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Papillary muscle repositioning for repair of anterior leaflet prolapse caused by chordal elongation.The Journal of Thoracic and... Sep 2006Anterior leaflet prolapse is still a challenge. Various techniques have been described, but very little is known of the long-term outcome. We describe the long-term...
OBJECTIVE
Anterior leaflet prolapse is still a challenge. Various techniques have been described, but very little is known of the long-term outcome. We describe the long-term results of papillary muscle repositioning, with up to 15 years' follow-up.
METHODS
From 1989 through 2005, 120 patients with anterior leaflet prolapse (97 bileaflet and 23 isolated anterior leaflet) were treated with papillary muscle repositioning when chordae were elongated. All patients had severe mitral regurgitation. The mean left ventricular end-systolic diameter on echocardiography was 39.4 +/- 5.2 mm. The predominant cause was degenerative: dystrophic disease in 62 and Barlow's disease in 43. Papillary muscle repositioning was carried out on the posterior papillary muscle in 92.5% and on the anterior papillary muscle in 31.7%. A ring annuloplasty was performed in 117 cases. Fifty-seven (47.5%) patients had a tricuspid annuloplasty.
RESULTS
There were no in-hospital deaths or patients lost to follow-up. Mean follow-up was 6.3 +/- 0.4 years (maximum, 15.6 years). Cumulative actuarial survival at 5, 10, and 15 years was 97.2%, 94.1%, and 81.4%, respectively. Two (1.7%) patients required reoperation at 1 and 5 years after repair. No significant risk factor was identified for late mortality or reoperation. At the latest assessment, 88 (73.3%) patients were asymptomatic. Echocardiography showed no or trivial mitral regurgitation in 89 (74.2%) patients, mild mitral regurgitation in 8 patients, and moderate mitral regurgitation in 9 patients.
CONCLUSIONS
Anterior leaflet prolapse caused by elongated chordae can always be addressed with papillary muscle repositioning. Results indicate that it is a safe and durable technique, providing good long-term results in the management of degenerative pathology of the anterior leaflet.
Topics: Cardiac Surgical Procedures; Chordae Tendineae; Female; Follow-Up Studies; Heart Valve Prolapse; Humans; Male; Middle Aged; Mitral Valve Insufficiency; Papillary Muscles; Postoperative Complications
PubMed: 16935113
DOI: 10.1016/j.jtcvs.2006.06.003 -
Innovations (Philadelphia, Pa.) 2022Subannular mitral valve (MV) repair techniques have been developed to address increased rates of recurrent mitral regurgitation (MR) in patients with secondary MR (SMR)...
Subannular mitral valve (MV) repair techniques have been developed to address increased rates of recurrent mitral regurgitation (MR) in patients with secondary MR (SMR) type IIIb. Endoscopic papillary muscle relocation (PMR) is feasible via minithoracotomy. Nevertheless, the periprocedural outcome of patients with severe left ventricular (LV) dysfunction remains unknown. A total of 98 consecutive patients with SMR type IIIb underwent PMR at our institution. Due to concomitant coronary artery bypass grafting, 62 patients underwent sternotomy and were excluded from the current analysis, whereas 36 patients were treated by a minimally invasive technique using 3-dimensional endoscopy. Of these, 18 patients had severely depressed LV ejection fraction (LVEF) ≤35% (study group) and were compared to the remaining 18 patients with LVEF >35% (control group). Periprocedural outcome was retrospectively analyzed. Although LVEF was significantly worse in the study group (30% ± 4% vs 43% ± 6%, < 0.001), the severity of SMR and the degree of MV leaflet tethering were similar. The prevalence of concomitant procedures and the duration of surgery, cardiopulmonary bypass, and aortic cross-clamp were comparable. Periprocedural low cardiac output syndrome was favorably low in both groups (16.7% vs 5.6%, = 0.29). Postoperative ventilation time (5.7 h [4.2 to 8.7 h] vs 6.0 h [4.6 to 9.8 h], = 0.43) and duration of intensive care unit stay (2 days [1 to 3 days] vs 2 days [1 to 3 days], = 0.22) were similar. There was no 30-day mortality in either group. Standardized endoscopic PMR resulted in favorable periprocedural outcomes in patients with severe LV dysfunction, suggesting that minimally invasive surgery can safely be extended to this patient population.
