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

Left ventricular dilation and remodelling occur in 35-40% of anterior transmural myocardial infarcts and these events are important antecedents to the development of late congestive heart failure. This process commences within the first 24 hours following myocardial infarction and may be steadily progressive over months to years. Both the infarcted and the uninfarcted regions of myocardium are equally involved in the process. Thinning of the left ventricular wall occurs mainly as a result of cell slippage. In addition, compensatory hypertrophy occurs in the uninfarcted segment of the myocardium. While this hypertrophy may initially be physiological, it ultimately appears to become a pathological process and thereby contributes to pump dysfunction. At the present time there are encouraging data to suggest that nitroglycerin, administered in the setting of the acute infarction, or the angiotensin converting enzyme inhibitor captopril, may ameliorate this process. Whether a patent infarct related artery further limits dilation is uncertain and is currently under investigation.
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PMID:The prevention of congestive heart failure: left ventricular dilation and its management. 215 39

Thinning and dilatation (expansion) of the infarct region and complete rupture of the ventricular wall are significant complications of acute transmural myocardial infarction associated with increased morbidity and mortality. The pathogenesis of these related events is unknown. Recent studies of myocardial connective tissue have delineated an extensive array of intercellular and pericellular structures which serve as a skeletal framework and which may modulate contractile activity. We have employed a modified silver impregnation method to visualize the connective tissue components by light microscopy. To explore whether the skeletal framework is altered in acute myocardial infarction with and without ventricular rupture, we studied 9 human hearts at autopsy, and 4 canine infarcts of known duration. The human infarctions included 4 nonruptured cases with infarcts 1-5 days old, and 5 ruptured cases with infarcts 3-10 days old. Sections from normal, lateral, and central infarct or ventricular rupture sites were stained with silver. The normal tissue from each heart served as a control. Silver staining was moderately decreased in the lateral infarct zones, and markedly decreased in the central non-ruptured infarct zones. In the 5 ventricular rupture cases, the rupture site had no silver staining. A similar pattern was observed in the 4 canine infarcts. Thus, we conclude that the skeletal framework is markedly altered in the central zone of acute myocardial infarction. The acute changes of silver stained connective tissue may contribute significantly to the development of infarct expansion or ventricular wall rupture.
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PMID:Alterations of the myocardial skeletal framework in acute myocardial infarction with and without ventricular rupture. A preliminary report. 245 17

The diagnostic accuracy of spin-echo Magnetic Resonance (MR) imaging in the detection and localization of a recent myocardial infarction (mean 4 days old) was compared to planar thallium-201 scintigraphy in 20 patients with a documented myocardial infarction. A control group of 10 subjects underwent a similar MR imaging procedure without thallium-201 scintigraphy. T1-weighted MR images (TE 30 msec) showed abnormal thinning of the infarcted left ventricular wall during systole (less than 50% of the opposite wall) in 11 patients (55%). On T2-weighted multi-echo MR images, (TE 30-60-90-120 msec) abnormally increased signal intensity was found in 17 patients and coincided with the location of the infarction. Thallium-201 scintigraphy detected the infarction in 18 patients. Comparison of T2-MR imaging and thallium-201 scintigraphy showed concordant findings in 82% of the left ventricular segments. In 9% of segments, thallium uptake was reduced with normal T2-MR and in 9% we found a normal thallium uptake with abnormal T2-MR findings. In all subjects of the control group, T1-MR images were normal, and only one subject showed increased signal intensity on T2-MR images. We conclude that the diagnostic accuracy of MR imaging in detecting a myocardial infarction is similar to that of T1-201 scintigraphy.
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PMID:Value of magnetic resonance imaging in patients with a recent myocardial infarction: comparison with planar thallium-201 scintigraphy. 250 44

