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At least 19 recordsLinked to original sources
PubMed1993

Scintigraphic recognition of papillary muscles and papillary muscle ischemia.

During stress thallium imaging, papillary muscles (anterolateral and posteromedial) appear scintigraphically as focal regions of enhanced activity in sites corresponding to their anatomic position. In the normal case, enhancement after exercise is greater than or equal to enhancement at rest. With papillary muscle ischemia, the involved papillary muscle demonstrates more enhanced activity at rest than at postexercise. This pattern change with papillary muscle ischemia was observed in four patients. Three cases demonstrated complete reversal of those ischemic changes after angioplasty and the remaining case failed to show any significant improvement after angioplasty.

Angioplasty, Balloon, Coronary↗
PubMed1981

Criteria for adequate oxygenation of isometric kitten papillary muscle.

Papillary muscles were taken from the right ventricles of hearts excised from chloroform-anesthetized kittens. Progressive 100-mmHg stepwise decreases in superfusate oxygen partial pressure (PO2) from control (95% O2 aeration, PO2, 620-650 mmHg) were produced, and subsequent changes in isometric active and resting tension were measured. If, under a given set of experimental conditions, the initial decrement in PO2 produced no decrease in active tensions development, it was concluded that complete oxygenation of the entire muscle cross section was achieved when bath PO2 was maximal. Accordingly, adequate muscle oxygenation during 95% O2 aeration occurred when temperature, stimulation rate, and mean muscle diameter were, respectively, 1) 37 degrees C, 30 beats/min, and 0.89 +/- 0.06 mm; 2) 30 degrees C, 30 beats/min, and 0.94 +/- 0.02 mm; and 3) 30 degrees C, 12 beats/min, and 1.15 +/- 0.09 mm. On the other hand, adequate oxygenation at either 30 or 37 degrees C was not demonstrable when rate was 60 beats/min and muscle diameter exceeded 0.60 mm. We conclude that very low stimulation rates are required for oxygen sufficiency unless the papillary muscle is extremely thin.

Animals↗
PubMed1985

Interaction between a normoxic and a hypoxic region of guinea pig and ferret papillary muscles.

Papillary muscles were mounted in a three-compartment bath. The tip of the muscle was exposed to hypoxic and glucose-free solution. The other parts of the preparation were superfused with Tyrode's solution, building a free-flow border between hypoxic and normoxic superfusates. The normoxic part of the bath was subdivided by a rubber membrane so that current pulses could be applied between segments of the preparation. Signs of electrotonic interaction between normoxic and hypoxic parts were observed a few minutes after the onset of hypoxia. Transmembrane action potentials in the normoxic part retained their plateau, but progressively shortened. Those in the hypoxic tip showed an early phase of rapid repolarization followed by a plateau phase near the resting potential. Terminal repolarization in the two parts coincided for many minutes. After 35 minutes, fast propagated activity ceased in the tip and was replaced first by conducted slow responses, then by decremental conduction. At 50 minutes, cells near the borderline had resting potentials of either -76 +/- 7 mV (SD, n = 9) in normoxic tissue or -16 +/- 3 mV (SD, n = 9) in hypoxic tissue. Concurrently, subthreshold potentials no longer appeared to spread into the tip. Unipolar electrograms remained diphasic over the normoxic part but lost their negative deflection near the borderline, implying the absence of axial current flow into the hypoxic part. Furthermore, electrotonic potentials generated by current flow across the rubber membrane did not spread beyond a line of demarcation. Reduced nicotinamide adenine dinucleotide fluorescence increased in the hypoxic part, and appeared to correlate with the development of electrical decoupling.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1977

[Biventricular massive infarction with rupture of a mitral papillary muscle and a tricuspid papillary muscle].

