SEARCH · PubMed Health

Results for “Papillary Muscles”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources

PubMed1984

Electrophysiological effects of alpha-adrenoceptor antagonists in rabbit sino-atrial node, cardiac Purkinje cells and papillary muscles.

The effects of prazosin, labetalol, and medroxalol were studied in the rabbit sino-atrial node, Purkinje cells and papillary muscles. At concentrations producing similar bradycardia, labetalol and medroxalol reduced the maximum rate of depolarization (Vmax) and overshoot potential in the sinus node. Prazosin had no such effects. These large and highly significant reductions in Vmax and overshoot in sinus node cells were observed at concentrations of medroxalol and labetalol which had no negative inotropic effect. If depolarization in the sinus node was due to the second inward current, this would imply that such currents in the sinus node and contracting cardiac muscle are pharmacologically distinct. All three drugs prolonged action potential duration in the sinus node, Purkinje cells and papillary muscles in a dose-related manner. Recovery after 1 h in drug-free solution from the effects of medroxalol and labetalol was only partial in the sinus node, but almost complete in Purkinje cells and papillary muscle. Recovery from prazosin was complete in all tissues. All three drugs depressed Vmax in Purkinje cells and papillary muscles in a dose-related manner, and recovery was complete. It is concluded that all three drugs had class 1 and class 3 antiarrhythmic actions, which could contribute to their protective effects in ischaemia and reperfusion independently of blockade of myocardial alpha-adrenoceptors.

Action Potentials↗

PubMed1995

Effect of perfusion pressure on diastolic stress-strain relations of isolated rat papillary muscle.

The effect of perfusion on diastolic muscle properties was investigated in six isolated right ventricular papillary muscles from rat hearts perfused with a crystalloid solution via the septal artery. Stress-strain relations were obtained at different perfusion pressures. Increased perfusion pressure caused an increase of stress at large strains but a decrease of stress at low strains. Thus stress-free strain increased with increasing perfusion pressure. Stress-strain relations of a given muscle at different perfusion pressures (range 12-122 cmH2O) intersected at a single "crossover" strain. Muscle stiffness, defined as the slope of the stress-strain relation, increased at all strains. Muscle diameter measurements indicated that the observed changes of the stress-strain relation occurred in association with vascular filling rather than with formation of edema. To explain the findings, the papillary muscle was modeled by two parallel compartments: muscle cells (together with the extracellular matrix) and vasculature. Perfusion was assumed to have an effect on the axial vascular properties but not on muscle cells. Combination of the stress-strain data of the muscle compartment and the vascular compartment (taken from literature) predicted stress-strain relations similar to those obtained in our perfused papillary muscles. We conclude that increased muscle stiffness at increased perfusion pressure is mainly caused by pressure-dependent changes in mechanical behavior of the vascular compartment.

Animals↗

PubMed1998

[A case report of infective endocarditis with total rupture of the posterior papillary muscle after aortic valve replacement].

We reported a case with severe mitral regurgitation caused by total rupture of the posterior papillary muscle two days after aortic valve replacement. A 62-year-old man was transferred to our hospital with high fever and dyspnea with severe aortic regurgitation caused by infective endocarditis. The left heart failure occurred suddenly two days after the initial operation. Echocardiogram revealed massive mitral regurgitation and rupture of the posterior papillary muscle. He underwent emergent mitral valve replacement. Histological examination of the papillary muscle showed typical ischemic necrosis without inflammation. The postoperative course was uneventful. We suggested the papillary muscle rupture in this case may be due to coronary artery emboli occurred in association with infective endocarditis.

Aortic Valve↗

PubMed2005

[Papillary muscle rupture due to acute myocardial infarction followed by cardiogenic shock, pulmonary edema, and acute renal failure].

AIM: The case of successfull surgical treatment of anterolateral papillary muscle rupture due to acute myocardial infarction with cardiogenic shock, pulmonary edema and acute renal failure. CASE REPORT: A 62-year old male from Belgrade with chest pain, hypotension and a new heart murmur refused hospitalization at the Military Medical Academy. On the third day of his illness he was readmitted to MMA as an emergency due to hemoptysis. Examination revealed mitral valve anterolateral papillary muscle rupture. The patient, with signs of cardiogenic shock and acute renal failure, was immediately operated on. The surgery was performed using extracorporeal circulation. An artificial mitral valve was implanted, and myocardial revascularization accomplished with one venous graft of the left anterior descending artery. On the second postoperative day, hemodialysis was carried out due to acute renal failure. On the 28th postoperative day, the patient was discharged from the hospital being hemodynamically stable with normal renal function and balanced anticoagulation. The case is interesting in terms of unrecognized papillary muscle rupture that led to the development of cardiogenic shock, hemoptysis and acute renal failure. CONCLUSION: Papillary muscle rupture is a fatal complication of acute myocardial infarction. Early recognition and urgent surgical intervention were life-saving in the case of complete papillary muscle rupture. Surgical treatment, regardless of high risk, is the procedure of choice.

