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We investigated a total of 15 mitral valves with myxomatous degeneration and compared these with normal mitral valves. In normal mitral valves, stromal cells located in the fibrosa and spongiosa showed small bipolar cytoplasmic processes and were found to be positive for CD34, suggesting a close relationship to CD34+ fibrocytes. In cases of myxomatous degeneration, stromal cells showed an altered morphology in that they exhibited multipolar cytoplasmic processes, appeared to be hyperplastic, and were increased in number. This study is the first to report on CD34+ fibrocytes making up the majority of mitral valve stromal cells. Major factors in the development of myxomatous valve degeneration are MMP-9, as well as collagen I and III, which have been reported to be secreted by CD34+ fibrocytes. Therefore, it is likely that CD34+ fibrocytes are involved in the pathogenesis of myxomatous mitral valve degeneration.

To determine if pimobendan, a phosphodiesterase III inhibitor and calcium sensitizer with positive survival benefits, has an effect on incidence of arrhythmias compared to placebo in small breed dogs with congestive heart failure (CHF) due to myxomatous mitral valve degeneration (MMVD).Eight client-owned small breed dogs (15 kg) with CHF due to MMVD.A prospective double-blind randomized placebo-controlled crossover study design was used. Data were recorded at baseline and 2 weeks post-administration of placebo or pimobendan. Average heart rate and incidence of arrhythmia were determined from 24 h Holter analysis. Owners completed a quality of life (QOL) questionnaire at each time point and recorded sleeping respiratory rates (SRR). Mixed effects analysis of variance, with dog as the random variable was used to compare values obtained between baseline, placebo, and pimobendan.Compared to baseline, QOL scores were significantly improved following administration of either placebo or pimobendan (p = 0.021 and p0.001, respectively). No significant differences in type or incidence of supraventricular or ventricular arrhythmia were identified. Average heart rate with pimobendan was significantly lower than baseline (p0.001). Compared to baseline, SRR was significantly lower with pimobendan (p = 0.004), and significantly different from placebo (p = 0.045).No significant difference between pimobendan and placebo was found on incidence of supraventricular or ventricular arrhythmia. The decrease in average heart rate and SRR may be reflective of superior heart failure control achieved with pimobendan therapy.

Background— Pathological processes underlying myxomatous mitral valve degeneration (MMVD) remain poorly understood. We sought to identify novel mechanisms contributing to the development of this condition. Methods and Results— Microarrays were used to measure gene expression in 11 myxomatous and 11 nonmyxomatous human mitral valves. Differential gene expression (thresholds P 1.5) and pathway activation (Ingenuity) were confirmed using quantitative reverse transcriptase polymerase chain reaction and immunohistochemistry. Contributions of bone morphogenetic protein 4 and transforming growth factor (TGF)-β2 to differential gene expression were evaluated in vitro. Contributions of angiotensin II to differential pathway activation were examined in mice in vivo. A total of 2602 genes were differentially expressed between myxomatous and nonmyxomatous valves. Canonical TGF-β signaling was increased in MMVD because of increased ligand expression and derepression of SMA mothers against decapentaplegic 2/3 signaling and was confirmed with quantitative reverse transcriptase polymerase chain reaction and immunohistochemistry. Myxomatous valves demonstrated activation of canonical bone morphogenetic protein and Wnt/β-catenin signaling and upregulation of their common target runt-related transcription factor 2. Our data set provided transcriptional and immunohistochemical evidence for activated immune cell infiltration. In vitro treatment of mitral valve interstitial cells with TGF-β2 increased β-catenin signaling at mRNA and protein levels, suggesting interactions between TGF-β2 and Wnt signaling. In vivo infusion of mice with angiotensin II recaptured several changes in signaling pathways characteristic of human MMVD. Conclusions— These data support a new disease framework whereby activation of TGF-β2, bone morphogenetic protein 4, Wnt/β-catenin, or immune signaling plays major roles in the pathogenesis of MMVD. We propose these pathways act in a context-dependent manner to drive phenotypic changes that fundamentally differ from those observed in aortic valve disease and open novel avenues guiding future research into the pathogenesis of MMVD.

