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At least 199 records · Page 11Linked to original sources
PubMed2004

Inverted L-shape sternotomy as a minimally invasive approach: re-do cardiac surgery for papillary muscle rupture.

We report a successful treatment of the complete papillary muscle rupture occurring 16 months after coronary artery bypass grafting (CABG). A 57-year-old man was admitted for the sudden onset of chest pain and cardiogenic shock. Emergency cardiac catheterization revealed severe mitral regurgitation and total occlusion in the right coronary artery, which was successfully revascularized by percutaneous coronary intervention under intra-aortic balloon pumping. The right internal thoracic artery grafted to the left anterior descending artery in the previous CABG was functioning well. An echocardiogram distinctly indicated the ruptured head of the papillary muscle. Since an emergency operation revealed complete rupture of the posterior papillary muscle, mitral valve replacement was carried out through an inverted L-shape sternotomy with T-shape left atriotomy. Our case indicates that the inverted L-shape sternotomy was a useful approach to preserve the function of grafts, and that T-shape left atriotomy offered a good exposure of the mitral valve in the limited surgical field.

Coronary Artery Bypass↗
PubMed1978

Effect of inhibitors of slow calcium current on rested state contraction of papillary muscles and post rest contractions of atrial muscle of the cat and rabbit hearts.

Effect of Ni, Co and Mn ions and of D-600 on rested state contractions (RSCs) of cat and rabbit papillary muscles and on post rest contractions (PRCs) of cat and rabbit atrial muscle was investigated. Ni and Co in concentration 2 mmol/l reduced the force of RSCs in papillary muscles by 78%, increased the dip between the phase 1 and 2 of respective action potentials (APs), lowered the level of plateau and decreased the total duration of AP. Strong PRCs in atrial muscle were reduced by Ni only by 25%, while the subsequent beats were strongly inhibited. Ni completely inhibited RSCs in papillary muscles increased by caffeine (10 mmol/1) or by reduction in Na concentration by 50%. Mn ions in concentration 1--2 mmol/l inhibited strongly both RSCs in papillary muscles and strong PRCs in atrial muscle, increased the dip between phase 1 and 2 and increased total duration of AP. Mn ions stimulated 45Ca efflux from papillary muscles and atrial strips. D-600 did not affect RSCs nor the shape of respective APs. It is concluded that RSCs in papillary muscles are directly activated by Ca inflow during the respective excitation while strong PRCs in atrial muscle are activated mostly by Ca released from intracellular stores.

Action Potentials↗
PubMed2002

[Nitric oxide mediates the inhibitory effects of interleukin-2 on the isolated ventricular papillary muscle and cultured neonatal rat cardiomyocyte]

OBJECTIVE: To explore the effects and mechanism of interleukin-2 on the isolated rat ventricular papillary muscle and cultured cardiomyocyte. METHODS: The isolated rat papillary muscle and cultured neonatal rat cardiomyocyte were used to determine the effects on contractile properties and spontaneous beating. RESULTS: IL-2 inhibited the contractile force of isolated rat papillary muscle and reduced the spontaneous beating rate of cultured neonatal rat cardiomyocytes in a dose-dependent manner. IL-2 at high concentration reduced the systolic duration and prolonged the diastolic duration. Pretreatment with L-NAME, an inhibitor of nitric oxide synthase,abolished the effects of IL-2. Heat inactivated IL-2 had no effect on papillary muscles and cardiomyocytes.CONCLUSION: Inhibitory effects of IL-2 on the contraction of isolated papillary muscle and spontaneous beating rate of cultured neonatal cardiomyocyte are mediated by nitric oxide.

Journal Article↗
PubMed1993

Inotropic and electrophysiologic effects of propofol and thiamylal in isolated papillary muscles of the guinea pig and the rat.