Topics: Endoscopy; Humans; Mitral Valve Annuloplasty; Mitral Valve Insufficiency; Papillary Muscles; Retrospective Studies; Treatment Outcome; Ventricular Dysfunction, Left
PubMed: 35983699
DOI: 10.1177/15569845221115419 -
The Journal of Thoracic and... Feb 2010Our objective was to evaluate long-term stability of mitral repair and reverse remodeling in patients with severe ischemic left ventricular dysfunction and functional...
OBJECTIVE
Our objective was to evaluate long-term stability of mitral repair and reverse remodeling in patients with severe ischemic left ventricular dysfunction and functional mitral regurgitation.
METHODS
Since June 2000, a total of 37 patients with ischemic functional mitral regurgitation have benefited from a double-level mitral repair that comprises an intraventricular peripapillary muscle sling completed by a classic intra-atrial mitral annuloplasty ring (mean age, 56 years; left ventricular end-diastolic diameter, 70 +/- 0 mm; left ventricular end-systolic diameter, 55 +/- 5.6 mm; ejection fraction, 15% to 45%; pulmonary hypertension > 60 in all patients; all were in New York Heart Association class III-IV). All patients had both papillary muscles encircled with a 4-mm polytetrafluoroethylene tube, correcting their lateral and downward displacement. Annuloplasty rings were moderately undersized or normal. Efficiency was evaluated on mitral stability, ventricular parameters, and functional status. According to the Leyden algorithm based on preoperative end-diastolic and end-systolic left ventricular diameters, only a minority of our patients were expected to experience reverse remodeling.
RESULTS
Regurgitation is none to trivial in 31 and mild to moderate in 4. Follow-up (3-84 months; mean, 55 +/- 22 months) shows stability of all initially successful double-level mitral repairs. Follow-up beyond 1 year shows improvements in ventricular diameters (56 +/- 5 mm), ejection fraction (49 +/- 6), volume (130 +/- 10 mL), and sphericity index (0.55). Two patients died during follow-up and 1 underwent transplantation.
CONCLUSION
Reapproximating the papillary muscles has an immediate effect on mitral leaflet mobility by suppressing the tethering resulting from displacement of the papillary muscles. It has an effect in preventing recurrent mitral regurgitation by avoiding further papillary muscle displacement. In this cohort of severely disabled patients, reverse remodeling can be expected with the double-level repair.
Topics: Adult; Aged; Comorbidity; Female; Heart Valve Prosthesis; Heart Valve Prosthesis Implantation; Humans; Male; Middle Aged; Mitral Valve Insufficiency; Myocardial Infarction; Papillary Muscles; Prosthesis Fitting; Secondary Prevention; Ventricular Dysfunction, Left
PubMed: 20106402
DOI: 10.1016/j.jtcvs.2009.08.007 -
American Journal of Physiology. Heart... Mar 2004Collagen degradation is suggested to be responsible for long-term contractile dysfunction in different cardiomyopathies, but the effects of acute and specific collagen...