The myxomatous mitral valve degeneration (DMVM) is the most common heart disease in dogs. The treatment of congestive heart failure (CHF) from DMVM is based on the use of angiotensin-converting enzyme inhibitors (ACE inhibitor) Receptor antagonists of angiotensin II (ARBs) promote complete blockade of angiotensin II, and are used in the treatment of CHF in humans, but is not common in dogs. The objective of this research was to compare the clinical responses of dogs carriers DMVM treated with enalapril-ACE inhibitors, losartan-ARBs. Thirteen dogs with DMVM and ICC class Ib were randomized into two groups as follows: G1-enalapril and G2-losartan. On physical examination, electrocardiogram and blood pressure were measured on days 0, 14, 28 and 56 after the begging of treatment. Radiographic measure, Vertebral Heart Size-VHS and ecodopplercardiográficas variables were obtained on days 0 and 56. Data were subjected to analysis of variance with repeated measures. There was no difference (P>0.05) for ecodopplercardiográficas, electrocardiographic and radiographic variables between the groups studied. In relation to time, there was a decrease (P

The heart valves play a crucial role in cardiovascular function by ensuring one-directional blood flow into and out of the heart. When heart valve tissues become diseased, structural changes lead to biomechanical insufficiency of the valves, which can have a major impact on blood distribution. Normal valvular homeostasis is tightly regulated by action of specialized cells residing within the valves; therefore, this article focuses on the known cellular changes that lead to pathological remodeling of heart valve extracellular matrix. At the end of the article, current and future therapeutic approaches are discussed.

A 13-year-old neutered male Maltese was referred for paroxysms of coughing and cyanosis, with radiographic evidence of bronchial disease and cardiomegaly. Investigation with echocardiography, bronchoscopy, fluoroscopy and bronchoalveolar lavage led to a diagnosis of myxomatous mitral valve degeneration with insufficiency, ISACHC class II heart failure and bronchomalacia with severe left mainstem bronchial collapse. Persistence of intractable cough despite medical therapy prompted placement of a stent in the left mainstem bronchus. Immediately after stent placement, severe pulmonary oedema developed, thought to be due to compression of the left atrium by the stent or acute lung injury related to stent placement. The dog recovered over a 3-day period with diuretic therapy and positive end expiratory pressure ventilation. Subsequently, the dog died from congestive heart failure 102 days after stent placement, during which time occasional, self limiting coughing episodes occurred.

Em cães com Doença Degenerativa Crónica da Válvula Mitral (DDCVM), de classe B1 de acordo com ACVIM, sem remodelação cardíaca, ou estenose aórtica, a pressão arterial sistémica, deve ser avaliada periodicamente, de forma a compreender a evolução da doença e decidir pela introdução de uma terapêutica considerada adequada. Como tal a determinação da pressão arterial é de extrema importância no exame clínico do animal. O presente estudo pretende comparar a medição da pressão arterial por dois métodos indiretos. Um dos métodos consiste no método Oscilométrico, frequentemente usado na prática clínica. O outro método em estudo é uma estimativa da pressão arterial sistólica, através do Gradiente de Pressão calculado durante a ecocardiografia, através da determinação da velocidade máxima do refluxo de regurgitação mitral. Uma vez que a ecocardiografia é considerada necessária para avaliação clínica deste grupo de indivíduos, pretendeu-se avaliar se este método é suficiente fiável para fazer uma avaliação da pressão arterial sistólica., Dogs undergoing Degenerative Chronic Mitral Valve Disease (DCMVD), class B1 according to ACVIM without cardiac remodeling or aortic stenosis, should be periodically submitted to systemic blood pressure evaluation in order to understand the evolution of the disease, and decide the introducing of appropriate therapy As such the determination of blood pressure is extremely important in clínical examination of the animal. The present study aims to compare the blood pressure measurement by two indirect methods. One of the methods is Oscillometric method, often used in clínical practice. Another method study is an estimated systolic blood pressure using the gradient calculated in echocardiography, by determining the speed of flow of mitral regurgitation. Since echocardiography is considered necessary for clínical evaluation of this group of individuals, we sought to evaluate whether this method is sufficient to make a reliable assessment of systolic blood pressure., Orientação : Nuno Gonçalo Ferreira Cardoso ; Co-orientação : Fausto Brandão

