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PubMed1983

Subxyphoid 2-dimensional echocardiographic identification of left ventricular papillary muscle anomalies in complete common atrioventricular canal.

Mitral valve dysfunction is probably the major cause of operative mortality from total repair of complete common atrioventricular (AV) canal in infancy. The presence of a solitary left ventricular (LV) papillary muscle appears to be 1 anatomic factor influencing the success of mitral reconstruction because suturing of the cleft between the superior and inferior components of the anterior mitral leaflet creates a parachute mitral valve deformity, which may result in stenosis or in unduly high tension on the components of the repair. This study reports on (1) the 2-dimensional (2-D) echocardiographic appearance of the LV papillary muscle architecture in patients with complete common AV canal compared with that in normal subjects, and (2) the incidence of solitary LV papillary muscle in patients with complete common AV canal. Two-dimensional echocardiography was performed in 31 infants with complete common AV canal, 14 normal infants, and 9 infants with a large ventricular septal defect not involving the AV canal region. Of 31 infants with complete common AV canal, 26 (80%) had 2 LV papillary muscles on 2-D echocardiography, 3 (10%) had 3 LV papillary muscles, and 3 (10%) had 1 LV papillary muscle. In patients with 2 LV papillary muscles, the anterolateral papillary muscle was displaced posteriorly compared with that in normal subjects and in patients with ventricular septal defect, whereas the posteromedial papillary muscle was in its normal location. Among the 25 patients with complete common AV canal with 2 LV papillary muscles, there was 1 operative death. Among the 6 infants with complete common AV canal with LV papillary muscle anomalies, 5 underwent surgical repair with 4 early deaths. Subxyphoid 2-D echocardiography is a useful technique for evaluating LV papillary muscle architecture in complete common AV canal and permits identification of patients who may be at higher risk for unsuccessful mitral reconstruction.

Echocardiography↗
PubMed1995

Papillary muscles split in the presence of 2,3-butanedione monoxime have normal energetic and mechanical properties.

A number of studies have used 2,3-butanedione monoxime (BDM) to avoid myocardial damage when small muscle preparations were cut from large hearts. The present study investigates the mechanical and energetic effects of varying muscle cross-sectional area (CSA) by dissection in physiological saline containing BDM. By use of adult rat hearts, three muscle groups were obtained: whole left ventricular papillary muscles (Whole) and left ventricular papillary muscles split longitudinally in the presence of 30 mM BDM, with removal of approximately 10% (BDMSP1) or 40-50% (BDMSP2) of the muscle (5 animals in each group). The isolated muscle preparations were studied at 27 degrees C and stimulated at 0.167 Hz. The Whole and BDMSP1 preparations had comparable CSAs; in isotonically contracting muscles working against a range of afterloads, work, enthalpy (energy use), and mechanical efficiency (work/enthalpy x 100%) were similar for the two groups. In addition, isometric performance [e.g., developed stress (force/CSA), length-tension relationship, and contraction time course] was also similar for the two groups. The thinner BDMSP2 preparations showed an enhanced mechanical performance compared with the Whole and BDMSP1 groups. This outcome was in accordance with data in the literature documenting a negative correlation between stress and CSA. The results suggest that BDM-split and intact papillary muscles of similar CSA have comparable energetic and mechanical properties.

Animals↗
PubMed1995

L-NMMA blocks carbachol-induced increases in cGMP levels but not decreases in tension in the presence of forskolin in rabbit papillary muscles.

OBJECTIVE: The purpose of the present investigation was to determine whether stimulation of the nitric oxide synthase pathway contributes to the muscarinic receptor-mediated elevation in cGMP levels and reversal of the positive inotropic response to the adenylyl cyclase activator forskolin in rabbit papillary muscles. METHODS: Intact rabbit papillary muscles suspended under tension in isolated tissue baths were incubated in the absence or presence of the nitric oxide synthase inhibitor L-NG-monomethyl arginine (L-NMMA) and then treated with forskolin followed by the muscarinic agonist carbachol. The developed tension of the preparations was monitored during their exposure to drug. Papillary muscles were then frozen and subsequently assayed for cGMP levels by radioimmunoassay. Tension and cGMP levels were also measured in some papillary muscles treated with forskolin followed by sodium nitroprusside. RESULTS: Incubation of papillary muscles with L-NMMA completely blocked increases in cGMP levels produced by carbachol, but had no effect on the reversal by carbachol of the increase in tension in response to forskolin. Sodium nitroprusside also caused a marked elevation of cGMP levels in rabbit papillary muscle, but had no significant effect on the forskolin-induced increase in tension. CONCLUSIONS: These data demonstrate that activation of muscarinic receptors results in increases in cGMP levels largely through the nitric oxide synthase pathway in rabbit papillary muscles. However, the cGMP produced through this pathway or by sodium nitroprusside does not appear to contribute to the reversal of the positive inotropic response to forskolin.