Collagen degradation is suggested to be responsible for long-term contractile dysfunction in different cardiomyopathies, but the effects of acute and specific collagen type I removal (main type in the heart muscle) on tension have not been studied. We determined the diastolic and developed tension length relations in isometric contracting perfused rat papillary muscles (perfusion pressure 60 cmH(2)O) before and after acute and specific removal of small collagen struts with the use of purified collagenase type I. At 95% of the maximal length (95%L(max)), diastolic tension increased 20.4 +/- 8.1% (P < 0.05, n = 6) and developed tension increased 15.0 +/- 6.7% after collagenase treatment compared with time controls. Treatment increased the diastolic muscle diameter by 7.1 +/- 3.4% at 95%L(max), whereas the change in diameter due to contraction was not changed. Diastolic coronary flow and normalized coronary arterial flow impediment did not change after collagenase treatment. Electron microscopy revealed that the number of small collagen struts, interconnecting myocytes, and capillaries was reduced to approximately 32% after treatment. We conclude that removal of the small collagen struts by acute and specific collagen type I degradation increases diastolic and developed tension in perfused papillary muscle. We suggest that diastolic tension is increased due to edema, whereas developed tension is increased because the removal of the struts poses a lower lateral load on the cardiac myocytes, allowing more myocyte thickening.
Topics: Animals; Collagen Type I; Collagenases; Coronary Circulation; Diastole; Edema; In Vitro Techniques; Male; Microscopy, Electron, Scanning; Papillary Muscles; Perfusion; Rats; Rats, Wistar
PubMed: 14576082
DOI: 10.1152/ajpheart.00967.2001 -
Journal of Investigative Medicine High... 2019Antiphospholipid syndrome (APS) is an autoimmune disorder that has a strong propensity for a hypercoagulable state and is known to be associated with venous and arterial...
Antiphospholipid syndrome (APS) is an autoimmune disorder that has a strong propensity for a hypercoagulable state and is known to be associated with venous and arterial thromboembolism. We describe an uncommon case of APS in the setting of non-Hodgkin's lymphoma, with thromboembolism, and a rare complication after an uncommon etiology of myocardial infarction. This case highlights the importance of early and appropriate type of anticoagulation to reduce the morbidity and mortality in patients with APS.
Topics: Antiphospholipid Syndrome; Heart Rupture; Heart Valve Prosthesis Implantation; Humans; Male; Middle Aged; Mitral Valve Insufficiency; Papillary Muscles; Thromboembolism
PubMed: 31010325
DOI: 10.1177/2324709619842247 -
Anesthesiology Jan 1993Etomidate has been shown to induce no significant inotropic effect on normal myocardium, but its effects on diseased myocardium remain unknown. (Comparative Study)
Comparative Study
BACKGROUND
Etomidate has been shown to induce no significant inotropic effect on normal myocardium, but its effects on diseased myocardium remain unknown.
METHODS
The effects of etomidate (1 and 5 micrograms/ml) on the intrinsic contractility of left ventricular papillary muscle from normal hamsters and those with cardiomyopathy (strain BIO 82.62, 6 months old) were investigated in vitro (Krebs-Henseleit solution, 29 degrees C, pH 7.40, Ca++ 2.5 mM, stimulation frequency 3/min).
RESULTS
The contractility of papillary muscles from hamsters with cardiomyopathy was less than that of controls, as shown by the decrease in maximum shortening velocity (-25%, P < .001), isometric active force (-45%, P < .01), peak power output (-57%, P < .01), and sarcoplasmic reticulum function (P < .01). Etomidate did not induce a significant inotropic effect, as shown by the absence of changes in maximum shortening velocity and active isometric force, except at 5 micrograms/ml in cardiomyopathic hamsters (+8 +/- 10%, P < .05). The effects of etomidate on these inotropic parameters were not different in normal and cardiomyopathic hamsters. Etomidate impaired contraction-relaxation coupling under low load in both groups, suggesting that etomidate decreased sarcoplasmic function. This impairment was less (P < .02) pronounced in cardiomyopathic muscles. The effects of etomidate on contraction-relaxation coupling under heavy load were not different between groups. In both groups, etomidate had no effect on the peak power output and the curvature of the total force-velocity curve, suggesting that it did not modify the muscle myothermal economy.
CONCLUSIONS
Etomidate had only a slight effect on the intrinsic mechanical properties of hamster cardiac papillary muscles, and these effects did not depend on the pathophysiologic state of the myocardium. These results may be clinically useful as, unlike etomidate, most anesthetics depress myocardial contractility.
