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

Nongated cardiac magnetic resonance imaging (MRI) has been reported previously to be inadequate for obtaining diagnostic information. This study explored the role of pulse sequence in the degradation of the nongated cardiac image. Images of diagnostic quality were obtained by using single spin-echo sequences with a very short echo time (10-20 msec TE) on a 0.12-T developmental MR unit. Marked degradation of the image was noted with longer TEs, and it is concluded that the previous unfavorable reports using a nongated technique may have been due to the longer TEs used in other units. Short-TE technique was used to examine 34 patients with a variety of cardiac diseases. Eleven patients had ventricular aneurysms. These cases showed thinning of the myocardium, and four of them showed increased signal within the aneurysm, perhaps related to regionally slower blood flow. Twenty patients had enlargement of one or more cardiac chambers. Three of these patients had thrombus within an enlarged chamber, which was readily identified on MRI. Twelve patients had left ventricular hypertrophy that was concentric in 11. One patient demonstrated asymmetric septal hypertrophy. All four pericardial effusions were low in signal intensity, but this was related to the pulse sequence used. Six patients had extrinsic masses displacing the heart and distorting the chamber contour. One patient showed intracardiac invasion of tumor; this finding was not evident on the CT. One patient with ventricular septal defect (VSD) and corrected transposition was scanned. In addition to identifying the VSD and chamber hypertrophy, the malposition of the great vessels at the base of the heart was seen. Four postoperative patients were scanned; wire suture artifact did not preclude imaging. In conclusion, diagnostic information can be obtained from nongated cardiac images provided that the TE is very short (10-20 msec). Although quantitative functional data are not available from nongated images, qualitative and diagnostic information is possible and may suffice in certain circumstances.
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PMID:Nongated cardiac magnetic resonance imaging: preliminary experience at 0.12 T. 623 9

The relation between ventricular function and the presence of electrocardiographic "strain" in patients with left ventricular hypertrophy was examined using digitised M mode echocardiography and 12 lead electrocardiograms in 64 patients with pressure overload, 21 with hypertrophic cardiomyopathy, and 14 athletes. Although all had increased left ventricular mass, those with strain had a prolonged interval from minimum cavity dimension to mitral valve opening and a reduced rate of early diastolic posterior wall thinning and dimension increase compared with those with normal ST segments and T waves. Both groups had normal systolic function (fractional shortening and peak velocity of circumferential fibre shortening), and the time between the termination of the T wave and minimum dimension was similar. In athletes, however, electromechanical systole was shorter than normal, and the end of the T wave and minimum cavity dimension were synchronous. It is concluded that abnormal electrical recovery in left ventricular hypertrophy is closely related to impaired early relaxation and may be dissociated from impaired systolic function, cavity dimension, interventricular conduction delay, and the presence of increased mass alone. The normal relation between electrical and mechanical systole is preserved even when the polarity of repolarisation is reversed.
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PMID:Relation between electrocardiographic repolarisation changes and mechanical events in left ventricular hypertrophy. 623 12

Knowledge of left ventricular chamber dynamics is central to our understanding of cardiac physiology. The complicated changes in left ventricular geometry observed in the dog during various phases of the cardiac cycle can be represented as distinct linear relationships between chamber eccentricity and intracavitary volume during diastole and ejection, and probably represent structural properties of the ventricular wall. Chamber geometry of the left ventricle is a major determinant of overall myocardial function. The slope of the radius of curvature (r) to wall thickness (h) relationship is a geometric constant that determines the mural force at any given transmural pressure. Chronic pressure and volume overload produce changes in this geometric relationship as a result of increased mural force resisting ejection. The adaptive mechanism of ventricular hypertrophy in this setting alters the r/h ratio and returns systolic mural force toward normal. Coronary occlusion induces acute changes in regional geometry characterized by holosystolic wall bulging and systolic wall thinning, which shift the r/h relationship upward and to the left. The geometric alteration during ischemia probably increases systolic mural force and could adversely affect myocardial function. Recent studies with patients have shown the r/h ratio to be of value in distinguishing between reversible and irreversible impairment of myocardial performance. Because most myocardial diseases produce major alterations in the structure of the ventricular wall, analysis of dynamic chamber geometry may prove of prognostic value in assessing patients with cardiac disorders.
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PMID:Dynamic geometry of the intact left ventricle. 645 23

