Magnetization transfer ratios of multiple sclerosis lesions with variable durations of enhancement

Papillary fibroelastomas are rare endocardial growths that most commonly occur on the cardiac valves. Whether papillary fibroelastomas represent true neoplasms, hamartomas, or degenerative changes is debatable. Whatever their origin, papillary fibroelastomas have a characteristic gross and microscopic appearance, are usually solitary, and are almost always incidental findings at autopsy or during cardiac surgery. We report a case of sudden death caused by occlusion of the right coronary artery ostium by a papillary fibroelastoma of the aortic valve. We discuss the gross and microscopic features, differential diagnosis, and etiology and pathogenesis of this rare and interesting cardiac lesion.     

Successful predilation of a resistant, heavily calcified lesion with cutting balloon for coronary stenting: a case report

Papillary fibroelastoma is a rare, benign cardiac tumor that can cause multiple emboli. We report herein a case of papillary fibroelastoma developing from the chordae of the tricuspid valve which was detected by echocardiography and confirmed by surgical resection. To our knowledge, this is only the fifth documented case of a tricuspid valve papillary fibroelastoma detected by echocardiography in a living patient.     

Rupture of the papillary muscle after percutaneous transvenous mitral commissurotomy (PTMC)--a case report

We experienced a rare case of the mitral regurgitation due to papillary muscle rupture after percutaneous transvenous mitral commissurotomy (PTMC). This case was a seventy years old female who underwent PTMC. The cardiac tamponade and mitral regurgitation occurred after PTMC. Pericardial drainage was done immediately, and the next day the emergency operation was required. Rupture of the posterior papillary muscle was found at the operation, and mitral valve replacement was performed. Her postoperative course was uneventful and she discharged on the 26th day after the operation. We should take the papillary muscle rupture into consideration if there are severe sub-valvular lesion and shorting of the chorda.     

Role of microtubules in the contractile dysfunction of hypertrophied myocardium

OBJECTIVES: We sought to determine whether the ameliorative effects of microtubule depolymerization on cellular contractile dysfunction in pressure overload cardiac hypertrophy apply at the tissue level. BACKGROUND: A selective and persistent increase in microtubule density causes decreased contractile function of cardiocytes from cats with hypertrophy produced by chronic right ventricular (RV) pressure overloading. Microtubule depolymerization by colchicine normalizes contractility in these isolated cardiocytes. However, whether these changes in cellular function might contribute to changes in function at the more highly integrated and complex cardiac tissue level was unknown. METHODS: Accordingly, RV papillary muscles were isolated from 25 cats with RV pressure overload hypertrophy induced by pulmonary artery banding (PAB) for 4 weeks and 25 control cats. Contractile state was measured using physiologically sequenced contractions before and 90 min after treatment with 10(-5) mol/liter colchicine. RESULTS: The PAB significantly increased RV systolic pressure and the RV weight/body weight ratio in PAB; it significantly decreased developed tension from 59+/-3 mN/mm2 in control to 25+/-4 mN/mm2 in PAB, shortening extent from 0.21+/-0.01 muscle lengths (ML) in control to 0.12+/-0.01 ML in PAB, and shortening rate from 1.12+/-0.07 ML/s in control to 0.55+/-0.03 ML/s in PAB. Indirect immunofluorescence confocal microscopy showed that PAB muscles had a selective increase in microtubule density and that colchicine caused complete microtubule depolymerization in both control and PAB papillary muscles. Microtubule depolymerization normalized myocardial contractility in papillary muscles of PAB cats but did not alter contractility in control muscles. CONCLUSIONS: Excess microtubule density, therefore, is equally important to both cellular and to myocardial contractile dysfunction caused by chronic, severe pressure-overload cardiac hypertrophy.     

Giant endocardial blood cyst in left ventricle resected by transaortic valve approach

A 57-year-old man had a histologically proven giant blood cyst in the left ventricle. An encapsulated mobile cystic tumor (3 x 3 x 4 cm), which was attached to the anterolateral papillary muscle by a stalk, was successfully resected by a transaortic valve approach for preserving cardiac function.     