Evidence of acute infarct expansion and the frequency of the acute infarct expansion syndrome (acute infarct dilatation and thinning associated with hypotension and left ventricular failure but no evidence of new necrosis) occurring at two days or more after a first acute Q-wave myocardial infarction were studied using serial two-dimensional echocardiography in 221 consecutive patients (100 anterior, 121 inferior). Patients with symptomatic pericarditis were treated with indomethacin (group 1, n = 73) or ibuprofen (group 2, n = 49) and those without symptomatic pericarditis received neither drug (group 3, n = 99). The overall frequency of the acute infarct expansion syndrome was 13% and 69% of these were among the pericarditis groups. The syndrome was significantly more frequent in group 1 (22%) than group 2 (8%) (P less than 0.05) or group 3 (9%) (P less than 0.025). Serial echocardiograms revealed more expansion with greater percentage increase in the infarct containing segment length in group 1 than group 2 or group 3 (18% versus 9% versus 9%, P less than 0.005). However, the decreases in infarct segment thickness were similar in groups 1 (24%) and 2 (25%) but greater (P less than 0.001) than in group 3 (7%). Despite similar infarct size and infarct thinning in groups 1 and 2, the degree of infarct expansion was greater and the infarct expansion syndrome more frequent in group 1. However, when allowance was made for the potential protective effect of prior use of intravenous nitroglycerin and concomitant use of nifedipine, indomethacin and ibuprofen had similar effects on expansion. Thus, indomethacin or ibuprofen should be used with caution after Q-wave infarction so as to avoid further expansion. The fact that short term use of other drugs might modify infarct remodelling should be considered in studies attempting to assess efficacy of one particular drug.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Myocardial infarct expansion during indomethacin or ibuprofen therapy for symptomatic post infarction pericarditis. Influence of other pharmacologic agents during early remodelling. 256 3

The time course of recovery of left ventricular wall motion after coronary reperfusion and how that relates to anatomical infarct size, wall motion abnormality, and the amount of cardiac myosin light chain II release were evaluated in conscious dogs. One week after the implantation of hydraulic occluders on the left circumflex arteries, myocardial infarction was induced. Coronary reperfusion was performed 3 h after the occlusion in 9 dogs (R) and occlusion was sustained in 9 dogs (C). All dogs underwent serial 2-dimensional echocardiograms and determination of serum cardiac myosin light chain II. The infarct size was identified at 14 days. Systolic wall thickening at the center of the ischemic area (SWT) at 3 h was -7.7 +/- 2.8% (C), -9.9 +/- 3.0% (R). Systolic thinning was observed even at 14 days in C. Significant recovery of contraction was observed in R, but the improvement continued for as long as 2 days. SWT at 14 days was -1.5 +/- 2.8% (C) and 7.0 +/- 4.6% (R) (p less than 0.05). All of SWT or the extent of systolic thinning (EST) 3-hour and 14-day were correlated well with infarct size in C. In group R, 14-day SWT and 14-day EST correlated with infarct size but 3-hour SWT and 3-hour EST did not. Total release of serum cardiac myosin light chain II levels correlated well with infarct size (r = 0.88), 14-day SWT (r = -0.90) and 14-day EST (r = 0.89) in all dogs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Infarct sizing after reperfusion by two-dimensional echocardiography and serum cardiac myosin light chain II in conscious dogs: dissociation between early left ventricular wall motion and ultimate infarct size. 260 Oct 4

MRI manifestations in 9 patients with old myocardial infarction (OMI) were analyzed and the results were compared with the changes seen in ECG (9 patients) and coronary angiography (6 patients). The authors found that: 1. Myocardial thinning was one of the important signs of OMI (78%); 2. Signal intensity was reduced which was remarkably lower than the adjacent normal myocardium (P less than 0.01). 3. MRI provided even more direct and accurate information for assessing the site and extent of infarction than ECG; 4. The results of LVEF calculated from MRI were closely correlated with that obtained from left ventriculography (r = 0.8245, 0.01 less than P less than 0.05). The authors preliminarily conclude that MRI is an accurate method for evaluating the site and extent of myocardial infarction, myocardial tissue characterization and left ventricular function.
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PMID:[A preliminary study on the diagnostic value of magnetic resonance imaging in old myocardial infarction]. 280 46

Infarct expansion and infarct extension are events early in the course of myocardial infarction with serious short- and long-term consequences. Infarct expansion, disproportionate thinning, and dilatation of the infarct segment probably begin within hours of acute infarction and usually reach peak extent within seven to 14 days. Clinical data suggest that infarct expansion occurs in approximately 35% to 45% of anterior transmural myocardial infarctions and to a lesser extent in infarctions at other sites. Although expansion usually develops in large infarcts, the extent of transmural necrosis rather than absolute infarct size predicts its occurrence. Expansion has an adverse effect on infarct structure and function for several reasons. Functional infarct size is increased because of infarct segment lengthening, and expansion results in over-all ventricular dilatation. Thus, patients with expansion of an infarct have poorer exercise tolerance, more congestive heart failure symptoms, and greater early and late mortality than those without expansion. Infarct rupture and late aneurysm formation are two additional structural consequences of infarct expansion. Experimental and clinical data suggest that the incidence and severity of expansion can be modified by interventions. Increased ventricular loading conditions and steroidal and nonsteroidal antiinflammatory agents make expansion more severe. Reperfusion of the infarct segment and pharmacologic interventions that decrease ventricular afterload lessen the severity of expansion. Previous myocardial infarction and preexisting ventricular hypertrophy may also limit the development of infarct expansion. Infarct extension is defined clinically as early in-hospital reinfarction after a myocardial infarction. The pathologic finding of infarct extension is necrotic and healing myocardium of several different recent ages within the same vascular territory. Although this pathologic criterion usually cannot be verified, studies employing invasive and noninvasive assessment of patients with early reinfarction provide evidence that the new myocardial injury is usually in the same vascular risk region as the original infarction. A variety of different criteria have been applied in the clinical diagnosis of infarct extension, and this has resulted in a large range of estimated frequencies from under 10% to as high as 86%. High estimates are found in studies using one or two nonspecific criteria such as ST segment shift or reelevation of total CK. The lowest rates have been found when combinations of criteria are used.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Myocardial infarct expansion, infarct extension, and reinfarction: pathophysiologic concepts. 288 58

