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Results for “HEART VALVE DISEASES”

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PubMed1985

[Hemodynamic effects of an etomidate-flunitrazepam or midazolam- fentanyl combination for induction of anesthesia in patients with heart valve diseases].

A comparison of the haemodynamic effects of 3 anaesthetic techniques, the combinations etomidate + fentanyl (I), flunitrazepam + fentanyl (II) or midazolam + fentanyl (III), respectively was carried out in 45 patients undergoing various types of cardiac valve replacement surgery. Haemodynamics were assessed by continuously measuring the heart rate as well as the blood pressure in the systemic and pulmonary circulations whereas the cardiac output was measured intermittently. In the first 30 minutes after induction of anaesthesia, a mean arterial blood pressure drop of 10% (I), 20% (II) or 15% (III) respectively, was observed; at the same time, the rate did not change significantly. Cardiac index, however, fell significantly in all 3 groups by 33% (I) 30% (II) or 28% (III), respectively. Pulmonary pressure, wedge pressure and systemic vascular resistance rose only in groups I and III and decreased in group II (flunitrazepam + fentanyl). On the other hand, pulmonary vascular resistance as well as left ventricular work index were significantly decreased in all 3 groups. We conclude that all 3 anaesthetic techniques investigated here may be effectively applied for safe induction of anaesthesia in patients with valvular lesions of the heart. On account of the effect of the combination flunitrazepam + fentanyl on decreasing pulmonary artery pressure and wedge pressure, this technique seems to be preferable in patients with pulmonary hypertension.

Adolescent↗
PubMed2002

Serotonin mechanisms in heart valve disease I: serotonin-induced up-regulation of transforming growth factor-beta1 via G-protein signal transduction in aortic valve interstitial cells.

Clinical disorders associated with increased serotonin [5-hydroxytryptamine (5-HT)] levels, such as carcinoid syndrome, and the use of serotonin agonists, such as fenfluoramine have been associated with a valvulopathy characterized by hyperplastic valvular and endocardial lesions with increased extracellular matrix. Furthermore, 5-HT has been demonstrated to up-regulate transforming growth factor (TGF)-beta in mesangial cells via G-protein signal transduction. We investigated the hypothesis that increased exposure of heart valve interstitial cells to 5-HT may result in increased TGF-beta1 expression and activity because of serotonin receptor-mediated signal transduction with activation of Galphaq, and subsequently up-regulation of phospholipase C. Thus, in the present study we performed a clinical-pathological investigation of retrieved carcinoid and normal valve cusps using immunohistochemical techniques to detect the presence of TGF-beta1 and other proteins associated with TGF-beta expression, including TGF-beta receptors I and II, latent TGF-beta-associated peptide (LAP), and alpha-smooth muscle actin. Carcinoid valve cusps demonstrated the unusual finding of widespread smooth muscle actin involving the interstitial cells in the periphery of carcinoid nodules; these same cells were also positive for LAP. Normal valve cusps were only focally positive for smooth muscle actin and LAP. In sheep aortic valve interstitial cell cultures 5-HT induced TGF-beta1 mRNA production and increased TGF-beta1 activity. 5-HT also increased collagen biosynthesis at the dosages studied. Furthermore, TGF-beta1 added to SAVIC cultures increased the production of sulfated glycan and hyaluronic acid. In addition, overexpression of Galphaq using an adenoviral expression vector for a constitutively active Galphaq mutant (Q209L-Galphaq) resulted in increased phospholipase C activity as well as up-regulation of TGF-beta expression and activity. These results strongly support the view that G-protein-related signal transduction is involved in 5-HT up-regulation of TGF-beta1. In conclusion, 5-HT-associated valve disease may be, in part, because of TGF-beta1 mechanisms.

Actins↗
PubMed2004

Valvular myofibroblast activation by transforming growth factor-beta: implications for pathological extracellular matrix remodeling in heart valve disease.

The pathogenesis of cardiac valve disease correlates with the emergence of muscle-like fibroblasts (myofibroblasts). These cells display prominent stress fibers containing alpha-smooth muscle actin (alpha-SMA) and are believed to differentiate from valvular interstitial cells (VICs). However, the biological factors that initiate myofibroblast differentiation and activation in valves remain unidentified. We show that transforming growth factor-beta1 (TGF-beta1) mediates differentiation of VICs into active myofibroblasts in vitro in a dose-dependent manner, as determined by a significant increase in alpha-SMA and the dramatic augmentation of stress fiber formation and alignment. Additionally, TGF-beta1 and increased mechanical stress function synergistically to enhance contractility. In turn, contractile valve myofibroblasts exert tension on the extracellular matrix, resulting in a dramatic realignment of extracellular fibronectin fibrils. TGF-beta1 also inhibits valve myofibroblast proliferation without enhancing apoptosis. Our results are consistent with activation of a highly contractile myofibroblast phenotype by TGF-beta1 and are the first to connect valve myofibroblast contractility with pathological valve matrix remodeling. We suggest that the activation of contractile myofibroblasts by TGF-beta1 may be a significant first step in promoting alterations to the valve matrix architecture that are evident in valvular heart disease.

Actins↗