Acute Kidney Injury↗

PubMed1984

Effects of fentanyl and nitrous oxide on contractility of blood-perfused papillary muscle of the dog.

The effects of fentanyl, nitrous oxide, and their combination on myocardial contractility were investigated in the papillary muscle preparation perfused by a donor dog. With a conscious donor, fentanyl infused directly into the arterial blood perfusing the papillary muscle produced a dose-related depression of developed tension. However, blood concentrations of fentanyl required to obtain the depression were in the range of 30-120 micrograms/ml. The ED50 for fentanyl for suppression of papillary muscle contractility was 89 +/- 9 micrograms/ml. When the donor dog was given nitrous oxide (N2O,80% and O2,20%), the developed tension of the papillary muscle decreased 25 +/- 5%. Fentanyl administered during nitrous oxide anesthesia caused a decrease in developed tension that was not significantly different from that obtained without N2O anesthesia (18 +/- 4% vs 13 +/- 4% for 30 micrograms/ml, and 61 +/- 5% vs 58 +/- 4% for 100 micrograms/ml). The results suggest that fentanyl produces a direct negative inotropic effect only in concentrations that are 2-3 orders of magnitude higher than its blood concentrations in fentanyl-induced anesthesia. When fentanyl and nitrous oxide are used together their interaction is not significantly different from additive.

Animals↗

PubMed1976

[Mechanical activity of the papillary muscles of the rat heart under high altitude conditions].

Mechanical activity of isolated papillary muscles in the left ventricle of rats was studied during permanent high altitude adaptation. The main computer parameters were: maximal developing tension, force of contraction, and capacity of papillary muscles at different periods of mountain adaptation (3, 15, 30 and 45 days). On the 15th day of mountain exposure, a statistically significant increase of maximal developing tension and papillary muscles activity was observed, which remained until the 45th day. Capacity was considerably increased on the 30th--45th day of adaptation. The data suggest positive effect of high altitude hypoxia on inotropic function of intact myocardium.

Actomyosin↗

PubMed1990

Single papillary muscle and ostium primum defect.

Parachute mitral valve (single papillary muscle) is commonly associated with complete atrioventricular (AV) canal. We report a case of ostium primum defect associated with single papillary muscle.

Echocardiography, Doppler↗

PubMed1990

Endothelin has no positive inotropic effect in guinea-pig atria or papillary muscle.

Endothelin is a recently discovered, highly potent vasoconstrictor peptide. In isolated atria from rat and guinea-pig, endothelin has been reported to elicit a positive inotropic effect. The purpose of the present study was to compare the effects of endothelin on electromechanical coupling in guinea-pig atrial and ventricular muscle. In isolated, electrically driven specimens of atria and papillary muscle, action potentials and isometric contractions were recorded in the basal state and 30 min following non-cumulative exposure to endothelin (100 nM). In the atria, endothelin reduced action potential overshoot and relaxation velocity, and increased resting tension. In the papillary muscle the peptide slightly shortened the duration of the action potential. Endothelin did not affect peak tension, either in the atria or in the papillary muscle. These data contrast with earlier reports on a positive inotropic effect of endothelin in guinea-pig atria.

Action Potentials↗

PubMed1998

Effect of papillary muscle position on mitral valve function: relationship to homografts.