Deferoxamine blocks interactions of fluoride and carbachol in isolated mammalian cardiac preparations

In papillary muscles, carbachol reduced the positive inotropic effects of isoprenaline (10 nmol/l). The negative inotropic effects of carbachol in isoprenaline-stimulated guinea pig papillary muscles were attenuated by additionally applied sodium fluoride (3 mmol/l). These effects of sodium fluoride were blocked by deferoxamine (200 micromol/l). In guinea pig left atria, sodium fluoride alone greatly reduced force of contraction. These effects in atria were blocked by 200 micromol/l deferoxamine, and positive inotropic effects of sodium fluoride were observed. It is suggested that the cardiac effects of muscarinic M2 receptor agonists in the ventricle involve, at least in part, the activation of phosphatases which are blocked by fluoride and reactivated by deferoxamine.     

Calcium-dependent toxic effects of digoxin in isolated myocardial preparations

On isolated guinea-pig papillary muscles as well as on electrically driven atria digoxin was infused into the bath fluid until cardiac arrest occurred. The concentration of digoxin which caused standstill is defined as the toxic one. The toxicity was determined under various Ca2+-concentrations. On the papillary muscle the increase of extracellular Ca2+ from 0.9 to 7.2 mM increased the toxicity of digoxin, i.e. significantly diminished its toxic concentrations. Likewise, on electrically driven atria an increase of Ca2+ from 0.45 to 7.2 mM increased the toxicity of digoxin. These results demonstrate that with regard to the toxicity Ca2+ and digoxin act synergistically.     

Effects of ONO-1101, a novel beta-antagonist, on action potential and membrane currents in cardiac muscle

Direct effects of ONO-1101 ?(-)-[(S)-2,2-dimethyl-1,3-dioxolan-4-yl]methyl-3-[4-[(S) -2-hydroxy-3-(2-morpholino carbonylamino)ethylamino] propoxy]phenylpropionate monohydrochloride), a novel beta-antagonist, on action potential parameters and membrane currents, and its beta adrenoceptor antagonism were examined in cardiac muscle. Action potential-parameters in papillary muscle of reserpinized animals and membrane currents recorded from single myocytes obtained from guinea pig and rabbit hearts were not affected by 1 to 100 microM ONO-1101. On the other hand, ONO-1101 markedly inhibited the potentiation of Ca current by isoproterenol in single cardiac myocytes of the guinea pig. The concentration-response relationship of Ca current for isoproterenol was shifted to the right. This effect resembled that of esmolol, which is also a beta adrenoceptor antagonist. A Schild plot analysis revealed the slope and pA2 value of each antagonist (ONO-1101, 0.94, 8.0; and esmolol, 0.98, 7.3, respectively) and demonstrated that ONO-1101 is about 5 times more potent than esmolol as a beta-antagonist. Two other effects of isoproterenol: 1) potentiation of delayed rectifier K current and 2) activation of chloride current, were also inhibited by ONO-1101. The time required for 50% removal of beta-antagonism of ONO-1101 and esmolol after the washout was estimated as 4 and 6 min, respectively, in depolarized papillary muscle. These results suggest that ONO-1101 is a potent beta-antagonist whose effects were removed quickly by washout. When applied at what is thought to be a clinical dosage, ONO-1101 had no direct effects on action potential-parameters and membrane currents in cardiac muscle. These characteristics of ONO-1101 suggest that this agent may be effective in clinical use.     

Relationship between myoglobin contents and increases in cyclic GMP produced by glyceryl trinitrate and nitric oxide in rabbit aorta, right atrium and papillary muscle

