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Papillary Muscles (papillary + muscle)

Distribution by Scientific Domains

Medical Sciences	76%
Life Sciences	20%

Kinds of Papillary Muscles

ventricular papillary muscle

Selected Abstracts

Octopus Papillary Muscle Associated with a Left Lateral Accessory Pathway

CONGENITAL HEART DISEASE, Issue 6 2009
Manisha S. Patel MD
ABSTRACT Left ventricular papillary muscle abnormalities are rare malformations. They have been related to significant mitral valve dysfunction and left ventricular midcavitary obstruction. We report our experience with a young adult who presented with palpitations. An echocardiogram on the patient showed an "octopus-like" left ventricular papillary muscle. Subsequent electrophysiologic testing showed evidence of supraventricular tachycardia via a left lateral accessory pathway associated with the abnormal insertion of the papillary muscle attachments. [source]

Real-time Integration of Intracardiac Echocardiography and Electroanatomic Mapping in PVCs Arising from the LV Anterior Papillary Muscle

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2009
Ph.D., TAKUMI YAMADA M.D.
A 54-year-old woman with idiopathic premature ventricular contractions (PVCs) underwent electrophysiological testing. Three-dimensional (3D) geometries of the papillary muscles and chamber of the left ventricle (LV) were reconstructed using a CARTO-based 3D ultrasound imaging system (Biosense Webster Inc., Diamond Bar, CA, USA) during the PVCs. Activation mapping in the LV was then performed during the PVCs and the activation map revealed the earliest ventricular activation on the anterior papillary muscle. An irrigated radiofrequency current delivered at that site with guidance from that system eliminated the PVCs. This case may suggest that the guidance system may be feasible and useful for catheter ablation of PVCs arising from uncommon sites. [source]

Reference Values Describing the Normal Mitral Valve and the Position of the Papillary Muscles

ECHOCARDIOGRAPHY, Issue 7 2007
Petrus Nordblom M.Sc.
In patients with functional mitral regurgitation (MR), the principal mechanisms are insufficient coaptation due to dilatation of the mitral annulus (MA), global ventricular dysfunction with tethering of leaflets, or restricted leaflet motion with incorrect apposition due to regional ventricular dysfunction and displacement of the papillary muscles (PMs). These different entities often coexist and for this reason, knowledge of the normal reference values describing the shape and size of the MA and the position of the PMs is essential. In the present study, we describe the MA dimensions and the position of the PMs in a group of normal individuals (n = 38, 60% women, age [mean ± SD] 51 ± 9 years and BSA 1.83 ± 0.16 m2) investigated with transthoracic echocardiography. The anteroposterior dimension (AP) of the ellipse-shaped MA was measured in a parasternal long axis, while the distance from the posteromedial (PoM) to the anterolateral (AL) commissure was measured in a parasternal short axis (CC). The annular area was calculated assuming elliptic geometry. The MA shape was described by the ratios AP/CC and AP/length of the anterior leaflet. The PMs' position was described by the following distances: (a) from the MA to the tip of the PoM and AL, PMs measured in a modified two-chamber view where both PMs could be identified, (b) the interpapillary distance, and (c) the tethering distance from the tip of the PM to the contralateral MA. These data on the normal mitral valve morphology should provide useful information when assessing the underlying mechanism of functional MR. [source]

Octopus Papillary Muscle Associated with a Left Lateral Accessory Pathway

Adenosine induces prolonged anti-,-adrenergic effects in guinea-pig papillary muscle