BACKGROUND: We used a finite element model to determine the effect of papillary muscle position on the stress distribution in the mitral valve. METHODS: A normal model was modified to move the posteromedial papillary muscle outward by either 2.5 mm or 5.0 mm. Next, the thickness was increased by 20%, simulating diseased tissue. Physiologic loading pressures were applied, and leaflet stress, chordal stress, and coaptation results were analyzed. RESULTS: Displacement of the posteromedial papillary muscle increased the leaflet stresses and altered the normal stress patterns. The displacement also restricted the leaflets from closing completely, allowing regurgitation. Combining increased thickness with papillary displacement decreased the stresses slightly. However, the amount of leaflet coaptation was further decreased, creating larger gaps for regurgitation. In all models, the stresses in the chordae were increased in the marginal chordae and decreased in the basal chordae, demonstrating a transfer of stress. CONCLUSIONS: Papillary muscle displacement creates abnormal valve stresses, and the potential for significant regurgitation. Papillary-chordal-leaflet geometry must be maintained in partial or complete mitral homograft replacement.

Blood Pressure↗

PubMed2004

Left ventricular outflow tract obstruction due to anomalous insertion of papillary muscle.

A 56-year-old man who complained of quadrantic hemianopsia was admitted to determine its etiology. Cerebral angiography revealed no organic stenosis. Echocardiography showed clear direct continuity between a hypertrophied anterolateral papillary muscle and the anterior mitral leaflet, and the left ventricular (LV) outflow tract (LVOT) was narrowed by the presence of an accessory papillary muscle. The LVOT obstruction caused an intra-LV pressure overload that resulted in LV concentric hypertrophy. Arrhythmia, such as paroxysmal atrial fibrillation (PAF), was thought to have caused a cerebral embolism. Mitral valve replacement (MVR), septal myectomy, and myectomy of the abnormal papillary muscle were performed, and complete release of the LVOT obstruction was accomplished. Anomalous insertion of papillary muscle is a rare cause of LVOT obstruction. Echocardiography was useful in identifying the papillary muscle malformation, and surgery was completely curative.

Cerebral Infarction↗

PubMed2006

The connection between the papillary muscles and leaflets of the tricuspid valve.

The tricuspid valve is more differentiated during evolutionary development than the mitral valve. In birds it is a muscular structure joined directly to the papillary muscles, although the mitral valve of birds resembles that of mammals. There have been well-known studies describing the evolutionary line of connection of the tricuspid valve with the papillary muscles. The present study was performed on a group of 107 formalin-fixed adult human hearts. The valves and papillary muscles were classified according to a scheme for human hearts drawn up earlier. The types of connection between leaflets of the tricuspid valve and the papillary muscles were classified according to a scheme drawn up earlier for vertebrates. We observed 3 types of connection between leaflets of the tricuspid valve and the papillary muscles in the group studied. The muscular and membranous connections were not linked with any one type of tricuspid valve. Atypical forms of distribution of the tendinous chords of the right ventricle were observed. It was found that valves with a higher number of leaflets were (with the exception of type 0) provided with a smaller number of tendinous chords. Atavistic features and atypical forms of distribution of the tendinous chords are present in a small percentage of samples of the human right valvular apparatus.

Adolescent↗

PubMed1985

Ruptured papillary muscle, a complication of myocardial infarction: clinical presentation, diagnosis, and treatment.

Ruptured papillary muscle due to myocardial infarction was encountered in 14 patients during the period 1975-1983. Five of the 14 patients had a history of angina pectoris and two had a history of prior myocardial infarction. Eleven patients with myocardial infarction developed additional pain due to myocardial ischemia and/or a murmur of mitral regurgitation and pulmonary edema within a week, 3 others had a prolonged course with intermittent pain due to myocardial ischemia and breathlessness for longer periods and then deteriorated. Thirteen of our 14 patients developed a murmur and all but one had pulmonary edema on the chest x-ray. Five patients had infarction patterns on the electrocardiogram, the remainder of the patients had only ST- and T-wave changes. Echocardiograms showed fine flutter and notching of the anterior mitral leaflets and vigorous contractions of the left ventricle. Only one patient was demonstrated to have a papillary muscle tip prolapsing into the left atrium on two-dimensional echocardiography. Twelve patients underwent surgery and 8 survived. Seven patients had single-vessel coronary disease, 4 involving the circumflex system and 3 involving the right coronary system. Four of the 7 patients with single-vessel coronary disease survived surgery. Five patients went to surgery with the intra-aortic balloon pump in place and only 3 survived. Three others had the pump inserted intraoperatively and 2 of these survived. Six of 9 patients who had mitral valve replacement and coronary bypass survived. Ejection fraction ranged from 40 to 79%. Surgical survival did seem to be related to the extent of papillary muscle rupture, with the best results occurring in the group with a small portion of the tip ruptured. Seven patients had a stormy clinical course and required surgery within 10 days of rupture. Four of these 7 survived. It seems reasonable to believe that these patients who often have small infarction and limited coronary disease have good potential for survival. Our approach has been to move toward surgery once the diagnosis is made to avoid the sudden deterioration that frequently occurs. The surgical mortality in this group remains in the 30 to 40% range.