Effects of glyceryl trinitrate (GTN) and nitric oxide (NO) on the cardiac functions and myocardial cyclic GMP (cGMP) contents were examined in comparison with those in the aorta and correlated with myoglobin (an inhibitor of soluble guanylate cyclase) contents using the preparations isolated from the reserpinized rabbit. GTN (10(-10)-10(-4) mol/l) produced a dose-dependent relaxation in the aorta. However, this compound exerted no effect on the rate of the spontaneous beat of the right atrium and the contraction of the papillary muscle. A transient and significant increase in cGMP was observed in the aorta with GTN (3 x 10(-6) mol/l). Although the increase was also observed in the right atrium, it was much smaller. No definite change was observed in papillary muscle. Increases in cGMP produced by NO (3 x 10(-6) mol/l) were larger and significant in all tissues; (AUCcGMP(GTN)/AUCcGMP(NO)) ratio was 30.1 for the aorta, 65.0 for the right atrium and 16.3% for the papillary muscle. Although higher concentrations of NO were necessary in the right atrium and papillary muscle to induce increases in cGMP, no differences were noted in the three tissues as regards the maximum accumulation of this substance. Furthermore, kinetic analysis of NO-induced increases in tissue cGMP indicated no marked difference in the production rate among the three tissues, while the rate of elimination of cGMP was lower in the aorta than in the atrium or the papillary muscle. The increases in cGMP observed in these three tissues were inversely related to the contents of myoglobin in respective tissues.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of Cerium on Cardiac Muscle of Rat and Guinea Pig

Rare earth elements (REE) have beenused in agriculture widely. But the mechanismof their biological effect is not very clear. REcould antagonize Ca2 in cardiac muslce[1]. Laand Gd could noncompetitively inhibit the ef-feet of Ca2 in cardiac muscular contraction,reduce the activity of adenosine triphosphatasein cardiac sarcoplasm and inhibit the contraction of atria and papillary muscle in guineapig, and cause the visible potential vibration.All these might be caused by the inhibition ofN…     

Dietary magnesium supplementation attenuates ethanol-induced myocardial dysfunction

Hypomagnesemia is positively correlated with a number of cardiovascular abnormalities and recent evidence suggests that magnesium supplementation prevents ethanol-induced development of hypertension. The purpose of our study was to assess whether dietary magnesium supplementation effectively reverses or attenuates chronic ethanol-induced cardiac dysfunction, both at the tissue and the cellular level. Therefore, the influence of dietary magnesium supplementation during chronic ethanol ingestion on the mechanical properties of cardiac muscle was studied using isolated papillary muscles and ventricular myocytes from rat heart. In addition, the acute effects of ethanol on cardiac muscle from animals chronically exposed to ethanol in the absence and presence of dietary magnesium supplementation were also examined. Chronic ethanol exposure caused significant cardiac, hepatic, and renal enlargement, increased systolic blood pressure, and produced hypomagnesemia. After chronic ethanol exposure, the baseline force generating capacity of papillary muscles was markedly depressed and was associated with a significant slowing in the maximum velocities of contraction and relaxation. By contrast, in isolated myocytes, long-term ethanol exposure increased the extent of cell shortening associated with a significant reduction in the duration of relengthening and an increase in both the maximum velocities of shortening and relengthening. Dietary magnesium supplementation among animals chronically ingesting ethanol effectively normalized heart size, systolic blood pressure, and reduced plasma ethanol concentration. Magnesium supplementation also attenuated chronic ethanol-induced depression of contractile force and increased the extent of cell shortening. As expected, acute ethanol exposure caused a dose-dependent inhibition of both isometric force and isotonic shortening associated with a decrease in the intracellular calcium transient. However, the extent of the acute ethanol-induced reduction in isometric force and isotonic shortening was always slightly greater among preparations from animals chronically exposed to ethanol. Dietary magnesium supplementation normalized the acute inhibitory action of ethanol on isometric force, isotonic shortening, and the intracellular calcium transient. Our results suggest that dietary magnesium supplementation may attenuate chronic ethanol-induced alterations in baseline myocardial mechanical function and normalize the cardiac response to acute ethanol exposure.     

Dose-effects and chemotherapy dose intensity of aggressive non-Hodgkin''s lymphomas in the adult

Papillary fibroelastoma is a rare, benign cardiac tumor. Before echocardiogram came into existence, it was diagnosed only by necropsy or incidentally at surgery. This kind of tumor may appear on the endocardial surface or in any of the valves. Although it is usually small in size, it is associated to embolic phenomena, thoracic pain and sudden death. This report presents the first case of papillary fibroelastoma in the presence of a mechanical valvular prosthesis in mitral position. In a patient 55 years old, presenting inactive rheumatic heart disease. The tumor was detected by means of transthoracic and transesophageal echocardiogram.     

