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PubMed1987

[Papillary muscle infarction: echocardiographic features and genetic factors].

To study the pathogenesis of papillary muscle infarction, its echocardiographic features were examined in 60 patients with old inferior infarction. Sixty-three healthy elderly persons served as the controls. 1. The papillary muscles were echocardiographically classified as fingerlike and non-fingerlike in configuration whose frequencies were 43% and 57%, respectively. In healthy subjects, the papillary muscles were less echogenic than the left ventricular wall. 2. In five patients, the posteromedial papillary muscle exhibited enhanced echo intensity and no contraction. The papillary muscles in two of these five patients were histologically examined and the diagnosis of papillary muscle infarction was verified. In these five patients, the papillary muscles were echocardiographically classified as fingerlike, and left ventricular infarction was observed to involve the attachment of the posteromedial papillary muscle. All five patients had mitral valve prolapse; posterior in four and anterior in one. Inferior infarction extended to the region just beneath the mitral annulus in the former four patients, but not in the latter one. 3. The echocardiographic features of papillary muscle infarction consisted of enhanced echo intensity of the papillary muscle and mitral valve prolapse, especially that of the posterior leaflet at the posteromedial commissural side, and extension of the asynergy region to the attachment portion of the papillary muscle. The fingerlike morphology of the papillary muscle and involvement of the attachment within the infarcted region are predispositions to the development of papillary muscle infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

[Surgical management of papillary muscle rupture following acute myocardial infarction].

Papillary muscle rupture is a rare but severe complication of acute myocardial infarction. Two cases successfully underwent mitral valve replacement and concomitant coronary artery bypass grafting (CABG) for acute myocardial infarction with the anterior papillary muscle rupture in cardiogenic shock. Each of them needed preoperative massive inotropic infusion, respiratory support and intraaortic balloon pumping assist. The first case was a 76-year-old female. Double vessel disease (seg 7 : 90%, seg 11 : 100%) was revealed by coronary angiography and rupture of the papillary muscle was confirmed by transesophageal echocardiography. The second case was a 69-year-old female. Double vessel disease (seg 2 : 90%, seg 11 : 100%) was revealed and severe mitral regurgitation due to prolapse of the anterior leaflet was confirmed by transthoracic echocardiography. To assess the diagnosis of postinfarction papillary muscle rupture, transthoracic and/or transesophageal echocardiography is mandatory. Coronary angiography is also desirable because concomitant myocardial revascularization may improve the prognosis.

Aged↗
PubMed1991

Caffeine rapid cooling contractures and negative force staircase in rat papillary muscle.

In rat papillary muscle, rapid cooling causes membrane depolarization which initiates action potentials that lead to a contraction. This rapid cooling contraction (RCC) can be blocked by TTX, Mn2+, Ni2+ or high K+ superfusion. In the presence of caffeine (0.5-1 mM), the rapid cooling contracture (caffeine-RCC) has an amplitude similar to that of a twitch elicited by field stimulation at 37 degrees C, but is not inhibited by these agents. As the caffeine-RCC appears to be independent of membrane depolarization and Ca influx but can be inhibited by increasing the bathing caffeine concentration to 20 mM, we consider that the amplitude of this contracture gives a good indication of the calcium content of the sarcoplasmic reticulum (SR). In Tyrode containing 1.8 mM Ca an increased stimulus frequency leads to a negative force staircase which is paralleled by a similar decrease in the amplitude of the caffeine-RCC. These effects are lost if the bathing Ca is reduced (0.18-0.45 mM) in a way which can be reversed by isoproterenol (100 nM). In verapamil (2 microM), however whilst the twitch responses may show a steeper dependence upon stimulus frequency, the negative frequency dependence of the caffeine-RCC is also lost. Low external Na+ also inhibits the frequency dependent reduction of the caffeine-RCC. The results suggest that if the amplitude of the caffeine-RCC is a good indication of the SR calcium content, then this Ca store is related reciprocally to membrane Ca current where activation of the Ca channels leads to a depletion of the store whereas inhibition of membrane Ca channels leads to a filling of the Ca store. We propose that on stimulation the size of the Ca influx determines the fraction of Ca released from the SR. This released Ca may be partially extruded from the cell by way of the Na/Ca exchange which acts in competition with the re-uptake mechanism of the SR to control SR Ca content.

