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

A complex angiographic examination was performed in 28 patients with rheumatic aortic valvular disease. The major mechanism of compensation in aortic failure was found to be an increase in left ventricular end-diastolic volume at the expense of added regurgitating blood volume. It was shown that isolated aortic failure was a good compensated defect with high functional myocardial reserves and coronary circulation along with adequate left ventricular dilatation and normal-stress nature of left ventricular hypertrophy. Left ventricular dilation at a regurgitation fraction of less than 30% and intramyocardial tension increase were demonstrated to be unfavorable predictive signs and to be indicative of profound myocardial dysfunction.
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PMID:[Intracardiac mechanisms of compensation of isolated aortic insufficiency]. 215 56

Coronary disease and left ventricular failure are the two main causes of death in haemodialysis patients. In these particular patients it is the accumulation of several risk factors rather than accelerated atherogenesis which seems to be the responsible for the frequent manifestations of a coronary disease which is sometimes difficult to diagnose. Independently of any cardiovascular history, the so-called "uraemic cardiopathy" is characterized by left ventricular dilatation associated with an increased myocardial mass but with a low mass/volume ratio. The systolic function is preserved whereas the ventricular diastolic compliance is altered due to the left ventricular hypertrophy.
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PMID:[Cardiovascular repercussions of chronic hemodialysis]. 232 88

Fetal cardiac changes due to ductal constriction by maternal ingestion of nonsteroidal anti-inflammatory drugs were studied morphologically in near-term rats as an animal model, and results were compared with values of control 1 (C1, twenty-first day) and control 2 (C2, twenty-second day). The fetal ductus was constricted (-70%) (p less than 0.05) by maternal administration of 10 mg/kg indomethacin. Dilatation of the right ventricle and evidence of congestive heart failure including increased pericardial effusion (+200%) (p less than 0.05) and an increase in water content in the abdominal wall were present at 1, 4, and 8 hours after drug administration. At 24 hours after drug administration, concentric right ventricular hypertrophy was shown by a diminished right ventricular cavity (-36% vs. C2) (p less than 0.05), increased right ventricular wall thickness (+70% vs. C2) (p less than 0.05), and increased right ventricular mass (+31% vs. C1) (p less than 0.05). Left ventricular dilatation was indicated by an increased cavity volume (+87% vs. C2) (p less than 0.05) and increased muscle mass (+29% vs. C1 [p less than 0.05] or +9% vs. C2 [p greater than 0.05]). Both the wet and dry weights of the ventricles were increased. In conclusion, fetal ductal constriction caused right ventricular hypertrophy, diminished right ventricular cavity, and left ventricular dilatation and hypertrophy at 24 hours after drug administration in rats after initial congestive failure.
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PMID:Right ventricular concentric hypertrophy and left ventricular dilatation by ductal constriction in fetal rats. 252 91

1. The circulating and tissue renin-angiotensin systems (RAS) contribute importantly to cardiovascular homeostasis. Systemic and/or local activation of the RAS is seen in many pathological conditions of the cardiovascular system (e.g. hypertension and congestive heart failure). Increased angiotensin production participates in the pathophysiology of these and other disease states. Accordingly, inhibitors of the renin angiotensin system have a broad spectrum of therapeutic efficacy. 2. Angiotensin-converting enzyme (ACE) inhibitors are effective antihypertensive agents that do not adversely affect serum lipid levels. In addition, they reduce left ventricular hypertrophy. 3. ACE inhibitors cause coronary vasodilation and reduce ventricular work and wall stress. They have been shown to reduce experimental infarct size and to increase anginal threshold in humans. 4. After experimental or human myocardial infarction that results in significant left ventricular dysfunction, ACE inhibitors prevent ventricular dilatation and development of congestive heart failure, and may improve survival. 5. ACE inhibitors can prevent ventricular fibrillation and contractile impairment (stunned myocardium) associated with reperfusion injury after experimental myocardial ischaemia. 6. ACE inhibitors reduce preload and afterload, improve exercise capacity, reduce ventricular arrhythmias, and improve patient survival in clinical cardiac failure. 7. Taken together, inhibition of the RAS may potentially result in primary as well as secondary protective effects on the cardiovascular system.
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PMID:Clinical implications for therapy: possible cardioprotective effects of ACE inhibition. 269 Sep 9