Animals↗
PubMed1977

Small cardiac lesions. Fibrosis of papillary muscles and focal cardiac myocytolysis.

Three types of small cardiac lesions were described and illustrated: (1) focal type of papillary muscle fibrosis, evidently a healed infarct of the papillary muscle present in 13% of autopsies, is a histologically characteristic lesion associated with coronary artery disease and healed myocardial infarction, (2) diffuse type of papillary muscle fibrosis, probably an aging change present in almost half of the autopsies, is associated with sclerosis of the arteries in the papillary muscle, is identifiable histologically, and apparently is not associated with any cardiac abnormality, and (3) focal cardiac myocytolysis, a unique histologic lesion, usually multifocal without predilection for any area of the heart, is associated with ischemic heard disease, death due to cancer complicated by nonbacterial thrombotic endocarditis and microthrombi in small cardiac arteries as well as with other diseases. Differentiation of the 2 types of papillary muscle fibrosis is important in the study of papillary muscle and mitral valve dysfunction. Focal cardiac myocytolysis may contribute to the fatal extension of myocardial infarcts.

Aged↗
PubMed1989

Mitral valve function after cryoablation of the posterior papillary muscle in the dog.

Extensive cryoablation of an arrhythmogenic left ventricular posterior papillary muscle associated with ventricular arrhythmias may affect mitral valve function. We studied the long-term effects of extensive cryoablation of the posterior papillary muscle and its ventricular attachment in 10 dogs. The dogs had hemodynamic, electrophysiological, and angiographic testing 1 month after operation. Seven dogs were then killed, and the hearts were examined at that time. Three dogs had repeat assessments 2 and 3 months after operation before they were killed. At 1 month, left ventricular angiography showed normal mitral valve function in all dogs. Pathological examination revealed that the posterior papillary muscle and its left ventricular attachment were replaced by a discrete dense, fibrous scar. The fibrous process involved the mitral valve in 2 dogs. At 3 months, pathological examination showed a marked fibrous scar with chondroid metaplasia and fibrous involvement of the mitral valve chordae and posterior leaflet in all 3 dogs. We conclude that extensive cryoablation of the posterior papillary muscle is not associated with long-term mitral valve dysfunction, and may be the best surgical technique to ablate an arrhythmogenic papillary muscle.

Animals↗
PubMed1996

The effects of sevoflurane on contractile and electrophysiologic properties in isolated guinea pig papillary muscles.

We examined, in guinea pig papillary muscles, whether the negative inotropic effect of sevoflurane is due to the depression of the influx of extracellular Ca2+ or to inhibition of the availability of intracellularly stored Ca2+. Sevoflurane decreased action potential duration and contractile force in a concentration-dependent fashion in normally polarized guinea pig papillary muscles. Sevoflurane produced a depression of contractile force with different rates or patterns of stimulation in the rested state and at low stimulation frequencies. In a potentiated state, sevoflurane did not depress contractile forces. Although sevoflurane decreased action potential duration and contractile force in a concentration-dependent fashion in normal Tyrode's solution, in high K+ Tyrode's solution, it caused a depression of contractile force without a shortening of action potential duration. Sevoflurane also depressed contractile force in normal and high K+ Tyrode's solution with ryanodine 1 microM. Our results suggest that in myocardial contractile force the negative inotropic effect of sevoflurane might be caused by depression of transsarcolemmal Ca2+ influx, accompanied by shortening of the action potential duration.

Action Potentials↗
PubMed2003

Electrophysiological effects of capsaicin on guinea pig papillary muscles.

The cardiac electrophysiological effects of capsaicin (CAP) were examined in guinea pig papillary muscles using intracellular microelectrode technique. The results obtained are as follows: (1) the duration of action potential (APD) in normal papillary muscles was decreased by CAP (30, 60, 120 micromol/L) in a concentration-dependent manner; (2) in partially depolarized papillary muscles, 60 micromol/L CAP not only reduced APD, but also decreased the amplitude of action potential, overshoot and maximal velocity of phase 0 depolarization; (3) pretreatment with L-type Ca(2+) channel agonist Bay K8644 (0.5 micromol/L) could completely block the effects of CAP (60 micromol/L); (4) pretreatment with ruthenium red (20 micromol/L), a vanilloid receptor (VR) blocker, did not affect the actions of capsaicin on papillary muscles. All these results suggest that the effects of CAP on papillary muscles are likely due to a decrease in calcium influx which is not mediated by VR.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1996

Automatic identification of papillary muscles in left-ventricular short-axis echocardiographic images.