Aged↗

PubMed1979

Effects of 2-nicotinamidoethyl nitrate (SG-75) on dog coronary artery and cat papillary muscle.

Effects of 2-nicotinamidoethyl nitrate (SG-75) on isolated dog coronary artery and cat papillary muscle were investigated. SG-75 dose-dependently relaxed the isolated coronary arterial strips contracted with potassium. Large doses of SG-75 depressed contraction of papillary muscle driven with electrical stimulation and inhibited enhancement of contraction of papillary muscle induced by calcium and isoproterenol. From these results it is suggested that SG-75 may have a weak Ca++-antagonistic action.

Animals↗

PubMed1986

Electrophysiologic effects of papillary muscle traction in the intact heart.

In this study we used transmural multipolar electrodes, sonomicrometers implanted within the left ventricular wall, and cardiac electrical stimulation techniques to examine the effect of transient mechanical posterior papillary muscle traction on local myocardial electrophysiologic characteristics. Nine open-chest dogs were atrially paced (cycle length 400 msec) followed by insertion of timed premature extrastimuli at left ventricular epicardial pacing sites either in the vicinity of (traction zone) or remote from (nontraction zone) the site of papillary muscle traction. Electrophysiologic recordings were made before and during periods of intermittent papillary muscle traction of predetermined timing, application rate (25 cm/sec), and duration (170 msec). Papillary muscle traction was applied in late diastole just before the last beat of each atrial drive train. In seven of nine dogs application of transient papillary muscle traction resulted in significantly earlier local ventricular activation (mean activation advancement 30 +/- 13 msec), altered QRS morphology of the last conducted atrial drive-train beat, and relative prolongation of ventricular functional refractory period in the traction zone. Conversely, in nontraction zones in these seven dogs, early activation did not occur and refractoriness remained unchanged as tested by a locally placed extrastimulus. In two of nine dogs traction failed to induce early activation and changes in refractoriness did not occur. Alterations in regional myocardial blood flow (assessed by radioactive microsphere technique) did not appear responsible for the observed changes, since there was no demonstrable traction-induced difference in regional blood flow between the traction and nontraction zones.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1998

Clinical experiences of surgical repair for mitral regurgitation secondary to papillary muscle rupture complicating acute myocardial infarction.

Mitral regurgitation secondary to ischemic heart disease carries a significant mortality even after emergency open heart surgery. From 1993 to 1997, four patients were operated on for ischemic mitral regurgitation secondary to papillary muscle rupture. These patients were between 58 and 69 years of age and all were in class III or IV of the New York Heart Association Classification. The responsible infarction area was located in the lateral wall in 2 patients, and inferior in others. The interval between the onset of acute myocardial infarction and the appearance of mitral regurgitation was from 1 to 10 days. Three patients had partial rupture (defined as only one or several heads of papillary muscle ruptured), and one had total papillary muscle rupture. Primary mitral plasty was performed in 3 patients, including 1 patient who had undergone patch closure of ventricular septal perforation at the onset of acute myocardial infarction. Mitral plasty combined with coronary artery bypass grafting was performed in 1 patient. Only one case, who had total papillary muscle rupture, required reoperation for recurrence of mitral regurgitation. We suggest that even in the case of ischemic mitral regurgitation, when a papillary muscle rupture is partial, mitral repair is performed because of its potential for improving therapeutic results.

Aged↗

PubMed1997

Prolonged ejection duration helps to maintain pump performance of the renal-hypertensive-diabetic rat heart: correlations between isolated papillary muscle function and ventricular performance in situ.