A 49-year-old woman with myxomatous mitral valve degeneration complicated by severe mitral regurgitation caused by endocarditis and left ventricular dilatation underwent successful mitral valve replacement using the Khonsari technique. Preoperative two-dimensional Doppler echocardiography showed severe mitral regurgitation, progressive left ventricular dilatation, left atrial enlargement, and marked calcification of the posterior anulus. Color-flow imaging revealed severe mitral regurgitation. Cardiac catheterization revealed normal coronary arteries. Postoperative findings detected by transthoracic two-dimensional and Doppler echocardiography are shown and a review of the procedure used in conjunction with mitral valve replacement is presented.

As doenças cardíacas são um achado frequente na prática clínica. Saber se pacientes assintomáticos com doença mixomatosa da válvula mitral necessitam ou não de medicação numa fase inicial da doença não é tarefa fácil. A ativação neuro-hormonal, apesar de ter um efeito benéfico compensatório a curto prazo, torna-se deletéria a longo prazo, sendo que para isso é necessária intervenção farmacológica para inibir a sua atividade O SRAA (sistema renina angiotensina aldosterona) tem importantes mecanismos patofisiológicos implicados no desenvolvimento da insuficiência cardíaca congestiva e tem como produto final a aldosterona, que contribui para a remodelagem cardíaca. Neste trabalho verifiquei a inexistência de uma diferença significativa de valores de aldosterona sérica de cães assintomáticos com Doença Mixomatosa Valvular Mitral (estadio B2 da classificação ACVIM) e os valores do intervalo de referência desta hormona. Concluí também não haver relação entre a idade, ureia, creatinina, rácio Proteina-Creainina, Pressões arteriais sistólica, média e diastólica, frequência de pulso, parâmetros de remodelagem cardíaca e padrão do fluxo transmitral com os valores da aldosterona medidos. É através da evidência destes achados que sugiro a não instituição de um IECA neste tipo de pacientes. O uso precoce de IECA pode não só não trazer vantagens terapêuticas nesta fase da doença como também vai promover o aparecimento precoce de fenómenos de “escape da aldosterona”., Heart disease is a common finding in clinical practice. Whether asymptomatic patients with myxomatous mitral valve disease need medication at an early stage of disease is no easy task. The neurohormonal activation, despite having a beneficial compensatory effect in a short term, it becomes deleterious in a long term and pharmacological intervention with ACE inhibitor is required to inhibit its activity. The RAAS (renin-angiotensin-aldosterone system) has important pathophysiological mechanisms involved in the development of congestive heart failure and aldosterona is it final product, leading to cardiac remodeling. In this work I checked the absence of a significant difference in the values of serum aldosterona in dogs with asymptomatic mitral valve regurgitation (stage B2 in ACVIM classification) and the reference values of this hormone. I also find no relationship between age, urea, creatinine, protein-creatinine ratio, systolic, mean and diastolic pressure, pulse rate, cardiac remodeling parameters and transmitral flow pattern with the measured aldosterona values. It is through these findings that I do not suggest the imposition of an ACEI in such patients. Early use ACE inhibitors may not only don’t bring therapeutic benefits at this stage of disease but also will promote the early onset of the phenomena of “aldosterone escape”., Orientação : Luís Lima Lobo ; Co-orientação : Pedro Morais de Almeida

