B-type natriuretic peptide in patients after percutaneous trans-coronary-sinus mitral annuloplasty

Functional mitral regurgitation affects a substantial proportion of patients with congestive heart failure due to myocardial infarction or dilated cardiomyopathy. Functional mitral regurgitation greatly increases morbidity and mortality. Surgical annuloplasty is the standard of care for symptomatic patients with moderate or severe functional mitral regurgitation; however, a large number of patients are refused surgery. Several percutaneous approaches have been developed to address the need for less invasive treatment of mitral annulus dilatation. Devices using coronary sinus to cinch the mitral annulus are relatively easy to use; however, a number of factors may limit their clinical application, such as suboptimal anatomical relationship between the coronary sinus and mitral annulus, risk of coronary artery compression, large variability in the coronary venous anatomy and conflict with other therapies such as ablation or cardiac resynchronisation. Direct mitral annuloplasty is anticipated to be more effective than the coronary sinus approaches; however, it has yet to prove its safety and efficacy in carefully designed clinical trials. The best candidates and the best timing for each percutaneous mitral annuloplasty therapy, whether direct or indirect, have yet to be identified.

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Simulated Deployment of Percutaneous Transvenous Mitral Annuloplasty Device Into Human Coronary Sinus Vessel

ASME 2011 Summer Bioengineering Conference, Parts A and B ◽

10.1115/sbc2011-53851 ◽

2011 ◽

Cited By ~ 1

Author(s):

Thuy M. Pham ◽

Qian Wang ◽

Milton DeHerrera ◽

Wei Sun

Keyword(s):

Coronary Sinus ◽

Ventricular Dysfunction ◽

Surgical Repair ◽

Critical Role ◽

Cost Effective ◽

Mitral Annulus ◽

Left Ventricular ◽

Functional Mitral Regurgitation ◽

Patient Specific ◽

Mitral Annuloplasty

Functional mitral regurgitation (MR) is the consequence of left ventricular dysfunction occurring after ischemic heart disease and often has poor prognosis. Surgical repair and replacement of the mitral valve are currently being used to treat severe functional MR However, the technique carries high mortality rate [1] and is not suitable for patients with comorbidities and advanced age [2]. Recently, a new non-surgical intervention, percutaneous transvenous mitral annuloplasty (PTMA), is emerging as an attractive endovascular alternative that is less invasive, less recovery time, and cost effective. The device is delivered percutaneously into the coronary sinus (CS) vessel and once embedded, it contracts and shortens the septo-lateral distance of the mitral annulus, hence improve MR. However, despite of its feasibility, current clinical trials reported severe adverse events, such as device fracture [3]. The biomechanical interaction between the CS wall and the stent plays a critical role in the outcome of the deployment and the device performance. In this study, we proposed to analyze this interaction by developing Finite Element (FE) models of the CS vessel and the PTMA anchors and analyzing the peak stresses, strains, interaction forces (shear, normal) after the deployment of the proximal and distal anchors into a realistic patient-specific CS model.

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Regional plasma levels of cardiac peptides and their response to acute neutral endopeptidase inhibition in man

Clinical Science ◽

10.1042/cs0950547 ◽

1998 ◽

Vol 95 (5) ◽

pp. 547-555 ◽

Cited By ~ 21

Author(s):

J. G. LAINCHBURY ◽

M. G. NICHOLLS ◽

E. A. ESPINER ◽

H. IKRAM ◽

T. G. YANDLE ◽

...