We compared the inotropic and electrophysiologic effects of propofol and thiamylal in isolated papillary muscles of the guinea pig and rat. Propofol applied in clinical 10% intralipid emulsion showed concentration-dependent negative inotropic effects, accompanied by decreased action potential duration, in the guinea pig. Intralipid alone had no effect. Although thiamylal showed a concentration-dependent depression similar to propofol in the guinea pig, depolarization of resting membrane potential was seen at 0.1 and 0.3 mM, and a slight prolongation of action potential duration at 90% repolarization at 0.1 mM, and then a decrease of action potential duration at 0.3 mM. In rat papillary muscles, propofol did not produce any depression of contractile force, whereas thiamylal produced a concentration-dependent negative inotropic effect. The important findings observed in the action potential in rat papillary muscles were the modest shortening of action potential duration after propofol application, and the significant decrease of resting membrane potential and the significant prolongation of action potential duration caused by thiamylal. Both propofol and thiamylal depressed slow action potentials and contractile force in guinea pig papillary muscles depolarized by 25 mM K+ solution. In conclusion, the negative inotropic effects of propofol and thiamylal might be caused by inhibition of trans-sarcolemmal Ca2+ influx accompanied by shortening of action potential duration in guinea pig papillary muscles. The action potential of thiamylal might be affected by the suppression of K+ current in guinea pig and rat papillary muscles that was never observed in the propofol-treated tissue.

Action Potentials↗
PubMed1997

Papillary muscle discoordination rather than increased annular area facilitates mitral regurgitation after acute posterior myocardial infarction.

BACKGROUND: Acute posterior myocardial infarction that produces immediate mitral regurgitation alters the mitral annulus and its spatial relationship with both papillary muscles. The precise deformations that cause valve insufficiency are not understood and impair efforts to repair the valve. METHODS AND RESULTS: In six Dorsett hybrid sheep, sonomicrometry transducers were placed around the mitral annulus (6) and at the tips and bases of both papillary muscles (4). Two weeks later, three branches of the circumflex coronary artery were occluded to infarct approximately 32% of the posterior left ventricle. This infarction produced acute 2 to 3+ mitral regurgitation in all animals, as determined by color flow Doppler velocity mapping. Before and after infarction, distance measurements between sonomicrometry transducers were used to produce the three-dimensional coordinates of each transducer every 5 ms. After infarction, the area of the annulus increased only 9.2+/-6.3% at end systole (ES). In addition, the normal shortening of the posterior papillary muscle was obliterated to allow its tip to move 1.4+/-0.6 mm closer to the centroid of the annulus at ES. After infarction, the anterior papillary muscle continued to shorten normally, but at ES, its tip and base were 0.9+/-0.7 mm and 1.3+/-0.7 mm farther from the centroid, respectively. CONCLUSIONS: These deformations tend to produce a relative prolapse of leaflet tissue attached to the posterior papillary muscle and restriction of leaflet tissue attached to the anterior papillary muscle. This papillary muscle discoordination with minimal annular dilatation distorts leaflet coaptation sufficiently to produce severe mitral regurgitation.

Animals↗
PubMed1994

Effects of isoproterenol on the mechanical activity of isolated papillary muscles and perfused rat hearts in various calcium concentrations.

The aim of the study was to examine, in papillary muscles and in a whole heart preparation, the effects of isoproterenol on the myocardial mechanical activity at different extracellular Ca2+ concentrations. Papillary muscles from left ventricles, contracting isometrically, and rat hearts perfused by the Langendorff technique developing isovolumetric pressure at a fixed rate (200 bpm) and diastolic pressure of 5 mmHg were studied at different Ca2+ concentrations for analysis of the effects of increasing doses of isoproterenol. Papillary muscles were treated with isoproterenol (0.5 to 8 ng ml-1) at four extracellular Ca2+ concentrations (0.25, 0.5, 1.25 and 2.5 mM) and Langendorff perfused hearts were stimulated by isoproterenol (0.05 ng ml-1 to 0.8 ng ml-1), also at four extracellular Ca2+ concentrations (0.5, 1.25, 2.5 and 3.75 mM). Both papillary muscles and perfused hearts showed that force and isovolumetric systolic pressure increase in response to isoproterenol at low Ca2+ concentrations. As Ca2+ concentration is increased, isoproterenol's positive inotropic effect subsides. However, papillary muscle isometric contractions showed a similar time to peak tension decrease in response to isoproterenol at all external Ca2+ concentrations used. The results suggest that the positive inotropic response to isoproterenol, in isolated preparations, changes as a function of extracellular Ca2+ concentration decreasing as external Ca2+ increases. Time to peak tension reduction reinforces the idea that this small positive inotropic response to isoproterenol of the rat myocardium, at the physiological Ca2+ concentration, is due to the Ca2+ saturation of the mechanical activity.