The authors report the case of a man of 62 who was admitted with a clinical and electrocardiographic picture of a posterior infarction which was very soon complicated by collapse and anuria. The findings on catheterisation of the right side of the heart were as expected. The cardiac index was very low, and the major abnormality was a type of adiastole with equal pressures in the right ventricle and the auricle of the right atrium. Despite an attempt to assist the circulation by an intra-aortic ballon, the patient died within a few hours. The postmortem examination confirmed the presence of a massive infarction of the left ventricle, but also of the right ventricle, together with rupture of the posterior papillary muscle of the mitral valve, and ischaemic rupture of one papillary muscle of the tricuspid valve.

Electrocardiography↗
PubMed1995

Papillary muscle perfusion pattern. A hypothesis for ischemic papillary muscle dysfunction.

BACKGROUND: The pathogenesis of posterior papillary muscle dysfunction is poorly understood. We hypothesized that papillary muscle perfusion pattern may explain the higher prevalence of posterior papillary muscle dysfunction after myocardial infarction. METHODS AND RESULTS: Twenty patients were monitored by transesophageal echocardiography during coronary surgery. Superselective coronary graft injections of 0.2 to 0.5 mL of sonicated albumin microbubbles were performed to assess graft patency and papillary muscle perfusion. Thirty-five graft injections were analyzed: 13 in the right coronary artery, 15 in an obtuse marginal branch, 1 in the left anterior descending coronary artery, and 6 in the first diagonal branch. The posterior papillary muscle was opacified in 16 patients, 11 from the right coronary artery and 5 from one obtuse marginal branch. In 10 of 16 patients (63%), the papillary muscle was perfused by one vessel, while in 6 of 16 (37%), it was perfused by two vessels. The anterior papillary muscle was opacified in 14 patients. Ten patients (71%) had double-vessel and 4 (29%) had single-vessel supply. In the subgroup of 10 patients with old inferior myocardial infarction, mitral regurgitation was present only among those 6 with single rather than double blood supply (P < .05). CONCLUSIONS: Myocardial infarction may cause papillary muscle dysfunction when the blood supply is provided by one rather than two vessels, as is more frequently the case with the posterior rather than the anterior papillary muscle.

Adult↗
PubMed2000

Thebesian sinusoids: forgotten collaterals to papillary muscles.

BACKGROUND: Papillary muscles of the left ventricle are prone to ischemic damage but seldom rupture, perhaps because they are protected by transendocardial diffusion and thebesian sinusoids as well as by arteries. Sinusoids are primitive vessels that precede coronary arteries as nutrient suppliers to all parts of the embryonic heart. OBJECTIVES: To determine whether sinusoids penetrate to the tips of papillary muscles. MATERIALS AND METHODS: Adult hearts with and without evidence of acute and chronic ischemic lesions were selected. Papillary muscle sinusoids were perfused by black ink from the apex of the left ventricle. Papillary muscles and the adjacent ventricular free walls were then excised and fixed before gross and microscopic examination for inked sinusoids. Some fixed specimens were cleared through methyl salicylate and examined stereoscopically. RESULTS: The meshwork of trabeculae and, importantly, intertrabecular spaces lining the apex of the left ventricle continue into the deeply undercut bases of papillary muscles. In most hearts, sinusoids can be shown to extend from the undercut bases to the tips of human papillary muscles, especially in ischemic hearts. The compact myocardium of the adjacent ventricular free wall contains few sinusoids. CONCLUSIONS: Sinusoids may supplement normal arterial flow to papillary muscles and mitigate the effects of coronary occlusion. The authors hypothesize that the apex of the human left ventricle is adapted for sinusoidal flow to papillary muscles.

Adult↗
PubMed1988

Ceftizoxime level in the myocardium (right atrial muscle and mitral papillary muscle) during open heart surgery.