Myxomatous degenerative mitral valve disease (MMVD) is a common heart disease in dogs. Although several morphological similarities occur between human and canine MMVD differences exist. However, in advanced stages the accumulation of proteoglycans is the main finding in both species. The extracellular matrix (ECM) in normal canine and human mitral valves is similar. In MMVD of both species proteoglycans is the major alteration, although specific changes in collagen distribution exists. The valvular expression pattern of matrix metalloproteinases (MMPs) and of their inhibitors (TIMPs) differs, in part, between dogs and humans. The MMPs and TIMPs expression patterns are similar in normal canine and human mitral valves, but they are quite different during degenerative progression. Valve endothelial cells (VEC) and interstitial cells (VIC) are phenotypically transformed in canine and human MMVD. Inflammation is an unlikely cause of valve degeneration in humans and dogs. There are several lines of evidence suggesting that transforming growth factor β1 (TGF β1) and serotonin signaling may mediate valve degeneration in humans and dogs. Although human and canine MMVD share structural similarities, there are some differences in ECM changes, enzyme expression and cell transformation, which may reflect a varied pathogenesis of these diseases.

Background Preclinical myxomatous mitral valve degeneration (MMVD) includes a heterogeneous group of dogs. Therefore, identifying risk factors for progression of the disease is of clinical importance. Objectives To investigate survival time and risk factors for clinical and echocardiographic variables taken at initial examination for clinical progression in preclinical MMVD dogs. Animals A total of 256 dogs with stage B1 or B2 MMVD. Materials and Methods Medical records of 256 dogs with preclinical MMVD were reviewed retrospectively. Long-term outcome was assessed by telephone interview. Dogs alive at the time of phone interview were asked to return to the hospital for re-evaluation of their cardiac status. Results Seventy of 256 (27.3%) dogs died during the observation period. The median survival time, regardless of cause of death, was 588 (range 75–1,668) days. The presence of a murmur was associated with an increased risk of death (AHR 2.14; 95% CI 1.12, 4.11; P = 0.022). Thirty (12%) deaths were considered cardiac related. LA/Ao > 1.4 was the only negative predictor (AHR 2.64; 1.13, 6.13; P = 0.024) for cardiac-related deaths. Eighty-three dogs were re-examined, of which 34 progressed to a more advanced stage of MMVD. The presence of Emax > 1.2 (AHR 2.75; 95% CI 1.01, 7.48; P = 0.047) and cough (AHR 7.89; 95% CI 3.18, 20.07; P

14. Ostan-Smith I, Silverman NH, Oddershaw P, Lincoln C, Shinebourne EA. Cor triatriatum sinistrum. Br Heart J 1984;51:211-19. Al Abdulla HM, Demany MA, Vimmerman HA. Cor triatriaturn: preoperative diagnosis in an adult patient. Am J Cardiol 1970;26:310-14. Miller GAH, Ongley PA, Anderson MW, Kincaid OW, Swan HJ. Cor triatriatum, hemodynamic and angiocardiographic diagnosis. AM HEART J 1964:68:298-308. MCi 31:263-72. Leung WH, Wong CK, Lau CP, Cheng CH. Cor triatriatum masked by coexisting chronic obstructive pulmonary disease in an adult. Chest 1989;96:776-8. Wong CK, Leung WH, Cheung CH, Lau CP. Myxomatous mitral valve degeneration complicating asymptomatic car triatriatum. Clin Cardiol 1989;12:48-50. Leavitt TW, Nixon JV. Cor triatriatum with mitral regurgitation in a 52-year-old male. Cathet Cardiovasc Diagn 1979; 5:75-g. Pate1 AK, Ninneman RW, Rahko PS. Surgical resection of car triatriatum in a 74-year-old man. J Am Sot Echocardiogr 1990; 3:402-7. Porter BA, Bogren HG, DeMaria AN. Cor triatriatum in an adult with mitral regurgitation and massive left atria1 enlargement. Cardiovasc Intervent Radio1 1983;6:37-40. Ludomirsky A, Erickson C, Vick GW, Cooley DA. Transesophageal color flow Doppler evaluation of car triatriatum in an adult. AM HEART J i$90;120:451-5. Marin-Garcia J. Tandon R. Lucas R. Edward JE. Cor triatriatum: study of 20 cases. Am J Cardiol 1975;35:59-66. Thilenius OG, Bharati S, Lev M. Subdivided left atrium: an expanded concept of car triatriatum sinistrum. Am J Cardiol 1976;37:743-52. Praagh PV, Corsini. Cor triatriatum: pathologic anatomy and a consideration of mophogenesis based on 13 postmortem cases and a study of normal development of the pulmonary vein and atria1 septum in 83 human embryos. AM HEART J 1969;78:379-405.