Left ventricular aneurysm is a common complication of myocardial infarction. The most common type of aneurysm is a true aneurysm which forms after transmural infarction by gradual thinning and expanding of the scarred left ventricular wall. Its distinctive features are that of a large-mouthed sac containing all layers of ventricular wall. A rare type of aneurysm is the "false" or pseudoaneurysm of the left ventricle that develops from rupture of recently infarcted myocardial wall forming a localized haemopericardium confined by parietal pericardium. Pathologically, there is a small narrow-necked channel connecting the ventricle with a large sac consisting of only clot and fibrous pericardial tissue without any myocardial elements. Pseudoaneurysms are distinguished from the true variety by their marked tendency to rupture. Because surgical repair of a pseudoaneurysm is often successful, it is important to make the diagnosis of this entity as early as possible. Two-dimensional echocardiography in combination with Doppler-flow is the mainstay of clinical diagnosis.
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PMID:[Ventricular pseudoaneurysm after acute myocardial infarction]. 292 62

Indexes of global ventricular function such as the ejection fraction (EF) and the peak diastolic filling rate (PDFR) are often used to assess the effects of coronary recanalization in patients with myocardial infarction. In this investigation we assessed the relationship between these global indexes and directly measured indexes of regional function during 15 minutes of coronary occlusion followed by 120 minutes of reperfusion in 22 open-chest dogs. A computerized nuclear cardiac probe was used to assess EF and PDFR. Indexes of regional function were measured by Doppler ultrasonic wall-thickening probes. During coronary occlusion, paradoxical systolic thinning occurred and the EF and PDFR decreased an average of 31.6% and 24.4%, respectively. During reperfusion the EF and PDFR improved rapidly and at 60 minutes were similar to baseline. Systolic wall thickening improved more gradually and remained abnormal throughout reperfusion. Likewise, indexes of diastolic function (mean rate to half end-diastolic thinning and late diastolic thinning fraction) recovered slowly and remained abnormal throughout reperfusion (78% and 69.7%, respectively). The correlation between the rate of change of global and regional function was poor during both coronary occlusion and reperfusion. Thus, during coronary occlusion the global and regional indexes of ventricular function undergo directionally similar changes. However, during coronary reperfusion the global indexes do not reflect the slow recovery of the stunned myocardium.
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PMID:Dissociation between global and regional systolic and diastolic ventricular function during coronary occlusion and reperfusion. 295 31

After acute transmural myocardial infarction, the heart may undergo major remodeling characterized by thinning and dilation of the infarct zone and overall enlargement of the heart. The effect of increased left ventricular pressure on infarct expansion and the extent to which it alters postinfarction remodeling were studied in a rat model. Rats with either aortic banding or a sham operation and a survival period of 3 weeks were further randomized to sham thoracotomy or left coronary ligation. Surviving rats were killed 7 days later and the hearts were fixed in diastole for morphologic analysis. Hearts with aortic banding had a mean peak to peak gradient of 20.7 +/- 4.9 mm Hg across the aortic band at death and a significantly thicker heart than that of the comparison group without an aortic band. Infarct size, as a percent of total left ventricular mass, at the time of death was less in the group with aortic banding, yet infarct expansion was more marked. However, when original infarct size was estimated taking into account the effects of aortic banding, scar formation, infarct expansion and infarct-induced hypertrophy, it was found to be similar in both infarct groups (45.50 +/- 4.2 versus 47.90 +/- 3.1%). Infarct expansion, as measured by cavity dilation and infarct thinning, occurred in both infarct groups but was greater in the group with aortic banding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased afterload aggravates infarct expansion after acute myocardial infarction. 297 4


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