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

Discrepancies exist regarding potential sex differences in the effects of ethanol on the myocardium. Therefore, the aims of this study were to determine if long-term ethanol consumption was associated with the development of a dilated cardiomyopathy (CM) in female rats and, second, to determine if the absence of ovarian hormones modulated this effect. Adult male and female (n=6-8/group) sham-operated and ovariectomized (OVX) Sprague-Dawley rats received the Lieber DeCarli ethanol-containing (8% vol/vol) or control liquid diet for 8 months. All ethanol groups showed echocardiographic evidence of a cardiomyopathy; however, more significant ethanol-elicited differences were found in the male ethanol group than in either the female or female OVX groups. In addition, the male ethanol group had significant reductions in in vivo measures of contractility, such as the maximum derivative of change in systolic pressure and preload recruitable stroke work. Sex differences were also apparent in the pattern and degree of posterior and septal wall thickness changes, in that the male ethanol group had more posterior and septal wall thinning. In conclusion, similar to male rats long-term ethanol consumption in gonad-intact and OVX female rats is associated with the development of a dilated cardiomyopathy.
Cardiovasc Toxicol 2007
PMID:Long-term effects of alcohol consumption in male and female rats. 1799 Jan 29

The aim of the study was to evaluate the cardioprotective and antiarrhythmic effects of intravenous Na+/H+ blockers (cariporide and SM-20550) in a rat model of ischemia and a long period reperfusion (14 days). This model allowed study of the role of Na+/H+ exchanger against late myocardial infarct expansion and left ventricular dysfunction. Each compound was administered 5 min before ischemia. Cariporide (from 0.16 mg/kg) and SM-20550 (from 0.04 mg/kg) significantly and dose-dependently reduced the number of ventricular premature beats during ischemia. The duration of ventricular tachycardia was importantly shortened in the presence of cariporide (0.63 mg/kg) and SM-20550 (0.16 mg/kg). Furthermore, cariporide (0.63 mg/kg) and SM-20550 (from 0.04 mg/kg) significantly reduced the infarct expansion: 43 +/- 2% in the cariporide group and 42 +/- 2% at 0.16 mg/kg SM-20550 versus 48 +/- 1% in the vehicle group. Cariporide and SM-20550 significantly prevented the left ventricular free wall thinning associated with the thickness ratio, suggesting a significant reduction of the ventricular dilation. Cariporide and SM-20550 significantly improved the negative dP/dtmax, suggesting a partial restoration of the cardiac relaxation. Collectively, Na+/H+ blockers administered before ischemia reduced arrhythmias and also prevented the remodeling process of the heart during postinfarction.
J Cardiovasc Pharmacol 2007 Nov
PMID:Effects of SM-20550 against myocardial infarction-induced arrhythmias, late infarct expansion, and left ventricular dysfunction. 1803 67

Cardiac tagging resolution for regional principal strains E1 and E2 has been a limiting factor for the study of dilated mouse hearts, in which the left ventricle (LV) wall thickness can drop to below 1 mm. Therefore, high resolution tagging was performed at 14.1 T to enable transmural principal strain measurements across the LV wall of normal mouse hearts and average principal strains in thinned LV walls of a transgenic mouse (PKCepsilon TG) that develops dilated LV. A modified DANTE tagging and fast gradient imaging method produced a tagging grid dimension of 0.33 x 0.33 mm and line thickness under 0.1 mm. In normal mice, average E1 strain in the epicardium was significantly higher than the endocardial E1 (epi = 0.22 +/- 0.10; endo = 0.13 +/- 0.07, p < 0.05), while magnitude of average endocardial E2 was greater than in the epicardium (endo = -0.12 +/- 0.03, epi = -0.08 +/- 0.03; p < 0.001). E1 strain averaged over four segments was reduced in dilated hearts compared to controls (PKCepsilon TG = 0.14 +/- 0.02; control = 0.18 +/- 0.02, p < 0.01), with specific reductions in septal (33%) and lateral (31%, p < 0.01) segments. E2 strain was similar between dilated and control hearts at -0.11 +/- 0.01. Thus, improved tagging resolution demonstrates that stretch (E1), but not compression strains (E2), are reduced as a result of significant LV wall thinning in a mouse model of dilated cardiomyopathy.
J Cardiovasc Magn Reson 2007
PMID:Improved cardiac tagging resolution at ultra-high magnetic field elucidates transmural differences in principal strain in the mouse heart and reduced stretch in dilated cardiomyopathy. 1806 48

