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[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

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

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

Leptomeric fibrils and T-tubule desmosomes in the Z-band region of the mouse heart papillary muscle.

The papillary muscle of the heart of adult white mice is investigated. Intrafibrillary located leptomeric fibrils, frequently encountered in the Z-band region of the myofibrils. The leptomeric fibrils are always running in a transverse direction and often in close proximity to the transverse tubules (which are also located at this level). There seems to be a close connection between the dense striae of the leptofibrils and the Z-bands of ordinary myofibrils. The leptomeric fibrils are spindle-shaped and have a length varying between 0.6 and 1.2 microgrometer. The banding periodicity of the fibrils is approximately 0.16 micrometer. Occasionally desmosomes are observed in the T-tubule system.

Animals

The time course of the effects of beta- and alpha-adrenoceptor stimulation by isoprenaline and methoxamine on the contractile force and cAMP level of the isolated rabbit papillary muscle.

In the isolated papillary muscle of the rabbit the time course of the effects of selective beta- and alpha-adrenoceptor stimulation by isoprenaline and methoxamine, respectively, on the contractile force and on the level of 3',5'-cyclic AMP (cAMP) was determined. 1. Isoprenaline (3 times 10(-7) M) increased significantly the content of cAMP at 15 sec and elevated it to the maximal level-about twice the control value-at 30 sec after its administration, while the developed tension of the papillary muscle was also increased significantly at 15 sec and reached gradually its maximum at 90 sec. 2. Compared with isoprenaline methoxamine (10(-4) M) increased the developed tension very slowly: the maximal response was reached after 20 min. The level of cAMP, on the other hand, was changed neither before nor during the induction of the positive inotropic effect of methoxamine. 3. The phosphodiesterase inhibitor papaverine (10(-5) M) inhibited the PDE activity of the papillary muscle by about 40% after an incubation of 1 hr, and increased the level of cAMP significantly. The effects of isoprenaline on the contractile forced and on the level of cAMP were considerably enhanced by papaverine: the content of cAMP was increased by isoprenaline (3 times 10(-7) M) to about 3 times the control value and also its positive inotropic effect was significantly greater than in controls without papaverine. On the other hand, the positive inotropic effect of methoxamine (10(-4) M) was not affected by papaverine (10(-5) M). Furthermore, in the papillary muscle treated with papaverine the level of cAMP was significantly reduced by methoxamine: the papaverine-induced increase of cAMP was abolished by methoxamine. 4. The present results are compatible with the hypothesis that cAMP is involved as a mediator in the positive inotropic effect induced by beta-adrenoceptor stimulation, and indicate further that the stimulation of alpha-adrenoceptors evokes its positive inotropic effec through a mechanism other than that elicited by beta-adrenoceptor stimulation, i.e., independent of cAMP.

Animals

External ATP antagonizes the effect of potassium channel openers in guinea-pig ventricular papillary muscle.

Right ventricular papillary muscles of the guinea-pig heart were electrically stimulated. Cromakalim 10-100 microM and Ro 31-6930 3 microM depressed the contractile force and shortened the duration of action potentials. Glibenclamide 0.3-3 microM, ATP 100 microM and alpha, beta-methylene ATP (alpha, beta-meATP) 30 microM antagonized these effects. Suramin 300 microM failed to reverse the alpha, beta-meATP-evoked antagonism of the action of cromakalim. It is concluded that both intra- and extracellular ATP may interfere with potassium channel openers and that extracellular ATP does not act via the known P2-purinoceptor subtypes.

Action Potentials

Effects of derivatives of cyclic amp and cyclic gmp on contraction force of cat papillary muscles.

Right ventricular kitten papillary muscles were incubated with dibutyryl adenosine 3',5'-monophosphate (dbcAMP) at varying concentrations as low as 1 X 10(-4)M. A positive inotropic effect was observed with all concentrations of dbcAMP. Concomitant administration of 5 X 10(-4)M monobutyryl guanosine 3',5'-monophosphate (mbcGMP) and 1-2 X 10(-4)M dbcAMP prevented the inotropic response observed when dbcAMP was used alone. When higher doses of dbcAMP were used (5 X 10(-4) M, 10 X 10(-4) M), there was no significant difference in the inotropic response seen between control tissues and papillary muscles pretreated with mbcGMP.

