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PubMedDate not supplied

Papillary muscle rupture caused by bacterial endocarditis: role of transesophageal echocardiography.

A 22-year-old man had severe pulmonary congestion and required mechanical ventilation. Endocarditis was suspected because a 2/6 systolic murmur was heard at the apex and because Osler nodes were present. Transthoracic and transesophageal echocardiography allowed correct diagnosis of papillary muscle rupture causing massive mitral regurgitation. To our knowledge, this is the first reported case of papillary muscle rupture caused by bacterial endocarditis diagnosed by transthoracic and transesophageal echocardiography.

Adult↗
PubMed1997

[A successful surgical repair of congenital mitral stenosis due to commissural papillary muscle fusion].

A case of congenital mitral stenosis, patent ductus arteriosus, pulmonary hypertension was reported. At one year of age, the patient underwent surgical division of PDA because of persistent left heart failure. She went well after the operation. At seven year of age, she was readmitted to our hospital for easy fatigability. The cardiac catheterization revealed remarkably elevated pulmonary arterial pressure and pulmonary capillary wedged pressure. She underwent a surgical intervention for the mitral stenosis at eight year of age. At operation, the mitral valve exhibited the characteristics of type IIc according to Carpentier's classification: thickened and dysplastic leaflet, extremely short chordae tendanae fused with papillary muscles, obliteration of interchordal space and hypertrophic two papillary muscles. We replaced the valve with 23 mm Carbomedicus prosthetic valve because it seemed to be difficult to repair the native valve satisfactorily without residual stenosis or insufficiency. Her postoperative course was uneventful and the pulmonary arterial pressure and pulmonary capillary wedged pressure decreased remarkably one year after the operation.

Child↗
PubMed2002

The inotropic effect of nitric oxide on mammalian papillary muscle is dependent on the level of beta1-adrenergic stimulation.

We tested the hypothesis that nitric oxide has a positive inotropic effect on mammalian cardiac muscle contractility and that this effect sums with the positive inotropic effect of beta1-adrenergic agonists when both are present. Feline right ventricular papillary muscles were stimulated to contract isometrically at 0.2 Hz in Krebs-Henseleit bicarbonate buffer (KREBS) gassed with 95% O2 and 5% CO2 (26 degrees C; pH 7.34). The nitric oxide (NO) donor, S-nitroso-N-acetylpenicillamine (SNAP, 10(-5) M), and the membrane permeable cGMP analog 8-bromoguanosine-3',5'-cyclophosphate sodium (Br-cGMP, 10(-5) M), significantly increased developed force by 13.3+/-1.5% (n = 11) and 7.8+/-2.8% (n = 7), respectively. SNAP, at 10(-5) M, significantly increased the force developed by papillary muscle treated with 10(-11) M or 10(-9) M dobutamine hydrochloride (a beta1-adrenergic agonist) (n = 25, 11.3+/-2.9% and 10.0+/-3.6%, respectively) when compared with the addition of KREBS (n = 27, 2.6+/-0.9% and 5.5+/-0.9%), but the increase was less than predicted by the sum of inotropic effects of SNAP and dobutamine. SNAP at 10(-5) M did not change developed force in muscles treated with 10(-7) M dobutamine but it significantly decreased developed force in muscles challenged with 10(-5) M dobutamine (n = 18, 29.3+/-5.0%) when compared with KREBS (n = 10, 41.5+/-6.8%). Similarly, 10(-4) M 8-bromo-adenosine cyclic 3',5'-hydrogen phosphate monosodium (a membrane permeable cAMP analog) increased developed force 14.9+/-3.3% and the addition of 10(-5) M Br-cGMP to those muscles significantly reduced developed force by 3.5%+/-1.1% (n = 7). Thus, the positive inotropic effect of NO decreased and ultimately became an attenuation as the level of beta1-adrenergic stimulation increased due at least in part, to an interaction between the cAMP and cGMP second messenger pathways.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1993

Cellular electrophysiological effects of hyperthermia on isolated guinea pig papillary muscle. Implications for catheter ablation.