We determined the level of sodium ceftizoxime (CZX) in the right atrium and mitral papillary muscle of 22 adults and 6 children undergoing open-heart surgery, 60 and 120 minutes after intravenous administration of this drug at the dosages of 2 grams for adults and 1 gram for children. The CZX level in the right atrial muscle after 60 minutes was 37.0 micrograms/g in adults and 51.0 micrograms/g in children. The CZX level in the papillary muscle of the mitral valve, determined at 120 minutes was 16.9 micrograms/g. In the present study, we measured the level of the antibiotic CZX in the myocardial tissue during open-heart surgery. The purpose of this was to determine the quantity in which the antibiotic is taken into the myocardial tissue.

Adult↗
PubMed1998

[The expression of proliferating cell nuclear antigen and alpha smooth muscle actin in papillary muscles of the patient with rheumatic heart disease and its significance].

OBJECTIVES: To reveal the change of chronic rheumatic cardiomyocyt phenotype and its relationship with myocardium fibrosis. METHODS: The papillary muscles samples were obtained from patients with rheumatic heart disease during mitral valve replacement. Normal papillary muscles samples obtained from adult and fetal heart during autopsy in control group. The specimens were examined using immunohistochemistry and immunoelectron microscopy observation with monoclonal antibody of antiproliferating cell nuclear antigen (PCNA) and anti-alpha smooth muscles actin (alpha-SMA), and imaging analysis was performed. RESULTS: The interstitial fibrosis (24.7% +/- 3.05%) and the ratio between inner and outer diamater of arteriolas (0.405 +/- 0.035) in rheumatic myocardium were higher significantly than those in normal myocardium. Immunohistochemical PCNA expression was not only in interstitial but also in hypertrophic cardiomyocytes of rheumatic heart disease. The positive expression in rheumatic myocardium increased. There were a lot of rough endoplasmic reticula, ribosomes and Golgi bodies in cytoplasm of PCNA and alpha-SMA positive cells. The degree of PCNA and alpha-SMA positive expression was increased with enlargement of fibrosis areas. CONCLUSIONS: There is not only a high expression of PCNA and alpha-SMA in the myocardium of patients with rheumatic heart disease but also in fetal myocardium. We suggested that pathological myocardial cells are constructive phenotype and synthetive phenotype. PCNA and alpha-SMA positive expression cells are in the proliferating stage, they take part in fibrotic progress and vascular reconstruction in the myocardium.

Adult↗
PubMed2003

Quantitation of papillary muscle function with tissue and strain Doppler echocardiography measures papillary muscle contractile functions.

UNLABELLED: It is well known that papillary muscle dysfunction may cause mitral regurgitation, however, there is not a standard technique to measure the papillary muscle function. The aim of this study is to investigate papillary muscle function by using tissue and strain rate Doppler echocardiography. METHOD: A study group (SG) of 42 patients (12 females, 30 males, mean age: 53.8 +/- 10.9 years) with coronary artery disease who have segmental left ventricular dysfunction and mitral regurgitation, and as a control group (CG) 20 patients (6 females, 14 males, mean age 52.5 +/- 10.2 years) who have no coronary artery disease and mitral regurgitation were studied. A subgroup 20 patients (7 females, 13 males, mean age 42.5 +/- 7.5 years) who have rheumatic mitral regurgitation was included to the study. The patients who have left ventricular and mitral annular dilatation were not included into the study. Longitudinal wall motion of mid-inferior segment (one point) and posterior papillary muscle (two point) of the left ventricle was assessed by tissue and strain rate Doppler echocardiography from the apical two-chamber view. Systolic tissue velocity (Sm), strain rate (SR), and strain (S) were measured from the two points in all patients. RESULTS: Comparing the one point values Sm, SR, and S were found less in SG than CG (respectively 4.2 +/- 1.4 vs 11.3 +/- 1.9 cm/sec, -1.0 +/- 0.4 vs -1.7 +/- 0.3 s-1, -13.5 +/- 5.0 vs -18.1 +/- 3.9%; P < 0.001 for all). Comparing the two point values Sm, SR and S were found less in SG than CG (respectively 2.8 +/- 1.2 vs 3.7 +/- 2.0 cm/sec, -0.8 +/- 0.4 vs -1.6 +/- 0.3 s-1, -9.7 +/- 4.6 vs -15.8 +/- 3.7%; P < 0.001 for all). Systolic mitral annulus, left ventricular systolic and diastolic dimensions were similar in two groups. Comparing the CG and subgroup, there were no significant differences with respect to Sm, SR, and S measured from the two points. CONCLUSIONS: Papillary muscle function may be assessed quantitatively by using tissue and strain rate Doppler echocardiography. Tissue velocity, strain rate, and strain values were found decreased in dysfunctional papillary muscle.