Animals↗
PubMed1989

The medial papillary muscle complex and its related septomarginal trabeculation. A normal anatomical study on human hearts.

The morphology of the medial papillary muscle complex of the right ventricle was studied in 81 normal hearts from subjects ranging in age from 20 weeks of gestation to 13 months. The position of the main medial papillary muscle (of Lancisi) was differentiated in terms of a root and a belly. The anterior aspect of the root was found in a constant position at the basal bifurcation of the septomarginal trabeculation, whereas its belly showed considerable positional variation. Three groups of minor papillary muscles were identified and localised in specific areas in the base of the right ventricle. Taken overall, they formed part of the medial papillary complex. The complex itself was found to be constantly related to the antero-septal commissure of the tricuspid valve. A separate group of septal papillary muscles could be differentiated from the medial papillary complex. The anchorage of the septal leaflet of the tricuspid valve to the ventricular septum was also studied. The antero-superior and postero-inferior portions of this leaflet were found to be supported by the medial and posterior papillary complexes, respectively. Its midportion was connected to the septal group of papillary muscles but much variability was evident. The portion of the septomarginal trabeculation supporting the medial papillary complex, namely the postero-basal division, was studied further. This showed considerable variability and did not form a continuous anatomical spectrum.

Fetus↗
PubMed1993

[Papillary muscle rupture. Diagnosis with transesophageal echocardiography].

Two patients with acute myocardial infarction and papillary muscle rupture are presented. The diagnosis of papillary muscle rupture was made by transesophageal echocardiography. The transesophageal echocardiographic findings and the usefulness of this technique in the diagnosis of papillary muscle rupture are described.

Adult↗
PubMed1990

Modulation of stimulation frequency responses and calcium dependency of functional parameters in hyperthyroid rat ventricular papillary muscles.

The effects of stimulation frequency (0.2-1.5 Hz) and extracellular calcium concentration ([Ca2+]o) (0.6-15.0 mM) on the contractile function of thin papillary muscles of euthyroid and hyperthyroid rats were studied. Hyperthyroidism led to a decrease in developed tension (DT) and time to peak tension (TPT), but it exhibited no influence on the maximal rates of contraction (+dT/dt) and relaxation (-dT/dt). Also, the mean rates of contraction were similar in euthyroid and hyperthyroid muscle groups. The increase in stimulation frequency brought about a marked decrease in DT, +dT/dt, and -dT/dt of euthyroid papillary muscles at lower frequencies in comparison to papillary muscles in the hyperthyroid group. At stimulation frequencies above 1.0 Hz, the absolute and relative levels of DT and -dT/dt of hyperthyroid myocardium were elevated over euthyroid preparations. At the same time, TPT was unchanged in any of the muscle groups. Hyperthyroidism modulated the relationships between contractile parameters and [Ca2+]o. At a [Ca2+]o of 1.0-4.0 mM, the DT of hyperthyroid papillary muscles was lower than in euthyroid muscle. At 4.0 and 8.0 mM of [Ca2+]o, the equal values of maximal DT were registered for euthyroid and hyperthyroid papillary muscles, respectively. An increase in the [Ca2+]o in the range of 1.0-15.0 mM was accompanied by an increase in TPT of both muscle groups, but to a greater extent in hyperthyroid myocardium. In conclusion, the myocardium of hyperthyroid rat appeared to exhibit decreased sensitivity to calcium as well as to the negative inotropic effect of enhanced stimulation frequency. Alterations of the processes of transsarcolemmal movement and intracellular recycling of Ca2 may be implicated.

