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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Postoperative echocardiogram often demonstrate persistent right ventricular dilatation and paradoxic ventricular septal motion after repair of an atrial septal defect. To determine the prevalence, causes and significance of these echocardiographic abnormalities, 31 patients were studied with catheterization and echocardiography before and after repair of an atrial septal defect. Before operation, every patient manifested right ventricular dilatation, and all but one had abnormal septal motion. After operation, right ventricular dilatation was noted in 24 (77%) and abnormal septal motion in 21 (68%) patients despite the absence of residual left to right shunting in 30 (97%). These echocardiographic abnormalities could be correlated with age at operation and length of postoperative follow-up study but did not correlate with the degree of preoperative right ventricular enlargement or with shunt size or right ventricular pressure before or after operation. There was no associated functional deficit as demonstrated by the normal maximal oxygen consumption in all 13 patients who underwent treadmill exercise testing 5 to 38 months after operation; these patients included 9 with persistent right ventricular enlargement and abnormal septal motion.
Am J Cardiol 1978 Feb
PMID:Abnormal right ventricular size and ventricular septal motion after atrial septal defect closure: etiology and functional significance. 14 24

To evaluate possible differences in the cardiac effects of different types of running training, 22 competing male runners--10 sprinters and 12 endurance runners--were studied with a physical examination, electrocardiography, chest X-ray film and echocardiography. Thirteen sedentary men served as control subjects. There were no differences between the athletic groups in physical findings. However, left ventricular hypertrophy in the electrocardiogram was more apparent in the endurance runners (P less than 0.05), whose relative heart size on chest X-ray examination was also greater than in the sprinters (P less than 0.02). On echocardiography the left ventricular end-diastolic volume was equally greater than normal in both groups of athletes (P less than 0.005), but in the endurance runners the percent chance of the minor axis diameter in systole was greater than in the sprinters or control subjects (P less than 0.02). Values for left ventricular wall thickness and mass were greater than normal in both groups of athletes but were higher in the endurance runners than in the sprinters (P less than 0.001). The left atrial diameter was apparently greater in the endurance runners than in the sprinters or control subjects (P less than 0.001), whereas that of the sprinters did not differ from normal. Thus, intensive sprinter training seems to dilate the left ventricle but causes less increase in wall thickness and mass than training for endurance running and no change in left ventricular function or left atrial size. Endurance running causes left ventricular dilatation equal to that of sprinter training, greater wall hypertrophy and improved systolic emptying of the left ventricle, and it also dilates the left atrium perhaps because of decreased left ventricular compliance.
Am J Cardiol 1979 Jul
PMID:Noninvasive evaluation of the athletic heart: sprinters versus endurance runners. 15 93

To examine problems in echocardiographic diagnosis of mitral valve prolapse, multiple crystal cross-sectional echocardiography and single crystal recordings derived from the multiple crystal array were used to study 45 clinically normal children aged 3 to 15 years (Group A), 26 children aged 2 to 10 years with known mitral valve prolapse (Group B), 12 children with a catheterization-proved large left to right shunt at the ventricular level (Group C) and 8 children with catheterization-proved left ventricular outflow tract obstruction (Group D). Children in Groups A and B were not studied hemodynamically. Children in Groups C and D had no evidence of mitral valve prolapse on angiography and were studied echocardiographically to determine the effect of changes in ventricular shape on the patterns of mitral valve motion. In the real time cross-sectional studies, normal patients demonstrated a spectrum of mitral valve motion in which the bodies of the anterior and posterior leaflets became slightly horizontal with systolic ejection. The mitral apparatus assumed a curvilinear funnel shape. Arching of the leaflets into a horizontal configuration was more striking in the presence of either left ventricular dilatation in left to right shunt or involvement of the anterior mitral anulus in subaortic stenosis (two patients) and was associated with false positive M mode tracings suggesting mitral valve prolapse. This latter configuration was easily differentiated from the superior motion of the body of the leaflets in true prolapse. Studies of single crystal M mode recordings derived form the cross-sectional array in known locations from six normal patients revealed M mode patterns of pseudoprolapse in tracings derived from the leaflet body and patterns of normal motion at the free edge. In contrast, superior-posterior prolapse visualized in cross-sectional studies in patients with the click-murmur syndrome was associated with abnormal M mode recordings from all parts of the leaflet, including the free edge, although the abnormalities were most striking in tracings derived from the leaflet body. The M mode echocardiographic findings of mitral valve prolapse in both normal patients and patients with the click-murmur syndrome were dependent upon transducer angulation and the portion of the valve examined. The critical differentiation of the spectrum of normal valve motion from prolapse requires careful evaluation of echoes from the free edge of the leaflet where the posterior and anterior leaflet echoes coapt in early systole.
Am J Cardiol 1977 Mar
PMID:Echocardiographic spectrum of mitral valve motion in children with and without mitral valve prolapse: the nature of false positive diagnosis. 55 83

