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

To examine the relations among hypertrophy, fibrosis and diastolic performance in early experimental hypertension, 18 control dogs and 12 dogs with experimental left ventricular hypertrophy were studied. Diastolic function was impaired in dogs with left ventricular hypertrophy, with decreased Doppler early to atrial inflow velocity ratio (E/A) (1.35 versus 1.72), increased atrial filling fraction (35% versus 29%), decreased sonomicrometric peak rates of wall thinning (-2.01 versus -3.37 liters/s) and filling (4.33 versus 6.64 liters/s) and prolonged time constant of isovolumetric relaxation (tau; 34.3 versus 28.1 ms). Neither chamber stiffness (k; P = AekV) nor passive elastic stiffness (E; E = k sigma, where sigma = stress) was increased. At postmortem examination, the hypertensive left ventricle weighed significantly more than normal (116 versus 80 g; p less than 0.01) and had greater muscle fiber diameter at endocardial and epicardial sampling sites in the apical free wall, basal free wall and septum (mean diameter 50 +/- 8 microns in hypertensive dogs, 37 +/- 8 microns in normal dogs; p less than 0.01). In contrast, neither percent fibrosis (1.2 +/- 0.8 versus 0.9 +/- 0.6 in normal dogs) nor fibrotic volume (1.21 +/- 0.63 versus 0.72 +/- 0.42%/g in normal dogs) was significantly increased. Peak volumetric filling rate was inversely related to fiber diameter (r = -0.74, p less than 0.001), although no variable of left ventricular function was significantly related to percent or volume fibrosis (all r less than 0.60, all p greater than 0.05). Thus, diastolic dysfunction may exist in the setting of hypertrophy without significant fibrosis. Increased myocyte size was associated with early diastolic filling abnormalities characteristic of the hypertensive left ventricle. Fibrosis appears to be a less important determinant of diastolic performance.
J Am Coll Cardiol 1991 Feb
PMID:Hypertrophy, fibrosis and diastolic dysfunction in early canine experimental hypertension. 182 98

Infarct expansion can be defined pathologically as a distortion of ventricular topography produced by thinning and disproportionate dilation of the infarct segment. Large transmural infarcts tend to be associated with greater propensity for infarct expansion. Two-dimensional echocardiography has made it feasible to detect these acute alterations in cardiac topography by serial examination of patients with acute myocardial infarction. A practical approach to the echocardiographic quantification of expansion involves analysis of end-diastolic cross-sectional echo views at the papillary muscle level, which can be used as fixed internal landmarks to divide the left ventricle into 2 segments, anterior and posterior. An off-line computer system can be used to track relative lengths of these segments as well as their thicknesses over time. In the initial clinical study, one third of patients with acute anterior transmural infarcts showed an average 50% increase in the infarct segment length beginning within the first 3 days of infarction, characterized by disproportionate progressive dilation and transmural thinning of this zone. These patients demonstrated a significantly higher mortality than those without expansion. Later studies demonstrated not only continuing dilation of the infarcted anterior wall, but also progressive dilation of the noninfarcted posterior wall, underscoring the importance of continuing long-term noninvasive follow-up. Not only is expansion associated with a poor clinical outcome; it has also been shown experimentally and clinically to be modifiable or even preventable by various therapeutic maneuvers, which may well improve survival. Because of the limitations of the echocardiographic window, it is often possible to obtain only a single cross-sectional view of high quality, and even then technical quality may not be sufficiently high to enable detailed quantitative analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1991 Nov 18
PMID:Myocardial infarct expansion: recognition, significance and pathology. 183 95