Animals

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

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

Influence of temperature on the positive inotropic effects mediated by alpha-and-beta-adrenoceptors in the isolated rabbit papillary muscle.

On the isolated rabbit papillary muscle experiments were carried out to determine whether the positive inotropic effects mediated by alpha- and by beta- adrenoceptors are brought about by different mechanisms or not.--For this reason the influence of temperature and the effect of the calcium antagonist D600 on the responses to phenylephrine and to isoprenaline were compared. 1. The maximal inotropic effects of phenylephrine, isoprenaline and calcium were not affected by raising the temperature of the organ bath from 37 degrees to 42 degrees C, wheras the basal developed tension of the muscle was significantly decreased. 2. The dose-response curve for phenylephrine was markedly shifted to the right by raising the temperature (pD2=0.89), while that for isoprenaline was also shifted to the right, but to a lesser extent (pD2=0.23). 3. In the presence of 1.5 times 10-8 M pindolol the shift of the dose-response curve for phenylephrine induced by elevation of temperature was more prominent (pD2=1,91), whereas phentolamine (3 times 10-6 M) inhibited the temperature-induced shift. 4. The positive inotropic effect of phenylephrine--mediated by alpha-adrenoceptors under blockade of beta-adrenoceptors by 1.5 times 10-8 M pindolol--was markedly depressed by D600 (10-7 and 3 times 10-7 M): the dose-response curve was shifted to the right ant the maximal response was depressed. On the other hand, the positive inotropic effect of isoprenaline--mediated by beta-adrenoceptors--was affected to a lesser extent by D600 and the maximal response was not changed. It indicates that the stimulation of alpha- adrenoceptors in the rabbit papillary muscle induces a positive inotropic response through a biochemical process different from that caused via beta- adrenoceptors, i. e., stimulation of alpha- adrenoceptors may increase the intracellular calcium level mainly by changing the transmembrane calcium flux.

Animals

Influence of temperature and frequency on the positive inotropic action of phenylephrine in the isolated rabbit papillary muscle.

On the isolated papillary muscle of the rabbit the maximal developed tension induced by phenylephrine bia alpha-adrenoceptors was not affected by changing the temperature, while the basal developed tension of the muscle was significantly increased or decreased by lowering the temperature from 37 degrees C to 32 degrees C or by raising it to 42 degrees C, respectively. When the temperature was lowered from 37 degrees C to 32 degrees C in the muscle stimulated at a frequency of 0.5 Hz, the dose-response curve for phenylephrine via alpha-adrenoceptors was shifted to the left (delta pD2-0.47), while that for phenylephrine via beta-adrenoceptors was also shifted to the left to a similar extent (delta pD2=0.43). When the temperature was raised from 37 degrees C to 42 degrees C, the dose-response curve for phenylephrine via alpha-adrenoceptors was markedly shifted to the right (delta pD2=1.58), whereas that via beta-adrenoceptors was not affected at all by this elevation of the temperature (delta pD2=0.04). The change of the stimulation frequency affected chiefly the intrinsic activity of phenylephrine but not the affinity of the drug for alpha-adrenoceptors expressed as the pD2-value.

Animals

[A case of mitral regurgitation caused by necrosis and total rupture of the papillary muscle].

Mitral regurgitation (MR) caused by total rupture of the papillary muscle has so ominous prognosis that it is treated by surgery exceedingly rarely. We recently experienced a case of MR caused by total rupture of the posterior papillary muscle that had presumably occurred after myocardial infarction. The patient was a 52-year-old male who was admitted to a hospital with liver dysfunction where he was noticed for the first time of his having cardiac murmurs and was diagnosed as having MR on the basis of echocardiography. With this diagnosis he was transferred to our department. Examination on admission revealed the patient to have an NYHA class III mitral incompetence with ECG evidence of old posteroinferior myocardial infarction. Cardiac catheterization demonstrated total occlusion of the segment 1 of the right coronary artery and MR, Sellers III. Abnormal echoes were noted in the left ventricle that moved almost synchronously with the posterior leaflet of the mitral valve, a finding leading to a suspected diagnosis of rupture of the posterior papillary muscle or chordae tendineae. Intraoperative findings were confirmative of total rupture of the posterior papillary muscle and mitral valve replacement was performed using a SJM prosthetic valve. Histological examination of the ruptured muscle revealed presence of necrosis, but no other specific inflammatory changes. Documented cases of surgically treated total papillary muscle rupture are quite limited in number, the present case being the 4th to be reported in Japan.

