Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The consequences of long-term O2 deprivation on heart development were analyzed morphometrically and ultrastructurally, utilizing the hearts of chicken embryos developed under hypoxia from the 3rd to the 18th incubation day. The results indicate that embryos kept under low O2 blood tension do not show disturbances in heart morphohistogenesis, but are characterized by a thicker epicardium and a thinner myocardium than the controls; moreover, both the number and calibre of the heart microvessels are increased. The thickening of the epicardium is due to hyperplasia of the mesothelial cells, increment in calibre of the submesothelial vessels, and to conspicuous perivascular infiltration of blood-derived cells. The thinning of the cardiac muscle seems to be dependent on myocardiocyte hypotrophy and myofibril reduction. The increase in the volume density of myocardium vessels, due to their dilatation and proliferation, may be considered expression of a vascular adaptive reaction to low oxygen tissue concentration.
 ...
PMID:The effects of long-term hypoxia on epicardium and myocardium in developing chick embryo hearts. 177 79

To explore relationship between hypertrophy of left ventricle and its shape, blood supply and calcium turnover, the study enrolled 105 male patients with ischemic heart disease or those suspected of its presence. All patients underwent contrast coronary ventriculography, M-mode echocardiography and sectorial scanning. Moderately limited myocardial blood supply was found to be a factor, stimulating its local hypertrophy. In the event of severely impaired blood supply, no substantial myocardial hypertrophy is detectable in corresponding regions, while dynamic observation not infrequently reveals thinning of the wall. Patients with intact coronary arteries, and having more elongated shape of left ventricular cavity, demonstrate larger thickness of walls along the long axis, that is probably due to dependence of intramyocardial tension on the radius of the wall curvature. While performing ventriculography in the patients with hypertrophic myocardium, disclosed elevated level of calcium in the blood and enhanced calcium uptake by cardiac muscle versus patients without left ventricular hypertrophy.
 ...
PMID:Significance of left ventricular shape, its blood supply and calcium turnover for evolving myocardial hypertrophy. 252 3

Twenty-one dogs were chronically instrumented with ultrasonic left ventricular dimension transducers and micromanometers to elucidate the effects of acute protein-calorie malnutrition on cardiac function. Ten dogs received a regular diet for 3 wk, whereas 11 dogs received a protein-calorie-deficient diet designed to achieve a mean weight loss of 20-25% over a 3-wk period. Studies of cardiac function were performed in awake intact animals at base line (1 wk postoperatively) and after 3 wk. In the malnourished dogs, cardiac mass was lost in proportion to total body mass loss. Mean cardiac mass fell from 115 to 91 g. This was largely due to wall thinning in this group. Heart rate dropped from 125 to 79 beats/min with malnutrition and ejection fraction increased from 29.8 to 34.6%. Cardiac output fell from 2.98 to 2.38 l/min, but cardiac index normalized to body surface area was unchanged. No significant changes in hemodynamics were observed in the control group. In the malnutrition group, global ventricular contractility, as measured by the load-independent index of systolic function or the slope of linear relationship between end-systolic pressure and end-systolic volume (EmaxPV), decreased slightly from 3.56 to 2.81 mmHg/ml (P = 0.07). However, Emax calculated from circumferential stress and strain data was unchanged. This indicates that depressed contractility was due to loss of cardiac muscle mass rather than any change in the myocardium per se. Response to beta-adrenergic stimulation was unchanged with starvation. Acute protein-calorie malnutrition causes significant cardiac atrophy that is reflected in decreased cardiac output and slightly reduced contractility but not in intrinsic properties of the myocardium.
 ...
PMID:Left ventricular function in malnutrition. 361 11

Fifteen selected hypothyroid patients without symptoms or signs of cardiovascular disease and an equal number of matched control subjects underwent simultaneous recording of electrocardiogram and phono-, apex-, and echocardiography to assess dynamic systolic and diastolic left ventricular function. Both the systolic preejection period and the isovolumic relaxation period were significantly increased in the hypothyroid group. However, whereas the rate of myocardial contraction, assessed from the echocardiograph of the left ventricular posterior wall, was identical in patients and control subjects, the diastolic thinning rate of the muscle was markedly slowed in the hypothyroid individuals. The abnormalities demonstrated were in the main completely reversed after 3 months of T4 therapy. These results demonstrate a relatively selective and readily reversible disturbance of the rate of myocardial relaxation in hypothyroidism, suggesting an intrinsic abnormality of cardiac muscle. This allows an intriguing parallel to be drawn with the delayed relaxation phase of voluntary muscle contraction, long recognized as a direct measure of tissue thyroid function in hypothyroidism. The abnormality of diastolic function we have described is of similar character to that found in patients with other cardiomyopathies and which has been shown to be a major cause of disturbance of global cardiac action.
 ...
PMID:Reversible abnormalities of myocardial relaxation in hypothyroidism. 400 7