Adult↗
PubMed1975

Papillary muscle dynamics: in situ function and responses of the papillary muscle.

Experiments were designed to 1) study in situ changes in papillary muscle length and force during the cardiac cycle, 2) investigate the relationship between papillary muscle length and maximal ventricular pressure, 3) study the effect of both positive and negative inotropic intervention on this relationship. A mercury gauge transduceror Walton-Brodie strain-gauge arch was sutured to the anterior papillary muscleand used to measure the extent of shortening or lengthening (deltaL) or force (APMF),.respectively. The anterior papillary muscle showed rapid increase of length and forcewhile contracting during isovolumic contraction and reached peak systolic length at end-isovolumic contraction or during the early injection phase. The papillary muscle was observed to shorten during the phases of ejection and isovolumic relaxation. It was concluded that changes in ventricular pressure during the cardiac cycle are associated with changes in papillary muscle length and force such that the resulting "lengthening contraction force" is appropiate for maintenance of normal atrioventricular valve function during isovolumic contraction. There was an inverse relationship between deltaL and maximal ventricular pressure such that for each increment in peak ventricular pressure there was a decrease in deltaL. The deltaL-force relationship was shifted upward and to the right by norepinephrine (NE) and isoproterenol and downward and to the left by occlusion of the posterior vena cava. Phenylephrine had little or no effect on this relationship.

Animals↗
PubMed1975

Sarcomere length-tension relations in living rat papillary muscle.

Small papillary muscles about 2 mm long and 0.2 mm thick were dissected from the right ventricles of 16-19 day-old rats. Resting (between twitches) and active (at twitch peaks) striation patterns were photographed in living muscles using a light microscope. External muscle length was varied from Lmax, the length at which peak twitch tension was maximum, to 0.75Lmax, the length at which peak twitch tension was about 10% of maximum. Resting and active tension versus muscle length curves were similar to those obtained from other papillary muscle preparations. Resting average sarcomere length at Lmax was about 2.23 mu; it decreased with decreasing muscle length in the range between Lmax and 0.75Lmax. Near 0.75Lmax, resting average sarcomere length was about 1.5-1.6mu. Considerable internal shortening occurred during contractions, and the active average sarcomere lengths measured at the twitch peaks were less than the resting values. At Lmax, the active average sarcomere length was 1.98mu. At 0.75Lmax, there was only about a 3-6% decrease in average sarcomere length at the twitch peaks. However, at external muscle lengths between Lmax and 0.75Lmax more internal shortening was present than there was at Lmax, since average sarcomere length decreases of about 15% were observed. The finding that peak active tension decreases as sarcomere length decreases below about 2.0mu suggests that some of the factors limiting force generation at short lengths in skeletal muscle may also limit it in mammalian cardiac muscle.

Animals↗
PubMed2006

Unusual anomalous single papillary muscle causing symptomatic mid-left ventricular cavity obstruction: octopus papillary muscle.

This report describes a patient with an unusual large anomalous papillary muscle within the left ventricular cavity causing symptomatic midventricular outflow obstruction. The obstructing papillary muscle comprised a large central core that extended multiple circumferential muscular arms to all the walls of the left ventricle, including the septum. The papillary muscle and the arms divided the left ventricle into apical and subaortic chambers. Flow communicated between the two chambers through multiple openings between the arms with a systolic peak Doppler gradient of 50 mm Hg.