We herein present an extremely rare case of a perforation of the ascending aorta with a hematoma extending into the left-side upper extrapleural cavity. A 62-year-old male with a sudden onset of severe chest pain was referred to our institution because of an abnormal shadow in the left-side upper lung field. Computed tomography revealed a small fusiform aortic arch aneurysm and a hematoma extending to the left-side upper extrapleural cavity. We diagnosed the patient to have acute aortic syndrome and urgent surgery was thus performed. Major bleeding which might be caused by a progression of the perforation was seen during a dissection of the aorta. The aortic arch was transected and a total arch replacement was performed with a 26 mm Dacron graft. No findings of a rupture of the aortic arch aneurysm or dissection were observed. The histopathology of the aorta revealed a severe atheromatous lesion with calcification and thinning disarrayed elastic fibers. The postoperative course was essentially good except for the development of pericardial effusion which required drainage.
Interact Cardiovasc Thorac Surg 2008 Apr
PMID:Perforation of the ascending aorta with a hematoma extending into the left-side upper extrapleural cavity. 1808 15

A 46-year-old man underwent emergency surgery for heart rupture after acute infarction of the posterior wall. Echocardiography revealed limited myocardial thinning, so rather than sutureless repair, a covering patch was used in view of the risk of recurrent rupture. Postoperative echocardiography showed the myocardial thinning had progressed to a wide defect, and computed tomography demonstrated that the covering patch had prevented a repeat rupture.
Asian Cardiovasc Thorac Ann 2008 Oct
PMID:Postinfarction heart rupture of posterior wall repaired by covering patch. 1881 51

Congenitally corrected transposition of the great arteries (CCTGA) is a rare and complex congenital anomaly characterized by atrial-ventricular (AV) discordance and ventricular-arterial discordance. Ventricular noncompaction (VNC) is a rare unclassified cardiomyopathy due to the arrest in intrauterine endomyocardial morphogenesis and it is characterized by numerous prominent trabeculations and intratrabecular recesses. We reported the case of a 47-year old female patient. When she was 35-year old an "isolated" CCTGA was diagnosed because of a heart murmur. Since then she attended periodically echocardiograms. She showed us 2 of them where right ventricle apical trabeculation was reported, without any others details. We performed a periodic evaluation in a patient still active, with a 6-month history of mild dyspnea occurring during exertion, no episodes of chest discomfort or palpitation. The ECG showed ectopic atrial rhythm, 83 bpm, normal QRS duration, QS complex in V1-V2 leads. The echocardiogram demonstrated: CCTGA, moderate enlargement and dysfunction of the right systemic ventricle, moderate to severe systemic AV valve regurgitation, severe thinning and dyskinesia of the basal segment of the septum, apical and mid-segments prominent and numerous trabeculations with deep intertrabecular recesses, better showed by color Doppler, in continuity with the ventricular cavity. This case presents some distinctive features: (1) the association between two rare congenital anomalies; (2) Striking right VNC, involving the apex and mid-segments, rarely described in literature; right VNC has been proposed according to the presence of 3 over 4 criteria proposed by Jenni et al. (Heart 86:666-671, 2001); (3) Severe thinning and dyskinesia of the basal segment of the septum, probably related to coronary artery abnormalities frequently described in CCTGA patients.
Int J Cardiovasc Imaging 2009 Aug
PMID:Unusual association between "congenitally corrected transposition of the great arteries" and "noncompaction" of the right systemic ventricle. 1968 Jul 80

Repair of complex valve pathological processes often requires the use of leaflet tissue or pericardium. The use of bovine photo-oxidized pericardium may be an alternative, a tissue less prone to calcification. The aim of this study is to evaluate the use of photo-oxidized bovine pericardial tissue in the reconstruction of atrioventricular valves in humans. Between July 2001 and September 2006, 21 patients with complex valve pathology underwent a reconstruction with photo-oxidized pericardium. The pericardial patch was used for the reconstruction of a tricuspid valve leaflet in two patients, the reconstruction of a mitral valve leaflet in six patients, the reconstruction of the tricuspid annulus in one patient and the reconstruction of the mitral annulus in 12 patients. The follow-up ranged from 13.9 to 43.2 months. There were five perioperative deaths. Four patients developed failure of the reconstruction, in one patient there was thinning and perforation of the pericardial patch without signs of infection or abrasion. The other patients were free from thromboembolism, endocarditis, hemorrhagic complications or echocardiographic signs of failure of the reconstruction. Photo-oxidized bovine pericardium is a versatile material for complex reconstruction of the atrioventricular valvular structures. Its durability should, however, be investigated in comparison with alternative tissues in a randomized trial.
Interact Cardiovasc Thorac Surg 2009 Nov
PMID:Reconstruction of atrioventricular valves with photo-oxidized bovine pericardium. 1968 31