Action Potentials↗
PubMed1986

Calcium and thiopental-induced spontaneous activity in rabbit papillary muscle.

Isolated rabbit papillary muscles exposed to 20 to 30 mg/l of thiopental developed spontaneous contractile activity. The spontaneous activity often appeared following the cessation of high frequency stimulation. The maximum rate of spontaneous beating decreased in parallel with the force of contraction when the extracellular Ca2+ concentration was lowered or when ryanodine, an inhibitor of sarcoplasmic reticular function, was added. Stretching of the muscles increased the incidence of thiopental-induced spontaneous activity. These results suggest that intracellular Ca2+ influences thiopental-induced spontaneous activity, analogous to arrhythmias associated with afterdepolarization.

Animals↗
PubMed1989

Developmental changes in the electrophysiologic properties of rabbit papillary muscles.

We studied the electrophysiological properties of adult (AD) and newborn (NB) rabbit papillary muscles in vitro with superfusion of normal Tyrode's solution, solutions with elevated [K+]o, and in solutions with various concentrations of tetrodotoxin. In control solutions, the NB papillary muscles had a more negative resting membrane potential (-83.6 +/- 1.2 versus -80.0 +/- 1.5 mV), a higher rate of rise of phase 0 (134 +/- 5 versus 120 +/- 5 V/S) and a higher, longer-lasting action potential plateau than the AD papillary muscles. Exposure to elevated [K+]o led to a significant post-repolarization refractoriness in AD papillary muscles that was more than that for NB papillary muscles even when NB papillary muscles were depolarized to the same resting membrane potential as the AD papillary muscles. The NB papillary muscles were comparatively resistant to tetrodotoxin in terms of percent reduction of conduction velocity and percent rise in the current threshold for excitation. The conduction velocity for AD papillary muscles in control solution (66 +/- 6 cm/s) was more than for NB papillary muscles (44 +/- 4 cm/s), which would not be expected from the data on the rate of rise of the action potential, suggesting that the cable properties of NB papillary muscles (specifically a greater surface to volume ratio of the ventricular cells) are also significantly different from the AD papillary muscles.

Action Potentials↗
PubMed1994

Receptor mediated presynaptic modulation of the release of noradrenaline in human papillary muscle.

OBJECTIVE: The aim was to determine the presynaptic modulation of noradrenaline (NA) release from the sympathetic nerve terminals in human isolated papillary muscle. METHODS: Papillary muscle and the right atrial appendage were obtained from operations on 22 patients (10 men and 12 women). The papillary muscle preparations were preincubated with [3H]NA and the release of [3H] at rest and in response to field stimulation was measured. RESULTS: Using an immunohistochemical method dopamine-beta-hydroxylase-positive neurones were found in the papillary muscle and right atrial appendage sample. The release of noradrenaline from the papillary muscle, associated with axonal activity, was enhanced by 7,8(methylenedioxy)-14-alpha-hydroxyalloberbane HCl (CH-38083), a selective alpha 2 adrenoceptor antagonist, and inhibited by xylazine, an alpha 2 adrenoceptor agonist, indicating that negative feedback modulation was functioning. In addition, the release of [3H]NA was enhanced by atropine, pancuronium, and 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP), a selective M3 muscarinic receptor antagonist, and reduced by oxotremorine, a selective muscarinic receptor agonist, indicating that acetylcholine released from the parasympathetic nerve ending was able to reach the varicose noradrenergic axon terminals that are equipped with inhibitory M3 muscarinic receptors. CONCLUSIONS: These findings, obtained for the first time in human papillary muscle, indicate that the release of noradrenaline is modulated by alpha 2 autoreceptors activated by noradrenaline and M3 muscarinic heteroreceptors. Thus during parasympathetic stimulation the release of noradrenaline from the sympathetic axon terminals is presynaptically controlled through muscarinic receptors.