Adult↗
PubMed2000

[A surgical case of papillary muscle reconstruction and double-CABGs for mitral regurgitation due to ruptured papillary muscle after myocardial infarction].

A 76-year-old female patient underwent papillary muscle reconstruction, and d-CABGs a month after the onset of myocardial infarction. Posterior papillary muscle (PPM) was recognized to be ruptured partially, its stump was sewn to original PPM. An ePTFE suture (CV 5) was placed from anterior mitral leaflet to anterior papillary muscle in attempt to reinforce PPM-repair. Carpentier-Edwards ring was inserted and d-CABGs (LITA to LAD and GEA to RCA) were performed, simultaneously. Postoperative examination revealed no regurgitation and no stenosis of bypass grafts during follow-up period of 5 months after the procedure. Papillary muscle reconstruction was effective procedure for MR due to the ruptured papillary muscle.

Aged↗
PubMed2001

Traumatic papillary muscle rupture.

Papillary muscle rupture caused by blunt chest trauma is a relatively rare cause of mitral incompetence. To date only 25 cases of surgically corrected posttraumatic mitral regurgitation have been reported, of which only eight resulted from rupture of the anterolateral papillary muscle.

Adult↗
PubMed1998

Collagenous skeleton of the human mitral papillary muscle.

The papillary muscles (PM) of the heart have been the subject of numerous structural and functional studies. However, despite the importance of the collagenous compartment of the heart in the mechanical and electrical properties of the myocardium, little information is available on the structural organization of collagen within the PM. We study here the structural organization of collagen within the mitral papillary muscles (PM) of the human heart. Fragments of human mitral PM from normal and hypertensive subjects were macerated in NaOH to eliminate the cellular components. Macerated and nonmacerated samples were then studied with the scanning electron microscope (SEM). SEM shows that cardiac myocytes and endomysial capillaries are ensheathed in a layer of collagenous tissue. The myocyte sheath wall is formed by thin collagen fibers oriented at right angles to the main cell axis. These sheaths are open structures, collagen fibers continuing into adjacent sheaths at the points of lateral communications. Thick perimysial septa do not divide the PM tissue into separate compartments. Hypertensive hearts show perivascular and interstitial fibrosis. In addition, the lumen of the coronary vessels is reduced or obliterated, and large areas of the myocardium are substituted by densely packed collagen. Endomysial sheaths constitute a continuous collagenous layer that replicates the myocyte network. The endomysium should play a complex role in myocardial mechanics, assuring the equal distribution of force during the cardiac cycle. The absence of insulating boundaries should facilitate lateral propagation of excitation. Fibrosis in hypertensive hearts appears to be both reactive and reparative. The increase in the amount of collagen should greatly impair contractile capabilities and electrical conductance, severely compromise heart function, and contribute to development of heart failure.

Aged↗
PubMed2004

[Papillary muscle rupture].

Papillary muscle rupture (PMR) is a rare, but catastrophic mechanical complication of acute myocardial infarction (AMI). Patients with PMR present in acute pulmonary edema and commonly in cardiogenic shock. The absence of new heart murmur after AMI dose not exclude the diagnosis. To diagnose PMR accurately, transesophageal echocardiography is the most useful and essential, coronary angiography is also necessary for appropriate surgical treatment. Based on these results of diagnostic procedure, combined myocardial revascularization and mitral operation should be performed without delay. Although mitral valve repair has the effects of improving left ventricular function, repairing could be undertaken successfully in limited cases, such as ruptured muscle tissue is not friable. If repair is technically more challenging, mitral valve replacement should not be hesitated. Postoperative early and late survival may relate to surgical correction of coronary artery revascularization, especially in multivessel disease, concomitant coronary artery bypass grafting is benefit theoretically and should be performed.

Cardiac Surgical Procedures↗