To delineate temporal changes in the integrity and function of mitochondria/cardiomyocytes in hearts from mice exposed in utero to commonly used nucleoside analogs (NRTIs), CD-1 mice were exposed in utero to 80 mg AZT/kg, 40 mg 3TC/kg, 80 mg AZT/kg plus 40 mg 3TC/kg, or vehicle alone during days 12-18 of gestation and hearts from female mouse offspring were examined at 13 and 26 weeks postpartum. Alterations in cardiac mitochondrial DNA (mtDNA) content, oxidative phosphorylation (OXPHOS) enzyme activities, mtDNA mutations, and echocardiography of NRTI-exposed mice were assessed and compared with findings in vehicle-exposed control mice. A hybrid capture-chemiluminescence assay showed significant twofold increases in mtDNA levels in hearts from AZT- and AZT/3TC-exposed mice at 13 and 26 weeks postpartum, consistent with near doubling in mitochondrial numbers over time compared with vehicle-exposed mice. Echocardiographic measurements at 13 and 26 weeks postpartum indicated progressive thinning of the left ventricular posterior wall in NRTI-exposed mice, relative to controls, with differences becoming statistically significant by 26 weeks. Overall, progressive functional changes occurred in mouse mitochondria and cardiac tissue several months after in utero NRTI exposures; AZT and 3TC acted in concert to cause additive cardiotoxic effects of AZT/3TC compared with either drug alone.
Cardiovasc Toxicol 2010 Jun
PMID:In utero exposure of female CD-1 mice to AZT and/or 3TC: II. Persistence of functional alterations in cardiac tissue. 2015 31

Microvascular dysfunction can be demonstrated in most patients with hypertrophic cardiomyopathy (HCM), both in the hypertrophied and nonhypertrophied myocardial walls, mostly due to intimal and medial hyperplasia of the intramural coronary arteries and subsequent lumen reduction. As a consequence, regional myocardial ischemia may be triggered by exercise, increased heart rate, or arrhythmias, in areas which are unable to increase myocardial blood flow. In patients with HCM, microvascular dysfunction leading to severe myocardial hypoperfusion during maximal hyperemia represents a strong predictor of unfavorable outcome, left ventricular remodeling with progressive wall thinning, left ventricular dysfunction, and heart failure. Accurate quantitative assessment of microvascular dysfunction and myocardial ischemia is not easily feasible in clinical practice. Although signs of inducible myocardial ischemia may be detected by electrocardiogram, echocardiography, or myocardial scintigraphy, the vasodilator response to dipyridamole by positron emission tomography is considered the method of choice for the assessment of maximal regional and global flow. Cardiac magnetic resonance provides further information, by late gadolinium enhancement (LGE), which may show areas where replacement fibrosis has occurred following microvascular ischemia and focal necrosis. LGE areas colocalize with severe regional microvascular dysfunction, are associated with increased prevalence of ventricular arrhythmias, and show more extensive distribution in the late stages of the disease, when heart failure is the dominant feature. The present review aims to provide a concise overview of the available evidence of microvascular dysfunction and ischemia eventually leading to disease progression and heart failure in HCM patients.
J Cardiovasc Transl Res 2009 Dec
PMID:Microvascular dysfunction, myocardial ischemia, and progression to heart failure in patients with hypertrophic cardiomyopathy. 2056 3

The secure and haemostatic implantation of the left ventricular assist device (LVAD) apex inflow cannula can sometimes be challenging, especially in the setting of an acute myocardial infarction or significant ventricular wall thinning, when the myocardial tissue may be friable and tissue strength may be compromised. In these cases, surgical complications from this site may present a challenge. We describe a modified suturing technique for the implantation of the left ventricular apical inflow cannula of the HeartMate II LVAD that may prevent surgical complications from the inflow cannula site.
Interact Cardiovasc Thorac Surg 2010 Oct
PMID:A modified suturing technique for the implantation of the apical cannula of the HeartMate II left ventricular assist device. 2064 20


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>