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)

Cardiac abnormalities were studied using the clinical, electrocardiographic and echocardiographic methods in 66 patients with systemic scleroderma. Abnormal ecg was seen in 41 patients (62.1%), most frequently in form ventricular extrasystole (21.2%), incomplete block of the right bundle branch (12.1%), left ventricular and right atrial hypertrophy (10.6%) each, and the pattern suggesting the history of past myocardial infarction (7.6%). Abnormal echocardiographic results were found in 38 patients (57.6%). The most usual changes, differentiating that group from the controls, were: sluggish diastolic movement of the posterior wall of the left ventricle (40.7%), pericardial effusion (37.0%), elongation of the isovolumic relaxation time diastole phase (99.3 s.m.v. 81.1 ms, p less than 0.001) and right ventricular dilatation. There were no significant differences between the scleroderma and the control group as regards the indices of the contractility of the left ventricle: ejection fraction (EF), velocity of circumferential fibres shortening (VCF), diastolic size of the left ventricle and of the left atrium. The prevalence of the electrocardiographic and echocardiographic abnormalities in particular types of scleroderma (diffuse, acroscleroderma, severe acroscleroderma, CREST) was roughly similar: 50-76%. Finding of the impaired diastolic rather than systolic function of the left ventricle and of the similar prevalence of the cardiac abnormalities in the particular types of scleroderma is new and contradictory to the commonplace opinions.
Pol Arch Med Wewn 1989 Feb
PMID:[Electrocardiographic and echocardiographic evaluation of cardiac changes in systemic scleroderma]. 261 59

Angiotensin-converting enzyme (ACE) inhibitors are now established drugs in the treatment of hypertension and heart failure. The renin-angiotensin-aldosterone system is complex and acts as a circulating hormonal system, a local endogenous tissue system and neuromodular. Current experimental evidence suggests that ACE inhibitors reduce the risk associated with atherosclerotic cardiovascular disease. The antiatherogenic action of ACE inhibitors is related to complex effects mediated by these agent, including an antiproliferative and antimitotic action, beneficial effects on endothelial function, plaque-stabilizing effects and the action of these agents on the sympathetic nervous system. The role of ACE inhibitors in preventing the clinical sequale of atherosclerotic cardiac disease has been evaluated in various patient populations. Several small trial assess the effects of ACE inhibitors in severity of angina pectoris have reported conflicting results, with benefit is some patients and no benefit or even exacerbation of angina in others, indicating that ACE inhibitors do not have consistent antianginal effects in short-term study. ACE inhibitors have the theoretical potential to prevent restenosis after PTCA but they do not prevent restenosis and has no effect on overall clinical outcome. New data suggest that ACE inhibitors may be effective therapy fir patients following acute myocardial infarction. The renin-angiotensin system, is activated during new myocardial infarction and has an impact on the process of remodeling of the left ventricle which causes ist dysfunction and heart failure. In most of the large mortality trials the rationale for early treatment with ACE inhibitors after myocardial infarction was stated. ACE inhibitors have a positive effect in preventing the ventricular dilatation and they reduce the rate of reinfarctions and the mortality rate.
Pol Merkur Lekarski 1998 Jan
PMID:[The significance of converting enzyme inhibitor angiotensin I to angiotensin II in treatment of patients with coronary disease]. 955 7

Mitral regurgitation may result from left ventricular dilatation and cause progression of heart failure. Percutaneous techniques for mitral valve repair are under development. Techniques utilizing a trans-coronary venous approach exploit the anatomical relationship between the mitral annulus and the venous system of the heart. The coronary sinus, great cardiac vein and the origin of the anterior interventricular vein surround the posterior mitral annulus. This enables percutaneous approaches to annuloplasty for mitral regurgitation. Devices can be implanted into the coronary veins that modify the shape and size of the mitral annulus. We present a case of ischaemic mitral regurgitation successfully treated by use of a percutaneous approach, the Carillon Mitral Contour System. Significant reduction of the mitral regurgitation jet was observed. The patient was discharged 4 days after the procedure. During the follow-up visits, the patient showed an improved general condition and increased exercise capacity. Procedural steps are shown in detail and the current status of the coronary sinus based technique is discussed. Percutaneous techniques for mitral valve repair may be an attractive alternative to cardiac surgery in heart failure patients with secondary mitral regurgitation. The Carillon Mitral Contour System is under ongoing clinical evaluation in the AMADEUS trial.
Kardiol Pol 2007 Mar
PMID:Percutaneous valve repair for mitral regurgitation using the Carillon Mitral Contour System. Description of the method and case report. 1743 55