Verapamil has a negative inotropic action in isolated cardiac muscle. Its effects on left ventricular function were tested in 25 patients with suspected coronary artery disease. A double-blind, randomized, placebo-controlled study design was used. Verapamil (0.2 mg/kg over 10 minutes) significantly lowered mean arterial pressure (from 105 to 89 mm Hg) while increasing the cardiac index (from 2.8 to 3.1 liters/min/m2). No statistically significant effect was seen on heart rate, left ventricular end-diastolic pressure or end-systolic volume index, ejection fraction, peak rates of systolic wall thickening or diastolic wall thinning, or percentage of hemiaxial shortening. However, there was a small increase in the left ventricular end-diastolic volume index (from 94 to 102 ml/m2). Important findings were a reduction in systemic vascular resistance (from 39 to 30 U . m2), an increase in left ventricular end-diastolic volume index consistent with a negative inotropic effect, and no evidence of improved regional wall dynamics in portions of the left ventricular wall considered hypokinetic because of myocardial ischemia.
 ...
PMID:Effect of verapamil on left ventricular function: a randomized, placebo-controlled study. 634 Apr 53

The calcium channel blocking agent, nifedipine, has been shown to improve indexes of left ventricular relaxation, diastolic filling and compliance in patients with hypertrophic cardiomyopathy. The mechanism of action of nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy is unclear and could result from an improvement in myocardial inactivation or from systemic vasodilation and left ventricular unloading. To distinguish between these mechanisms, the effects of nifedipine and the vasodilator nitroprusside on left ventricular diastolic properties were compared in 10 patients with nonobstructive hypertrophic cardiomyopathy using simultaneous micromanometer left ventricular pressure and echocardiographic measurements. Left ventricular peak systolic pressure was comparable during nitroprusside infusion (132 +/- 38 mm Hg) and after nifedipine (132 +/- 32 mm Hg). During nitroprusside infusion, the decrease in left ventricular end-diastolic pressure (22 +/- 11 to 17 +/- 11 mm Hg, p less than 0.05) was associated with a decrease in left ventricular end-diastolic dimension. In contrast, the decrease in left ventricular end-diastolic pressure after nifedipine (22 +/- 11 to 18 +/- 10 mm Hg, p less than 0.05) was associated with no reduction of left ventricular end-diastolic dimensions, suggesting an increase in left ventricular distensibility. Compared with nitroprusside, nifedipine was associated with less prolongation of the left ventricular isovolumic relaxation time and less depression of the peak left ventricular posterior wall thinning rate and peak left ventricular internal dimension filling rate. These data suggest that the effects of the calcium channel blocker, nifedipine, on diastolic mechanics in hypertrophic cardiomyopathy result not only from systemic vasodilation but also from improved cardiac muscle inactivation.
 ...
PMID:Comparison of the effects of nitroprusside and nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy: altered left ventricular loading or improved muscle inactivation? 668 50

Two cases of perforation of the cardiac wall during central venous catheterization are reported. One patient, a women, died 6 weeks after perforation of the anterior wall of the right ventricle; the other, also a woman, died immediately following perforation of the posterior wall of the right atrium by a polyethylene catheter. Both cases prove that even a seemingly correct technique and the use of soft catheters cannot entirely exclude the possibility of perforation. Relative weakness of the cardiac muscle due to lipomatosis could have been a pre-disposing factor in one case, and thinning of the atrial wall between the pectinate muscles in the other case. There is also the possibility that the spaces between the trabeculae carneae act as a trap for the catheter. Radiological control of the placement of the catheter should also be performed in those cases where the catheter had to be withdrawn because of malposition in order to make sure of its correct extracardial location.
 ...
PMID:[Perforation of the cardiac wall during central venous catheterization - muscular defects as a contributing factor (author's transl)]. 730 69