A 69-year-old Hispanic male came to the Coney Island Hospital emergency room with complaints of dyspnea for 2 days, reduced exercise tolerance, orthopnea, and paroxysmal nocturnal dyspnea. The patient denied any cough, loss of weight, night sweat, chest pain, palpitations, diaphoresis, or fever. The patient said his private physician had diagnosed a murmur a year ago but no work-up was done. He had no prior history of valvular heart disease or prior myocardial infarction. In the ER, the patient was noticed to have a temperature of 98 degrees Fahrenheit, a pulse of 112 beats per minute, regular, a blood pressure of 130/80 mm Hg with no Kussmaul9s sign, and a respiratory rate of 30 per minute. He had jugular venous distention with regular S1 and S2 hear sounds. A systolic murmur 4/6 was appreciated in mitral area radiating to the axilla. A systolic murmur in the tricuspid area 4/6 was also appreciated radiating to the carotids. Peripheral pulses were regular. Lung field auscultation revealed bibasal rales. The chest x-ray revealed acute pulmonary edema and no pleural effusion. The electrocardiogram showed sinus tachycardia and P pulmonale. Arterial blood gas showed oxygen saturation of 98% on 3 liters of oxygen. Serum chemistry including electrolytes and renal and liver function tests were normal. Urine toxicology was negative. Serial creatinine phosphokinase was normal. The patient was admitted to a monitored unit and a transesophageal echocardiogram (TEE) was performed. It documented mitral and tricuspid valve prolapse with moderate to severe mitral regurgitation and moderate tricuspid regurgitation with pulmonary hypertension. There was thickened, myxomatous, and prolapsing mitral valve posterior leaflets into the left atrium with flail segment. The chordae were intact. Interior leaflets are slightly thickened but otherwise normal in structure. The tricuspid valve posterior leaflet was also thickened, redundant, and myxomatous. Posterior leaflet was also prolapsing into the left atrium with flail segment. Tricuspid valve leaflet chordae are also intact. Left ventricle was mild to moderately dilated with global hypokinesis. Left ventricular ejection fraction was moderately compromised and visually estimated 35%. Left atrium was severely enlarged. The patient was transferred to cardiac care unit and was given diuretics, ACE inhibitors, digoxin, and prophylaxis for infective endocarditis. The patient underwent emergency mitral valve replacement. He recovered well postoperatively and noted to be stable on discharge and on follow-up. Conclusion Myxomatous prolapsing mitral valve may present late in a patient9s life as acute pulmonary edema.

This a report of myxomatous mitral valve degeneration in a child with Turner syndrome. The diagnosis was first suspected at 7 months of age. At 5 years of age, ultrasonic and angio-cardiographic confirmation prompted a successful mitral valve replacement with a Starr prosthesis. The child also had partial anomalous pulmonary venous return and a dysplastic right kidney. The child has remained well for 4 years after surgery.

Cor triatriatum presenting in adulthood is extremely rare. This paper reports a case of cor triatriatum initially masquerading as mitral stenosis, which was later complicated by myxomatous mitral valve degeneration with severe regurgitation, which necessitated mitral valvular replacement. To the authors' knowledge, such a combination has not been reported in the literature.

