Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the mirror of the pertinent literature, we present our experiences gained in 161 operations for pectus carinatum. The Type I (keel chest) deformity is corrected by bilateral resection of the costal cartilages, transverse osteotomy of the sternum, detachment of the xiphoid process, and resection of the lower end of the body of the sternum. The sternum is maintained in its corrected position by utilizing the pulling force of the rectus muscles through the reattached xiphoid and by tacking the pectoralis muscles together in front of the breast bone. Type II (pouter pigeon breast) is handled by double transverse osteotomy, chiseling off the protuberant portion of the strernomanuberial junction, and by supporting the lower sternal body with either the suspended xiphoid process or with Marlex mesh. Limited forms of Type III (asymmetrical or lateral pectus carinatum) are managed with simple resection of the involved cartilages only. If the anomaly is more extensive, bilateral resection of the cartilages and correction of the sternal axis is carried out.
J Thorac Cardiovasc Surg 1979 Jul
PMID:Pectus carinatum. 37 53

The heart is able to adapt itself to a demanded load by increasing (hypertrophy) or decreasing (regression of hypertrophy) its muscular mass within a wide range. Overstressing of the ability of adaptation is accompanied by degenerative changes of myocytes. Semiquantitative investigations of endomyocardial biopsies (EMCBs) of patients with dilative cardiomyopathy (DCM) and hypertrophic nonobstructive cardiomyopathy (HNCM) show a fibrosis of the interstitial space, as well as almost similar changes of myofibrils and mitochondria. A reduced number of myocytes in hearts with DCM could explain the decreased functional capacity. Quantitative investigations of endomyocardial biopsies and myectomy specimens in patients with hypertrophic obstructive cardiomyopathy have revealed that hypertrophy and, to a certain extent, hyperplasia of muscle fibers cause asymmetrical thickening of the septum. Experimental investigations of the regression of training-induced hypertrophy in rats have shown that nearly all parameters (cardiac weight, thickness of muscle fibers, myofibrillar mass, interstitial space, and capillary width) returned to the values of controls 14 days after termination of a swimming training regimen. A significantly higher density of capillaries after regression of muscle fiber hypertrophy compared to controls points to a temporal dissociation in the regression of myocyte size and capillary network. Decrease in RNA concentration and an increased number of autophagic vacuoles give evidence for decreased anabolism and increased catabolism may occur during regression. In humans, fibrosis of the myocardium and scar formation explain the irreversibility of cardiac hypertrophy, as observed in some patients with valvular heart disease, despite valve replacement.
J Cardiovasc Pharmacol 1987
PMID:Morphologic criteria of progression and regression of cardiac hypertrophy. 248 27

A factorial experimental design was used to quantify the changes in heart rate produced by stimulation of the cardiac sympathetic and vagal nerves in eleven adult dogs and four puppies, and to quantify the extent of the peripheral sympathetic-vagal interactions. The chronotropic responses to autonomic stimulation were significantly less in the puppies than in the adult dogs, which suggests that autonomic regulation is functionally incomplete in the puppies. In both adult dogs and puppies, the chronotropic responses to autonomic nerve stimulation were bilaterally asymmetrical. The heart rate responses to a given level of right-sided stimulation of either the sympathetic or vagal nerves were greater than those to comparable left-sided stimulation. In both adult dogs and puppies, there were significant sympathetic-vagal interactions, such that the sympathetic enhancement of heart rate was less effective the higher the background level of vagal activity. The sympathetic-vagal interactions were prominent in the puppies as well as in the adult animals, regardless of whether the stimulated sympathetic and vagal nerves were located ipsilaterally or contralaterally to one another. Thus, the mechanisms responsible for the sympathetic-vagal interactions appear to be fully developed in puppies. Also, the cardiac sympathetic nerve endings that originate from one side of the body must lie in close apposition to the cardiac vagal nerve endings that originate from either the same side or from the opposite side of the body.
Cardiovasc Res 1983 Sep
PMID:Autonomic nervous control of heart rate: sympathetic-parasympathetic interactions and age related differences. 662 75

The effectiveness in reversing ventricular fibrillation of 30 s duration of asymmetrical, bidirectional, rectangular waveforms in which the lagging half-cycle has the same duration but lower amplitude than the leading portion of the waveform was evaluated in a 2160-episode study involving anaesthetised calves. An additional 480-episode auxiliary study involved the interlacing of unidirectional and bidirectional wave episodes. The leading half-cycles of the 18 bidirectional waveforms evaluated were 35 A at 8 and 16 ms, 50 A at 4 and 8 ms, and 70 A at 2 and 4 ms. Associated with each of the six leading half-cycle configurations were lagging half-cycles having reverse current levels of 1/8th, 1/4th, and 1/2 of the leading half-cycle current amplitudes. Six waveforms were successful in 97% or more of the transthoracic episodes. Of these, three were 100% successful. Our data, when combined with those from earlier unidirectional and symmetrical, bidirectional, rectangular waveform studies, suggest that a broad category of bidirectional rectangular shocks are superior to the most favourable unidirectional rectangular shock.
Cardiovasc Res 1984 Jul
PMID:Defibrillation of 100 kg calves with asymmetrical, bidirectional, rectangular pulses. 674 62

A 2-year-old girl with asymmetrical upper limbs and underdevelopment of the bones of the left forearm, wrist and hand with associated muscular and osteal hypoplasia is described. Doppler ultrasonography of the arterial trunks of the upper limb suggested a normal ulnar trunk in the left upper arm, an arterial vessel extending from the bend of the elbow to the distal third of the forearm, and the absence of any other arterial trunks in the radial region. Angiography confirmed that vascularization of the forearm was sustained by the ulnar artery, which supported the dorsal arch of the carpus and digital arteries arising from it. The interosseal artery was morphologically normal but there was aplasia of the radial artery. It is suggested that this malformation is the result of suppressed development of the vascular system of the left radial segment as other pathologies normally associated with the condition were absent.
Cardiovasc Surg 1993 Jun
PMID:Aplasia of the radial artery. 807 44