An automatic method for identifying the location of the papillary muscles in two-dimensional (2-D) short-axis echocardiographic images is described. The technique uses both spatial and temporal information to identify the presence and track the location of the muscles in the left ventricle from end-diastole to end-systole. The three main steps of the method are spatial preprocessing, spatial processing, and temporal processing. The spatial preprocessing step includes a region of search estimation. The spatial processing step includes a papillary muscle existence test and an initial approximation of the papillary muscle points. The temporal processing includes motion-pattern evaluation and final papillary muscle location. The estimates of existence and position for the automatic method were compared with estimates made by an independent expert observer. Two hundred and ten frames, three taken from each of 70 image sequences, were evaluated. Since two regions of search were processed for each frame (one for the posterior-inferior and one for the anterior-lateral papillary muscle), a total of 420 approximations were made. Of this total, 340 automatic estimates were judged to be in close agreement with estimates made by the expert. Of the remaining 80 approximations, 54 estimates were made by the expert when the computer determined that no papillary muscle was present, 17 estimates provided poor results, and nine estimates were made by the computer when the observer concluded that no papillary muscle was present.

Algorithms↗
PubMed1997

Induction of calcium-dependent action potentials by 4-aminopyridine in potassium depolarized guinea-pig papillary muscle.

Exposure of guinea-pig papillary muscle to 22 mM K+ resulted in loss of electromechanical excitability accompanied by an elevation of mean electrical threshold by 8.96 V and a membrane depolarization of about 47.3 mV. After setting the threshold to a new sensitive level for stimulation, 4-AP (1.25-5 x 10(-3) M) could restore both the propagated action potentials typical for Ca2+ (e.g. resting potential: -46 mV; action potential amplitude: 74.25 mV; upstroke velocity: 11.4 V/sec; abolition by Ca(2+)-channel blokers) and contractions to papillary muscle cells, with further elevation of resting potential from -51.2 mV to -46 mV. Restoration of electromechanical activity by 4-AP was dose-dependent and susceptible to blockade with D600 (5 x 10(-7) M). From these data, it was concluded that 4-AP restored electrical and mechanical excitability by increasing membrane conductance to Ca2+ (gCa2+).

4-Aminopyridine↗
PubMed1986

Contractile properties of papillary muscle from young cardiomyopathic hamsters: effects of isoprenaline.

Papillary muscles isolated from the left ventricle of 17-20 day old Syrian hamsters with genetic cardiomyopathy (BIO 14.6 strain) were examined for their mechanophysiological response to the beta adrenoceptor agonist isoprenaline. The indices of isometric twitch for both myopathic and aged matched normal (BIO RB strain) hamster papillary muscles were statistically the same before exposure to catecholamine. Isoprenaline, however, elicited an exaggerated degree of positive inotropism in myopathic papillary muscles. In addition, the characteristic relaxing effect of beta adrenoceptor agonists (abbreviation of twitch duration) was virtually absent in myopathic muscles. These results suggest that under conditions resembling sympathetic stimulation sarcolemma and perhaps sarcoplasmic reticulum become inadequate regulators of calcium, predisposing young myopathic heart cells to accrue damaging concentrations of sarcoplasmic calcium.

Animals↗
PubMed1989

Anatomic findings in acute papillary muscle necrosis.

To investigate the consequences of acute papillary muscle necrosis of the left ventricle, 25 cases from a total of 133 autopsies of acute myocardial infarction were studied. Cardiac hypertrophy was found in 84%. The anterior papillary muscle was involved in four cases, the posterior in 13, and both muscles in eight. Left ventricular subendocardial infarction was found in 32% of cases. The size of left ventricular necrosis ranged from 11% to 75% of the left ventricular mass. Associated right ventricular infarction was observed in 68%. There were 19 cases of cardiogenic shock, four cases of pulmonary edema, and two cases of sudden death. We conclude that papillary muscle necrosis is usually associated with cardiac hypertrophy, posterior necrosis of both ventricles, and subendocardial infarction. Acute mitral regurgitation is probably an important contributing factor to clinical impairment and death, mostly in cases of small necrosis.

