contributes significantly to remodeling of the fetal heart during evolution of cardiac chambers and correct routing of the great vessels, it has been believed that apoptosis does not occur in terminally differentiated adult cardiac muscle cells. However, apoptosis has recently been demonstrated in animal models of heart failure as well as in explanted hearts from patients with end-stage heart failure undergoing cardiac transplantation. Ventricular dilatation and neurohormonal activation, the hall-marks of heart failure, lead to upregulation of transcription factors, induce muscle cell hypertrophy and prepare cells for entry into the cell-division cycle. However, since terminally differentiated myocytes cannot divide, they die by apoptosis. It has been proposed that low-grade apoptosis in failing heart may be responsible for inexorable decline in left ventricular function. Better understanding of the molecular and cellular basis of apoptosis in the failing myocardium may lead to development of strategies aimed at preventing progressive myocyte loss and deterioration in left ventricular function.
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PMID:Apoptosis in heart failure: a tale of heightened expectations, unfulfilled promises and broken hearts em leader. 1464 78

Dilated cardiomyopathy is a disorder of the cardiac muscle in which myocyte cytoskeletal weakness leads to ventricular dilatation and congestive cardiac failure. Most commonly, the etiology of non-ischemic cardiomyopathy is unknown (idiopathic) and, in our practice, the second most common cause is advanced valvular heart disease. Functional mitral valve regurgitation occurs in up to 40% of patients with heart failure due to dilated cardiomyopathy and contributes to a vicious cycle of volume overload, further left ventricular dilatation, and worsening mitral valve regurgitation and heart failure. Surgical management of mitral valve regurgitation in dilated cardiomyopathy may carry a high risk and can be very challenging. However, operative risk is mitigated by continued vigorous medical management and judicious perioperative care. For example, at our Clinic, mortality for mitral valve repair or replacement in 43 patients with non-ischemic cardiomyopathy having operation between 1993 and 2002 was 2.3%. Additional procedures to reverse cardiac remodeling have not proven to be uniformly successful and continue to undergo scientific scrutiny. Clinical outcome of mitral valve surgery in non-ischemic dilated cardiomyopathy compares well with cardiac transplantation in the early-to-intermediate term, but the long-term results are less satisfactory. For our patients having mitral valve repair, the 1-, 3-, and 5-year survivorships were 84%, 80% and 33%. Evolving technology and research that focus on methods of altering or reversing cardiomyopathy; e.g., cell transplant, may have significant impact on the future management of this debilitating illness.
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PMID:Mitral valve surgery in non-ischemic cardiomyopathy. 1573 70

A 35-year-old woman has suffered from faintness with cardiovascular failure at the end of a sclerotherapy session for varix management. The injected product was Aeloxisclerol (DCI lauromacrogal 400). The death came up very quickly. The autopsy didn't reveal any traumatic lesion. The anaphylactic choc could be ruled out. Macroscopically, the heart showed a right ventricular dilatation. The toxicological analysis didn't reveal any medicinal substances. Histology showed the presence of lipid degeneration of all the right-ventricle wall The discussion is carried out on the role played by this previous health-state on the onset of death, and also on the incidence of sclerotherapy using this product. and the onset of death. We are carrying out this discussion by taking in mind the nature of the product injected and the information available in the literature concerning the lipid degeneration of cardiac muscle. Quickly after this case, the AFSSAPS (The French Agency for Sanitary Security of Health Products) has emitted an written alert which correlates with the requirements of principles of precaution although it is not founded on the totality of investigation results done for this medicolegal case.
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PMID:[Case of death occurred after an injection of aetoxisclerol. The responsibility of the product should be discussed]. 1670 Jan 52

Induction of cardiac muscle regeneration following myocardial infarction (MI) represents a major challenge in cardiovascular therapy, as the current clinical approaches are limited in their ability to regenerate a new muscle tissue and to replace infarcted myocardium. Here, we describe the conception of two strategies based on bio-inspired materials, aimed at myocardial repair after MI. In the first strategy, alginate biomaterial was designed with affinity-binding moieties, enabling the binding of heparin-binding proteins and their controlled presentation and release. The combined features of this unique alginate hydrogel, as a temporary extracellular matrix replacement and a depot for bio-molecules such as insulin-like growth factor-1 and hepatocyte growth factor, led to improvements in cardiac structure and function, as demonstrated by the biomaterial's abilities to thicken the scar and prevent left-ventricular remodeling and dilatation. Endogenous regeneration occurring at the infarct as manifested by the enhanced angiogenesis, cardiomyocyte proliferation, and appearance of cardiac-related stem cells is likely to have contributed to this. In the second strategy, phosphatidylserine (PS)-presenting liposomes were developed to mimic apoptotic cells bodies, specifically their capability of immunomodulating activated macrophages into anti-inflammatory state. In a rat model of acute MI, targeting of PS-presenting liposomes to infarct macrophages after injection via the femoral vein was demonstrated by magnetic resonance imaging. The treatment promoted angiogenesis, the preservation of small scars, and prevention of ventricular dilatation and remodeling. Collectively, the two bio-inspired material-based strategies presented herein represent unique and clinical accessible approaches for myocardial infarct repair.
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PMID:Bioengineering the infarcted heart by applying bio-inspired materials. 2165 74

Myocarditis is a multifactorial disorder, characterized by an inflammatory reaction in the myocardium, predominantly triggered by infectious agents, but also by antigen mimicry or autoimmunity in susceptible individuals. Unless spontaneously resolved, a chronic inflammatory course concludes with cardiac muscle dysfunction portrayed by ventricular dilatation, clinically termed inflammatory cardiomyopathy (Infl-CM). Treatment strategies aim to resolve chronic inflammation and preserve cardiac function. Beside standard heart failure treatments, which only play a supportive role in this condition, systemic immunosuppressants are used to diminish inflammatory cell function at the cost of noxious side effects. To date, the treatment protocols are expert-based without large clinical evidence. This review describes concept and contemporary strategies to alleviate myocardial inflammation and sheds light on potential inflammatory targets in an evidence-based order.
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PMID:A Toolbox of Potential Immune-Related Therapies for Inflammatory Cardiomyopathy. 3244 Sep 11


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