BACKGROUND: The primary mechanism of tissue injury by radiofrequency catheter ablation is presumed to be thermally mediated. However, the myocardial cellular electrophysiological effects of hyperthermia are not well characterized. We used an in vitro model of isolated guinea pig right ventricular papillary muscle to investigate the acute cellular electrophysiological effects of hyperthermia. METHODS AND RESULTS: Excised guinea pig right ventricular papillary muscles were pinned in a high-flow tissue bath and superfused with Tyrode's solution at 37.0 +/- 0.5 degrees C. The superfusate temperature was rapidly changed to 38.0 to 56.0 degrees C for 60 seconds and then returned to 37.0 degrees C. Conventional microelectrodes were used to measure membrane potential (Vm), maximum rate of rise of the action potential (dV/dtmax), and action potential (AP) amplitude and AP duration at 50% (APD50) and 90% (APD90) repolarization. Hyperthermia resulted in (1) a progressive depolarization of Vm at temperatures > or = 40.0 degrees C, which became more prominent at temperatures > or = 45.0 degrees C; (2) changes in the AP characterized by a temperature-dependent increase in dV/dtmax and a temperature-dependent decrease in AP amplitude, APD50, and APD90; (3) reversible loss of cellular excitability within a temperature range of 42.7 to 51.3 degrees C (median, 48.0 degrees C); (4) irreversible loss of cellular excitability and tissue injury at temperatures > or = 50.0 degrees C; and (5) the development of abnormal automaticity at temperatures > 45.0 degrees C. CONCLUSIONS: Hyperthermia causes significant changes in myocardial cellular electrophysiological properties that include membrane depolarization, reversible and irreversible loss of excitability, and abnormal automaticity. There appear to be specific temperature ranges for reversible and irreversible electrophysiological changes. These observations may have important implications for tissue temperature monitoring during radiofrequency catheter ablation.

Animals↗
PubMed1994

Endocardial endothelium selectively modifies relaxation in rat papillary muscle.

The selective removal of endocardial endothelium of rat left ventricular papillary muscles by 1-second immersion in 0.5% Triton X-100 showed little influence on resting tension and only a small decrease in peak isometric tension (8.3 +/- 1.4 vs 9.6 +/- 2.4 mN/mm2 at Lmax, p > 0.05) with no reduction in maximal rate of tension development (+dT/dtmax; 136 +/- 21 vs 137 +/- 18 mN/mm2/s, p > 0.05). In contrast, there was a marked increase in maximal rate of tension decline (-dT/dtmax) from 71 +/- 14 to 92 +/- 15 mN/mm2/s (p < 0.05), so that the ratio between +dT/dtmax and -dT/dtmax fell from 1.98 +/- 0.27 to 1.51 +/- 0.13 (p < 0.01). Removal of endocardial endothelium led to a significant shortening of isometric twitch contractions. Time to peak tension was abbreviated from 111 +/- 20 to 84 +/- 8 ms (p < 0.05) and the half relaxation time from 92 +/- 9 to 68 +/- 8 ms (p < 0.01). Time to +dT/dtmax was also shortened from 31 +/- 6 to 44 +/- 9 ms (p < 0.05) and time to -dT/dtmax from 90 +/- 12 to 62 +/- 10 ms (p < 0.01). These effects were not influenced by alterations in stimulation frequency or muscle length. The early onset of relaxation and abbreviated duration of relaxation together with an increased rate of decline in tension led to a shorter total twitch which may explain the slightly lower peak tension once the endocardial endothelium was removed. Our findings confirm that endocardial endothelium modulates myocardial contraction, with a predominant influence on relaxation.

Analysis of Variance↗
PubMed1998

[The effect of antibodies on the Ca2+ release from the sarcoplasmic reticulum of the papillary muscle of the rat heart].

In experiments of skinned with saponin papillary muscles (PM) of the rat's heart we studied the effects of antibodies (AB), which are specific for the sarcoplasmic reticulum's membranes (SPR). AB (1-5 mg protein/ml) have been established to enhance the amplitude of the isometric PM tension. Inhibition of the Ca2+ release from SPR and its previous release prevented the development of the exciting effect of AB. Thus, AB increase the amplitude of PM contraction due to their intracellular mobilizing action.

Animals↗
PubMed2001

[Isolated left ventricular papillary muscle rupture: a rare event after blunt thoracic trauma].

We report about a 20-year old man, who suffered from a car accident under the influence of ecstasy. Although he had no visible injuries at the chest, the accident caused an isolated rupture of a papillary muscle of the mitral valve. A review of the literature shows the rarity of this kind of injury. The mechanisms of traumatic papillary muscle rupture, the diagnosis, therapy and complications are discussed.

Accidents, Traffic↗
PubMed1994

Hypertrophic obstructive cardiomyopathy in combination with anomalous insertion of papillary muscle directly into anterior mitral leaflet and "sawfish" systolic narrowing of the left anterior descending coronary artery.

This report describes an unusual case of subaortic stenosis in which hypertrophic obstructive cardiomyopathy was found in combination with both anomalous insertion of papillary muscle directly into the anterior mitral leaflet and "sawfish" systolic narrowing of the left anterior descending coronary artery. Definitive diagnosis was made on operation. We freed the left anterior descending coronary artery by incising the muscular bridge, resected both papillary muscles, and replaced the mitral valve.