Keyword(s):

Atrial Natriuretic Peptide ◽

Brain Natriuretic Peptide ◽

Natriuretic Peptide ◽

Coronary Sinus ◽

Femoral Artery ◽

Natriuretic Peptides ◽

Plasma Levels ◽

Neutral Endopeptidase ◽

Brain Natriuretic Peptides ◽

Atrial Natriuretic

1.The cardiac natriuretic peptides, atrial natriuretic peptide and brain natriuretic peptide, are degraded via clearance receptors and the enzyme neutral endopeptidase (EC 3.4.24.11). We studied the regional plasma concentrations of these peptides and their response to acute neutral endopeptidase inhibition in a consecutive series of patients with a broad spectrum of severity of cardiac dysfunction who were undergoing diagnostic right and left heart catheterization (24 patients, mean age 62.6 years). 2.Baseline blood samples were obtained for hormone analysis from femoral artery, femoral vein, renal vein, hepatic vein, superior vena cava, coronary sinus and pulmonary artery, and initial haemodynamic measurements were made. Twelve patients then received a neutral endopeptidase inhibitor (SCH 32615, 200 ;mg intravenously) and 12 received vehicle alone. The cardiac catheterization procedure was then completed and haemodynamic and hormone measurements were repeated. 3.Haemodynamic status was similar at baseline in both groups, and at repeated measurement (post-procedure after placebo or active drugs) haemodynamic variables were not significantly different from baseline values. Plasma levels of atrial and brain natriuretic peptides exhibited an arteriovenous increment (344% and 124% respectively) across the heart (femoral artery to coronary sinus) and decrement (by 28–54% and 9–16% respectively) across all other tissue beds (P< 0.05 for all) except the lung (no change). Final levels of atrial natriuretic peptide rose above initial levels at all sites in both groups (P< 0.05) except coronary sinus levels in the vehicle group (no change). The increase was consistently greater in the inhibitor group at all sites (P< 0.05 versus placebo). Levels of brain natriuretic peptide rose at all sites in the inhibitor group only (P< 0.05). The transcardiac step-up in atrial natriuretic peptide was markedly augmented after the administration of neutral endopeptidase inhibitor. Other tissue gradients were not significantly altered by neutral endopeptidase inhibitor. 4.Atrial and brain natriuretic peptides in plasma are degraded by a number of tissues, and respond differently to cardiac catheterization. Neutral endopeptidase has a significant role in determining plasma levels of natriuretic peptides, in part perhaps by influencing the amount of intact peptide reaching the circulation after secretion from the heart.

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Fatal coronary sinus and aortic erosions following percutaneous transvenous mitral annuloplasty device

EuroIntervention ◽

10.4244/eijv7i1a24 ◽

2011 ◽

Vol 7 (1) ◽

pp. 148-150 ◽

Cited By ~ 15

Author(s):

Stephane Noble ◽

Raquel Vilarino ◽

Hajo Muller ◽

Henri Sunthorn ◽

Marco Roffi

Keyword(s):

Coronary Sinus ◽

Mitral Annuloplasty

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Release of atrial natriuretic peptide by atrial distension

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y85-121 ◽

1985 ◽

Vol 63 (6) ◽

pp. 739-742 ◽

Cited By ~ 246

Author(s):

J. R. Ledsome ◽

N. Wilson ◽

C. A. Courneya ◽

A. J. Rankin

Keyword(s):

Heart Rate ◽

Atrial Natriuretic Peptide ◽

Pulmonary Vein ◽

Natriuretic Peptide ◽

Coronary Sinus ◽

Femoral Artery ◽

Left Atrial ◽

Cervical Vagotomy ◽

Atrial Receptors ◽

Atrial Natriuretic

A heterologous radioimmunoassay was used to measure the concentration of immunoreactive atrial natriuretic peptide (iANP) in plasma from the femoral artery of eight chloralose anaesthetized dogs. Mitral obstruction which increased left atrial pressure by 11 cmH2O increased plasma iANP from 97 ± 10.3 (mean ± SE) to 135 ± 14.3 pg/mL. Pulmonary vein distension increased heart rate but did not increase plasma iANP. Bilateral cervical vagotomy and administration of atenolol (2 mg/kg) did not prevent the increase in iANP with mitral obstruction. Samples of blood from the coronary sinus had plasma iANP significantly higher than simultaneous samples from the femoral artery confirming the cardiac origin of the iANP. Release of iANP depends on direct stretch of the atrium rather than on a reflex involving left atrial receptors.

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