Anthracyclines, potent cytotoxic agents used to treat a broad spectrum of malignancies, are limited in their use by an attendant risk of cardiotoxicity. Malignancies affect all age ranges, and anthracyclines are used in all age ranges, thereby exposing a broad population of patients to the development of heart disease. For some treated patients, anthracyclines affect cardiac muscle, resulting in cardiomyopathy. The type and degree of cardiomyopathy, as well as when during or after treatment the condition occurs, are dependent on what risk factors are present. Age is a major risk factor. Children and adults may develop restrictive and dilated cardiomyopathy. The length of subsequent survival and amount of subsequent somatic growth may influence late anthracycline-associated cardiac outcome. Early cardiotoxicity, occurring during or within 1 year of completion of treatment, is the largest risk factor for the development of late cardiotoxicity, which occurs beyond a year of completion of treatment. Risk factors, which appear to be specific for early cardiotoxicity in children, include black race, trisomy 21, and the use of amsacrine therapy after anthracycline therapy. More cardiotoxic effects are seen in survivors of childhood cancer, the longer from completion of treatment a patient is followed. Cumulative as well as peak anthracycline doses affect adults and children alike, and cardiotoxicity occurs early and late. In adults, left ventricular contractility is affected by anthracyclines. Children may manifest impairment of left ventricular contractility and increased afterload due to thinning of left ventricular walls. Patients with an early presentation of depressed left ventricular contractility are likely to show progression of cardiac disease with time. In addition, female gender appears to affect early and late cardiotoxicity in both adults and children, although this risk factor has been described predominantly in the survivors of childhood cancer. Thus, although anthracycline chemotherapy has improved overall survivorship of patients with cancer, there is a significant risk of cardiotoxicity associated with this class of drugs.
 ...
PMID:Epidemiology of anthracycline cardiotoxicity in children and adults. 976 28

To investigate how insulin-like growth factor I (IGF-I) modulates cardiovascular function and myocardial apoptosis in heart failure, the therapeutic effects of IGF-I were determined in a canine model of dilated cardiomyopathy. The animals were paced at 220 beats/min, and the left ventricular (LV) chamber became dilated after 2 weeks. A subset of paced dogs was treated with s.c. injections of IGF-I from week 3 to week 4. After 4 weeks of pacing, untreated paced dogs developed significant ventricular dysfunction. IGF-I-treated paced dogs showed better cardiac output, stroke volume, LV end-systolic pressure, and LV end-diastolic pressure. Moreover, pulmonary wedge pressure and systemic vascular resistance were increased in the untreated group and decreased in the IGF-I-treated group. IGF-I treatment was associated with less thinning of the ventricular wall. Compared with the controls, untreated paced dogs showed increased apoptosis of cardiac muscle cells, which was partially suppressed by IGF-I treatment. The myocardial apoptotic index was negatively related to the thickness of the ventricular wall and to cardiac output, suggesting that ventricular remodeling/dysfunction involves the occurrence of myocardial apoptosis. Due to the close resemblance between this experimental model of dilated cardiomyopathy and human heart failure, the results of this study provide evidence that IGF-I may be a potential therapeutic agent for the failing human heart.
 ...
PMID:Insulin-like growth factor I improves cardiovascular function and suppresses apoptosis of cardiomyocytes in dilated cardiomyopathy. 1049 43

The cardiac muscle architecture lies at the basis of the mechanical and electrical properties of the heart, and dynamic alterations in fiber structure are known to be of prime importance in healing and remodeling after myocardial infarction. In this study, left ventricular remodeling was characterized using diffusion tensor imaging (DTI) in a mouse model of myocardial infarction. Myocardial infarction was induced in mice by permanent ligation of the left anterior descending coronary artery. Serial ex vivo DTI measurements were performed 7, 14, 28, and 60 days after ligation. Apparent diffusion coefficient, fractional anisotropy, the three eigenvalues of the diffusion tensor, and the myofiber disarray served as readout parameters. After myocardial infarction, the mouse hearts displayed extreme wall thinning in the infarcted area, which covered large parts of the apex and extended into the free wall up to the equator. Average heart mass increased by 70% 7-60 days after infarction. Histological analysis showed that the infarct at 7 days consisted of unstructured tissue with residual necrosis and infiltration of macrophages and myofibroblasts. At 14 days after infarction, the necrotic tissue had disappeared and collagen fibers were starting to appear. From 28 to 60 days, the infarct had fully developed into a mature scar. DTI parameters showed dynamic changes as a function of time after infarction. The apparent diffusion coefficient in the infarcted region was lower than in remote regions and increased as a function of time after infarction. The fractional anisotropy was higher in the infarcted region and was maximum at 28 days, which was attributed to the development of structured collagen fibers. Myofiber disarray, which was analyzed by considering the alignment of fibers in neighboring voxels, was significantly higher in infarcted regions. DTI provides a valuable non-destructive tool for characterizing structural remodeling in diseased myocardium.
 ...
PMID:Diffusion tensor imaging of left ventricular remodeling in response to myocardial infarction in the mouse. 1878 Feb 84


1 2 Next >>