Regional and global left ventricular function was assessed in 23 neonates with persistent pulmonary hypertension using computer assisted analysis of their left ventricular echocardiograms and compared with that in 50 healthy neonates. End diastolic left ventricular dimension was normal and end systolic dimension increased while percentage left ventricular shortening and peak velocity of circumferential fibre shortening decreased indicating impaired systolic performance. The peak rate of increase in left ventricular diameter in early diastole was significantly decreased and the durations of the rapid filling and isovolumic relaxation periods were prolonged suggesting resistance to left ventricular filling due to changes in diastolic myocardial properties. This abnormal left ventricular cavity function may have been due to a combination of increased diastolic wall thickness, reduced percentage systolic wall thickening, increased relative wall thickness, and pronounced reduction in peak rates of systolic wall thickening and diastolic wall thinning Seven neonates with persistent pulmonary hypertension died, and of the three examined at necropsy all had left ventricular hypertrophy and two extensive subendocardial haemorrhage and infarction affecting the right and left ventricular papillary muscles. Thus left ventricular dysfunction appears to be a common feature in neonates with this disorder and may be readily detected using computer analysis of left ventricular echocardiograms. Unfortunately, no single echo measurement was useful prognostically. Left ventricular dysfunction in persistent pulmonary hypertension probably results from a combination of hypoxaemia, acidaemia, and pulmonary hypertension, and although it may contribute to the high mortality in this syndrome, a correlation between the severity of left ventricular dysfunction and clinical outcome could not be shown.
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PMID:Left ventricular function in persistent pulmonary hypertension of the newborn. Computer analysis of the echocardiogram. 665 97

Six hundred and twenty-five patients with diabetes mellitus were studied by standardised clinical methods, resting and exercise electrocardiography (ECG) and digitised echocardiography to determine the prevalence of coronary and non-coronary heart disease. Clinical evidence of coronary artery disease (angina and infarction) was present in 110 (18 per cent) normotensive patients. Hypertension (blood pressure greater than 165/95 mmHg) was present in 172 (27 per cent) of whom 32 had cardiac symptoms. Heart failure or left ventricular dilatation was seen in 18 of whom 11 had either hypertension or coronary artery disease and six asymptomatic patients had unexplained ventricular hypertrophy. Echocardiograms in 245 of 290 asymptomatic patients with normal ECG showed that relaxation was prolonged (p less than 0.001) and mitral valve opening delayed (p less than 0.001) from normal especially in those with severe microangiopathy (proliferative retinopathy and/or heavy proteinuria). The peak rates of cavity dimension increase and posterior wall thinning were reduced from normal (both p less than 0.001) and patients with severe microangiopathy had the most marked changes. Redivision of these 245 diabetics by abnormalities of left ventricular function showed that 147 had normal function in whom only one of 23 (random 15 per cent sample) had a positive exercise ECG. Prolonged relaxation or delayed mitral valve opening alone (a nonspecific abnormality) was present in 41 and only three of 28 had a positive exercise ECG. Thirty-one had delayed mitral valve opening with inco-ordinate relaxation (abnormalities very suggestive of coronary artery disease) of whom 20 of 29 had a positive exercise ECG. Twenty-six had delayed mitral valve opening with slow cavity dimension increase or wall thinning (without hypertrophy) of whom 21 of 25 had a negative exercise ECG. This is a relatively specific abnormality similar to that found in left ventricular hypertrophy. Coronary artery disease is common in symptomatic and asymptomatic forms in diabetes mellitus. Non-coronary left ventricular diseases, such as dilation and hypertrophy, are probably no more common in diabetics than non-diabetics. A small number of diabetics with severe microangiopathy had abnormal relaxation and reduced peak rate of dimension increase or wall thinning which may represent left ventricular disease due to microangiopathy.
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PMID:A prospective study of heart disease in diabetes mellitus. 670 23

The remodeling of the spared non-ischemic left ventricular myocardium after different time intervals from the occlusion of the left coronary artery was examined in rats. In the presence of large infarcts, ventricular failure developed two to three days after surgery, because of chamber dilation and thinning of the wall, resulting in an average 7.5-fold increase in diastolic stress on the surviving myocardium. Mural thinning of the ventricular wall remote from and bordering the infarction occurred through side-to-side slippage of myocytes and capillaries within the wall. Although an average hypertrophic growth of 22% of the spared myocytes has been found, this amount of hypertrophy was insufficient to restore normal myocardial function. Long-term cardiac restructuring after infarction was characterized by the persistence of chamber dilatation and thinning of the ventricular wall. In addition to the side-to-side slippage, lengthening of the myocytes was an important cause of ventricular changes. As the reactive hypertrophy of the unaffected ventricle was insufficient to re-establish the ratio of ventricular mass to chamber volume, the diastolic stress remained elevated and decompensated eccentric ventricular hypertrophy developed. The anatomical remodeling of the spared left ventricular myocardium is an important conditioning factor in the short- and long-term outcome of ischemic cardiomyopathy.
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PMID:Cellular basis of ventricular remodeling after myocardial infarction in rats. 757 6

