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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibromuscular dysplasia (FMD) is found in various arteries but the common iliac arteries and the coronary arteries are seldom involved. A 49-year-old woman was referred to our hospital with a pulsatile mass in her right lower quadrant. She had subdural hemorrhage in a postpartum state at the age of 27. After admission angiography diagnosed the bilateral iliac artery aneurysms and coronary angiography revealed a coronary artery aneurysm, the size of which was 12 mm x 19 mm in the region of the left main trunk. The bilateral iliac artery aneurysms were resected and Y-shaped vascular prosthesis was replaced. Microscopic sections of the aneurysm showed remarkable decrease of elastic fibers and thinning of the media, but no increase occurred in the smooth muscle. Histopathological diagnosis was FMD (periarterial fibroplasia). To our knowledge, no patient with a iliac arterial aneurysm caused by FMD has been reported and only a few cases with coronary arterial FMD have been described. This is the first report of iliac arterial aneurysm due to FMD. Since this case has multiple aneurysms, a long-term follow-up is definitely required, especially focusing on the coronary aneurysm.
J Cardiovasc Surg (Torino) 1995 Dec
PMID:Bilateral common iliac artery aneurysms secondary to fibromuscular dysplasia accompanied with a coronary aneurysm. A case report. 863 31

Rupture of the left-ventricular free wall may not always result in immediate irreversible hemodynamic collapse. We report a series of five patients (4 male, 1 female; age 59-79 years) successfully operated for postinfarction free-wall rupture with good long-term results. Two patients presented with syncopy and acute tamponade three days after an acute myocardial infarction. In two patients with atypical chest pain and congestive heart failure, a large pericardial effusion and an extreme localized thinning of a myocardial scar region was seen several weeks after an uncomplicated myocardial infarct. In one patient a pseudoaneurysm was detected, which developed asymptomatically within three weeks after a posterior myocardial infarct. In all cases myocardial rupture was suspected after an echocardiographic examination. At surgery a hemopericardium and a localized rupture site were found. The surgical procedure included closure of the defect by direct suture or patch, CABG in 3 cases, and mitral valve replacement in one patient. The postoperative course was uneventful, only one patient needed IABP for 24 hours. Three patients returned to NYHA functional class I, one patient to class II, and one patient to class III. The latter patient died of heart failure 17 months postoperatively, and the other patients are still alive 4,18,24, and 26 months postoperatively. Thus clinical representation of left-ventricular free-wall rupture after myocardial infarction can be highly variable. But close cooperation between experienced echocardiographers and surgeons may allow successful corrections with good long term-results.
Thorac Cardiovasc Surg 1996 Apr
PMID:Clinical presentation of rupture of the left-ventricular free wall after myocardial infarction: report of five cases with successful surgical repair. 878 31

Radiofrequency catheter ablation of symptomatic ventricular ectopy guided by unipolar mapping was successfully accomplished at the right ventricular outflow tract in a patient who did not exhibit apparent structural heart disease. A "QS" morphology with a fast slope of the downstroke deflection at the successful ablation site was observed on the unipolar electrogram. Focal thinning of the lateral wall of the right ventricular outflow tract was shown in the magnetic resonance image, similar to that reported in patients with "idiopathic" right ventricular outflow tract tachycardia.
J Cardiovasc Electrophysiol 1998 Jan
PMID:Unipolar mapping and magnetic resonance imaging of "idiopathic" right ventricular outflow tract ectopy. 947 81