Aged↗
PubMed2002

[Electrophysiological effects of phytoestrogen genistein on guinea pig papillary muscles].

The cardiac electrophysiological effects of genistein (GST) were examined in guinea pig papillary muscle using intracellular microelectrode technique. The results obtained are as follows. (1) Duration of action potential (APD) in normal papillary muscles was decreased by GST (10 100 micromol/L) in a concentration-dependent manner. (2) In partially depolarized papillary muscles, 50 micromol/L GST not only reduced APD, but also decreased the amplitude of action potential, overshoot and maximal velocity of phase 0 depolarization. (3) Pretreatment with N( )-nitro-L-arginine (L-NNA, 5 mmol/L) failed to affect the above effects of GST (50 micromol/L)on papillary muscles. (4) 17beta-estradiol (E(2), 5 micromol/L) or GST (10 micromol/L) alone did not affect action potential, while GST combined with E(2) at the same doses shortened APD significantly. All these results indicate that the effects of GST on papillary muscles are likely due to a decrease of calcium inflow which is not mediated by NO and that GST has a facilitative or synergetic action with E(2).

Action Potentials↗
PubMed1980

Systolic quick releases of nonexcised blood-perfused canine papillary muscle.

Systolic stiffness was studied in five coronary perfused twitching papillary muscles of canine right ventricles. The muscles beat at regular sinus rhythms at 37 degrees C. They were shortened quickly at about 10 muscle lengths/s in the middle of isometric contractions. Systolic force decreased exponentially with the shortening in the force-length diagram. Relating Lagrangian stress (sigma) and strain change (delta epsilon) relative to isometric length calculated from the force-length relationship curve during quick release, I found a linear relationship between ln sigma and delta epsilon. This indicates that the systolic stres-strain relationship of the canine papillary muscle can be approximated by an exponential curve, sigma = sigma m exp(k . delta epsilon), where sigma m = isometric stress at the onset of quick release. The mean +/- SE of the stiffness constant k was calculated to be 55 +/- 8 (dimensionless). These k values are greater than those of excised cat papillary muscles at 37 degrees C reported in literature. This difference in k values may be ascribed to the difference in the mechanical property of the uncut pinned end of the present preparation as opposed to the cut clamped end of the conventional preparation, although the canine and feline papillary muscles may simply have the different k values.

Animals↗
PubMed1981

Papillary muscle hypertrophy in chronic rheumatic mitral valve stenosis. A clinicopathologic study.

A quantitative pathologic study was performed on papillary muscles in 15 cases of chronic rheumatic mitral stenosis. The papillary muscles were grossly hypertrophied as compared with papillary muscles in 10 normal specimens. Hypertrophy of papillary muscles was associated with pronounced fibrosis. Angiographically, these hearts were remarkable in small left ventricular cavity with almost complete cavity elimination at end systole. Left ventricular wall dyskinesia was also present. It is probable that derangement of the mitral valve structure due to rheumatic process leads to more stress on the supporting elements, thus resulting in papillary muscle hypertrophy.

Adolescent↗
PubMed1999

Analysis of the atypical characteristics of adenosine receptors mediating negative inotropic and chronotropic responses of guinea-pig isolated atria and papillary muscles.

1. Adenosine receptor(s) mediating negative inotropy of paced left atria, isoprenaline-stimulated paced left atria and papillary muscles, and negative chronotropy of spontaneously beating right atria were characterized. 2. Isometric tension of guinea-pig isolated paced left atria and left ventricular papillary muscles and rate of contraction of spontaneously beating right atria were recorded. Papillary muscles were pre-stimulated with isoprenaline (1x10-8 M). Concentration-response curves (CRCs) for tension or rate reduction by N6-cyclopentyladenosine (CPA), the stereoisomers of N6-(2-phenylisopropyl)adenosine ((+)-PIA and (-)-PIA), 5'-(N-carboxamido)adenosine (NECA), N6-2-(4-aminophenyl)ethyladenosine (APNEA) and N6-(3-iodobenzyl)adenosine-5'-N-methyuromide (IB-MECA) revealed a potency order of CPA=(-)-PIA>NECA in right atria and papillary muscles, which is consistent with involvement of A1-receptors. The potency order in left atria was CPA=NECA>(-)-PIA>(+)-PIA>APNEA, which is not typical of A1 adenosine receptors. Weak activity of APNEA and IB-MECA discounts involvement of A3 receptors. 3. pA2 values for the antagonism of CPA by 8(p-sulfophenyl)theophylline (8-SPT) were calculated from Schild plots (log concentration-ratio against log 8-SPT concentration), the unity slopes of which indicated competitive antagonism. The pA2 value in the papillary muscles was significantly higher than for atrial preparations, indicating a possible difference in receptor characteristics between atrial and papillary muscle responses. 4. In left and right atria there was a limit to the displacement of the CPA CRCs at higher concentrations of 8-SPT. The 8-SPT-resistant component of the response is suggested to arise from duality of coupling of a common A1 receptor through either different G proteins or G protein subunits to independent transduction pathways. The results with papillary muscles can be explained by a typical A1 receptor coupled to a single transduction pathway.

