Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously shown that a peptide corresponding to the sequence of the second extracellular loop of the human muscarinic-2 (M2) receptor (M2-peptide) was able to induce an autoimmune cardiomyopathy in rabbits. In this study, we investigated the effect of M2-antagonist (otenzepad) on M2-peptide-induced cardiomyopathy in rabbits. New Zealand White rabbits were divided into four groups: 1) control group, saline injection; 2) M2-peptide group, M2-peptide injection; 3) M2-antagonist group, otenzepad (30 mg/day) orally and saline injection; and (4) M2-antagonist + M2-peptide group, otenzepad (30 mg/day) orally and M2-peptide injection. The study duration was 1 year. Saline or peptide was injected once a month. All rabbits in both the M2-peptide group and the M2-antagonist + M2-peptide group had high titers of anti-M2-autoantibodies in their sera. Rabbits in the M2-peptide group showed an increase in heart weight, wall thinning and dilatation of the right ventricle. On the contrary, rabbits in the M2-antagonist + M2-peptide group had normal heart weight and shape. All rabbits in the M2-peptide group showed multifocal degeneration and necrosis of myocardial cells with moderate infiltration of inflammatory cells, while four rabbits in the M2-antagonist + M2-peptide group showed slight infiltration of inflammatory cells with normal myocardial cells and interstitium, and another three showed no histological changes in the hearts. In conclusion, M2-antagonist protects the myocardium from injury induced by autoimmune mechanism against M2-muscarinic receptor.
J Cardiovasc Pharmacol 2001 Oct
PMID:Beneficial effect of muscarinic-2 antagonist on dilated cardiomyopathy induced by autoimmune mechanism against muscarinic-2 receptor. 1181 58

Most of the serious clinical manifestations (such as unstable angina, acute MI, and many cases of sudden death) of coronary atherosclerosis result from thrombosis, usually occurring on a disrupted atherosclerotic plaque. Plaques prone to disruption have large lipid-rich cores with evidence of cap-thinning and active inflammation. Inflammatory cells may contribute to both plaque disruption and subsequent thrombosis. Here we review the evidence for the involvement of inflammation in plaque disruption and thrombosis and the potential clinical implications of this pathophysiologic paradigm.
Rev Cardiovasc Med 2001
PMID:The role of inflammation in plaque disruption and thrombosis. 1243 85

We describe a case of false aneurysm due to loosening of the anastomotic sutures 5 years after graft replacement for subacute type A aortic dissection. Leakage from the graft was controlled by tightening the suture slack indicating that suture loosening was the cause of the aneurysm. The mechanism was probably the progressive thinning of the edematous swollen aortic wall over the years causing the sutures to loosen.
Asian Cardiovasc Thorac Ann 2002 Dec
PMID:False aneurysm due to suture loosening after aortic arch replacement. 1253 85

A 53 year old man was referred for a contrast enhanced cardiovascular magnetic resonance (CMR) scan for assessment of anterior myocardial wall viability. An earlier coronary angiogram had shown a mid left anterior descending artery (LAD) occlusion, and echocardiography had shown mildly reduced global left ventricular function without any other abnormalities. Cine CMR images (steady state free precession sequence) showed a dilated left ventricle (LV) with reduced global systolic function [End-diastolic volume 224 mls (NR 77-195 mls); end-systolic volume 124 mis (NR 19-72 mls); ejection fraction 45%]. There was wall thinning and akinesis of the anteroapical wall and severe hypokinesis of the mid anteroseptal wall. Postgadolinium images (segmented inversion recovery turboFLASH sequence) revealed a prominent LV apical thrombus which measured 1.4 cm at greatest diameter (Figure 1). Using the late gadolinium technique there was extensive (mainly transmural) hyperenhancement (HE) involving the mid and apical septum and the apex. The patient was commenced on warfarin. A second CMR scan repeated after 4 months of warfarin therapy showed complete resolution of the thrombus in the early and late post-gadolinium images (Figures 2 and 3). CMR imaging post-contrast administration is a sensitive tool in the detection of left ventricular thrombi, and overcomes some of the near-field limitations of 2D echocardiography.
Int J Cardiovasc Imaging 2004 Oct
PMID:Resolution of ventricular thrombus identified by contrast enhanced cardiac MRI. 1576 59

Aortic valve replacement options are limited in children, and all of them have disadvantages. Aortic valve repair techniques have evolved slowly and have not gained wide acceptance; however, large series using a variety of techniques demonstrate that valve repair is possible with excellent early hemodynamics and satisfactory intermediate durability. The results of aortic valve repair at the Children's Hospital of Wisconsin are presented. Simple repairs (blunt valvotomy, commissurotomy, or commissurotomy with leaflet thinning) directed at congenital aortic stenosis resulted in 86% +/- 5% freedom from reintervention at 10 years. Repair of aortic insufficiency with ventricular septal defect (VSD) resulted in 93.3% +/- 6% freedom from reoperation at 10 years. Complex repairs included a combination of techniques and yielded 5-year freedom from reintervention of 83% +/- 7% compared with 73% +/- 11% for patients undergoing aortic valve replacement (P = .62). Aortic valve repair provides an alternative to aortic valve replacement in selected patients. The utility of aortic valve repair and aortic valve replacement must be measured not only in freedom from reintervention but also in regression of left ventricular mass and exercise testing. Improvement in outcome depends on better patient selection and suitable bioprosthetic materials.
Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu 2005
PMID:Aortic valve repair. 1581 66