Adult↗
PubMed2002

Papillary muscles identified by myocardial contrast echocardiography in preparation for percutaneous transluminal septal myocardial ablation.

In patients with hypertrophic obstructive cardiomyopathy (HOCM), percutaneous transluminal septal myocardial ablation (PTSMA) supplemented by myocardial contrast echocardiography (MCE) can provide a therapeutic benefit. We report a 33-year-old woman with HOCM in which MCE revealed a septal branch artery supplying the postero-medial papillary muscles. Thus, PTSMA was aborted because of the risk of acute mitral regurgitation secondary to papillary muscle dysfunction.

Adult↗
PubMed1997

Comparison of patients with and without papillary muscle rupture during acute myocardial infarction.

Seventeen of 31 patients with papillary muscle rupture (PMR) were admitted with a >24-hour delay since onset of acute myocardial infarction (AMI) in contrast to 81 of 1,012 with AMI without cardiac rupture; in 8 of 11 patients with in-hospital PMR it was preceded by new anginal pain in 5 and/or by strenuous exercise in 4; mortality was higher in those with anterior PMR, previous infarction, or 3-vessel disease than in those without PMR. Thus, persistence of physical activity before or during hospitalization, as well as postinfarction ischemia/infarct extension, appear to be relevant triggers of PMR, whereas mortality is more often associated with existence of a previous infarction, 3-vessel disease, and/or anterior PMR.

Aged↗
PubMed2001

Regional myocardial function at the papillary muscle insertion site.

The importance of the mitral apparatus to the global left ventricular (LV) function has been suggested in several clinical studies. One recent study reported that chordal transsection induced an unloading of myocardium at the papillary muscle insertion site. We hypothesized that the regional response for afterloading at this site with intact mitral apparatus was different from that at the free wall. We investigated the end-systolic pressure-regional segment length relations (ESPLR) in two anterior LV sites, free wall (FREE) and the papillary muscle insertion site (PAP), during an increasing afterload by aortic occlusion in 7 anesthetized open-chest dogs. To measure the regional segment length at FREE and PAP, two sets of the pair of sonomicrometer crystals were implanted in the same midwall depth at the same circumferential hoop by using an echocardiographic guide. ESPLR both at FREE and PAP were always highly linear in a physiological range (r > or = 0.9). The slope of this relation at FREE (274 +/- 164 mmHg/mm) was significantly steeper than that at PAP (157 +/- 118 mmHg/mm) for each dog (p < 0.05). These data indicate that the regional response for afterloading at PAP loaded by chordal tension is different from that at FREE in the same heart.

Animals↗
PubMed2002

Original histologic findings in arteries of the right ventricle papillary muscles in human hearts.

In this study we describe original histologic findings of the right ventricle papillary muscle (PM) arteries in people under 30 years old. We examined 666 samples taken from the tip, mid-portion, and base of the PM in 56 males and 55 females, as well as samples from the rest of the right ventricle. The amount of smooth muscle cell (SMC) fibers in the tunica media (TM) led to their division into three groups: Group 1: 351 samples (53%); normal amount, normal lumen. The amount of SMCs increased from the tip (20%) to the base (48%). Group 2: 226 samples (34%); mild to moderately increased amount of SMCs, with narrowness, eccentric displacement, and uneven lumen shape. They decreased from the tip (42%) to the base (23%). Group 3: 89 samples (13%), with abundant SMCs that duplicated the arterial size, contrary to the other two groups. Their shape was round and their extremely narrow, centrally located lumen had a round or oval shape. These changes were restricted only to PM arteries and decreased from the tip (65%) to the mid-portion (35%). This type of artery predominated compared to the other two groups, probably because of the narrow lumen. No inflammatory reaction or chronic ischemic changes were found in the PM and its arteries. The SMC changes in groups 2 and 3 were found in subjects older than 2 months. The above findings will provide anatomists, cardiologists, and physiologists with valuable knowledge.

Adolescent↗
PubMed2004

Assessment of papillary muscle function using myocardial velocity gradient derived from tissue Doppler echocardiography.