Adrenergic beta-Antagonists↗
PubMed1965

CAT HEART MUSCLE IN VITRO. VI. POTASSIUM EXCHANGE IN PAPILLARY MUSCLES.

The exchange of cell K with K(42), J(K), has been measured in cat right ventricular papillary muscle under conditions of a steady state with respect to intracellular K concentration. Within the limits of the measurement, all of cell K exchanged at a single rate. Cells from small cats are smaller and have larger surface/volume ratios than cells from large cats. The larger surface/volume ratio results in larger flux values. J(K) increases in an approximately linear manner as the external K concentration is increased twentyfold, from 2.5 to 50 mM, at constant intracellular K concentration. The permeability for K ions, P(K), calculated from the influx and membrane potential, remains very nearly constant over this range of external K concentrations. J(K) is not affected by replacement of O(2) by N(2), or by stimulated contractions at 60 per minute, but K influx decreases markedly in 10(-5)M and 10(-8)M ouabain.

Cats↗
PubMed2006

Considerations on the left papillary muscles microangioarchitecture.

The aim of the present study was to bring macroscopic and microscopic evidence on the left papillary muscles blood supply in human hearts. For the study were used human adult hearts from patients without clinically known cardiac ischemic history. Ten hearts were used for injecting China ink in the coronary arteries and other twenty hearts were dissected to evidence the characteristics of the main arteries of the left papillary muscles. Pieces - left papillary muscles - were drawn from the injected hearts and diaphanised. In all dissected hearts the left anterolateral papillary muscles were supplied by the left coronary system: anterior interventricular artery, second diagonal branch and left (obtuse) marginal artery. In 70% the left posteromedial papillary muscles were supplied by the right coronary system (posterior interventricular artery, left retroventricular artery) and in 30% by the left coronary system (circumflex artery). The left papillary muscles were supplied each by one or two main arteries that penetrated the muscles longitudinally. The ventricular wall attaching the papillary muscles was supplied by the subepicardial vessel sending the main arteries of the papillary muscles but also by neighbor subepicardial vessels distributed in that wall. The mural vessels were finer than the papillary muscles main arteries. Injected papillary muscles presented each with two systems of blood perfusion: one represented by segmental centers of arterial branching and distribution of the main arteries of the muscle and other represented by capillary extensions of the mural networks at that level. From the segmental branching centers were perfused the neighbor segments of the papillary muscles and intrasegmental anastomoses were recognized. The microvascular study of the left papillary muscles proves the usual overlapping of sources for segmental supply; this overlapping is reinforced by the high capillary density to ensure the vascularisation of the papillary muscles.

Adult↗
PubMed2001

[Spontaneous rupture of the papillary muscle with angiographically normal coronary vessels].

Papillary muscle rupture is an unusual pathology, commonly being a mechanical complication of an acute myocardial infarction or a blunt chest trauma. In this case report we describe a patient with a spontaneous complete posteromedial papillary muscle rupture, secondary to an isolated papillary muscle infarction, in the absence of coronary artery disease, resulting in severe mitral regurgitation, cardiogenic shock and uneventful urgent mitral valve replacement. The clinical and histopathologic literature, and mechanisms to explain this kind of rupture, are reviewed.

Aged↗
PubMed1993

Two-dimensional echocardiographic assessment of papillary muscle contractility in patients with prior myocardial infarction.

