The necessity for measurement of left atrial pressure after cardiac valve surgery.
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Twenty-one patients who underwent cardiac valvular replacement procedures were studied to determine the perioperative changes of plasma endothelin-1 (ET-1) concentration and disposition of ET-1 in the pulmonary and systemic vasculature between patients with elevated (over 20 mmHg) mean pulmonary artery pressure and patients with normal pulmonary artery pressure. The overall profile alterations of plasma ET-1 concentration did not differ between the two groups of patients. The plasma ET-1 levels in the pulmonary artery and right atrium were significantly higher in patients with high pulmonary artery pressure than in patients with normal pulmonary artery pressure. Before cardiopulmonary bypass, significant pulmonary extraction of the plasma ET-1 existed in patients with high pulmonary artery pressure but the pulmonary extraction was not seen after bypass. There was no transpulmonary difference of the plasma ET-1 concentration in patients with normal pulmonary artery pressure either before or after bypass. The high levels of ET-1 in the pulmonary circuit and the pulmonary extraction of the ET-1 in patients with high pulmonary artery pressure might be a protective mechanism for rheumatic valvular patients with elevated pulmonary artery pressure.
Since the introduction by Gorlin and Gorlin of the hydraulic formulae for calculating valve area, it has become the best parameter for quantitating valve stenosis. Recently Hakki et al proposed a simplified formula for valve area calculation that does not take into account either heart rate (HR) or left ventricular filling or ejection time. The purpose of this study was to analyze the validity of Hakki's formulae under different physiological conditions and to propose an easy correction to improve its accuracy. Our study suggests: (1) that an easy correction for heart rate in certain cases, dividing by 1.35 when HR less than 75 beats per min in mitral stenosis and when HR greater than 90 beats per min in aortic stenosis, significantly improves the accuracy and validity of Hakki's formulae (p less than 0.02 and p less than 0.05); (2) the instantaneous valve gradients (peak gradient for aortic stenosis and average of instantaneous early, middle, and late diastolic gradients for mitral stenosis) are as valid as mean planimetric gradients for valve area calculation. Thus the simplified formulae proposed in this study allow mitral and aortic valve area calculations by means of instantaneous gradients, cardiac output, and heart rate.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
With the recent advancement and experience in minimally invasive coronary artery bypass surgery in selected patients, minimally invasive valve surgery using similar techniques is promising. Coupled with the movement in cardiac surgery to decrease costs, hospital lengths of stay and recovery time, minimally invasive techniques for both mitral and aortic valve surgery are promptly being pursued. This article reviews various minimally invasive surgical techniques for mitral and aortic valve surgery. Mitral valve surgery by means of port-access technology is detailed. Techniques for minimally invasive aortic valve surgery via a ministernotomy and a parasternal incision are described.
Explore the source record for details and available documents.
Papillary fibroelastomas are rare, primary, benign cardiac tumours most frequently located in the heart valves. They are a potential cause of systemic emboli, stroke, myocardial infarction and sudden death. We present two cases of papillary fibroelastomas located in the mitral and aortic valves of patients who had suffered multiple strokes. The fibroelastomas were diagnosed using transoesophageal echocardiography and the patients were treated surgically, with broad excision of the tumours and preservation of the valves. The echocardiographic and microscopic characteristics of the fibroelastomas are analysed and methods for their differential diagnosis from other cardiac tumours are discussed in the context of the available literature.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND AND AIM OF THE STUDY: The roles of cardiac valvular interstitial cells (VIC) in extracellular matrix remodeling in fetal development, adaptation and response to injury are largely unknown. METHODS: The phenotype of VIC was studied in health (normal adult human and sheep), development (fetal human and sheep), disease (human mitral valves with myxomatous degeneration), adaptation (clinical pulmonary to aortic valve autografts) and tissue-engineered heart valves matured in vitro and remodeled in vivo. Cell phenotype was assessed using expression of vimentin (V), alpha-smooth muscle actin (SMA, A), matrix metalloproteinase (MMP)-13/collagenase-3 (M), and SMemb (S). RESULTS: VIC in normal adult valves were predominantly quiescent fibroblasts immunoreactive to vimentin (89.7 +/- 2.5%), but not MMP-13 or SMemb, with only 2.5 +/- 0.4% of alpha-SMA-positive cells ('normal/quiescent' phenotype: V+/A-/M-/S-). In contrast, fetal VIC were mostly activated myofibroblasts ('developing/activated' phenotype: V+/A+/M+/S+), with 62.1 +/- 5.0% of cells staining positive for alpha-SMA. VIC in myxomatous valves, short-term autografts and engineered valves in vitro were also activated myofibroblasts with coexpression of vimentin, alpha-SMA (36.2 +/- 3.7%, 19.3 +/- 2.4%, and 60.3 +/- 9% positive cells, respectively), strong MMP-13 activity indicative of collagen remodeling, and SMemb ('remodeling/activated' phenotype: V+/A+/M+/S+). In contrast, VIC in long-term pulmonary autografts and engineered valve explants had a mostly fibroblast-like phenotype, with sparse alpha-SMA expression (6.0 +/- 1% and 5.4 +/- 1.0% positive cells) (V+/A-/M-/S-). CONCLUSION: Most VIC in normal valves were quiescent with a fibroblast-like phenotype. VIC in developing, diseased, adapting and engineered valves adjust to a dynamic environment through VIC activation and secretion of proteolytic enzymes mediating extracellular matrix remodeling ('developing/ remodeling/activated' phenotype), followed by a normalization of phenotype.
A retrospective review of 115 patients who underwent cardiac surgery demonstrated a marked reduction in postoperative atrial fibrillation (8% vs 32%, p <0.05) in patients who received carvedilol versus metoprolol or atenolol immediately after surgery. A prospective study examining the possibility of carvedilol's greater efficacy in preventing postoperative atrial fibrillation appears warranted.