Papillary muscle (PM) function is vital to mitral valve competence. However, quantitative assessment of the function is difficult due to the complexity of the mitral apparatus. We hypothesized that myocardial velocity gradient (MVG) could be applied to assess PM function. We studied MVG-PM in 123 patients with left ventricular dysfunction (ejection fraction <40%) and 123 normal subjects throughout a systolic phase. MVG-PM in normal subjects was significantly higher than in patients with left ventricular dysfunction (3.6/s vs 1.4/s, p <0.001). MVG-PM reached its peak at early systole and correlated well with PM thickening (r = 0.89). MVG-PM in patients with left ventricular dysfunction correlated with the severity of apical tenting of the mitral valve (y = 0.8x - 0.07, r = 0.72). Patients with lower MVG-PM tended to have less severe mitral regurgitation (y = 0.03x + 0.3, r = 0.83). PM contractility can be quantitatively assessed by calculating the MVG derived from tissue Doppler imaging. PM dysfunction, indicated by lower MVG-PM, decreased mitral leaflet tethering, thus paradoxically decreasing mitral regurgitation severity. MVG is a useful tool in determining the role of PM in functional mitral regurgitation.

Aged↗
PubMed1997

Action potential duration and contraction after rest at room temperature in guinea pig papillary muscle.

Simultaneous recordings of action potential and isometric tension of right papillary muscles were performed. After regular stimulation at 1 Hz, pauses of 10 min were allowed. In the first beat after rest, we measured action potential duration at the 90% of the repolarization (APD90), maximal twitch tension (T), time to peak of contraction (TTP), and rate of development of tension (+dT/dt) and relaxation (-dT/dt). Values were normalized against pre-rest ones. No significative changes were observed after rest at 35 degrees C. After rest at 25 degrees C APD90 and TTP were prolonged but T was reduced. Post-rest +dT/dt were slower, dT/dt did not show significative changes. Nifedipine 10 microM prevented post-rest APD90 lengthening, and produced a further reduction of mechanical response. Substitution of external Na+ by Li+ shortened APD90, increased T of either regular or post-rest beats and led to calcium overload signs. When pause were allowed during Na+ substitution, calcium overload signs were attenuated. We conclude that the combination of rest and room temperature diminished [Ca++]i mainly by Na+/Ca++ mechanism. The reduction of [Ca++]i in turn could delay the inactivation of iCa. As a consequence, longer APs were obtained, accompanied by weaker and slower mechanical responses. Changes in TTP and + dT/dt could suggest that post-rest contractions in room temperature, are dependent of extracellular Ca++ rather than a deplected RS.

Action Potentials↗
PubMed1981

Effects of diethyl-stilboestrol on contractile response and action potential of rabbit papillary muscle.

The effects of diethyl-stilboestrol (DES) were studied on isolated papillary muscles from rabbits (37 degrees C). The preparation was paced at a frequency of 0.67 Hz and the muscle length was adjusted to 95% of the length of optimum force production. Membrane potentials and the isometric force production were recorded. DES (10 microM) reduced peak isometric force by 44.5% (mean of 6 preparations) and maximum rate of force development was reduced to approximately the same degree. The time to peak force, the time from peak force to half relaxation and the action potential duration were not significantly affected by DES. The results are consistent with the idea that DES reduces the calcium influx during the cardiac action potential without significantly influencing the calcium reuptake during relaxation. The data are compared to the effects of DES on uterine and skeletal muscles and the differences in metabolism of activator calcium in different kinds of muscles are discussed.

Action Potentials↗
PubMed2005

[Mitral valve replacement for mitral regurgitation caused by papillary muscle head rupture complicating acute myocardial infarction: report of a case].

A 71-year-old female was admitted for acute posterolateral infarction. On the next day of the successful emergency perctaneous coronary intervention, she developed severe dyspnea and was intubated at intensive care unit. Massive mitral regurgitation was detected on color Doppler imaging and left ventricular cardiac failure was increasingly developed. The urgent operation was performed for papillary muscle rupture 18 days after first episode. Head rupture of the posterior papillary muscle was found during surgery and the mitral valve was replaced by a prosthetic valve (SJM # 25). The postoperative course was uneventful and she discharged on 52 days after surgery.

Aged↗
PubMed1989

[Effects of FeSO4 on electrical and mechanical activity of guinea pig papillary muscles].

FeSO4 0.1-0.7 mmol/L shortened the action potential duration, decreased the action potential amplitude (APA) and maximal upstroke velocity of 0 phase (Vmax), and reduced the contractile force of myocardium in a concentration-dependent manner. FeSO4 0.2 mmol/L depressed the APA and Vmax of papillary muscles in Tyrode's solution containing MnCl2 3 mmol/L, and reduced the APA, Vmax and duration of slow action potentials in potassium-depolarized papillary muscles. These results suggest that Fe2+ may inhibit the transmembrane movement of Ca2+ and Na+ in myocardial cells. This may be one of the mechanisms of heart failure and circulatory collapse in acute iron poisoning.

Action Potentials↗