OBJECTIVES: This study was performed to assess the length and contractile performance of human left ventricular papillary muscles and to determine the relation between papillary muscle dysfunction and mitral regurgitation. BACKGROUND: Assessment of human papillary muscle contractility remains a clinical challenge. METHODS: Two-dimensional echocardiographic examinations were performed in 16 normal subjects and 31 patients with prior myocardial infarction. Apical echocardiograms were used to obtain long-axis views of the anterior and posterior papillary muscles. The end-systolic and end-diastolic lengths of the papillary muscles were measured and fractional shortening was calculated. RESULTS: Fractional shortening in normal subjects was 27 +/- 8% for the anterior papillary muscle and 30 +/- 8% for the posterior papillary muscle. In patients with prior myocardial infarction, a significant decrease in fractional shortening was observed in proportion to the severity of left ventricular wall motion abnormalities at the site of papillary muscle implantation. Moderate or severe mitral regurgitation was significantly more frequent in patients with combined anterior and posterior papillary muscle dysfunction than in those with isolated anterior or posterior dysfunction or with normal function of both papillary muscles (p < 0.05). CONCLUSIONS: Two-dimensional echocardiography is useful for demonstrating abnormal contractility of human left ventricular papillary muscles. Papillary muscle contractility should be analyzed in each case to elucidate the mechanism of mitral regurgitation in patients with papillary muscle dysfunction.

Adult↗
PubMed1996

Comparison of cleft and papillary muscle position in cleft mitral valve and atrioventricular septal defect.

Differentiation of cleft mitral valve from atrioventricular septal defect (AVSD) is surgically important because of different conduction pathways. The purpose of this study was to find echocardiographic markers for differentiating cleft mitral valve from AVSD. We examined 11 children with cleft mitral valve, 11 children with AVSD, and 11 normal children. We defined a fixed reference point (0 degrees of arc) at the medial junction of the right ventricular free wall with the posteroinferior ventricular septum. Left ventricular papillary muscle and cleft position was measured clockwise in degrees of arc from 0 degrees around a point representing the center of the left ventricle in the parasternal short-axis views. Mural leaflet size was expressed by the arc between the bases of the papillary muscles. Papillary muscle position in cleft mitral valve was similar to that in normals (anterolateral ventricular papillary muscle:cleft mitral valve 194 +/- 10 degrees, normals 191 +/- 8 degrees; posteromedial ventricular papillary muscle:cleft mitral valve 329 +/- 10 degrees, normals 329 +/- 14 degrees). In AVSD, both left ventricular papillary muscles originated closer to each other and were rotated counterclockwise (anterolateral papillary muscle: 182 +/- 7 degrees; posteromedial papillary muscle: 287 degrees +/- 17 degrees). The mural leaflet size was similar in cleft mitral valve and in normal children. In AVSD, the mural leaflet was significantly smaller than in cleft mitral valve and in normals. The cleft position did not permit distinction between cleft mitral valve and AVSD. In conclusion, echocardiographic measurements of papillary muscle position and mural leaflet size permit differentiation of cleft mitral valve from AVSD.

Child↗
PubMed1969

The ultrastructure of the cat myocardium. I. Ventricular papillary muscle.

The ultrastructure of cat papillary muscle was studied with respect to the organization of the contractile material, the structure of the organelles, and the cell junctions. The morphological changes during prolonged work in vitro and some effects of fixation were assessed. The myofilaments are associated in a single coherent bundle extending throughout the fiber cross-section. The absence of discrete "myofibrils" in well preserved cardiac muscle is emphasized. The abundant mitochondria confined in clefts among the myofilaments often have slender prolongations, possibly related to changes in their number or their distribution as energy sources within the contractile mass. The large T tubules that penetrate ventricular cardiac muscle fibers at successive I bands are arranged in rows and are lined with a layer of protein-polysaccharide. Longitudinal connections between T tubules are common. The simple plexiform sarcoplasmic reticulum is continuous across the Z lines, and no circumferential "Z tubules" were identified. Specialized contacts between the reticulum and the sarcolemma are established on the T tubules and the cell periphery via subsarcolemmal saccules or cisterns. At cell junctions, a 20 A gap can be demonstrated between the apposed membranes in those areas commonly interpreted as sites of membrane fusion. In papillary muscles worked in vitro without added substrate, there is a marked depletion of both glycogen and lipid. No morphological evidence for preferential use of glycogen was found.

Animals↗
PubMed1981

Incomplete mitral leaflet closure in patients with papillary muscle dysfunction.