To determine the effects of chronic constriction of the left coronary artery on the function and structure of the heart, coronary artery narrowing was surgically induced in rats and ventricular pump performance, extent and distribution of myocardial damage, and the hypertrophic and hyperplastic response of myocytes were examined. Alterations in cardiac hemodynamics were found in all rats, but the characteristics of the physiological properties of the heart allowed a separation of the animals into two groups which exhibited left ventricular dysfunction and failure, respectively. Left ventricular hypertrophy occurred in both groups and was characterized by ventricular dilatation and wall thinning which were more severe in the failing animals. Multiple foci of myocardial damage across the wall were seen in all animals but tissue injury was more prominent in the endomyocardium and in failing rats. The anatomical and hemodynamic changes resulted in a significant increase in diastolic wall stress which paralleled the depression in ventricular performance. Myocyte cell loss and myocyte cellular hypertrophy were more severe with ventricular failure than with dysfunction. Finally, diastolic overload appeared to be coupled with activation of the DNA synthetic machinery of myocytes and nuclear mitotic division. In conclusion, a fixed lesion of the left coronary artery leads to abnormalities in cardiac dynamics with marked increases in diastolic wall stress and extensive ventricular remodeling in spite of compensatory myocyte cellular hypertrophy and hyperplasia in the remaining viable tissue.
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PMID:Ventricular remodeling in global ischemia. 757 15

In hypertensive cardiomyopathies, diastolic function is abnormal due to impaired relaxation associated with left ventricular hypertrophy, and a variable degree of reduction in left ventricular compliance may also be present. Abnormal relaxation can be indicated from prolonged isovolumic relaxation time and reduced early diastolic mitral inflow velocity, as well as from a reduced rate of posterior wall thinning and the neg dp/dt estimated from a continuous wave recording of mitral regurgitation. Reduction in left ventricular compliance can be assessed from shortening of the mitral A-wave, and from increased flow reversal in the pulmonary veins at atrial contraction. Non-invasive assessment of LV diastolic function is therefore possible by recording mitral and pulmonary venous flow velocities and posterior LV wall motion.
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PMID:Doppler echocardiographic evaluation of diastolic function in hypertensive cardiomyopathies. 828 71

Arterial hypertension leads to left ventricular hypertrophy. In proportion to increased left ventricular systolic pressure, left ventricular hypertrophy is considered to be of adaptive nature from the point of view of wall stress regulation. In the beginning, left ventricular function is normal, whereas diastolic filling is already compromised by the process of hypertrophy and altered ventricular geometry. In case of ventricular dilation and wall thinning, wall stress increases and leads to an increment in myocardial oxygen demand and a decrease of left ventricular ejection fraction. This is followed by a further decline in intrinsic myocardial contractility and a decrease in the elastic material properties of the myocardium. The structure of the myocardium is characterized by myocyte hypertrophy, a process of reactive and reparative fibrosis and alterations of the coronary microcirculation. Coronary vasodilator reserve is markedly impaired and is likely to initiate a process of malperfusion and malnutrition under increased metabolic demands. Particularly, the combined involvement of myocytes, interstitium, and intramyocardial vasculature appears to predispose to late heart failure after prolonged exposure to chronic pressure overload in arterial hypertension.
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PMID:Heart failure on the basis of hypertension. 848 35

Decompensated eccentric ventricular hypertrophy characterizes the transition from compensated pressure or volume over-load hypertrophy to myocardial dysfunction and failure. Myocyte loss is the major etiologic factor of wall thinning and chamber dilation and may condition the progression of the cardiac myopathy. Myocyte death can occur by apoptosis or necrosis, but the activation of the suicide program of myocytes exceeds necrotic cell death in the pathologic heart of ischemic origin. Whether reactive fibrosis constitutes a primary event in the initiation of ventricular dysfunction or a secondary reaction to myocyte death is an important unanswered question.
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PMID:Myocyte death in heart failure. 883 66


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