Heart Rupture

Clinical and pathologic factors contributing to acute papillary muscle ischemia.

Hearts from 110 consecutive adult autopsies were examined to determine the frequency and predisposing clinical and pathologic features of acute left ventricular papillary muscle ischemia. Acute infarcts of papillary muscles were present in 23% of the hearts and were more frequent than acute infarcts of their corresponding ventricular walls. Patients with acutely infarcted papillary muscles were more likely to have significant stenosis of the corresponding coronary artery than were patients with normal papillary muscles. Increasing heart weight was also associated with increased frequency of papillary muscle acute infarction. Patients with acutely infarcted papillary muscles were more likely to have had hypertension and to have suffered significant hypotension prior to death than were patients with normal papillary muscles.

Adult

[Evaluation of elasticity by means of length-tension relationships in a model of isolated ventricular myocardium from rat and cat papillary muscle under conditions of contracture (author's transl)].

Increase of Ca2+ concentration to 7.5 mM in the presence of 10 mM or 20 mM caffeine shifted length-tension relationships of 5 rat trabecular muscles and 5 cat papillary muscles to higher tensions. At 1max diastolic tension was enhanced from (formula: see text), for all measured points of stress-strain relationships after the increase of diastolic tension by caffeine and Ca2+ as well as under control conditions. The function E = f (sigma) = b (sigma - c) was computed by linear regression analysis (0.99 greater than r2 greater than 0.96). The average value of constant b was 13.89 +/- 2.01 in control curves of rat trabecular muscles and 13.42 +/- 1.98 in curves with 10 mM caffeine and 7.5 mM Ca2+. Likewise, in cat papillary muscles 20 mM caffeine and 7.5 mM Ca2+ did not alter the stiffness constant b in a statistically significant manner (control: 16.63 +/- 3.03, caffeine: 16.43 +/- 3.02). The results demonstrate that the stiffness constant b cannot indicate acute variations of the length-tension relationships due to caffeine and Ca2+ and may result in overestimating of myocardial distensibility. However, if the tangent modulus (E) is related to strain (epsilon), the alterations of diastolic elasticity are detectable. Mathematical considerations of these experimental results imply a new base for evaluation of diastolic elasticity of the heart by means of the tangent modulus (E). These results are of substantial importance in clinical evaluation of distensibility of myocardial tissue, as the tangent modulus related to wall stress apparently is not appropriate to realize alterations in "passive" myocardial properties due to contracture.

Animals

A comparison of contractile function between papillary muscles and isolated myocytes from the same human hearts.

The contractile function in response to increasing extracellular calcium and isoprenaline has been investigated using papillary muscles from seven human hearts (failing and non-failing) obtained at the time of transplant. Myocytes have been enzymatically isolated from adjacent myocardium, and their contractile characteristics measured in parallel to those of the intact papillary muscle. Similar experiments were performed on rabbit hearts, but in this case separate animals were used for the papillary muscles and cells. For human myocardium, the EC50 (concentration for half-maximal effect) for calcium, and the percentage increase in amplitude between basal (1.3mM) and maximally activating calcium, was similar between papillary muscle and cells. Variability of absolute responses was 4-5 times greater for papillary muscle than for myocytes. Isoprenaline accelerated the time to peak tension, time to 50% relaxation and time to 90% relaxation in papillary muscle; a similar effect on shortening was seen for time to peak tension and time to 50% relaxation in cells. Time to peak tension and time to 50% relaxation were not significantly different between the human preparations with isoprenaline, but the time to 50% relaxation with high calcium was faster for myocytes than for papillary muscle (p less than 0.05). Isoprenaline induced after-contractions in some cells, prolonging the time to 90% relaxation. This was not observed in papillary muscle preparations. Papillary muscles were less sensitive to the stimulatory effects of isoprenaline than cells taken from the same hearts. EC50 values were higher (p less than 0.05) and increases in contraction were lower (p less than 0.05) in whole tissue. This difference between cells and papillary muscle was not seen in rabbit hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

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

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

Aged

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

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

Animals

Anatomic findings in acute papillary muscle necrosis.

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

Aged