Animals↗
PubMed2005

A new classification of the mitral papillary muscle.

BACKGROUND: Mitral valve homograft implantation and reconstruction of the left ventricular subvalvular apparatus requires a good knowledge of the morphology of the left papillary muscles. A comprehensive description of the left ventricular subvalvular apparatus is presented to aid in this procedure and to support conventional and endoscope-assisted reconstruction of the chordae tendineae. MATERIAL/METHODS: The subvalvular apparatuses of 100 unfixed human hearts were investigated. Papillary muscles were endoscopically examined on the hearts in situ, then the hearts were explanted and the subvalvular apparatus was macroscopically inspected. The geometrical arrangement of the chordae tendineae was determined. RESULTS: We defined three groups of the left ventricular papillary muscle. In group I the basal part and the apex of the muscle were undivided. In group II there were two heads; in subgroup II/A the base of the papillary muscle was undivided and in II/B it was divided into two separate parts. In group III the papillary muscle had three heads. In subgroup III/A the base was undivided, while in III/B it was made up of two and in III/C three separate parts. CONCLUSIONS: We propose a classification of the left ventricular subvalvular apparatus based on the macroscopic and endoscopic investigations. It emphasizes the morphology of the apical and basal parts of papillary muscles and includes the geometrical arrangement of the chordae tendineae. Thus it may be of a great value in endoscopic and conventional mitral valve replacement or reconstruction of the chordae tendineae and in mitral valve homograft implantation.

Adult↗
PubMed2004

Effects of endogenous adenosine and adenosine receptor agonists on hypoxia-induced myocardial stunning in Guinea-pig atria and papillary muscles.

The effects of endogenous adenosine and adenosine receptor agonists were examined on hypoxia-induced myocardial stunning of guinea-pig isolated paced left atria and papillary muscles. Hypoxia (30 minutes) reduced developed tension and increased diastolic tension (contracture) of left atria (41.8 +/- 11.5%) and papillary muscles (17.7 +/- 6.2%). Developed tension recovered to 80.8 +/- 3.15 and 77.2 +/- 5.3% 15 minutes after reoxygenation (stunning). Recovery of left atria was unaffected by adenosine deaminase (1 IU mL) but was depressed in papillary muscles (15 minutes, 48.6 +/- 4.3%) and contracture (46.1 +/- 7.5%) increased. Endogenous adenosine therefore protects from ventricular but not atrial stunning. Adenosine receptor agonists were introduced at 10 minutes into hypoxia. CPA (A1 selective, 3 x 10 M) impaired left atrial recovery (5 minutes, 38.1 +/- 5.0%), through direct negative inotropy, but did not affect papillary muscles. CGS21680 (A2A selective, 3 x 10 M) did not affect recovery. APNEA (A1/A3 receptor agonist, 10 M), increased recovery rate of left atria. Improved rate and extent of recovery of papillary muscles by APNEA (15 minutes, 94.8 +/- 3.1%) was prevented by the A3 receptor antagonist, MRS-1220 (10 M). IB-MECA (A3 selective, 3 x 10 M) increased atrial recovery rate but not the maximum developed tension reached in either tissue. However, when added at reoxygenation, IB-MECA caused complete recovery of both tissues, in the absence or presence of adenosine deaminase. Thus, A3 receptor stimulation reverses myocardial stunning of isolated atria and papillary muscles.

Adenosine↗
PubMed1993

[Papillary muscle rupture complicating with acute myocardial infarction: a case report].