ACTA PHYSIOLOGICA, Issue 1 2002
L. ARVOLA
ABSTRACT A sustained anti- , -adrenergic effect of adenosine has been reported. This study was initiated to investigate this topic and especially elucidate the role of protein kinase C (PKC). Contractile force amplitude and action potential duration at 90% repolarization (APD90) were measured in guinea-pig papillary muscles before and after 5 min challenge with 5 nm isoproterenol. Protocols contained 30 min exposure to the test agents adenosine 33 ,m (ado), adenosine + PKC-inhibitor bisindolylmaleimide 20 nM (ado + BIM), PKC-activator 1,2-dioctanoyl-sn-glycerol 10 ,m (DOG) and , -agonist phenylephrine 5 ,m (phe). Isoproterenol was given at the end of test exposure and after 15 min washout. Results are mean ± SEM of percentage-change, P , 0.05 considered significant and labelled *. The first isoproterenol challenge significantly increased contractile force (27 ± 7%*) in the control group. Responses in the test groups were 2 ± 4 (ado), 1 ± 5 (ado + BIM), 14 ± 4* (DOG), 0 ± 2% (phe). After washout of adenosine, DOG and phenylephrine, isoproterenol induced 3 ± 8 (ado), 23 ± 5* (ado + BIM), 13 ± 5* (DOG), 15 ± 7% (phe) increase in test groups compared with 22 ± 5%* increase in contractile force in the control group. After 45 min washout of adenosine the inotropic response was still significantly reduced compared with control (29 ± 4 vs. 79 ± 8%*). Isoproterenol stimulation shortened APD90 in controls at both time points (5 ± 1%* and 4 ± 1%*), with no significant shortening in test groups. Adenosine induces sustained anti- , -adrenergic effects on contractile force as well as APD90. A role for PKC in signal transduction is supported with respect to contractile force. [source]

The Double Jeopardy of Blunt Chest Trauma: A Case Report and Review

ECHOCARDIOGRAPHY, Issue 3 2006
Subha L. Varahan M.D.
Cardiac injury, specifically valvular rupture, must be considered after blunt chest trauma even in previously healthy patients. Isolated mitral regurgitation (MR) and tricuspid regurgitation (TR) due to blunt chest trauma are rare phenomena. More unique is simultaneous complete papillary muscle rupture of the mitral valve (MV) and tricuspid valve (TV) with only four patients being previously reported in the literature. This case describes a patient with complete transection of the posteromedial papillary muscle of the MV with severe MR and a concomitant flail TV with severe TR following a motor vehicular accident. The importance of transthoracic and transesophageal echocardiography in the early evaluation of patients following blunt chest trauma is also highlighted by this case. [source]

3 ISCHEMIC MITRAL VALVE REPAIR: THE IMPACT OF THE MECHANISM OF MITRAL REGURGITATION ON LATE POSTOPERATIVE RESULTS

ECHOCARDIOGRAPHY, Issue 1 2004
E. Ereminien
Aim: The aim of our study was to establish the anatomical-functional mechanisms of ischemic mitral regurgitation (MR) and to analyse its impact on late results after mitral valve (MV) reconstructive surgery. Methods: The study included 53 patients with ischemic MR, who underwent CABG and MV repair. MV surgery consisted of subvalvular apparatus repair and/or annuloplasty. 2D Doppler investigations performed pre-, 10,14 days, and 12 months after surgery included evaluation of MV and left ventricular (LV) geometry and function. Results: Analysis of the mechanisms of ischemic MR permitted dividing patients into two groups: group 1,29 patients with inferobasal scar and posterior papillary muscle (PM) displacement, including 22 patients with PM infarction and 7 patients without it, and group 2,24 patients with isolated mitral annulus (MA) dilation. In the case of PM infarction two different mechanisms of MR were stated: (a) P3 restriction and A3 prolapse due to chordal tethering, (b) A3 P3 (commissural) prolapse due to chordal papillary elongation. Preoperatively LV geometry and function were better preserved in group 1 and late MV repair results were better versus (vs.) group 2: LV end-systolic diameter index decreased from 22.9 ± 3.1 mm/m2 to 20.9 ± 3.6 mm/m2 at 1 year, p < 0.05, LV ejection fraction increased from 34.9 ± 8.4 to 41.8 ± 8.1%, respectively, p < 0.05. No significant changes in LV geometry and function were noted in group 2. Conclusions: The underlying mechanism of ischemic MR has an impact on MV repair results. In patients with MR due to posterobasal infarction MV repair resulted in more favorable postoperative effect-marked improvement in LV geometry and function late after surgery versus MR due to isolated MA dilation. [source]