Clinical acceptance of an association between papillary muscle dysfunction and mitral regurgitation is widespread, despite the lack of objective support. To evaluate a possible association, we performed echocardiographic examinations on 22 patients with prior myocardial infarction and clinical evidence of papillary muscle dysfunction, 40 patients with prior myocardial infarction and no clinical evidence of papillary muscle dysfunction, and 20 normal subjects. There was a unique pattern of incomplete mitral leaflet closure in a high percentage (91%) of infarct patients with mitral regurgitation. In these patients, one or both leaflets were effectively arrested within the cavity of the left ventricle during ventricular systole. Dyskinetic wall motion in the region immediately surrounding one of the papillary muscles was present in 23 of 24 patients (96%) with demonstrated incomplete closure. This study provides the first objective evidence that de novo mitral regurgitation in patients with prior myocardial infarction is due to dyskinesis involving the left ventricular myocardium beneath one of the papillary muscles, producing increased tension on the mitral leaflets and preventing normal closure.

Aged↗
PubMed1994

Preconditioning in isolated superfused rabbit papillary muscles.

Preconditioning has only been demonstrated in arterially perfused myocardium. Our aim was to develop a model of preconditioning in isolated, superfused, isometrically contracting rabbit right ventricular papillary muscle. This would eventually allow us to evaluate isolated human muscles. Papillary muscles were suspended in an organ bath, superfused with oxygenated Tyrode solution, and field stimulated at 1 Hz. Muscles were assigned either to control or to preconditioning groups. Preconditioning was induced with 3 min of rapid pacing (3 Hz) with substrate-free hypoxic buffer and was followed by 15 min of reoxygenation with substrate. Subsequently, both groups were exposed to 45 min of substrate-free hypoxia followed by 120 min of reoxygenation with substrate. Preconditioning protected the myocardium with better recovery of developed force (50.6 +/- 6.7 vs. 27.4 +/- 4.2% of baseline developed force, P < 0.01). This effect could be blocked by 8-(p-sulfophenyl)theophylline (SPT) given during preconditioning at a dose that did not increase hypoxic damage in controls (percent developed force compared to baseline: preconditioned muscles + SPT = 30.9 +/- 2.8% and control muscles + SPT = 27.1 +/- 2.3%). In addition, pretreatment with (-)N6(2-phenylisopropyl)adenosine similarly protected the myocardium (49.5 +/- 5.5% recovery, P < 0.01). We conclude that isolated superfused muscles can be preconditioned. This preconditioning does not depend on coronary flow and involves activation of adenosine receptors.

Animals↗
PubMed1965

CAT HEART MUSCLE IN VITRO. 8. ACTIVE TRANSPORT OF SODIUM IN PAPILLARY MUSCLES.

The cells of cat right ventricular papillary muscles were depleted of K and caused to accumulate Na and water by preincubation at 2-3 degrees C. The time courses of changes in cellular ion content and volume and of the resting membrane potential (V(m)) were then followed after abrupt rewarming to 27-28 degrees C. At physiological external K concentration ([K](o) = 5.32 mM) recovery of cellular ion and water contents was complete within 30 minutes, the maximal observable rates of K uptake and Na extrusion (Deltammol cell ion/(kg dry weight) (min.)) being 3.4 and 3.6, respectively. The recovery rate was markedly slowed at [K](o) = 1.0 mM. Rewarming caused V(m) measured in cells at the muscle surface to recover within from <1 to 9 minutes, but only slight restoration of cellular ion contents (measured in whole muscles) had occurred after 10 minutes. Studies of recovery in NaCl-free sucrose Ringer's solution made it possible to separate the ouabain-insensitive outward diffusion of Na as a salt from a simultaneous ouabain-sensitive Na extrusion which is associated with a net cellular K uptake. A hypothesis consistent with these observations is that rewarming may activate a ouabain-sensitive "electrogenic" mechanism, most probably the net active transport of Na out of the cell, from which net K uptake may then follow passively.

Biological Transport↗
PubMed1987

Acute mitral regurgitation with papillary muscle rupture in a dog.

Papillary muscle rupture is uncommon in the dog. Two-dimensional echocardiography provides a rapid, noninvasive test in the diagnosis of acute, severe mitral regurgitation resulting from papillary muscle rupture. This report illustrates the usefulness of echocardiography to determine the cause of acute mitral regurgitation.