Low-dose intravenous nitroglycerin infusion can be safely administered during acute myocardial infarction to unload the left ventricle and salvage ischemic myocardium and left ventricular geometry and function. In an experimental conscious dog model, low-dose infusion titrated to decrease mean blood pressure by 10% over the first 6 hours after coronary artery ligation resulted in 51% decrease in infarct size, 54% decrease in preload, and more than 50% increase in collateral blood flow. The same benefits were seen when methoxamine was given to counteract that 10% decrease in blood pressure. Similar short-term nitroglycerin infusion also limited remodeling in the dog model. More important, no myocardial salvage was seen with excessive nitroglycerin-induced hypotension to levels less than 80 mm Hg. Clinically, prolonged low-dose nitroglycerin infusion was evaluated in a prospective, randomized, single-blinded, placebo-controlled study of 310 patients with acute infarction: 154 received nitroglycerin and 156 received placebo. Nitroglycerin was titrated to reduce mean blood pressure by 10% in normotensive patients and up to 30% in hypertensive (blood pressure greater than 140/90 mm Hg) patients, but not to less than 80 mm Hg. Nitroglycerin produced several benefits compared with placebo: (1) smaller creatine kinase infarct size; (2) less regional left ventricular dysfunction, better global ejection fraction, and less infarct expansion and thinning; (3) better clinical functional status and hemodynamics; (4) fewer inhospital complications such as acute left ventricular failure and dilation due to marked infarct expansion, left ventricular thrombus, cardiogenic shock, and infarct extension; and (5) fewer deaths up to 1 year in patients with anterior Q-wave infarction.
Am J Cardiol 1991 Nov 18
PMID:Intravenous nitroglycerin unloading in acute myocardial infarction. 183 97

A 56-year-old male patient was submitted to coronary artery bypass graft surgery. Pericarditis and dilatation of the right ventricle with thinning of the walls of the right ventricle was observed. Intraoperative right ventricle biopsy revealed fibro-adipose tissue. The diagnosis of concomitant Uhl's syndrome was made.
Arq Bras Cardiol 1991 Nov
PMID:[Uhl's anomaly in adults associated with coronary disease]. 184 Apr 65

Restenosis is the most important problem limiting the success of coronary angioplasty. Clinically, restenosis is seen in approximately one-third of patients undergoing percutaneous transluminal coronary angioplasty. Several clinical and angiographic risk factors have been identified which may contribute to the development of restenosis. Histopathologic studies indicate that restenosis is characterized by intimal proliferation of smooth muscle cells in a loose connective tissue matrix. These intimal lesions are associated predominantly with the nonatheromatous portion of the vessel wall. Thinning of the media of the plaque-free wall and marked fragmentation of the internal elastic lamina are also seen. Traumatic injury of the vessel wall during angioplasty probably triggers a series of cellular and subcellular events which may ultimately lead to myointimal proliferation and restenosis. Although the exact mechanism by which this occurs is unknown, several factors may enhance smooth muscle cell growth and therefore may play a role in the development of restenosis. These include platelet deposition, mechanical stretching of the media, inflammation of the vessel wall, the activity of growth factors, and alterations in vessel geometry. These possible mechanisms of restenosis suggest several potential ways to limit the proliferative response to vascular injury. Anticoagulants and platelet antagonists, direct inhibitors of smooth muscle proliferation, anti-inflammatory agents, growth factor inhibitors, and new devices which improve final vessel geometry are currently being tested as methods to curb restenosis. Unfortunately, no treatment has yet been shown to reduce significantly the rate of restenosis following angioplasty. The problem of restenosis will most likely be solved by better understanding of the basic molecular and biologic phenomena involved in vascular injury and repair.
Clin Cardiol 1991 Oct
PMID:Restenosis following coronary angioplasty. 195 87

Left ventricular dimensions were measured in Cd2+ arrested (presumably diastolic), open-chest rats. Aortic pressure was maintained at 137 cm H2O (100 mm Hg) and left-ventricular (luminal) pressures were established and maintained at their chosen values, each by means of reservoir systems. The selected left-ventricular pressures were chosen to be within or to even broaden the range of conceivable diastolic pressures (-3 to 48 cm H2O). After in situ fixation with 4% formaldehyde and gelatin embedding, the hearts were serially sectioned in the apex base direction to obtain information at 11 levels (10, 20, . . . 90, 100%). Tracings of selected sections were made along the edge of the left ventricular lumen and the pericardial surface. Volumes, surface areas, and mean external and internal radii of the left ventricle were derived. To quantify the circularity of sections a form factor (FF) was introduced (FF = 1 for a circular cross-section and less than one for other shapes). Ventricular lengths, radial dimensions, endocardial and epicardial surface areas, and total and luminal volumes increased with the increasing intraventricular pressures; as expected, the wall simultaneously thinned. Though its appearance was altered by the wall thinning, the curving muscle fascicular pattern was present over the entire pressure range examined. Endocardial surface areas increased more than did the epicardial surface areas. The endocardial FF value increased (more circular) at each section level as the pressure increased. The epicardial FF relationship was apparently constant (0.798 +/- 0.014) for all section levels from 10% through 90%, regardless of luminal pressure. These results, when taken in conjunction with the results of our previous published studies, prompted the following speculation. The wall of the diastolic ventricle is a fluid-filled chamber with intramyocardial pressures that may be higher than ventricular pressures.
Basic Res Cardiol
PMID:Left ventricular shape-luminal pressure relationship. An open-chest study. 195 75