Nifedipine enhances cGMP production through the activation of soluble guanylyl cyclase in rat ventricular papillary muscle

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 4 2005
Kazuhiko Seya
It is known that nifedipine, an L-type calcium channel blocker, increases cGMP production, which partially contributes to the relaxation of vascular smooth muscle. The aim of our investigation was to clarify whether or not nifedipine regulates cGMP production, which has a physiological role in cardiac muscle. To measure contractile responses and tissue cGMP levels, left ventricular papillary muscles prepared from male Wistar rats (350,400 g) were mounted in the isolated organ chamber under isometric conditions and electrically paced by means of platinum punctate electrodes (1 Hz, 1 ms duration). In papillary muscle preparation, the negative inotropic effect induced by nifedipine (30 to 300 nm) was significantly inhibited in the presence of ODQ (1H-[1,2,4]oxidazolo[4,3-a]quinoxaline-1-one; 10 ,m), a soluble guanylyl cyclase inhibitor. Furthermore, nifedipine (100 nm) strongly increased the tissue cGMP level, which was significantly decreased in the presence of ODQ. On the other hand, NG -monomethyl-l-arginine (100 ,m), a nitric oxide synthase inhibitor, did not inhibit either the negative inotropic effect or cGMP production induced by nifedipine. These results indicate that in rat left ventricular papillary muscle, nifedipine augments its negative inotropic effect at least partly through direct activation of cardiac soluble guanylyl cyclase but not nitric oxide synthase. [source]

Real-time Integration of Intracardiac Echocardiography and Electroanatomic Mapping in PVCs Arising from the LV Anterior Papillary Muscle

Modelling covariance structure in ascending dose studies of isolated tissues and organs

PHARMACEUTICAL STATISTICS: THE JOURNAL OF APPLIED STATISTICS IN THE PHARMACEUTICAL INDUSTRY, Issue 2 2003
Richard John Brammer
This paper describes the analysis of two pharmacology assays: the guinea pig papillary muscle assay (an example of an isolated tissue assay) and an assay looking at pressure changes in isolated rat lungs. Both assays use an ascending dose design to minimize carryover effects. This is often necessary in these studies, due to the limited life span of the tissues. Various mixed models, with different covariance structures, are fitted to find the most appropriate model. These are then compared to two other possible methods of analysis: paired t-tests and two-way analysis of variance. For both assays, the mixed model was found to be the best approach. These examples illustrate the importance of modelling covariance structure correctly in any ascending dose study, whether in isolated organs/tissues, in animals or phase I volunteers. Copyright © 2003 John Wiley & Sons, Ltd. [source]

A metabolic approach to the treatment of dilated cardiomyopathy in BIO T0,2 cardiomyopathic Syrian hamsters

BIOFACTORS, Issue 1-4 2005
Rino Mancinelli
Abstract Mechanisms underlying dilated cardiomyopathy (DCM) are poorly understood and effective therapy is still unavailable. The aim of this study was to examine the heart ultrastructure and dynamic of BIO T0,2 cardiomyopathic hamsters, an animal model of DCM, and to study in these animals, the effects of a co-formulation (HS12607) of propionyl-L-carnitine, coenzyme Q10 and omega-3 fatty acids on cardiac mechanical parameters. Sarcomere length, Frank-Starling mechanism and force-frequency relations were studied on isolated ventricular papillary muscle from age-matched BIO F1B normal Syrian hamsters, BIO T0,2 control and BIO T0,2 HS12607-treated cardiomyopathic Syrian hamsters. At the optimum length to maximum active force, electron microscopy of left ventricular papillary muscle revealed that seven out of ten muscles studied showed shorter sarcomeres (1.20 ± 0.29,m), and the remaining three showed longer sarcomeres (2.80 ± 0.13,m), compared to those of normal hamsters (2.05± 0.06,m, n=10). Severe alterations of the Frank-Starling mechanism, force-frequency relations and derivative parameters of contractile waves were also observed in vitro in the BIO T0,2 control hamsters. Long-term (8 weeks) treatment with HS12607 prevented alterations in sarcomere length in the BIO T0,2 cardiomyopathic hamsters; the Frank-Starling mechanism and force-frequency relations were also significantly (P<0.05) improved in these hamsters. Therefore results of the present study strongly suggest the need for clinical studies on metabolic therapeutic intervention in the effort to stop the progression of dilated cardiomyopathy. [source]

