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Results for “HEART ENLARGEMENT”

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At least 19 recordsLinked to original sources
PubMed1997

The clinical significance of fetal right heart enlargement with a structurally normal heart.

Isolated right heart enlargement of the fetus without cardiac structural abnormalities appears to be associated with growth retardation or abnormal perinatal outcome. We report the outcome of eight fetuses with subjective enlargement of the right heart. All cases were diagnosed antenatally from a standard four-chamber view on an ultrasound scan. All fetuses had otherwise normal cardiac anatomy. Seven out of the eight fetuses ultimately had outcomes which deviated from the norm. An isolated finding of fetal right heart enlargement warrants close antenatal fetal surveillance.

Female↗
PubMed1991

Effect of dimethyl sulfoxide on enlarged hearts of copper-deficient rats.

The purpose of this study was to examine, by transmission electron microscopy (TEM), the nature of the protective effect of dimethyl sulfoxide (DMSO) on hearts of copper-deficient (CuD) rats. Male, weanling Sprague-Dawley rats were fed, in a two-way design, CuD (0.45 micrograms/g) or copper-sufficient (CuS, 5.4 micrograms/g) diets with or without 5% DMSO in their drinking water. After 28 d, CuD rats showed typical signs of copper deficiency, including reduced liver and heart Cu, enlarged hearts, and anemia. DMSO-treated, CuD rats had lower heart weights and higher hematocrits than CuD rats. DMSO enhanced organ Cu concentrations in CuS, but not in CuD rats. TEM of CuD hearts showed myofibrillar distortion and enlarged, vacuolated mitochondria with fragmented cristae; morphometric measurements indicated an enhanced mitochondrial/myofibrillar ratio (mito/myo), but an increase of both mitochondrial and myofibrillar mass relative to CuS hearts. Compared to CuD hearts, DMSO-treated CuD hearts showed better mitochondrial morphology and myofibrillar organization, as well as a greater mito/myo, but lower mitochondrial and myofibrillar masses. Its function as a hydroxyl radical scavenger indicates that DMSO could protect CuD hearts, in particular their mitochondria, against oxidative damage. However, because measurements of thiobarbituric acid reactive substances were not consistent with this theory, other metabolic mechanisms, direct and indirect, must be examined.

Animals↗
PubMed1998

[Heart enlargement in an athlete--a diagnostic challenge].

Endurance training can result in an enlargement of the heart. These athlete's hearts are rarer than generally assumed. Pathological causes, resulting in an eccentric hypertrophy, have to be considered. We report on a 32 year old athlete performing approximately 10 hours of endurance training weekly. He consulted a physician because of a drop in performance. The eccentric left ventricular hypertrophy, diagnosed by means of echocardiography, was not interpreted as a solely physiological cardiac adaptation because the ejection fraction did not increase during exercise (stress-echocardiography), the left ventricular diastolic function (maximum E/A-ratio) was impaired at rest, and the ergometric performance was reduced in comparison to the heart size. The invasive diagnostics including myocardial biopsy demonstrate histologically a focal fibrosis as the result of former myocarditis. The fibrosis was possibly involved in the genesis of the eccentric hypertrophy based on structural dilatation through a preferably mesenchymal lesion. It remains open whether the long-term endurance training had forced the dilatation. This case demonstrates that pathological causes must be excluded if in athletes an enlarged heart does not concur together with a clearly increased ergometric performance. Stress-echocardiography and endomyocardial biopsy can considerably contribute to the differential diagnosis between physiological and pathological cardiac hypertrophy.

Adult↗
PubMed1988

[Interrelations between cardiac rhythm disorders and heart enlargement in patients with exertion-induced stenocardia and pain-free forms of ischemic heart disease].

Data from 24-h ECG monitoring of 137 patients with angina of effort or painless IHD were compared with respective X-ray evidence of heart enlargement. The patients were identified at an epidemiological screening for multifactorial IHD prevention among male residents of Kaunas, aged 40-59 yrs. A correlation was established between the enlargement of the cardiac volume and left compartments and the severity of arrhythmias.

Adult↗
PubMed1989

Radiological heart enlargement in treated hypertensive men: a comparative study of chest X-ray examination and M-mode echocardiography.