Cardiogenic shock caused by papillary muscle rupture in acute myocardial infarction is potentially reversible by surgical treatment. A case of posterior myocardial infarction in a 79-year-old woman is reported. She was admitted to the hospital in cardiogenic shock. She had been suffered from chest pain for three days before admission. On physical examination diffuse rales and a grade 4/6 holosystolic apical murmur were present. The diagnosis of an acute posterior myocardial infarction was based on the electrocardiographic findings and serum creatine kinase level. Coronary angiography visualized subtotal occlusion of the left circumflex coronary artery. Transesophageal echocardiography demonstrated severe mitral regurgitation and the ruptured anterior papillary muscle connected to normal chordae tendineae and posterior mitral leaflet. In systole, the head of the ruptured papillary muscle moved like a whip in the left atrium. At operation, the ruptured papillary muscle was confirmed. Mitral valve replacement with a 27 mm St. Jude Medical prosthesis and coronary artery bypass grafting to the left circumflex coronary artery was performed. Postoperatively she was weaned intraaortic balloon pumping after 4 days and recovered uneventfully.

Aged↗
PubMed1960

Cat heart muscle in vitro. I. Cell volumes and intracellular concentrations in papillary muscle.

Methods have been developed for the simultaneous determination of total water, inulin space, and K and Na content in muscles of 0.5 to 10 mg. wet weight. These methods have been used to define steady state conditions with respect to intracellular K concentration in papillary muscles from cat hearts perfused and contracting isometrically at 27-28 degrees C. and at 37-38 degrees C. Cell volumes and intracellular ionic concentrations have been followed as a function of the external K concentration and compared with values predicted on the basis of electroneutrality and osmotic equilibrium.

Animals↗
PubMed1975

Changing haemodynamics in patient with papillary muscle dysfunction.

A patient with papillary muscle disease caused by myocardial infarction was studied before and after injection of phenylephrine. The pulmonary wedge pressure was normal at rest. However, pressures and murmur changes, occurring spontaneously and after injection of phenylephrine, suggested that intermittent severe mitral regurgitation contributed significantly to the recurrent episodes of acute left heart failure presented by this patient.

Blood Pressure↗
PubMed1994

Endothelin-1 does not alter Ca2+ responsiveness in saponin-skinned ferret papillary muscles.

Endothelin is a potent vasoconstrictor and a positive inotropic agent in myocardium. Endothelin has been reported to increase myocardial contractility with little or no increase in intracellular Ca2+, thus apparently enhancing myofilament responsiveness to Ca2+. We investigated the effects of endothelin on tension development and Ca2+ responsiveness in both intact and saponin-skinned ferret right ventricular papillary muscles. Isolated ferret papillary muscles were stimulated for 2 h in the presence or absence of endothelin (100 nM). The muscles were then chemically skinned with saponin and exposed to relaxing and contracting solutions containing varying amounts of Ca2+, and the developed force of contraction was measured. The [Ca2+] required for half-maximal activation (pCa50) was determined by fitting force versus Ca2+ data to the Hill equation. In isometrically contracting muscles, endothelin (100 nM) caused a mean percent increase in developed tension of 34.7% +/- 11.3% (mean +/- S.E.). In muscles that were exposed to endothelin for 2 h and then skinned, neither the pCa50 nor the maximal Ca(2+)-activated force (Fmax) were significantly different from control skinned papillary muscles. After skinning, when endothelin (100 nM) was added to the Ca2+ buffers, both pCa50 and Fmax were significantly decreased. When papillary muscles were pretreated with phorbol 12-myristate 13-acetate (PMA) and then skinned, there was a significant increase in the pCa50. These results indicate that endothelin acts directly on the myofilaments to impair force development by directly decreasing the Ca2+ responsiveness of myofilaments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

Adenosine antagonizes the positive inotropic action mediated via beta-, but not alpha-adrenoceptors in the rabbit papillary muscle.