In the pathogenesis of dilated cardiomyopathy (DCM) in Emery-Dreifuss muscular dystrophy (EDMD) matrix metalloproteinases (MMPs) are supposed to be involved and may have diagnostic/prognostic value. Serum levels of MT1-MMP, MMP-2 and MMP-9 were quantified by ELISA and zymography in 22 EDMD patients and 15 age-matched controls. In the autosomal-dominant EDMD MMP-2 and MT1-MMP were increased in all cases, and MMP-9 was increased in two of the eight examined patients. In the X-linked EDMD MMP-2 expression was increased in all the cases, MMP-9 level was elevated in 3 of the 14 cases, and MT1-MMP was decreased in eight of these patients. There was no evident correlation between the MMPs level and the different cardiac parameters including left-ventricular end-diastolic diameter, left atrial diameter and left ventricular ejection fraction in either form of EDMD. The presented results indicate that a changed level of matrix metalloproteinases, especially that of MMP-2 in serum, may be of value for detection of cardiac involvement in EDMD patients, especially in those patients with no evident subjective cardiac symptoms. Further follow-up studies of MMPs are needed to check if their determination is of value for monitoring of the progression of atrial/ventricular dilatation. MMPs determinations may also be useful for monitoring DCM treatment by synthetic MMPs inhibitors.
Acta Biochim Pol 2009
PMID:Matrix metalloproteinases in serum of Emery-Dreifuss muscular dystrophy patients. 1999 54

Coordinated functional balance of negative and positive transcription complexes maintain and accommodate gene expression in hearts during quiescent and hypertrophic conditions, respectively. Negative elongation factor (Nelf) complex has been implicated in RNA polymerase II (pol II) pausing, a widespread regulatory transcriptional phenomenon observed across the cardiac genome. Here, we examine the role of NelfA aka, Wolf-Hirschhorn syndrome candidate 2 (Whsc2), a critical component of the negative elongation complex in hearts undergoing pressure-overload induced hypertrophy. Alignment of high-resolution genome-wide occupancy data of NelfA, Pol II, TFIIB and H3k9ac from control and hypertrophied hearts reveal that NelfA associates with active gene promoters. High NelfA occupancy is seen at promoters of essential and cardiac-enriched genes, expressed under both quiescent and hypertrophic conditions. Conversely, de novo NelfA recruitment is observed at inducible gene promoters with pressure overload, accompanied by significant increase in expression of these genes with hypertrophy. Interestingly, change in promoter NelfA levels correlates with the transcript output in hypertrophied hearts compared to Sham, suggesting NelfA might be playing a critical role in the regulation of gene transcription during cardiac hypertrophy. In vivo knockdown of NelfA (siNelfA) in hearts subjected to pressure-overload results in early ventricular dilatation and dysfunction, associated with decrease in expression of inducible and cardiac-enriched genes in siNelfA hypertrophied compared to control hypertrophied hearts. In accordance, in vitro knockdown of NelfA in cardiomyocytes showed no change in promoter pol II, however significant decrease in in-gene and downstream pol II occupancy was observed. These data suggest an inhibited pol II progression in transcribing and inducible genes, which reflects as a decrease in transcript abundance of these genes. These results indicate that promoter NelfA occupancy is essential for pol II -dependent transcription. Therefore, we conclude that NelfA is required for active transcription and gene expression during cardiac hypertrophy.
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PMID:Acute NelfA knockdown restricts compensatory gene expression and precipitates ventricular dysfunction during cardiac hypertrophy. 3227 32