Clinical and morphologic features of transmural myocardial infarction (associated with insignificant or absent atherosclerosis of the extramural coronary arteries) are described in seven patients with hypertrophic cardiomyopathy. Marked chronic congestive heart failure associated with supraventricular arrhythmias occurred in six of the seven patients, each of whom had no or mild left ventricular outflow tract obstruction under basal conditions. No patient had typical angina pectoris, and only one patient had clinically evident acute myocardial infarction. Infarction may have caused cardiac arrest in one other patient, but was "silent" in the remaining five patients. At necropsy, six of the seven patients had extensive myocardial scarring involving the ventricular septum, left ventricular free wall and one or both left ventricular papillary muscles; in four patients portions of the right ventricular wall were also scarred. Six patients had dilated ventricular cavities, including two who were known to have nondilated ventricular cavities earlier in their clinical course. It is concluded that transmural myocardial infarction in the absence of significant coronary atherosclerosis is a not uncommon finding (prevalence rate 15 percent) in a population of patients who had died from hypertrophic cardiomyopathy. Although transmural infarction is possibly a secondary event, it more likely contributes causally to the clinical deterioration of some patients with hypertrophic cardiomyopathy, leading to ventricular dilatation and progressive fatal cardiac failure.
Am J Cardiol 1979 Jun
PMID:Hypertrophic cardiomyopathy and transmural myocardial infarction without significant atherosclerosis of the extramural coronary arteries. 57 70

In a series of 840 cases of unselected complete LBBB, 2 groups were compared with each other, one of 174 cases of complete LBBB with a QRS axis markedly deviated leftward, from minus50 to minus 90 degree (group A), the other 434 complete LBBB with a normal QRS axis included between minus20 and plus30 degree (group B). Group A differed from group B by the etiological predominance of primary cardiomyopathies, the lesser frequency of hypertensive and/or coronary heart disease, the rarity of idiopathic complete LBBB. It was commonly combined with marked enlargement of the X-ray heart shadow, with marked widening of QRS complex and had a definitely more severe prognosis. The anatomical study performed in 88 cases (52 group A, 36 group B) showed on thw whole a slightly more enlarged heart and a more marked left ventricular dilatation in group A. There were no differences in the state of the coronary arteries and in the frequency of myocardial infarction. Microscopical examination of the left bundle branch, performed in 42 cases (25 group A, 17 group B), showed the habitual and intense changes of the bundle branch, but without obvious difference between the 2 groups concerning the topographical distribution of the lesions.
Adv Cardiol 1975
PMID:Complete left bundle branch block with marked left axis deviation of qrs clinical and anatomical study. 113 88

We studied 11 patients with severe mitral regurgitation (MR). With 2-D echocardiogram we could obtain the septal and posterior wall thickness, left ventricular internal dimensions and ventricular function. With parasternal short axis view we calculate the h/r ratio (left ventricular thickness/radius). The results were compared with normal values: we found important left atrial and ventricle dilatation with significative difference from the normal values (P < 0.001), the diastolic and systolic h/r ratio was significative lower than the normal values (P < 0.005): the systolic wall stress was significative higher in relation to normal values (P < 0.001). We conclude that patients with severe (MR) initially have an important ventricular dilatation but no hypertrophy despite volume overload. The possible explanation is that in early stages of the disease, the afterload of the left ventricle is low and does not trigger the development of hypertrophy. The hypertrophy appears only when the systolic stress is high secondary to myocardial failure. The excessive dilatation of the left ventricle probably damages the myocardial fibers by excessive stretch. This mechanism probably explains the poor late surgical evolution of patients with mitral prosthesis. This we propose that the optimal surgical timing for such patients is when the systolic wall stress elevates over the normal limits, because this is an early sign of myocardial failure.
Arch Inst Cardiol Mex
PMID:[The thickness/radius ratio (h/r) of the left ventricle in pure mitral insufficiency]. 128 61