We reported a patient with a saccular ascending aortic aneurysm located just above the non-coronary sinotubular junction. The aneurysm produced severe aortic regurgitation and two episodes of cardiac tamponade. By intraoperative inspection, the border between the aneurysmal wall and non-dilated portion of the normal aortic wall was distinct, and the aortic valve leaflets and aortic annulus appeared normal. Aortic valve dysfunction appeared to be caused by dilation of the noncoronary sinotubular junction and mild distortion of the noncoronary sinus because of the aneurysmal formation. We performed patch closure of the aneurysmal ostium and repaired the dilated noncoronary sinotubular junction. Postoperative echocardiography and aortography demonstrated a good coaptation of the aortic valve leaflets with trivial aortic regurgitation. Although a rupture site, dissection or carcinomatous pericarditis which is attributable to the two episodes of cardiac tamponade could not be found, pathologic examination of the aneurysm wall revealed intramural blood leakage between the mucoid degenerated media and notably thickened adventitia. In addition, there was thinning and interruption of the elastic fibers of the media. These findings are consistent with a leaking aneurysm which cause the slow development of cardiac tamponade.
Jpn J Thorac Cardiovasc Surg 1999 Mar
PMID:Surgical treatment for a supra sinotubular junctional saccular aneurysm associated with aortic regurgitation. 1022 13

We have previously demonstrated that turkey poults fed furazolidone (Fz) in high concentrations (700 ppm) develop dilated cardiomyopathy (DCM) which approximates the human condition [1-3]. We wanted to study the effects of a calcium channel blocker in an animal model with a documented decrease in beta-receptor density, increased levels of circulating catecholamines, and abnormal calcium metabolism. The effects of a third generation calcium channel blocker has not been studied in our model. We hypothesized that the model would be predictive of the human condition and provide additional insights into the potential use of Ca2+ channel blockers in the setting of DCM. In the present study, we examined the effect of pranidipine, a new dihydropyridine calcium antagonist, in the setting of DCM on the gross and microscopic morphology of the heart and the overall contractile performance of the myocardium. A state of symptomatic to mild cardiomyopathy was induced in Broad-Breasted White turkey poults by administration of Fz for three weeks. Blood pressure, heart rate, fractional shortening, and body weight were monitored and compared in DCM animals treated with pranidipine and those given a placebo. After four weeks of treatment or no treatment with pranidipine, animals were euthanized and heart weight, cardiac dimensions, and microscopic morphology were compared. Progressive left ventricular (LV) dilatation and wall thinning was prevented with pranidipine treatment. In addition, microscopic examination demonstrated myocyte hypertrophy regression in DCM animals treated with pranidipine. In DCM animals, treatment with pranidipine resulted in significantly smaller left ventricular dimensions. We conclude that the calcium channel blocker pranidipine was not detrimental to global cardiac function in animals with dilated cardiomyopathy.
Cardiovasc Drugs Ther 1999 Sep
PMID:Effects of pranidipine, a calcium channel antagonist, in an avian model of heart failure. 1054 27

We developed a new approach to quantitative coronary angiography (QCA), which overcomes several limitations of available programs, such as dependence on operator input; limited tracking ability; fixed correction of the point spread function (PSF); and different calibration on empty vs. contrast-filled catheters. The program (Intelligent Images QCA, version 1.4) provides absolute reproducibility by deterministic, operator-independent identification of the skeleton and the edges of the coronary tree. The algorithm works as follows: application of a matched filter to emphasize selectively the coronary arteries; adaptive threshold binarization; binary thinning and skeletonization; perpendicular resampling with sub-pixel interpolation; derivative filtering; minimal cost edge detection; and automatic identification and quantification of the stenosis. Operator's interaction is restricted to definition of a region of interest; editing of either skeleton or edges is not allowed. PSF correction is fine-tuned to the actual frequency response of the imaging chain by calibration on a contrast-filled conical lucite phantom. Catheter calibration is carried out by a second derivative-based edge detection much less sensitive to the presence of contrast. In vitro phantom analysis (0. 5 to 5.0 mm) showed accuracy of 0.028-0.031 mm and precision of 0. 054-0.062 mm on nonmagnified images from the angio TV chain and the cine projector, respectively. In vivo evaluation on a series of consecutive diagnostic angiograms yielded correct contour detection of 70/73 stenoses (96%); interobserver intraframe MLD variability 0. 00 mm; correct tracking of catheter edges 100%; interobserver variation coefficient of catheter calibration 3.3%; and mean difference of calibration factor on contrast-filled vs. empty catheters 2.7%. This new approach significantly improves reproducibility with respect to conventional QCA, maintaining high accuracy, precision, and applicability. Cathet. Cardiovasc. Intervent. 48:435-445, 1999.
Catheter Cardiovasc Interv 1999 Dec
PMID:A deterministic approach to automated stenosis quantification. 1066 Mar 63