A Review of HNS-32: A Novel Azulene-l-Carboxamidine Derivative with Multiple Cardiovascular Protective Actions

CARDIOVASCULAR THERAPEUTICS, Issue 4 2001
Yoshio Tanaka
ABSTRACT HNS-32 [N1,N1 -dimethyl- N2 -(2-pyridylmethyl)-5-isopropyl-3,8-dimethylazulene-1-carboxamidine] (CAS Registry Number: 186086-10-2) is a newly synthesized azulene derivative. Computer simulation showed that its three dimensional structure is similar to that of the class Ib antiarrhythmic drugs, e.g., lidocaine or mexiletine. HNS-32 potently suppressed ventricular arrhythmias induced by ischemia due to coronary ligation and/or ischemia-reperfusion in dogs and rats. In the isolated dog and guinea pig cardiac tissues, HNS-32 had negative inotropic and chronotropic actions, prolonged atrial-His and His-ventricular conduction time and increased coronary blood flow. In the isolated guinea pig ventricular papillary muscle, HNS-32 decreased maximal rate of action potential upstroke (V,max) and shortened action potential duration (APD). These findings suggest that HNS-32 inhibits inward Na+ and Ca2+ channel currents. In the isolated pig coronary and rabbit conduit arteries, HNS-32 inhibited both Ca2+ channel-dependent and -independent contractions induced by a wide variety of chemical stimuli. HNS-32 is a potent inhibitor of protein kinase C (PKC)-mediated constriction of cerebral arteries. It is likely to block both, Na+ and Ca2+ channels expressed in cardiac and vascular smooth muscles. These multiple ion channel blocking effects are largely responsible for the antiarrhythmic and vasorelaxant actions of HNS-32. This drug may represent a novel approach to the treatment of arrhythmias. [source]

Adenosine induces prolonged anti-,-adrenergic effects in guinea-pig papillary muscle

CASE REPORTS: Trepopnea Associated with Paroxysmal Severe Tricuspid Regurgitation Triggered at Left Lateral Decubitus Position

ECHOCARDIOGRAPHY, Issue 8 2010
David Wolf M.D.
A 78-year-old male patient was referred cardiovascular risk evaluation before elective resection of a bronchial carcinoma. A myocardial infarction with a subsequent coronary artery bypass revascularization and a mitral prosthetic valve surgery were known. Left lateral decubitus (LLD) was permanently avoided because of significant trepopnea since several years. No signs of heart failure were found in the physical examination. A mitral valve prosthesis presented normal characteristics at examination. Left ventricular dimensions and function were normal. A severe tricuspid regurgitation could be documented during examination in the LLD, with changing characteristics in dorsal decubitus, when it could be graded as moderate. Trepopnea associated with severe paroxysmal tricuspid regurgitation was never described before in the literature. Sympathetic/parasympathetic modulation of papillary muscles of the tricuspid valve can be proposed as a probable cause of this dynamic valvular dysfunction. (Echocardiography 2010;27:E77-E79) [source]

Reference Values Describing the Normal Mitral Valve and the Position of the Papillary Muscles

Role of Echocardiography in Assessing the Mechanism and Effect of Ramipril on Functional Mitral Regurgitation in Dilated Cardiomyopathy