During 241 consecutive percutaneous mitral valvotomy (PMV) procedures performed with the Inoue balloon, 16 patients (6.6%) developed severe mitral regurgitation (MR). Baseline clinical, echocardiographic (Doppler mitral valve area and Wilkins' score) and hemodynamic data were not different from those of patients without this complication. Severe MR occurred during the first inflation in 7 patients and after several stepwise inflations in 9. Although maximal balloon size was similar in both groups, unusual indentations and subvalvular inflations were more frequently observed in patients who developed severe MR. Early mitral valve replacement was required in 6 patients. All of them had a leaflet rupture either along the midportion (2 patients), along a commissure (4 patients), or both. Commissural calcium was present in 5 valves and 5 also had severe subvalvular involvement that had been underestimated by echocardiography. Of the 10 nonsurgically treated patients, 4 had chordal rupture by echocardiographic criteria, whereas in the remaining 6 the precise mechanism of MR could not be determined. During follow-up (11.4 +/- 4 months, range 1 to 30), 1 patient required surgery for symptoms and the remaining 9 were symptomatically improved and free of left ventricular dilatation. In conclusion, severe MR complicated 6.6% of PMV procedures with the Inoue balloon, and its mechanism was leaflet or chordal rupture. Although one third of the patients required early mitral surgery, most of the remaining obtained midterm symptomatic benefit.
Am J Cardiol 1992 Nov 01
PMID:Predictors, mechanisms and outcome of severe mitral regurgitation complicating percutaneous mitral valvotomy with the Inoue balloon. 141 41

Serial electrocardiograms as well as echocardiographic studies of 51 pilgrims suffering from acute heat stroke (mean rectal temperature 41.6 degrees C) were performed. All patients were examined immediately after cooling and 24 h later whenever possible. Regional wall motion abnormalities were detected in 9 cases (17.6%) while pericardial effusion was observed in 13 cases (25%) and asymmetrical septal hypertrophy was detected in 8 cases (15.6%). Other cardiac abnormalities included right ventricular dilatation and increased in left ventricular internal dimensions in 4 cases (7.8%), respectively. Thirteen cases (25.5%) had normal echocardiographic findings. Forty (78%) patients had sinus tachycardia while 8 cases (15.7%) showed atrial fibrillation with uncontrolled ventricular rate, and 3 (5.8%) had sinus bradycardia. Heat stroke electrocardiograms showed tracings demonstrating ST segment depression, compatible with ischaemia in 9 cases, while in 6 cases there were nonspecific T wave changes, whereas in another 4 cases the tracings demonstrated different conduction abnormalities. The collected data were analysed and compared to those of 43 control patients. The adverse effects of heat stroke on the heart are multifactorial requiring the utmost attention and understanding, as they reflect the patient's cardiovascular status.
Int J Cardiol 1992 Nov
PMID:Non-invasive evaluation of cardiac abnormalities in heat stroke pilgrims. 145 70

We describe a simple, non-invasive and practical method to determine the peak velocity of tricuspid regurgitant flow (and hence derive systolic pulmonary artery pressure) from examination of the dynamics of retrograde tricuspid flow on Doppler. Based on a previously described relationship between right ventricular systolic pressure and the time interval between pulmonary valve closure and tricuspid valve opening, our technique does not require the peak tricuspid regurgitant velocity to be recorded; nor, as in previous studies does it rely upon recording the jugular venous pulse, right ventricular apexcardiogram or invasive pressure measurements. We have studied 65 patients with right ventricular disease (53 with pulmonary hypertension), and 24 with dilated cardiomyopathy, with M-mode, two-dimensional echocardiography, Doppler, and phonocardiography. The peak tricuspid regurgitant velocity could be predicted from the interval between pulmonary closure and the end of the tricuspid regurgitant signal on Doppler in patients with pulmonary hypertension and those with right ventricular disease with normal pulmonary artery pressure, but not in patients with dilated cardiomyopathy. In patients with pulmonary hypertension or right ventricular dilatation, this may be a useful alternative method in estimating pulmonary artery pressure from Doppler, in cases where it is not possible to record the peak tricuspid regurgitant velocity.
Int J Cardiol 1992 Mar
PMID:Assessment of the peak tricuspid regurgitant velocity from the dynamics of retrograde flow. 156 51

Early in the acute phase of myocardial infarction the phenomenon of expansion may occur, with regional thinning and dilatation of necrotic region. This complication may be detected by echocardiography since the first hours of infarction. During the two subsequent weeks, an additional increase of left ventricular volume may occur, due to an increase of length of the infarcted segments and, as well, of the contractile segments which suffer a "volume overload hypertrophy". This is the phenomenon of remodeling. Finally during the first year post infarction, a progressive left ventricular dilatation may develop. This late dilatation seems to be due to an increase of perimeter of the contractile regions only. By the time this topographic changes have occurred, the left ventricle assumes a more spheric configuration. Left ventricular dilatation affects adversely cardiac function, with higher incidences of heart failure and death. Experimental and clinical studies show that, in selected patients, remodeling and ventricular dilatation may be attenuated by the administration of angiotensin-converting-enzyme inhibitors, with better indices of left ventricular function. Final results of several on-going multicenter studies are awaited for; they will allow a better definition of the role of ACE inhibitors on prevention and treatment of left ventricular dysfunction after myocardial infarction.
Rev Port Cardiol 1992 Mar
PMID:[Expansion of infarction, dilatation and ventricular remodelling. Therapeutic potential of angiotensin-converting enzyme inhibitors]. 161 Jun 13


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