To evaluate the feasibility of detecting denervated myocardium in the infarcted canine heart, the distribution of sympathetic nerve endings using I-123 metaiodobenzylguanidine (MIBG) was compared with the distribution of perfusion using thallium-201, with the aid of color-coded computer functional map in 16 dogs. Twelve dogs underwent myocardial infarction by injection of vinyl latex into the left anterior descending coronary artery (transmural myocardial infarction, n = 6), or ligation of the left anterior descending coronary artery (nontransmural myocardial infarction, n = 6). Four dogs served as sham-operated controls. Image patterns were compared with tissue norepinephrine content and with histofluorescence microscopic findings in biopsy specimens. Hearts with transmural infarction showed zones of absent MIBG and thallium, indicating scar. Adjacent and distal regions showed reduced MIBG but normal thallium uptake, indicating viable but denervated myocardium. Denervation distal to infarction was confirmed by reduced norepinephrine content and absence of nerve fluorescence. Nontransmural myocardial infarction showed zones of wall thinning with decreased thallium uptake and a greater reduction or absence of MIBG localized to the region of the infarct, with minimal extension of denervation beyond the infarct. Norepinephrine content was significantly reduced in the infarct zone, and nerve fluorescence was absent. These findings suggest that 1) MIBG imaging can detect viable and perfused but denervated myocardium after infarction; and 2) as opposed to the distal denervation produced by transmural infarction, nontransmural infarction may lead to regional ischemic damage of sympathetic nerves, but may spare subepicardial nerve trunks that course through the region of infarction to provide a source of innervation to distal areas of myocardium.
J Am Coll Cardiol 1991 May
PMID:Scintigraphic assessment of sympathetic innervation after transmural versus nontransmural myocardial infarction. 201 61

The effects of reperfusion on myocardial infarct healing in the rabbit were analyzed using two morphometric indexes: the ratio of the volume of the organized portion of infarct to the volume of the whole infarct (%O/I), and the ratio of the minimal thickness of the infarct zone to the normal zone thickness (thinning ratio). In the nonreperfused infarcts, %O/I increased from 43.8 +/- 3.1% (mean +/- SEM) at 48 h to 85.7 +/- 2.5% at seven days, which supported the validity of this index. The thinning ratio was 0.50 +/- 0.03 at 48 h and did not change during the following five days. In other groups of rabbits, the coronary artery was temporarily occluded for 30 mins (early reperfusion) or 60 mins (late reperfusion), and the hearts were analyzed at 72 h or seven days. Early reperfusion limited infarct size as a percentage of the area at risk (%I/AAR) by approximately 50%, but late reperfusion did not. In both nonreperfused and reperfused infarcts, %O/I correlated significantly with absolute infarct size. Furthermore, the regression lines of the relationship of infarct size to %O/I of early and late reperfused infarcts shifted towards higher %O/I values compared with that of nonreperfused infarcts at seven days, which suggested accelerated organization. However, such a regression line shift by reperfusion was not detected at 72 h after infarction. The thinning ratio was higher in early reperfused infarcts compared to nonreperfused or late perfused infarcts, and there was a weak inverse correlation between thinning ratio and %I/AAR when the data of reperfused and nonreperfused infarcts were pooled.(ABSTRACT TRUNCATED AT 250 WORDS)
Can J Cardiol 1991 Apr
PMID:Effects of early and later reperfusion on healing speed of experimental myocardial infarct. 204 18