Twenty-five hypertensives with no history of myocardial infarction and with a radiologically determined heart enlargement were examined with M-mode echocardiography and compared with a normotensive control group (n = 41). All except two of the hypertensive patients were on a beta-blocker based antihypertensive treatment regime. The relative heart volume on X-ray was significantly larger in the hypertensives, 562 ml m-2 body surface area (BSA), compared to the normotensives, 408 ml m-2 BSA (P less than 0.001). Both left ventricular diameter (LVD) in end-diastole and end-systole and left arterial (LA) diameter were significantly larger in the hypertensives (56 vs. 51 mm, P less than 0.01; 35 vs. 31 mm, P less than 0.01; 46 vs. 42 mm, P less than 0.01, respectively) as was the LV mass (296 vs. 203 g, P less than 0.001). The end-systolic wall stress (ESWS) was significantly greater in the hypertensives. Despite these findings resting left ventricular fractional shortening was the same and showed a similar correlation with ESWS (r = 0.79 and r = 0.77, respectively) in both groups. Hence, left ventricular systolic performance was not impaired in the hypertensives compared to the normotensives. These results show that an enlarged cardiac silhouette on the chest X-ray in hypertensive subjects with beta-blocker based drug therapy must be interpreted with caution and must not, a priori, be judged as a sign of an impaired systolic cardiac function.

Adrenergic beta-Antagonists↗
PubMed2001

Resolution of right heart enlargement after closure of secundum atrial septal defect with transcatheter technique.

OBJECTIVES: The purpose of this study was to prospectively characterize the reduction in right atrial (RA) area and right ventricular (RV) volume after transcatheter closure of atrial septal defect (ASD) and to investigate factors that may predict magnitude of resolution in right heart enlargement. BACKGROUND: Secundum ASD can cause volume overload of the right side of the heart with the potential for development of late complications. Little is known about reduction in right heart size after closure of ASD. METHODS: Transthoracic echocardiography was performed in 38 patients undergoing transcatheter closure of ASD. The RA area and RV volume were measured prior (n = 38), within 24 hours (n = 37), at 3 to 6 months (n = 24), at 12 months (n = 20) and at 24 months (n = 10) after closure of ASD. Change over time within the study group was assessed and the study group was compared to a control group of 19 patients with structurally normal hearts. RESULTS: Indexed RA area decreased from baseline to 3- to 6-month follow-up (p = 0.004) as did indexed RV volume (p < 0.0001). Indexed RV volume was similar to that in the control group at 24 months (p = 0.3); however, indexed RA area remained greater than in the control group (p = 0.006). Decrease in indexed RA area over the first 12 months of follow-up was related to young age at time of closure by regression analysis (r = 0.55, p = 0.013). CONCLUSION: Closure of secundum ASD results in decreased indexed RV volume comparable to that in control subjects at 24 months following closure. Indexed RA area remains increased compared to that in control subjects but does decrease over time. Decrease in RA area is inversely proportional to age at time of ASD closure. Long-term follow-up is required to evaluate the clinical impact of persistently increased RA size.

Adolescent↗
PubMed1980

[Ultrastructural-morphometric characterization of adaptive and compensatory myocardial changes using heart enlargement as an example].

A morphometric analysis of the heart muscle cell shows significant differences in the reaction of different cellular structures in different experimental stress models of the myocardium (swimming exercise and ligature infarction) in the rat. For instance, the number of mitochondria is 44% higher only 2 days after infarction than after 45 h of swimming exercise over a period of 4 weeks. The mitochondria/myofibrils ratio is higher than in the case of training. But later on in the course of the experiment the number of mitochondria and their membrane surface density diminishes compared with training. The differences in the rate of formation and in the kind and intensity of the changes are probably attributable to different adaptive mechanisms by means of which the heart reacts to acute and chronic loads.

Adaptation, Physiological↗
PubMed1989

[Experience of valve replacement in 16 cases of heart enlargement].

From July 1985 to 1988 Feb. 16 patients with large heart (C-T ratio 65-85%) underwent valve replacements with mechanical valve. Isolated mitral valve replacement was performed in 15 cases and combined aortic and mitral valve replacement in 1. The valvular lesions was rheumatic in origin. The heart function (NYHA) was grade III in 5 cases (32.5%), and IV in 11 (67.5%), 60% of the cases were suffered from moderate or severe pulmonary hypertension. 1 patient died postoperatively. In the survivals the cardiac function was improved and the heart-size reduced distinctly. Some points about the operative results, selection of the time for operation and the postoperative management were discussed.

Adolescent↗
PubMed1976

[Heart enlargement and arterial hypertension in renal arteriovenous fistula].

In a patient hospitalized for progressive congestive heart failure the findings were hypertension, cardiomegaly and a mass in the left upper abdomen. A murmur was audible over the tumor. Clinical suspicion of a renal newgrowth with an arteriovenous fistula was confirmed by renal angiography. After nephrectomy the heart size became normal but the hypertension could only be controlled by drugs. The causes, symptoms and signs, and pathophysiology of arteriovenous shunts are discussed. Therapy is surgical. Surgery eliminates the congestive heart failure.

Adenocarcinoma↗