OBJECTIVE: The purpose of this study was to examine the degree to which mechanical alterations in left ventricular papillary muscles of renal hypertensive-diabetic rat hearts correlate with functional measurements made on the same hearts in situ. METHODS: Female Wistar rats weighing 170-200 g were made hypertensive by placing a 0.24 mm clip on the left renal artery, and made diabetic 1 week later by a single intravenous injection of streptozotocin (60 mg/kg). Approximately 3-5 months later hemodynamic measurements including left ventricular pressure and dP/dtmax, arterial pressure and aortic flow were made on control and hypertensive-diabetic hearts in situ and correlated with mechanical measurements in left ventricular papillary muscles isolated from the same hearts. Body and tissue weights and biochemical and histological measurements were made at the time of sacrifice. RESULTS: Hypertensive-diabetic rats which survived to the time of study had decreased body weights, increased left ventricular weights and increased right ventricular weight to body weight and lung weight to body weight ratios. Those rats which died before the scheduled in-situ measurements had significantly more severe hypertension, greater left ventricular hypertrophy, increased right ventricular and lung weights, and more interstitial fibrosis than either surviving hypertensive-diabetics or controls. Rates of isometric tension development (normalized) and relaxation as well as shortening and relaxation velocities were significantly depressed in papillary muscles from hypertensive-diabetic rat hearts despite unchanged developed tension and peak shortening. Time to peak tension and time to peak shortening were markedly prolonged. Mean aortic flow was maintained in the hypertensive-diabetic group despite significant depression of left ventricular dP/dtmax (normalized), peak aortic flow, peak aortic flow acceleration and heart rate. There was also significant depression of left ventricular-dP/dtmax. Ejection duration was markedly prolonged and correlated with both time to peak shortening in vitro and with stroke volume in vivo. CONCLUSIONS: Surviving hypertensive-diabetic rats were not in overt congestive heart failure; nevertheless, their hearts showed abnormal contractile performance which was qualitatively and quantitatively similar to that of left ventricular papillary muscles obtained from them. Depression of peak aortic flow, peak aortic flow acceleration and heart rate in the hypertensive-diabetic group was offset by increased ejection duration, resulting in normal mean aortic flow. The close correlation of ejection duration with time to peak shortening of the isolated papillary muscles suggests that it is a manifestation of an intrinsic change in the myocardium. To the extent that this prolongation is already maximized, further decreases in contractile speed would be expected eventually to cause depressed pump function and congestive heart failure. The possibility that this sequence of events occurred in the dying animals needs to be examined by evaluating in-vitro and in-vivo myocardial function at various stages of this disease model.

Animals↗

PubMed1988

Morphometry of right ventricular papillary muscle in rat during development and regression of hypoxia-induced hypertension.

Morphometric analyses of the right ventricular papillary muscle, as well as measurements of right ventricular pressure and weight, were carried out in the rat during the development and recovery of hypoxic pulmonary hypertension. Animals were divided into hypoxic and normobaric control groups. The hypoxic rats were placed in hypobaric chambers for 1, 2, and 3 wks; and after 3 wks exposure, subgroups of hypoxic rats were allowed to recover in normoxia for 1 to 9 wks. Hematocrit (HCT) and right ventricular systolic pressure (RVSP) were measured prior to sacrifice. The heart was perfused, and the right ventricle (RV) was separated from the left ventricle and septum (LV+S) and weighed. The papillary muscles were dissected and processed for ultrastructural morphometry. Results showed that HCT, RVSP, and RV weight increased in the rats during the hypoxic exposure and then gradually returned to control levels after 3 to 4 wks of normobaric recovery. The papillary muscle of the hypoxic rats showed increased volume density of interstitium, increased diameter and cross sectional area of the cardiac myocytes, reduced volume density of mitochondria, and reduced mitochondria to myofilament ratio. During normoxic recovery, these morphometric indices returned toward control values at various periods of time ranging from less than 3 wks to 9 wks. The results indicate that the adaptive ultrastructural changes of the papillary muscle in RV hypertrophy paralleled the RVSP changes, and also demonstrate the reversibility of these changes in ambient oxygen.

Animals↗

PubMed1985

[Features of the angioarchitectonics of the papillary muscles and the chordae tendineae of the human heart].

In persons of mature, elderly and old age vascularization of the papillary muscles and tendinous chordae in the right and left cardiac ventricles has been studied depending on peculiarities of their structure and sources of their blood supply using injection, macro-microscopical, roentgenoangiographic methods, and silver nitrate impregnation. Certain data concerning the distribution zones in the papillary muscles of the coronary artery branches at various types of the cardiac blood supply are presented. Angioarchitectonics of the papillary muscles are described along their whole extention--in the basal area, in the middle part and at the apex. Architectonic peculiarities of the blood vessels in the muscular-tendinous part of the papillary muscles and in some tendinous chordae are described.

Adult↗