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

The study was performed in 33 patients with echocardiographic diagnosis of mitral valve prolapse (PVM), without any other associated heart disease. A 19 derivations electrocardiogram (ECG) was performed a direct inscription 4 channel Samborns 150 machine at 25 and 50 mm/sec. The purpose of the study was determine the alterations in ventricular depolarization and repolarization, and to correlate them with valve prolapse, as well as with cavitary and parietal dimensions, as measured by M mode and/or two-dimensional echocardiography. Left ventricular hypertrophy detected by ECG agreed with the ECO test in 77%; the sensitivity was of 86% and specificity of 67.5%. Left ventricular hypertrophy detected by ECG was not related with the type of prolapse. Ventricular repolarization alteration was very frequent (84.8%). Association of this parameter with initial notch of R in a VF becomes important for diagnosis suspicion (p less than 0.01). When the abnormal repolarization affected the anterolateral wall, posterior valve prolapse was frequent; when the posteroinferior region was the affected one, the prolapse occurred more frequently in both valves. An important correlation (p less than 0.01) was found between left ventricular dilatation detected by ECO and the abnormal ventricular repolarization.
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PMID:[Electro-echocardiographic correlation in mitral valve prolapse]. 295 79

The basic criteria for the electrical diagnosis of left ventricular and biventricular enlargements are discussed on the basis of the myocardial depolarization and repolarization sequence. Left ventricular dilatation secondary to isolated diastolic overloading increases the manifestation of the main vectors resulting from the activation of this ventricle. These changes reflect the proximity of the left ventricular walls to the exploring electrodes. The above mentioned vectors appear as tall R waves and wide ventricular curves with counterclockwise rotation on the three planes. If the diastolic overload is a isolated phenomenon, T waves are positive and asymmetric on the left leads while the T loop, of secondary type, is concordant in its orientation with the R loop. This fact is due to a prolonged duration of the repolarization phase of the left ventricle. Global left ventricular hypertrophy produced by a sustained systolic overloading increases the magnitude and manifestation of all the vectors resulting from the depolarization of this ventricle (I, II l, III l) owing to the prolonged duration of the corresponding activation fronts. When LBBB is also present, the first septal vector is not evident. In extreme degrees of the systolic overload, the T wave is inverted and shows morphologic secondary characteristics in left leads, and the T loop opposes the R loop on frontal and horizontal planes. The directional changes of the repolarization fronts of free left ventricular walls can satisfactorily explain these features. Left ventricular hypertrophy of a segmentary type, such as that observed in idiopathic myocardiopathy, generally increases the magnitude and manifestation of septal vector I and II left. When both ventricles are hypertrophied, the electromotive forces originating in the more severely affected heart chamber predominate in electrical records.
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PMID:[Electrovectocardiographic manifestations of left ventricular and biventricular growth]. 296 67

Confusion may exist at the time of postmortem examination as to whether the diseased heart is dilated, hypertrophied, or both. Ventricular dilatation and ventricular hypertrophy were therefore evaluated by cardiac partition techniques in 441 subjects at autopsy to determine their relationship. Specific weight and surface area of each ventricle were obtained and patients were divided into categories of disease. Wall thickness measurements, a parameter routinely used in the ordinary autopsy, were found to be unreliable in defining hypertrophy. Ventricular surface area (an index of dilatation) was highly correlated with ventricular weight in most disease categories. Exceptions were cardiomyopathy and aortic stenosis, in which hypertrophy predominated. We conclude from these data that dilatation and hypertrophy occur proportionately in the postmortem heart in most disease categories except in cardiomyopathy and aortic stenosis. These findings clarify the relationship of dilatation and hypertrophy at the time of autopsy in most cases. Therefore, uncertainty as to whether cardiac dilatation or hypertrophy is present or which predominates is usually related to the inability to assess these states critically at the time of autopsy when the ordinary pathological methods are used.
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PMID:The relationship between hypertrophy and dilatation in the postmortem heart. 296 21