Topics: Animals; Cardiomyopathies; Cricetinae; Etomidate; Female; In Vitro Techniques; Male; Mesocricetus; Muscle Contraction; Papillary Muscles; Reference Values
PubMed: 8424576
DOI: 10.1097/00000542-199301000-00013 -
American Journal of Physiology. Heart... Mar 2010Rewarming patients after profound hypothermia may result in acute heart failure and high mortality (50-80%). However, the underlying pathophysiological mechanisms are...
Rewarming patients after profound hypothermia may result in acute heart failure and high mortality (50-80%). However, the underlying pathophysiological mechanisms are largely unknown. We characterized cardiac contractile function in the temperature range of 15-30 degrees C by measuring the intracellular Ca(2+) concentration ([Ca(2+)](i)) and twitch force in intact left ventricular rat papillary muscles. Muscle preparations were loaded with fura-2 AM and electrically stimulated during cooling at 15 degrees C for 1.5 h before being rewarmed to the baseline temperature of 30 degrees C. After hypothermia/rewarming, peak twitch force decreased by 30-40%, but [Ca(2+)](i) was not significantly altered. In addition, we assessed the maximal Ca(2+)-activated force (F(max)) and Ca(2+) sensitivity of force in skinned papillary muscle fibers. F(max) was decreased by approximately 30%, whereas the pCa required for 50% of F(max) was reduced by approximately 0.14. In rewarmed papillary muscle, both total cardiac troponin I (cTnI) phosphorylation and PKA-mediated cTnI phosphorylation at Ser23/24 were significantly increased compared with controls. We conclude that after hypothermia/rewarming, myocardial contractility is significantly reduced, as evidenced by reduced twitch force and F(max). The reduced myocardial contractility is attributed to decreased Ca(2+) sensitivity of force rather than [Ca(2+)](i) itself, resulting from increased cTnI phosphorylation.
Topics: Animals; Body Temperature; Calcium; Electric Stimulation; Fluorescent Dyes; Fura-2; Hypothermia; Male; Models, Animal; Myocardial Contraction; Papillary Muscles; Phosphorylation; Rats; Rats, Sprague-Dawley; Troponin I
PubMed: 20023122
DOI: 10.1152/ajpheart.00805.2009 -
Japanese Journal of Pharmacology Dec 1976Effects of bufetolol and propranolol, adrenergic beta-receptor blocking and anti-arrhythmic drugs, on active and passive membrane properties of the dog papillary muscle...
Effects of bufetolol and propranolol, adrenergic beta-receptor blocking and anti-arrhythmic drugs, on active and passive membrane properties of the dog papillary muscle were investigated with microelectrode and sucrose-gap methods. Bufetolol (10(-5) to 10(-4) g/ml) and propranolol (10(-6) g/ml) significantly decreased the maximum rate of rise of the action potential. The maximum responsive frequency to driving stimulus was decreased in the presence of bufetolol (3 X 10(-5) g/ml) and propranolol (10(-5 g/ml), whereas the effective refractory period was not affected. The critical threshold potential was shifted to more positive potential in the presence of the drugs. The passive membrane property, the space constant (lambda), the time constant (tau) and the current-voltage relations of the muscle membrane were not significantly altered by the drugs. It is concluded that bufetolol and propranolol suppress the excitability of the muscle membrane and this action may be ascribed to the decrease in the sodium conductance (gNa) and to the rise of gNa onset potential without alteration in the passive membrane property.
Topics: Action Potentials; Adrenergic beta-Antagonists; Animals; Anti-Arrhythmia Agents; Dogs; Electric Stimulation; Heart Conduction System; In Vitro Techniques; Membrane Potentials; Papillary Muscles; Propanolamines; Propranolol; Refractory Period, Psychological
PubMed: 15153
DOI: 10.1254/jjp.26.639 -
Toxins Jan 2022Cardiotoxins (CaTxs) are a group of snake toxins that affect the cardiovascular system (CVS). Two types (S and P) of CaTxs are known, but the exact differences in the...