ECHOCARDIOGRAPHY, Issue 4 2005
D.M. (Card), F.I.A.E., F.I.A.M.S., F.I.C.C., F.I.C.P., I.B. Vijayalakshmi M.D.
The objectives of this article are to determine the possible mechanism of functional mitral regurgitation in patients with dilated cardiomyopathy (DCM) and to know the effect of ramipril on left ventricle (LV) and mitral regurgitation by ECHO. Several postulates are put forth for functional mitral regurgitation in DCM, and mitral annular dilatation is said to be the primary mechanism in the past, but the exact mechanism is not clear. Though angiotensin converting enzyme (ACE) inhibitors are known to remodel the LV, their beneficial effect in patients with DCM with functional mitral regurgitation is not known. Various cardiac dimensions and degree of mitral regurgitation were measured by echocardiography in 30 normal control group and in 30 patients with DCM of various etiologies except ischemic, before and after ramipril therapy. There was a significant difference in all parameters especially sphericity of left ventricle and position of papillary muscles (P < 0.0003) in DCM patients, but mitral valve annulus did not show significant change (P < 0.3) compared to control group. In 50% of the patients, the functional mitral regurgitation totally disappeared. In 30% of patients, it came down from grade II to I or became trivial. In 20% of patients, it remained unchanged. There was remarkable improvement in sphericity, LV dimension, volumes, and EF%, which increased from 31 ± 9.81 to 39.3 ± 8.3% (P < 0.0003). It is concluded that echocardiography clearly demonstrates the increased sphericity of LV in DCM. The lateral migration of papillary muscles possibly plays a major role in functional mitral regurgitation. Ramipril significantly reduces not only sphericity but also functional mitral regurgitation. [source]

High extracellular [Mg2+]-induced increase in intracellular [Mg2+] and decrease in intracellular [Na+] are associated with activation of p38 MAP kinase and ERK2 in guinea-pig heart

EXPERIMENTAL PHYSIOLOGY, Issue 12 2008
Shang-Jin Kim
High extracellular Mg2+ concentrations ([Mg2+]o) caused a remarkable concentration-dependent and reversible increase in intracellular Mg2+ concentrations ([Mg2+]i) in beating and quiescent guinea-pig papillary muscles, accompanied by a definite decrease in intracellular Na+ concentrations ([Na+]i). A change in 1 mm[Mg2+]o evoked a direct change in 0.0161 mm[Mg2+]i and an inverse change in 0.0263 mm[Na+]i. Imipramine completely abolished the high [Mg2+]o -induced decrease in [Na+]i and remarkably diminished the high [Mg2+]o -induced increase in [Mg2+]i in papillary muscles. High [Mg2+]o also produced a significant activation of p38 mitogen-activated protein (MAP) kinase and extracellular signal-related kinase 2 (ERK2) that was inhibited by pretreatment with imipramine. These results suggest that the high [Mg2+]o -induced increase in [Mg2+]i could be coupled with the decrease in [Na+]i, which might involve activation of the reverse mode of Na+,Mg2+ exchange, accompanied by activation of p38 MAP kinase and ERK2 in the guinea-pig heart. [source]

Papillary Muscle Approximation for Ischemic Mitral Valve Regurgitation

JOURNAL OF CARDIAC SURGERY, Issue 6 2008
Akhtar Rama M.D.
Several procedures were described to restore a more normal alignment between the mitral annulus and the laterally displaced papillary muscles. We report a new approach to relocate the displaced papillary toward the mitral annulus and to reduce tethering. This procedure is believed to be technically easy and beneficial in terms of mitral repair. [source]

Characteristics of Hypertrophic Obstructive Cardiomyopathy Refractory to Medical Treatment and Selection of Surgical Methods