To evaluate pathologic features of myocardial infarction of the right ventricle (MI-RV), we analyzed 106 autopsy cases with transmural myocardial infarction (MI) (fresh in 46 cases and healed in 60). Anterior MI was observed in 47, posterior MI in 54 and lateral in 5. There were 13 cases (12%) with MI-RV (anterior in 1 case and posterior in 12), which included 10 cases with fresh MI and 3 with healed MI. All cases with MI-RV had associated transmural interventricular septal infarction. Of the 13 cases with MI-RV, 9 (69%) had right ventricular dilatation (RVD) and 2 had right ventricular hypertrophy. Extensive MI-RV (more than 1/3 of the right ventricle) was observed in 8 (89%) of those with RVD. Of 93 cases of MI without MI-RV, 14 (16%) had RVD. The incidence of RVD was greater in cases with MI-RV than in those without (p less than 0.005). All 12 cases with posterior MI-RV had significant (greater than or equal to 75%) narrowing of the right coronary artery (RCA), and 19 cases (87%) of those with posterior MI without MI-RV, had similar lesions. In conclusion, the incidence of RVD and significant narrowing of RCA was greater in cases with posterior MI-RV than in those with posterior MI.
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PMID:Pathologic study of myocardial infarction of the right ventricle. 296 27

Myocardial hypertrophy may influence coronary hemodynamics variably. Therefore, coronary sinus blood flow (gas chromatic argon technique) was determined in patients with left ventricular hypertrophy, with or without dilatation, associated with entirely normal coronary arteriographic results: 12 patients with hypertrophic obstructive cardiomyopathy (left ventricular mass-to-volume ratio, 3.66 +/- 0.52 g/ml), 22 patients with hypertensive heart disease due to essential hypertension (left ventricular mass-to-volume ratio, 2.12 +/- 0.26 g/ml), 18 patients with hypertensive dilatation (left ventricular mass-to-volume ratio, 1.6 +/- 0.48 g/ml), six patients with aortic stenosis (left ventricular mass-to-volume ratio, 1.99 +/- 0.41 g/ml), 12 patients with aortic incompetence, and 20 patients with normal heart function. Coronary sinus blood flow was determined as a control value and as the value following intravenous injection of dipyridamole (0.5 mg/kg of body weight). Coronary reserve was calculated as the ratio of coronary resistance before and after dipyridamole. Normal coronary reserve averaged 4.89 +/- 0.11. Similar values, despite marked left ventricular hypertrophy, were present for both hypertrophic obstructive cardiomyopathy (4.4 +/- 0.19) and aortic stenosis (4.66 +/- 0.12), whereas coronary reserve was considerably reduced in the concentrically hypertrophied hypertensive hearts (3.22 +/- 0.19) (p less than 0.001). Moderate decrease in coronary reserve was found in aortic incompetence and in dilated essential hypertension. These results indicate that patients with nonhypertensive hypertrophy, despite left ventricular mass augmentation, may have normal coronary reserve, whereas at a comparable degree of left ventricular hypertrophy, patients with hypertensive hypertrophy have a specific reduction in coronary reserve. Independent from vascular effects, ventricular dilatation may result in deterioration of coronary reserve because of an abnormal component of coronary vascular resistance. These results were also verified in experimental hypertension. Moreover, prevention and/or regression of the impaired coronary circulation in experimental hypertensive heart disease, most probably due to the reduction of smooth muscle layers of the media of coronary resistance vessels, could be achieved by long-term vasodilator therapy.
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PMID:Coronary hemodynamics in hypertensive heart disease. Basic concepts, clinical consequences, and experimental analysis of regression of hypertensive microangiopathy. 297 65


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