In the isolated rabbit papillary muscle, adenosine (1-300 microM) alone scarcely affected the basal tension developed. The positive inotropic action of isoprenaline, mediated via beta-adrenoceptors, was inhibited by adenosine in a concentration-dependent manner. Atropine (0.3 microM) abolish the inhibitory action of carbachol on the isoprenaline-induced positive inotropic action but not affect the inhibitory asction of adenosine. Adenosine failed to inhibit the positive inotropic action exerted by phenylephrine via stimulation of alpha-adrenoceptors in the presence of pindolol (30 nM). The present results indicate that the positive inotropic action was mediated via alpha-adrenoceptors whose subecllular mechanism was not susceptible to the inhibitory action of adenosine as are beta-adrenoceptors.

Adenosine↗
PubMed1998

Papillary muscle shortening for mitral valve reconstruction in patients with ischaemic mitral insufficiency.

AIMS: To evaluate the feasibility of papillary muscle shortening in a specific group of high risk patients with ischaemic mitral regurgitation undergoing mitral valve reconstruction. BACKGROUND: From January 1996 to December 1997, 712 (10.1%) out of a total of 7042 open heart patients underwent mitral valve surgery in our hospital. Mitral valve reconstruction was performed in 408 of these patients (57.3%) and valve replacement had to be performed in 304 patients (42.7%). METHODS: A specific technique of papillary muscle reconstruction was performed in 32 patients undergoing valve reconstruction (7.8%). These cases had degenerated and had developed fibrotic elongated papillary muscles, which resulted in prolapses of one or more parts of the mitral valve leaflets. The aetiology in this group of patients was ischaemic, requiring concomitant myocardial revascularization in 28 patients (87.5%) with a mean of 2.7 grafts/patient. All patients underwent papillary muscle shortening using a pericardium pledget-reinforced Polytetrafluoroethylene suture and annuloplasty with a Carpentier-Edwards Physio Annuloplasty Ring. Of these 32 patients, 17 (53.1%) were male, the mean age was 67.1+/-9.7 years (range 41 to 81 years) and all but one were in pre-operative NYHA class III or IV. RESULTS: There were two hospital deaths (6.2%). Postoperative Doppler echocardiography indicated satisfactory mitral valve function in all patients. Within the short mean follow-up period of 9.6+/-5.4 months (3 to 26 months) there was one non-cardiac-related death (3.1%). There was no need for reoperation, and no cases of thromboembolic and bleeding complications in the postoperative period. All patients were in NYHA functional class I or II at the time of follow-up. CONCLUSION: Our results indicate that mitral valve repair is a safe treatment for this group of high risk patients, and that papillary muscle shortening is a valuable tool in these patients with ischaemic mitral regurgitation undergoing surgery.

Adult↗
PubMed1992

Comparative ultrastructure of the tip of ventricular papillary muscle.

Electron microscopic studies of the tips of left ventricular papillary muscles from seven human, two monkey, three sheep, and two chicken hearts were done to elucidate the fine structure of myotendinous junctions. The human specimens were from normal hearts obtained 3 to 9 hours postmortem from persons aged 7 months to 30 years (mean, 13.3 years). We found no significant ultrastructural differences between the human hearts and those of monkey, sheep, and chicken. Myocardial fibers were elongated and thinner (tapered) in the tips of papillary muscles. In addition to usual working myocardial cells, the distal end of narrowing muscle fibers also contained small pale cardiocytes containing fewer myofibrils and smaller mitochondria. These cells were similar to P cells or transitional cells in the conduction system. Nerve axons and Schwann cells were commonly seen in the interstitium, usually in association with capillaries. Fibroblasts and axon varicosities were occasionally seen extremely close to the cardiocytes. These specialized myocardial cells associated with rich neural tissue in the papillary muscle tip possibly function as foci of local automaticity. This histologic organization may also represent neurosensory function responding to and monitoring local pressure changes, efferent adrenergic or cholinergic neural activity, or both.

Adolescent↗