JOURNAL OF CARDIAC SURGERY, Issue 1 2005
Yujiro Hirasawa M.D.
Using the classification of systolic anterior movement (SAM) which has been previously reported, we tried to identify the characteristics and use them to treat HOCM appropriately. Methods: The clinical, echocardiographic, catheterization, and surgical data of 29 hospitalized patients with HOCM during 1980 to 1999 were analyzed retrospectively. We classified SAM in all patients by echocardiography. Ninteen patients improved with medical treatment (medical group), and 10 patients underwent surgical treatment because of ineffectiveness of medication (surgical group). We studied the relation between types of SAM and medical/surgical groups, and examined the relation between types of SAM and the surgical methods. Results: Type I SAM was significantly more frequent in the medical group, while type II SAM was more frequent in the surgical group (p = 0.047). Patients in the surgical group underwent mitral valve replacement (MVR), myectomy, or a combination of MVR and myectomy. Left ventricular outflow gradient (LVOG) of over 100 mmHg was recognized in almost all patients with type II SAM. Conclusions: It was suggested that patients with medication-responsive HOCM tended to have type I SAM and those with refractory HOCM tended to have type II SAM. We consider that in type I SAM, if the position of the papillary muscles changed with medication or myectomy, shift of the chordae and type I SAM were reduced or disappeared. However, in type II SAM, even if the position of the papillary muscles changed, SAM did not disappear because lifting of the mitral leaflets remained. It is therefore suggested that patients with type II SAM should undergo at least MVR. [source]

Nifedipine enhances cGMP production through the activation of soluble guanylyl cyclase in rat ventricular papillary muscle

Real-time Integration of Intracardiac Echocardiography and Electroanatomic Mapping in PVCs Arising from the LV Anterior Papillary Muscle

Aspects of Left Ventricular Morphology Outperform Left Ventricular Mass for Prediction of QRS Duration

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2010
Nina Hakacova M.D., Ph.D.
Background: The knowledge of the case-specific normal QRS duration in each individual is needed when determining the onset, severity and progression of the heart disease. However, large interindividual variability even of the normal QRS duration exists. The aims of the study were to develop a model for prediction of normal QRS complex duration and to test it on healthy individuals. Methods: The study population of healthy adult volunteers was divided into a sample for development of a prediction model (n = 63) and a testing sample (n = 30). Magnetic resonance imaging data were used to assess anatomical characteristics of the left ventricle: the angle between papillary muscles (PMA), the length of the left ventricle (LVL) and left ventricular mass (LVM). Twelve-lead electrocardiogram (ECG) was used for measurement of the QRS duration. Multiple linear regression analysis was used to develop a prediction model to estimate the QRS duration. The accuracy of the prediction model was assessed by comparing predicted with measured QRS duration in the test set. Results: The angle between PMA and the length of the LVL were statistically significant predictors of QRS duration. Correlation between QRS duration and PMA and LVL was r = 0.57, P = 0.0001 and r = 0.45, P = 0.0002, respectively. The final model for prediction of the QRS was: QRSPredicted= 97 + (0.35 × LVL) , (0.45 × PMA). The predicted and real QRS duration differed with median 1 ms. Conclusions: The model for prediction of QRS duration opens the ability to predict case-specific normal QRS duration. This knowledge can have clinical importance, when determining the normality on case-specific basis. Ann Noninvasive Electrocardiol 2010;15(2):124,129 [source]

Is serum troponin T a useful marker of myocardial damage in newborn infants with perinatal asphyxia?

ACTA PAEDIATRICA, Issue 2 2007
S. Costa
Abstract Aim: To assess the correlation of echocardiographic signs of myocardial damage to serum cardiac troponin T (cTnT) concentrations in newborn infants with perinatal asphyxia. Methods: Electocardiograms (ECG) and echocardiograms (Echo) were obtained during the first 24 h of life from 29 asphyxiated and 30 control infants and correlated with cTnT concentrations. The echocardiographic parameters included systolic ventricular performance, preload, afterload, diastolic function, stroke volume (SV), left ventricular output (LVO), hyperechogenity of the papillary muscles and insufficiency of the atrioventricular valves. Results: LVO and SV were lower but CTnT were significantly higher in asphyxiated than in control infants: 0.15 (010,0.23) vs. 0.05 (0.02,0.13), p < 0.001). Asphyxiated infants with signs of myocardial damage were associated with significantly higher cTnT than those without, 0.20 (0.11,0.28) and 0.11 (0.05,0.14 ug/L), p = 0.04. Conclusion: Cardiac troponin may prove to be valuable in evaluating myocardial damage in birth asphyxia. However, the degree of prematurity may complicate the assessment. [source]