Transesophageal echocardiographic localization of an aortic valve papillary fibroelastoma during routine coronary artery bypass surgery

Papillary fibroelastomas are rare, primary cardiac tumors most often diagnosed incidentally at autopsy. These tumors have been associated with embolism, neurologic injury, coronary ischemia and sudden death. We report a case of clinical detection of an asymptomatic aortic valve papillary fibroelastoma by transesophageal echocardiography. The mass was an incidental finding during routine coronary artery bypass surgery. This finding dictated a change in the operative approach to include resection of the aortic valve mass in addition to coronary revascularization.     

Left ventricular volume reduction for end-stage heart failure: intrapapillary or extrapapillary resection, mitral valve repair or replacement?

We report on two patients with end-stage dilated cardiomyopathy and functional mitral valve insufficiency who underwent left ventricular volume reduction. Intrapapillary resection and correction of the mitral valve regurgitation produced inadequate reduction of the ventricular cavity and resulted in inability to wean the patients from cardiopulmonary bypass. Following extension of the resection to include the papillary muscles and mitral valve replacement, there was a significant improvement in cardiac function. Both patients survived surgery; subsequent echocardiography provided evidence of improved myocardial function and NYHA functional class.     

Left ventricular fibroma in an aged patient: report of a case

We report herein the case of a 77-year-old man with a left ventricular tumor originating from the papillary muscle of the left ventricular wall, in whom a successful tumor resection with mitral valve replacement was performed. The pathological diagnosis of the tumor was confirmed as cardiac fibroma. His postoperative course was uneventful and he is currently well with no signs of recurrence 2 years after surgery.     

Efficient gene transfer into cardiac myocytes using adeno-associated virus (AAV) vectors

Adeno-associated virus (AAV) vectors, derived from a non-pathogenic parvovirus, are considered to be an appropriate gene transfer vehicle for both dividing and non-dividing cells. In the present study, we investigated whether the rat heart could be efficiently transduced with AAV vectors. Rat cardiac myocytes (CM) were infected with AAV-lacZ vector containing beta-galactosidase (beta-gal) gene in vitro, and the expression of beta-gal in CM was evaluated by X-gal staining and beta-gal ELISA. With increasing multiplicities of infection (MOI), more than 60% of CM were stained positively with X-gal, and the beta-gal expression increased to 31.1 +/- 4.6 ng/mg protein in a MOI-dependent manner (MOI: 10(4) to 10(6) particles/cell). The beta-gal expression was also increased in an incubation period-dependent manner (1-24 h). beta-gal expression was maximal at day 3 and then gradually decreased with time. However, beta-gal expression at day 14 was almost the same level as that at day 1 (45.5 +/- 5.9 v 55.2 +/- 6.2 ng/mg protein). Excised rat right ventricular papillary muscles were also infected with AAV-lacZ ex vivo. When the beta-gal expression was evaluated by X-gal staining, more than 80% of CM in the papillary muscles were stained positively, indicating efficient gene transfer into CM using AAV vectors. These findings suggest that AAV vectors are promising for cardiac gene therapy.     

Conserved residues amino-terminal of cytoplasmic tyrosines contribute to the SHP-1-mediated inhibitory function of killer cell Ig-like receptors

The heart has been recognized as a major target of thyroid hormone action. Our study investigates both the regulation of cardiac-specific genes and contractile behavior of the heart in the presence of a mutant thyroid hormone receptor beta1 (T3Rbeta1-delta337T) derived from the S kindred. The mutant receptor was originally identified in a patient with generalized resistance to thyroid hormone. Cardiac expression of the mutant receptor was achieved by a transgenic approach in mice. As the genes for myosin heavy chains (MHC alpha and MHC beta) and the cardiac sarcoplasmic reticulum Ca2+ adenosine triphosphatase (SERCA2) are known to be regulated by T3, their cardiac expression was analyzed. The messenger RNA levels for MHC alpha and SERCA2 were markedly down-regulated, MHC beta messenger RNA was up-regulated. Although T3 levels were normal in these animals, this pattern of cardiac gene expression mimics a hypothyroid phenotype. Cardiac muscle contraction was significantly prolonged in papillary muscles from transgenic mice. The electrocardiogram of transgenic mice showed a substantial prolongation of the QRS interval. Changes in cardiac gene expression, cardiac muscle contractility, and electrocardiogram are compatible with a hypothyroid cardiac phenotype despite normal T3 levels, indicating a dominant negative effect of the T3Rbeta mutant.     