Acute Disease↗
PubMed1998

Solitary papillary muscle hypertrophy as a possible form of hypertrophic cardiomyopathy.

Patients can present with hypertrophied papillary muscles in the left ventricle, even without hypertrophy in other segments, and they have electrocardiographic (ECG) abnormalities suggestive of hypertrophic cardiomyopathy (HCM). This study was performed to evaluate whether the solitary papillary muscle hypertrophy was related to HCM. By analyzing 6731 echocardiographic studies between 1990 and 1994, the incidence of patients with papillary muscle hypertrophy was retrospectively examined, as well as the ECG features and family history related to HCM in these patients. After the normal size of the anterolateral and posteromedial papillary muscles was obtained from echocardiographic studies in 40 healthy subjects (0.7 +/- 0.2 cm for each of the vertical and horizontal axis), papillary muscle hypertrophy was defined as follows: either the vertical or horizontal diameter of at least one of the 2 papillary muscles was more than 1.1 cm (mean+2SD in the normal subjects). Using this definition, 29 patients with papillary muscle hypertrophy were identified, of whom 14 (48%) showed high voltage QRS complexes, 10 (34%) showed T wave inversion, and 6 (21%) showed abnormal Q waves. Ten patients (34%) had a family history of HCM. In 2 patients that were followed for 18 and 11 years, respectively, the voltages of the QRS complexes and inverted T waves progressed with the hypertrophy of the papillary muscle. These findings suggest that solitary papillary muscle hypertrophy is related to HCM and that papillary muscle hypertrophy is a newly identified subtype of or an early form of HCM.

Adolescent↗
PubMed1997

Severe mitral regurgitation complicating acute myocardial infarction. Clinical and angiographic differences between patients with and without papillary muscle rupture.

AIMS: To assess the differential clinical and angiographic characteristics of patients with severe mitral regurgitation related (n = 31) or unrelated (n = 16) to papillary muscle rupture complicating acute myocardial infarction. METHODS AND RESULTS: The clinical and angiographic features of patients with myocardial infarction and severe mitral regurgitation were evaluated. Patients with papillary muscle rupture were older (67 vs 60 years, P < 0.005) and had a lower rate of diabetes (7% vs 38%, P < 0.005) and of previous angina or infarction (24% vs 50%, P < 0.05). Frequency of inferior infarction was high and comparable in both groups (papillary muscle rupture, 72% vs non-papillary muscle rupture, 88%, ns) whereas in-hospital rate of angina/infarct extension prior to mitral regurgitation, also high, tended to be higher in patients without than in those with papillary muscle rupture (67% vs 39%, ns). Incidence of multivessel disease tended to be higher in patients without papillary muscle rupture (87% vs 56%, P < 0.06) and they had a lower ejection fraction (46 +/- 15 vs 61 +/- 14%, P < 0.03), whereas the culprit artery was mainly the right or the circumflex coronary artery in both groups (papillary muscle rupture, 100% vs non papillary muscle rupture, 93%, ns). Valve replacement was performed earlier in patients with papillary muscle rupture (1 (1; 14) vs 25 (5; 45) days, median, P < 0.002) but was associated with a similar mortality (papillary muscle rupture 11/24, 46% vs non-papillary muscle rupture, 7/15, 47%, ns). The main cause of death was cardiogenic shock in patients without papillary muscle rupture (5/7, 71%), and respiratory insufficiency--sepsis in those with papillary muscle rupture (7/11, 64%). CONCLUSIONS: Severe mitral regurgitation in myocardial infarction with or without papillary muscle rupture is mostly related to inferior infarction and often follows reinfarction, particularly in non-papillary muscle rupture cases. The main contributors to surgical mortality appear to be respiratory insufficiency in patients with papillary muscle rupture and cardiogenic shock, facilitated by a lower ejection fraction, a higher frequency of diabetes and more extensive coronary disease, in patients without papillary muscle rupture.

Aged↗