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aortic valve stenosis/hypoxie
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Nuclear factor-κB-hypoxia-inducible factor-2 pathway in aortic valve stenosis.
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OBJECTIVE
Valvular calcification is a prominent feature of aortic valve stenosis (AS), and calcified aortic valves share several features with bone tissue. Hypoxia-inducible factor-2 (HIF-2) is activated by nuclear factor-κB (NF-κB) and plays a critical role in an osteoblastic differentiation. The
Major alterations in relaxation during cardiac hypertrophy induced by aortic stenosis in guinea pig.
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Left ventricular hypertrophy (LVH) was produced in guinea pigs after aortic stenosis (AS). The percentage of LVH in AS was determined by normalizing left ventricular (LV) weight by the mean LV weight of sham-operated controls (n = 12). After 3 weeks of cardiac overload, a mild LVH (30 +/- 3%) was
Aortic regurgitation associated with critical aortic stenosis in a fetus.
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Aortic regurgitation in association with aortic stenosis is rare in the fetus. Findings have shown that severe aortic regurgitation is worsened by the increase in systemic vascular resistance after birth, resulting in low cardiac output, hypoxemia, and neonatal death. This report describes a unique
Functional polymorphism of the renalase gene is associated with cardiac hypertrophy in female patients with aortic stenosis.
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Renalase decreases circulating catecholamines concentration and is important in maintaining primary cellular metabolism. Renalase acts through the plasma membrane calcium ATPase 4b in the heart, which affects pressure overload but not exercise induced heart hypertrophy. The aim of this study was to
Oxygen delivery and uptake relationships in patients with aortic stenosis.
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Previous studies have reported finding supply-dependent O2 uptake (VO2) in patients with the adult respiratory distress syndrome, sepsis, chronic obstructive lung disease, sleep apnea, and other cardiopulmonary diseases. A common element among these diverse conditions is the potential to reduce
Valve replacement for aortic stenosis: the curative potential of early operation.
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Concentric hypertrophy of the left ventricular wall is the primary consequence of acquired aortic stenosis (AS). Reduced left ventricular (systolic) function usually returns to normal after aortic valve replacement (AVR) in AS. Afterload mismatch prior to AVR, and not reduced contractility, is
Anoxia-induced changes in ventricular diastolic compliance in two models of hypertension in rats.
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OBJECTIVE
The effects of a brief period of anoxia upon myocardial distensibility and coronary vascular resistance (CVR) were evaluated in two models of pressure overload in the rat.
METHODS
A similar degree of left ventricular hypertrophy was obtained by using deoxycorticosterone acetate (DOCA)-salt
Hypoxia-driven glycolytic and fructolytic metabolic programs: Pivotal to hypertrophic heart disease.
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Pathologic cardiac growth is an adaptive response of the myocardium to various forms of systemic (e.g. pressure overload) or genetically-based (e. g. mutations in genes encoding sarcomeric proteins) stress. It represents a key aspect of different types of heart disease including aortic stenosis (AS)
Importance of SERCA2a on early isolated diastolic dysfunction induced by supravalvular aortic stenosis in rats.
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Cardiac remodeling is defined as changes in shape and function of the heart in response to aggression (pressure overload). The sarcoplasmic reticulum calcium ATPase cardiac isoform 2a (SERCA2a) is a known factor that influences function. A wide spectrum of studies report a decrease in SERCA2a in
Mechanisms of aortic stenosis.
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The pathobiology of degenerative aortic valve stenosis (AS) is complex and involves multiple features such as fibrosis, inflammation, oxidative stress, angiogenesis, hemorrhage, and osteogenic differentiation. We summarize the mechanism of valve calcification and angiogenesis which is necessary for
Truncal or aortic valve stenosis in functionally single arterial trunk. A clinical, hemodynamic and pathologic study of six cases.
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Stenosis of the semilunar valve in the presence of a functionally single arterial trunk is uncommon. Three patients with truncus arteriosus, two with tetralogy of Fallot and pulmonary atresia and one with pulmonary atresia and intact septum were diagnosed as having stenosis of the truncal or aortic
Relaxation of mammalian heart muscle during chronic cardiac overload.
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Cardiac relaxation was studied in rat papillary muscle during hypertrophy induced by different chronic volume and/or pressure overload (aortic insufficiency, aorto-caval fistula, aortic stenosis, spontaneously hypertensive rat). Maximum velocity of lengthening did not depend upon the degree of
Elastin insufficiency predisposes to elevated pulmonary circulatory pressures through changes in elastic artery structure.
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Elastin is a major structural component of large elastic arteries and a principal determinant of arterial biomechanical properties. Elastin loss-of-function mutations in humans have been linked to the autosomal-dominant disease supravalvular aortic stenosis, which is characterized by stenotic
Histoenzymological Characteristics of Smooth Muscle Cells in Myocardial Vessels: A Comparative Study under Conditions of Increased Left or Right Ventricular Afterload.
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Histoenzymological methods were used to study metabolism of smooth muscle cells of intramural myocardial arteries during experimental aortic or pulmonary artery stenosis. Aortic stenosis was accompanied by changes in smooth muscles of the left ventricle manifested by deceleration of tricarboxylic
Management of neonatal critical pulmonic stenosis in the balloon valvotomy era.
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We evaluated our recent experience with management of neonatal critical pulmonic stenosis and intact ventricular septum between 1982 and 1988. Thirty-nine patients (aged less than 3 months) were treated initially by operation (group A, n = 19) or with balloon pulmonary valvotomy (group B, n = 20).
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