Cardiotoxins (CaTxs) are a group of snake toxins that affect the cardiovascular system (CVS). Two types (S and P) of CaTxs are known, but the exact differences in the effects of these types on CVS have not been thoroughly studied. We investigated cellular mechanisms of action on CVS for cobra CaTxs CTX-1 (S-type) and CTX-2 (P-type) focusing on the papillary muscle (PM) contractility and contraction of aortic rings (AR) supplemented by pharmacological analysis. It was found that CTX-1 and CTX-2 exerted dose-dependent effects manifested in PM contracture and AR contraction. CTX-2 impaired functions of PM and AR more strongly than CTX-1. Effects of CaTxs on PM were significantly reduced by nifedipine, an L-type Ca channel blocker, and by KB-R7943, an inhibitor of reverse-mode Na/Ca exchange. Furthermore, 2-aminoethoxydiphenyl borate, an inhibitor of store-operated calcium entry, partially restored PM contractility damaged by CaTxs. The CaTx influence on AR contracture was significantly reduced by nifedipine and KB-R7943. The involvement of reverse-mode Na/Ca exchange in the effect of CaTxs on the rat aorta was shown for the first time. The results obtained indicate that CaTx effects on CVS are mainly associated with disturbance of transporting systems responsible for the Ca influx.
Topics: Animals; Aorta; Cardiotoxins; Elapid Venoms; Male; Muscle Contraction; Naja naja; Papillary Muscles; Rats, Wistar; Vasoconstriction; Rats
PubMed: 35202116
DOI: 10.3390/toxins14020088 -
The Journal of Physiology Jul 19891. Heat and force were measured from isometrically contracting (0.2 Hz) rabbit papillary muscles at 21 degrees C during a single contraction-relaxation cycle using...
1. Heat and force were measured from isometrically contracting (0.2 Hz) rabbit papillary muscles at 21 degrees C during a single contraction-relaxation cycle using antimony-bismuth thermopiles and a capacitance force transducer. 2. Tension-independent heat (TIH) associated with excitation-contraction coupling was isolated from the initial heat by eliminating tension and tension-dependent heat with a Krebs-Ringer solution containing 2,3-butanedione monoxime (BDM) and mannitol. 3. A strategy for testing the validity of this new method for measuring TIH in heart muscle is described and the test confirms that the BDM-hypertonic solution partitioning method properly estimates the magnitude of the TIH component of initial heat. 4. TIH at the time of complete mechanical relaxation is 1.00 +/- 0.17 mJ/g wet weight and the data suggest that calcium cycling is complete by this time. Conversion of TIH to calcium cycled, assuming that 87% of TIH is due to calcium pumping by the sarcoplasmic reticulum, indicates that approximately 52 nmol calcium/g wet weight are required to support a single cycle of mechanical activity (0.2 Hz, 21 degrees C). 5. The length and frequency dependence of excitation-contraction coupling were demonstrated. TIH is reduced by shortening muscle length and by increasing the interval between stimuli. These steady-state data suggest that only a portion (approximately 40%) of TIH is directly related to activation of the contractile apparatus. 6. TIH in the first twitch following a 45 min rest period is significantly reduced by approximately 30%. 7. With subsequent twitches in the positive treppe following the rest period, TIH does not increase as steeply as expected suggesting that tension rise in twitches 1-10 may be modulated by competitive binding of calcium rather than increased calcium delivery.
Topics: Animals; Chromogenic Compounds; Diacetyl; Electric Stimulation; Evaluation Studies as Topic; Hot Temperature; Hypertonic Solutions; Isotonic Solutions; Male; Methods; Myocardial Contraction; Papillary Muscles; Rabbits; Rest; Time Factors
PubMed: 2607437
DOI: 10.1113/jphysiol.1989.sp017697