Animals↗
PubMed1997

[A case of scheduled mitral valve replacement for mitral regurgitation caused by papillary muscle rupture after acute myocardial infarction].

Mitral regurgitation caused by papillary muscle rupture after acute myocardial infarction has poor prognosis, and it is the usual course for such cases in cardiogenic shock to be performed early mitral valve replacement. However, we recently experienced a case of successful scheduled mitral valve replacement for mitral regurgitation caused by rupture of the posterior papillary muscle after acute inferior myocardial infarction. The patient was a 63-year-old woman who admitted to a hospital with back pain and dyspnea and was diagnosed as pulmonary edema due to mitral regurgitation after acute myocardial infarction. She was treated with dopamine and diuretic agents effectively, but not weaned from these drugs. Then, she was transferred to our hospital. At the admission, she was in the NYHA class II due to mitral regurgitation and inferior myocardial infarction with papillary muscle rupture revealed by transesophageal echocardiography. Cardiac catheterization demonstrated total occlusion of the proximal right coronary artery (segment #2) and mitral regurgitation in Sellers III. The patient underwent a successful scheduled mitral valve replacement with SJM 27M concomitant with coronary artery bypass grafting 47 days after the onset of acute mitral regurgitation. There are few reports that successful surgical treatment for papillary muscle rupture was done more than 4 weeks after the onset of mitral regurgitation in Japan.

Female↗
PubMed2001

Effects of melittin on isolated papillary muscles of guinea pig.

AIM: To investigate the effect of melittin (Mel) on papillary muscles of guinea pigs. METHODS: Contraction of papillary muscles were examined by conventional method and action potentials (AP) were recorded by standard glass microelectrode technique. RESULTS: Mel (0.5, 3 micromol/L) significantly increased the contractility of guinea pig papillary muscles while 5 micromol/L exerted dual action with a transient decrease followed by an increase of the contractility. Mel shortened the functional refractory period (FRP) at concentrations of 0.5, 3, and 5 micromol/L and increased the automaticity induced by adrenaline (Adr) at 3 and 5 micromol/L. Mel shifted the duration-intensity curve upward at 3 micromol/L. It shortened the action potential duration (APD) of fast action potential (FAP), decreased the action potential amplitude (APA) and resting potential (RP) at 0.5 and 3 micromol/L. As to slow action potential (SAP), Mel 0.8 micromol/L shortened APD20 and APD50, and decreased APA and RP. CONCLUSION: Mel increased the contractility and automaticity of papillary muscles, shortened the FRP, decreased the excitability, shortened the APD, and decreased APA and RP of AP.

Action Potentials↗
PubMed1987

Ischemic myocardial necrosis and papillary muscle dysfunction in infants and children.

Ischemic myocardial and papillary muscle dysfunction has considerable implication in newborn infants and children with normal or malformed hearts. Papillary muscle dysfunction in adults primarily involves coronary artery occlusion and ischemic necrosis in the left ventricle and papillary muscles. Infants and children rarely develop coronary artery occlusion. Their myocardial dysfunction and injury occurs with nearly equal frequency in both ventricles as a result of underperfusion from a wide range of causes, including severe birth asphyxia, congenital heart disease, and complications of premature delivery. A history of cardiogenic shock, acute congestive heart failure with cyanosis and atrioventricular murmur, or persistent fetal circulation in a newborn without congenital heart disease should alert the pathologist to the possibility of ischemic myocardial necrosis (IMN). Older infants with ventricular hypertrophy, persistent pulmonary hypertension (PPHN), bronchopulmonary dysplasia (BPD), and those with malformed hearts involving severe ventricular hypertension due to outflow obstruction or pulmonary hypertension may have IMN, fibrosis, or dystrophic calcification alone or in combination. Animal models of adult ischemic cardiac injury may not be suitable for study of the newborn.

Cardiomyopathies↗