Familial hypertrophic cardiomyopathy (FHC) is a cardiomyopathy that occurs in 0.2% of the general population. It is characterized by asymmetrical hypertrophy of the ventricle, predominantly the intraventricular septum. FHC is caused by genetic mutations in several of the sarcomeric proteins, such as myosin heavy chain, troponin T, troponin I, alpha-tropomyosin, essential and regulatory light chains of myosin, and the cardiac myosin-binding protein C. FHC is genetically heterogeneous, and, therefore, it is associated with a very diverse clinical presentation in terms of altered cardiac structure and clinical manifestations. The most severe manifestation is sudden death. The purpose of this article is to provide the reader with new insights into the genetic mutations that give rise to FHC and to discuss risk factors that are associated with severe hypertrophy and sudden death in this population.
J Cardiovasc Nurs 1999 Jul
PMID:Familial hypertrophic cardiomyopathy. 1038 71

Predictors for a reintervention following a successful first re-do surgical revascularization (CABG) were examined. Success and limitations of the reintervention procedures were evaluated. Between 3/88 and 3/95, 16.81% (302/1796) patients who had undergone a first re-do CABG surgery in the authors' center, required a reintervention. Graft angioplasty was performed in 158 (52.32%) patients and a second re-do CABG in 47.68% (n = 144). Graft angioplasty was preferred over surgery in patients aged 70 years or older (43% versus 24.3%, P<0.001) and in patients with unstable angina (55.6% versus 33.3%, NS) or a Left Ventricular Ejection Fraction (LVEF) <30% (34.8% versus 20%, P<0.05). Re-do CABG was preferred over graft angioplasty for multivessel revascularization (3+/-0.3 versus 1+/-0.6, P<0.001), proximal occlusive disease (P<0.001) and for graft disease of a longer duration (7.18+/-1.7 years versus 3+/-0.6 years, P<0.01). The independent predictors of a reintervention were (i) lack of arterial revascularization and (ii) inability to achieve a complete revascularization in a previous operation. The predictors of a failed graft angioplasty were diameter stenosis >70%, long occlusive lesions (multivariate), angulation, calcification and asymmetrical lesions (univariate). Failed graft angioplasty required a re-do CABG (n = 48: early 21, late 27), repeat graft angioplasty (n = 34: early 8, late 26) or transplant (n = 1). Recurrent symptoms following a second re-do CABG required a graft angioplasty (n = 6: early 2, late 4), a subsequent re-do CABG (n = 32) or a transplant (n = 4). Cumulative incidence of cardiac events at 1 month, and 1 and 8 years were: 20, 40.45 and 66.44% following graft angioplasty and 5.5, 10 and 56.55% following a second re-do CABG, respectively (P<0.05). Actuarial survival at 1 month and 6 years following graft angioplasty were 97.15 and 77.22%, and 94.7 and 83.26% after a second re-do CABG, respectively (NS). Re-do CABG was more effective and durable. Graft angioplasty provided a good palliation in suitable cases and also postponed the need for a high-risk surgical intervention for more favorable conditions.
Cardiovasc Surg 1999 Apr
PMID:Reinterventions for recurrent ischemic heart disease following a successful first re-do myocardial revascularization: predictors, indications and results. 1038 58

Lateralized looping of the heart tube, with associated torsion of the embryo axis, is the first structural sign of the consistent left-right asymmetrical organization that characterizes all vertebrate embryos. Rare failures or reversals of this asymmetry in humans lead to clinically important syndromes of malformation in heart and great blood vessels. Recently, elements of the genetic control sequence underlying this left-right aspect of development have been uncovered. The normal sequence of transmission for asymmetry information can now be traced to a point close to the actual execution of right-hand looping in the heart tube, with the hope that the further sequence of gene activity, within the heart itself and directing these events, may soon be uncovered.
Trends Cardiovasc Med 1998 Jul
PMID:A cascade of gene action controlling heart asymmetry and torsion in embryonic development. 1498 67

A patient with aortic regurgitation, stenosis, and calcification of the septum is reported. Results of echocardiography revealed asymmetrical septal hypertrophy without other features of idiopathic hypertrophic subaortic stenosis. There was no subaortic obstruction evident on cardiac catheterization and angiography. This case serves to emphasize that calcification of the interventricular septum is another possible cause of asymmetrical septal hypertrophy.
Cardiovasc Dis 1980 Mar
PMID:Unusual findings of asymmetrical septal hypertrophy associated with calcification of the interventricular septum: Case report. 1521 85

A 27 year old female with Noonan syndrome and hypertrophic cardiomyopathy underwent cardiovascular magnetic resonance imaging. These images showed asymmetrical septal hypertrophy with maximal left ventricular end-diastolic wall thickness of 25 mm. Following administration of gadolinium, areas of hyperenhancement were seen in the anterior, anteroseptal and lateral walls. This is the first report of focal gadolinium hyperenhancement in hypertrophic cardiomyopathy due to Noonan syndrome and suggests that myocardial fibrosis can be imaged by MR hyperenhancement as seen previously in sarcomeric hypertrophic cardiomyopathy.
Int J Cardiovasc Imaging
PMID:Hypertrophic cardiomyopathy in Noonan Syndrome closely mimics familial hypertrophic cardiomyopathy due to sarcomeric mutations. 1626 21


1 2 3 Next >>