Myxomatous degeneration of the mitral valve is a common pathological finding in mitral valve surgery and the most common reason for severe mitral valve regurgitation. Considering the importance of right ventricular remodeling and global function after mitral valve surgery we tried to elucidate a possible association of myxomatous mitral valve and impairment of right atrial and ventricular function, which might have an impact on global ventricular performance after mitral valve surgery. Right atrial tissue was harvested from 47 patients undergoing mitral valve surgery. We took the trabeculae from the right auricle, which was resected at the right auricle for implementation of extracorporal circulation. The tissue was skinned and prepared in a 24 h-lasting procedure to create small fibers for hinging them in the "muscle machine", an experimental set-up, created for pCa-force measurements. Patients without myxomatous mitral valve developed significantly more force (4.0 mN ± 0.8 mN) at the highest step of calcium concentration compared to 2.7 mN ± 0.4 mN in group of patients with myxomatous valve degeneration (p 0.03). Calcium sensitivity in the myxomatous valve group was at pCa 6.0 and in the non-myxomatous group at pCa 5. Furthermore we observed a significant difference in ejection fraction (EF) among the groups: 49% in the non-myxomatous group versus 57% in the myxomatous group (p 0.03). In the non-myxomatous group 5 patients had diastolic dysfunction grade I-II (22,7%), in group I 10 patients (40%). This was also significant (p 0.04). Patients with myxomatous mitral valve degeneration seem to have reduced force capacities. Calcium sensitivity is higher compared to the non-myxomatous group, which might be a compensatory mechanism to cover the physiological demand. Furthermore we suggest a higher incidence of diastolic dysfunction in patients with myxomatous mitral valve degeneration, which might have an impact on ventricular remodeling after mitral valve surgery.

A principal etiologia de insuficiência cardíaca congestiva em canídeos é a doença degenerativa mixomatosa mitral (DDMM). Aquela conduz a uma diminuição no débito cardíaco e consequentemente à disfunção de vários órgãos, nomeadamente os rins. O conhecimento sobre o eixo cardiorenal permitiu entender de que modo é que a disfunção num destes órgãos conduz à disfunção do outro, provocando o síndrome cardiorenal. Neste estudo retrospectivo aborda-se o síndrome cardiorenal em canídeos com insuficiência cardíaca grau C e grau D de acordo com o Colégio Americano de Medicina Interna Veterinária (ACVIM) por DDMM. Os dados foram recolhidos usando o sistema QVET do Hospital Veterinário do Restelo e são relativos ao período de tempo entre 2006-2012. O presente estudo tem como principal objectivo determinar a incidência de azotemia em canídeos com insuficiência cardíaca resultante de DDMM, tendo também como objectivo investigar a existência de um possível efeito da furosemida sobre o desenvolvimento/agravamento da azotemia nestes pacientes. Verificou-se que existe uma relação entre padecer de insuficiência cardíaca (IC) e sofrer alterações na função renal, aumentando a frequência e a gravidade da azotemia com o avançar do grau da IC. A predisposição dos pacientes com IC para sofrerem de azotemia é independente do momento em que se institui o tratamento. Também se verificou que, apesar da dose de furosemida ser semelhante em todos estes pacientes, estes manifestavam diferentes concentrações de BUN e de creatinina sérica, podendo isto ser justificado pelo grau de disfunção renal, induzido pela IC., The main cause of congestive heart failure in dogs is a degenerative myxomatous mitral valve disease (MMVD). That leads to a decrease in cardiac output and consequently the dysfunction of various organs, including kidneys. Through the cardio-renal axis we can understand how the dysfunction in these organs leads to dysfunction of the other, causing the cardiorenal syndrome. This retrospective study refers the cardiorenal syndrome in dogs with heart failure grade C and grade D (ACVIM) by MMVD. Data were collected through the system QVET from Veterinary Hospital Restelo during the period between 2006-2012. The present study has as main objective determine the incidence of azotemia in dogs with heart failure resulting from MMVD and to realize what the effect of furosemide on the development/worsening of azotemia in these patients. It was found that exists a relationship between suffering from heart failure (HF) and renal failure. Moreover the frequency and severity of azotemia increases with the degree of HF. The predisposition of patients with HF to suffer from azotemia is independent of time when treatment was initiated. It was also found that, despite the dose of furosemide administered being similar in all the patients, these showed different concentrations of BUN and serum creatinine levels, which could perhaps be explained by the degree of renal dysfunction induced by HF., Orientação : Joana de Oliveira ; Co-orientação : Manuel Monzo