Infarct scar, a requisite to the rebuilding of necrotic myocardium following myocardial infarction (MI), has long been considered inert. Earlier morphologic studies suggested healing at the infarct site was complete within 6-8 weeks following MI and resultant scar tissue, albeit necessary, was acellular and simply fibrillar collagen. Utilizing molecular and cellular biologic technologies, recent studies indicate otherwise. Infarct scar is composed of phenotypically transformed fibroblast-like cells, termed myofibroblasts (myoFb) because they express alpha-smooth muscle actin (alpha-SMA) and these microfilaments confer contractile behavior in response to various peptides and amines. These cells are nourished by a neovasculature and are persistent at the MI site, where they are metabolically active expressing components requisite to angiotensin (Ang) peptide generation, including converting enzyme, receptors for AngII and transforming growth factor (TGF)-beta1. They continue to elaborate fibrillar type I collagen. Their generation of these peptides contribute to ongoing scar tissue collagen turnover and to fibrous tissue formation of noninfarcted myocardium. Infarct scar contraction accounts for its thinning and its tonus may contribute to abnormal ventricular chamber stiffness with diastolic dysfunction. Infarct scar is a dynamic tissue: cellular, vascularized, metabolically active and contractile. Pharmacologic interventions with angiotensin converting enzyme inhibitor or AT1 receptor antagonist has proven effective in attenuating scar tissue metabolic activity and minimizing adverse accumulation of fibrous tissue in noninfarcted myocardium.
Cardiovasc Res 2000 May
PMID:Infarct scar: a dynamic tissue. 1077 28

The phenomenon of left ventricular (LV) remodeling with dilatation, wall thinning, and increased muscle mass has previously been reported in pigs with 7-day myocardial hibernation. This study investigated cellular and extracellular basis and reversibility of the structural LV remodeling with hibernating myocardium. Five groups of pigs were included: Group A: 7-day myocardial hibernation with a fixed coronary stenosis; Group B: 7-day hibernation with subsequent 3-week reperfusion by release of the stenosis; Group C: control group with sham operation; Group D: 24-hour myocardial hibernation to define structural mechanism of initial wall thinning in the hibernating region without confounding factors of cell loss or hypertrophy, Group E: 4-week myocardial hibernation to exclude the possibility of spontaneous regression of LV remodeling with hibernation. LAD flow decreased by 38+/-12% (p<0.01) with a significant decrease in systolic wall thickening at 7 days of hibernation with severe coronary stenosis (Group A). End-diastolic wall thickness decreased by 19% (p<0.01) accompanied by a decrease in myocyte number across the wall (44%) and in myocyte density (24%), a significant increase in myocyte width (17%), a mild increase in interstitial tissues in hibernating region, and significant increases in LV diastolic volume and in LV mass at 7 days. After reperfusion (Group B), LV volume decreased, LV ejection fraction improved, and myocyte hypertrophy regressed with a decreased LV mass index without a significant change in interstitial tissue. LV remodeling progressed with further increases in LV volume, mass, and interstitial fibrosis in 4-week hibernation. In pigs undergoing 24 hours of myocardial hibernation (Group D), end-diastolic LV wall thickness decreased significantly in the hibernating region with a proportional decrease in the transmural myocyte number but without changes in myocyte width, myocyte density, or interstitial tissues. Therefore, progressive gross LV remodeling associated with hibernating myocardium is accompanied by increasing myocyte hypertrophy and interstitial fibrosis. In hibernating myocardial region, wall thinning is proportional to a decreased myocyte number across the LV wall, indicating slippage of myocytes as a preponderant mechanism for the wall thinning. Myocyte hypertrophy develops within 7 days in hibernating myocardium, causing an increase in LV mass. These changes are partially reversible after reperfusion.
Cardiovasc Pathol
PMID:Reversibility and pathohistological basis of left ventricular remodeling in hibernating myocardium. 1114 2