In clinical and experimental studies we assessed images of digital subtraction coronary angiography (DSA) for evaluating regional myocardial perfusion. Myocardial perfusion was assessed by injecting contrast medium into the coronary artery, and by imaging the regional myocardium using DSA. On the time-density curve obtained from the myocardial region of interest, we calculated the time to peak concentration (TPC) and the exponential washout rate (T). TPC and T were measured in five patients with stable effort angina pectoris (AP) and left anterior descending (LAD) lesions before and after percutaneous transluminal coronary angioplasty (PTCA). The values of 1/T increased significantly from 0.09 +/- 0.02 l/sec to 0.21 +/- 0.04 l/sec (p less than 0.01) after PTCA, but l/TPC did not change. No significant difference in ejection fractions was observed between the patients with AP and the normal subjects (n = 7), while the regional percent area shrinkage in the anterolateral and apical regions supplied by the LAD was significantly decreased in the patients with AP compared with those of normal subjects (anterolateral: 39.8 +/- 8.8% vs 51.3 +/- 6.8%, apical: 36.6 +/- 8.4% vs 52.4 +/- 13.4%, both p less than 0.01). In 10 anesthetized dogs with varying degrees of reduction in the left circumflex coronary artery (LCX) blood flow (CBF: categories of stenosis (S1-S5), we compared 1/TPC and 1/T with regional myocardial function (systolic wall thickening: %WTh). With varying LCX stenosis, there were no significant changes in heart rate and mean aortic pressure and significant linear correlations were observed between %WTh and 1/TPC (r = 0.51), between %WTh and 1/T (r = 0.55). At S1 (CBF: 100-90% of the control), neither %WTh nor 1/TPC differed from that of the controls, but 1/T was significantly decreased (80% of the controls, p less than 0.01). From S3 (CBF: 79-60%) to S5 (CBF: 39-0%), %WTh, 1/TPC and 1/T were significantly decreased from those of the control levels (all p less than 0.01). However, at S5 (CBF: 39-0%) the values of 1/TPC (71% of controls) and 1/T (33%) did not differ from those at S4; whereas, %WTh was markedly reduced and the systolic thinning of the ventricular wall occurred at S5. Therefore, in critical coronary stenosis, 1/T was more sensitive than 1/TPC or wall dynamics for assessing myocardial ischemia. Both 1/TPC and 1/T, as well as %WTh, were useful for assessing moderate myocardial ischemia; however, these DSA indices had considerable limitations for evaluating the severity of myocardial ischemia when CBF was markedly reduced.
J Cardiol 1990
PMID:[Comparison of myocardial perfusion assessments by digital subtraction angiography with those of left ventricular wall dynamics]. 213 31

An abnormal elevation in collagen concentration or myocardial fibrosis occurs in the hypertrophied left ventricle of the rat with renovascular hypertension (RHT). The structural nature and functional consequences of this fibrosis and the mechanisms involved in its appearance were reviewed for various phases of hypertrophy. Within days after the onset of renal ischemia, type I collagen messenger ribonucleic acid is expressed. An interstitial fibrosis follows, characterized by an increased dimension of existing perimysial fibers and the appearance of fibrillar collagen in spaces previously devoid of collagen, together with a perivascular fibrosis of intramyocardial coronary arteries. These expressions of myocardial fibrosis are associated with an increase in diastolic and systolic myocardial stiffness. Endomyocardial fibrosis serves to further increase diastolic stiffness while myocytes encircled by fibrillar collagen become atrophic. Each of these consequences of myocardial fibrosis reduce myocyte length-dependent force generation. At 32 weeks of RHT there is an obvious diastolic and systolic dysfunction of the ventricle together with heart failure that includes ventricular dilatation, wall thinning and reduced ejection fraction. The mechanisms involved in mediating fibrosis in RHT appear to be multiple. Myocyte necrosis and fibroblast proliferation have been associated with elevated circulating angiotensin II. Necrosis in RHT was not seen with captopril pretreatment or in the hypertension and hypertrophy that accompanied infrarenal aorta banding. An alteration in coronary artery permeability may be responsible for the perivascular fibrosis that is not seen with captopril pretreatment. Thus in RHT, the hemodynamic status of the ventricle determines myocyte hypertrophy while the elevation in circulating angiotensin II is responsible for the remodeling of nonmyocyte compartments, including the appearance of myocardial fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1990 Apr 03
PMID:Myocardial fibrosis and pathologic hypertrophy in the rat with renovascular hypertension. 213 51


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