The chronic elevation in ventricular wall stress secondary to ventricular volume or pressure overload leads to structural remodeling of the muscular, vascular and extracellular matrix components of the myocardium. While initially a compensatory response, the progressive hypertrophy and ventricular dilatation induced by this condition ultimately have a detrimental effect on ventricular function, resulting in heart failure. Fibrillar collagen provides the skeletal framework which interconnects the cardiomyocytes, thereby maintaining ventricular shape and size and contributing to tissue stiffness. Accordingly, these myocardial collagen fibers must be disrupted for ventricular dilatation, sphericalization and wall thinning to occur. The presence of an abundant, latent matrix metalloproteinase (MMP) population which coexists with myocardial fibrillar collagen has been documented. Thus, the potential for collagen degradation to exceed synthesis exists should there be significant activation of this latent MMP system. Mast cells are known to store and release a variety of biologically active mediators including TNF-alpha and proteases such as tryptase and chymase, which can induce MMP activation. Increased cardiac mast cell density has been implicated in the pathophysiology of human end-stage cardiomyopathy and experimental myocardial infarction, hypertension and chronic volume overload secondary to mitral regurgitation and aorto-caval fistula. The potential role of cardiac mast cells in activating MMPs, which then results in fibrillar collagen degradation and adverse myocardial remodeling secondary to chronic volume and pressure overload will be the subject of this review.
Cardiovasc Res 2006 Feb 15
PMID:Cardiac mast cell regulation of matrix metalloproteinase-related ventricular remodeling in chronic pressure or volume overload. 1637 24

The aim of conducting this study was to assess the clinical relevance of matrix metalloproteinase (MMP) inhibition by doxycycline, an effective MMP inhibitor, in a rat model of extensive myocardial infarction (MI) and left ventricular (LV) dysfunction. Rats (n = 22) were subjected to extensive anterior MI. Doxycycline (25 mg SC, daily) or saline (control) injections were started for nine days thereafter. The effect of doxycycline on MMP activity in the infarcted and remote myocardium was measured by zymography, in another subgroup (n = 8), nine days after MI. Echocardiography and magnetic resonance imaging (MRI) studies were performed at one and thirty days after MI to assess LV remodeling and function. After 4 weeks, hearts were fixed, and subjected to morphometric and histological analysis. Compared with control, doxycycline treatment attenuated MMP-9 and -2 activity in both infarcted and remote myocardium. Serial echocardiography studies showed that doxycycline failed to attenuate scar thinning, LV dilatation and dysfunction. MRI study showed that doxycycline impaired LV compensatory hypertrophy. Furthermore, compared with control, doxycycline reduced vessel density (/mm(2) +/- SEM) in the infarcted myocardium (84 +/- 16 vs. 46 +/- 9/mm(2), respectively; p < 0.05). Our work suggest that effective MMPs' inhibition in the infarcted and remote myocardium by doxycycline does not prevent LV remodeling and dysfunction but impairs angiogenesis and compensatory LV hypertrophy. Our findings caution against aggressive, non-selective inhibition of MMPs in the early healing phase after MI.
Cardiovasc Drugs Ther 2005 Dec
PMID:Effect of matrix metalloproteinase inhibition by doxycycline on myocardial healing and remodeling after myocardial infarction. 1643 72

Aneurysms of the coronary arteries are uncommon occurrences that usually develop secondary to atherosclerosis and are often asymptomatic. They are usually diagnosed incidentally during investigation for ischemic heart disease or at autopsy for sudden death. We present a case of a "giant" right coronary artery aneurysm (CAA) discovered incidentally at surgery. Pathological examination confirmed that this was a true aneurysm showing marked thinning of the media and fibrocalcific plaques with small, multifocal areas of lymphocytic infiltrates.
Cardiovasc Pathol
PMID:A giant coronary artery aneurysm in the right coronary artery. 1669 28

Hypertension, wall thinning and aortic enlargement are the most important factors increasing wall stress and causing aortic aneurysms to rupture. Computed tomography, especially with contrast image enhancement, usually shows the aortic anatomy with great clarity and distinguishes a ruptured aortic aneurysm from an acute aortic syndrome.
Cardiovasc J Afr
PMID:Thoracic aortic aneurysm: direct sign of rupture. 1761 51

Between January 1988 and December 2003, 898 patients with rheumatic heart disease (mean age 22.4+/-10.1 years) underwent mitral valve (MV) repair. Five hundred and sixty-five patients (63%) had pre-operative atrial fibrillation. Six hundred and ten (68%) patients were in NYHA class III or IV. Four hundred and twelve (45.9%) had pure mitral regurgitation (MR) and 486 (54.1%) had mixed mitral stenosis and MR. The pathology was leaflet prolapse (n=270, 30%), annular dilatation (n=717, 79.8%) and calcification (n=39, 4.3%). Reparative procedures included annuloplasty (n=793, 88%), commissurotomy (n=530, 59%), chordal shortening (n=225, 25%), cusp excision/plication (n=41, 4.5%), cuspal thinning (n=325, 36%), cleft suture (n=142, 16%), decalcification (n=30, 3.3%), chordal transfer (n=13, 1.4%), and neo chordae construction (n=3, 0.3%). Early mortality was 32 (3.6%). Follow-up ranged from 6 to 180 months (mean 62.7+/-31.8 months) and was 96% complete. Six hundred and twenty-one patients (69%) had no, or trivial, or mild MV. Two hundred and seventy-seven of the 866 survivors had MR which was moderate in 153 (18%) and severe in 124 (14%) patients. Thirty-five patients underwent re-operation. There were 21 late deaths (2.4%). Actuarial and re-operation-free survival at 10 years were 92+/-1.1% and 81+/-5.2%, respectively. Freedom from moderate or severe MR was 32+/-3.9%. MV repair in the rheumatic population is feasible with acceptable long-term results.
Interact Cardiovasc Thorac Surg 2006 Aug
PMID:Results of mitral valve repair in rheumatic mitral regurgitation. 1767 May 93


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