Calcium channel antagonists (CCAs) have been proposed to prevent cardiac events after myocardial infarction (MI). However, unwanted effects, such as negative inotropy, limit their use in many cases. The aim of this study was to compare the effects of long-term treatment with the CCAs, mibefradil, verapamil, and amlodipine, administered before and after chronic MI on myocardial remodeling and cardiac function. MI was induced by permanent ligation of the left coronary artery in male Wistar rats. Infarcted animals were treated with placebo, mibefradil (10 mg/kg/d po), verapamil (8 mg/kg bid po), or amlodipine (4 mg/kg/d po). Treatment was started 7 days before or 3 h after MI induction. Six weeks after MI, mean arterial blood pressure (MAP), heart rate (HR), left ventricular end diastolic pressure (LVEDP), and cardiac contractility (dP/dt(max)) were measured. Morphometric parameters such as infarct size (IS), left ventricular dilation (LVD), septal thickness (ST), and cardiac fibrosis were determined in picrosirius red-stained hearts. Six weeks after MI, MAP and dP/dt(max) were decreased, whereas LVEDP and HR were increased in placebo-treated controls. The hearts featured an IS of 45%, left ventricular dilation, cardiac fibrosis, and septal thinning. MAP of all CCA-treated animals was increased, whereas LVEDP was decreased and dP/dt(max) increased 7-day pre- and 3-h post-MI started in mibefradil- and amlodipine-treated animals, but not in verapamil-treated animals. In contrast to amlodipine treatment, before and after MI started mibefradil and verapamil treatment decreased HR. Pretreatment with all CCA reduced IS and increased ST, whereas only mibefradil and amlodipine pretreatment prevented LVD and cardiac fibrosis. After MI started treatment with mibefradil and amlodipine reduced IS and cardiac fibrosis, and increased ST. Long-term treatment with the CCAs mibefradil, verapamil, and amlodipine reduced myocardial remodeling and improved cardiac function in MI-induced heart failure in rats.
J Cardiovasc Pharmacol 2001 Jan
PMID:Calcium channel blockade limits cardiac remodeling and improves cardiac function in myocardial infarction-induced heart failure in rats. 1115 76

We have shown that a peptide corresponding to the sequence of the second extracellular loop of the human beta1-adrenoceptor (beta1-peptide) was able to induce an autoimmune cardiomyopathy in rabbits. In this study, we examined the effect of angiotensin-converting enzyme inhibitor (ACEI) on beta1-peptide-induced cardiomyopathy. Rabbits were divided into four groups: (1) control group (n= 6) receiving saline injection; (2) beta1-peptide group (n = 8) immunized with beta1-peptide; (3) ACEI group (n = 6), lisinopril (3 mg/day) given orally and receiving saline injection; and (4) ACEI + beta1-peptide group (n = 7), lisinopril (3 mg/day) given orally and immunized with beta1-peptide. Our results showed that, after 1 year, all rabbits in the beta1-peptide group had an increase in heart weight, wall thinning and dilatations of both ventricles as compared with rabbits in the ACEI + beta1-peptide group that had normal heart weight and shape. All rabbits in the beta1-peptide group exhibited multifocal degeneration and necrosis of myocardial cells with moderate infiltration of inflammatory cells. In the ACEI + beta1-peptide group, three rabbits showed focal degeneration and necrosis of myocardial cells accompanied by mononuclear cells. The lesions in this group were apparently less marked than those in the beta1-peptide group. In conclusion, ACEI protects the myocardium from injury induced by an autoimmune mechanism against beta1-adrenoceptor.
J Cardiovasc Pharmacol 2000
PMID:Beneficial effect of angiotensin-converting enzyme inhibitor on dilated cardiomyopathy induced by autoimmune mechanism against beta1-adrenoceptor. 1120 19


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