Traumatic tricuspid valve insufficiency

We report a case of tricuspid insufficiency in connection with blunt chest trauma. The patient was involved in a car accident. The central venous catheter showed a right ventricular pressure curve, suggestive of a tricuspid valve insufficiency. A transoesophageal echocardiographic examination supported this by revealing a papillary muscle rupture. This kind of injury has been seen more frequently during the last 35 years, partly because of better diagnostic procedures and a better understanding of the pathology. The decelerating force in the right ventricular chamber produces a regurgitation thereby initiating rupture of the papillary muscle and/or the chordae tendinae. In a literature study twelve out of thirteen patients were involved in car accidents. Some of them had a dominant V-wave in the venous pulse curve, but no clinical observation is directly diagnostic. Therefore, cardiac lesions should be kept in mind whenever there is a history of blunt chest trauma. The best diagnostic approach is echocardiography.     

Structure-activity relationships of alkylxanthines: alkyl chain elongation at the N1- or N7-position decreases cardiotonic activity in the isolated guinea pig heart

Relationships between the alkyl substitutions (C1-C6) and cardiac inotropic activities of xanthine derivatives were studied in isolated guinea pig heart muscles. Most of the alkylxanthines exhibited positive inotropic activity on the left atrium, which was increased with an elongation of alkyl chain at the N3-position but decreased by substitution of a long alkyl group at the N1- or N7-position of the xanthine skeleton. Although positive inotropic activity in the right ventricular papillary muscle was also increased by longer alkyl groups at the N3-position, the inotropic activity became negative with an increment in alkyl chain length at the N1- or N7-position. The positive inotropic activity of alkylxanthines was correlated with their inhibitory activity on the phosphodiesterase (PDE) III isoenzyme. Adenosine A1 antagonism and PDE IV inhibitory activity were also partly associated with the inotropic activity because H-89, an inhibitor of cyclic AMP-dependent protein kinase, diminished the positive inotropic action and potentiated the negative inotropic action. These results indicate that the positive inotropic activity of alkylxanthines becomes weak with elongation of alkyl chains at the N1- and N7-positions; In particular, xanthines having two long alkyl chains show a negative inotropic activity on the right ventricular papillary muscle, an effect that could not be elucidated from their cyclic AMP-dependent action.     

Protective effect of clentiazem against epinephrine-induced cardiac injury in rats

We investigated the effects of clentiazem, a 1,5-benzothiazepine calcium antagonist, on epinephrine-induced cardiomyopathy in rats. With 2-week chronic epinephrine infusion, 16 of 30 rats died within 4 days, and severe ischemic lesions and fibrosis of the left ventricles were observed. In epinephrine-treated rats, left atrial and left ventricular papillary muscle contractile responses to isoproterenol were reduced, but responses to calcium were normal or enhanced compared to controls. Left ventricular alpha and beta adrenoceptor densities were also reduced compared to controls. Treatment with clentiazem prevented epinephrine-induced death (P < .05), and attenuated the ventricular ischemic lesions and fibrosis, in a dose-dependent manner. Left atrial and left ventricular papillary muscle contractile responses to isoproterenol were reduced compared to controls in groups treated with clentiazem alone, but combined with epinephrine, clentiazem restored left atrial responses and enhanced left ventricular papillary responses to isoproterenol. On the other hand clentiazem did not prevent epinephrine-induced down-regulation of alpha and beta adrenoceptors. Interestingly, clentiazem, infused alone, resulted in decreased adrenergic receptor densities in the left ventricle. Clentiazem also did not prevent the enhanced responses to calcium seen in the epinephrine-treated animals, although the high dose of clentiazem partially attenuated the maximal response to calcium compared to epinephrine-treated animals. In conclusion, clentiazem attenuated epinephrine-induced cardiac injury, possibly through its effect on the adrenergic pathway.