Insuficiência Mitral Isquêmica 2 - by Fábio Soares

Dr. Luis Cláudio Lemos lembrou algo importante a ser reconhecido, nomeado e servir de orientação ao clínico e cirurgião. Abaixo, algumas definições de Insuficiência Mitral Isquêmica, segundo os grandes estudiosos do tema:

Ischaemic mitral regurgitation: mechanisms and diagnosis

Thomas H Marwick,1 Patrizio Lancellotti,2 Luc Pierard2

"Ischaemic mitral regurgitation (MR) is defined as MR caused by changes of left ventricular structure and function related ultimately to ischaemia. However, the acute manifestation of MR following infarction (which usually presents as a haemodynamic crisis) is related to rupture or stretching of the papillary muscle, and is normally categorised with complications of infarction. The term ischaemic MR is usually understood to relate to chronic MR, occurring .2 weeks after infarction and in the absence of structural mitral valve disease. In terms of pathogenesis, this should be considered a disease of abnormal left ventricular (LV) shape and function with a valvular manifestation."

Ischaemic mitral regurgitation: pathophysiology, outcomes and the conundrum of treatment

Luc A. Pie´rard1* and Blase A. Carabello2

"Appropriate systolic coaptation of the anterior and posterior mitral leaflets depends on normal anatomy and function of the different components of the mitral valve apparatus: annulus, leaflets, chordae, papillary muscles, and the left ventricular (LV) wall. Mitral regurgitation (MR) consists in systolic retrograde flow from the LV to the left atrium (LA) because of the lack of adequate coaptation of the leaflets and a pressure gradient between the two cavities. It is important to distinguish between primary MR due to organic disease of one or more components of the mitral valve apparatus and secondary MR which is not a valve disease, but represents the valvular consequences of a LV disease. Secondary MR is defined as functional MR, due to LV remodelling by idiopathic cardiomyopathy or coronary artery disease. In the latter clinical setting, secondary functional MR is called ischaemic MR."

Surgical Management of Ischemic Mitral Regurgitation

Mitesh V. Badiwala, MD; Subodh Verma, MD, PhD; Vivek Rao, MD, PhD

"The pathophysiology of IMR is complex. Coronary artery disease results in myocardial ischemia and culminates in an infarction. These acute and chronic insults set the stage for maladaptive left ventricular remodeling (with apical and posterior displacement of the papillary muscles), which in turn leads to altered left ventricular function and underlies the pathophysiology of IMR.13–18 Indeed, in as many as 19% of patients who experience an acute MI, IMR then develops.2,3 The remodeling of the left ventricle further results in subvalvular apparatus dysfunction with leaflet tethering caused by papillary muscle displacement and also results in loss of mitral annular contraction with annular dilatation. 13–18 As leaflet tethering occurs, the leaflets fail to coapt during systole and on echocardiographic examination are usually found to have restricted motion resulting in Carpentier type IIIb mitral regurgitation. As mitral annular dilatation secondary to left ventricular enlargement occurs, the leaflets also fail to coapt centrally, resulting in Carpentier type I mitral regurgitation. These changes ultimately lead to what is known as functional mitral regurgitation. Mitral regurgitation, in turn, leads to left

ventricular volume overload and exacerbates maladaptive left ventricular dilatation, completing the vicious circle of IMR and left ventricular remodeling. The majority of patients with IMR have functional MR with structurally normal mitral leaflets and subvalvular apparatus. The remaining patients with IMR have “structural” MR with either papillary muscle rupture or papillary muscle infarction with an intact papillary muscle, each requiring differing surgical repair techniques.5,19,20".

Mitral regurgitation
Maurice Enriquez-Sarano, Cary W Akins, Alec Vahanian

The ischaemic form of this disease rarely results from an organic mechanism (papillary-muscle rupture)25 and is rarely acute. Frequently, it is functional (structurally normal leafl ets) and chronic, epitomising left-ventricular disease that causes valvular dysfunction. Papillarymuscle dysfunction plays little part in the generation of functional mitral regurgitation, which is mostly caused by apical and inferior-papillary-muscle displacement due to ischaemic left-ventricular remodelling


How to manage ischaemic mitral regurgitation
Patrizio Lancellotti,1 Thomas Marwick,2 Luc A Pierard3


Ischaemic heart disease is becoming an increasingly frequent cause of ischaemic mitral regurgitation (IMR). Three different clinical entities of IMR, which deeply affect the clinical decision making, are distinguishable: the acute IMR complicating an acute myocardial infarction, the true IMR secondary to a transient ischaemic phenomenon, and the chronic functional IMR (FIMR). The incidence of the two first entities is low; the third is much more frequent.

Insuficiência Mitral Isquêmica - by Fábio Soares

- A insuficiência mitral resulta do desbalanço entre o aumento das forças de tração (tethering forces), e redução das forças de fechamento, estas últimas incluem redução da contratilidade do VE, contração sistólica anular anormal, assincronia entre os músculos papilares e intraventricular, principalemnte nos segmentos basais.

- Uma característica importante da IM isquêmica é seu componente dinâmico. A área do orifício regurgitante efetivo (ERO) pode mudar durante a sístole, sendo maior na proto e telesístole. (observe esta inferência no modo M color)

- Uma observação interessante é a alteração do grau da IM determinada pelo esforço físico. Em alguns pacientes com IM moderada ou grave em repouso, uma diminuição do ERO pode ser observado com o exercício e usualmente resulta da reserva contrátil do VE, em particualr do segmento ínfero-látreo-basal, e/ou uma redução da assincronia intraventricular. Ao contrário, cerca de 30% dos pctes pioram o grau de IM e PSAP durante o esforço

Lancellotti P, Lebrun F, Pie´rard LA. Determinants of exercise-induced changes in mitral regurgitation in patients with coronary artery disease and left ventricular dysfunction. J Am Coll Cardiol 2003;42:1921–1928.

Lancellotti P, Pie´rard LA. Chronic ischaemic mitral regurgitation: exercise testing reveals its dynamic component. Eur Heart J 2005;26:1816–1817.

- O consenso europeu recomenda a graduação da IM baseado no cálculo do orifício regugitante pelo método de PISA e o volume regurgitante pela equação da continuidade, devendo a análise semiquantitativa (área do jato regurgitante) ser abandonada.

Lancellotti P, Moura L, Pierard LA, Agricola E, Popescu BA, Tribouilloy C, Hagendorff A, Monin J-L, Badano L, Zamorano JL. European Association of Echocardiography recommendations for the assessment of valvular regurgitation. Part 2: mitral and tricuspid regurgitation (native valve disease). Eur J Echocardiogr 2010;11:307–332.

- IM isquêmica grave, segundo alguns autores, deveria ser definida pela presença de volume regurgitante > 30ml e ERO>20mm2.

Grigioni F, Enriquez-Sarano M, Zehr KJ, Bailey KR, Tajik AJ. Ischemic mitral regurgitation: long-term outcome and prognostic implications with quantitative Doppler assessment. Circulation 2001;103:1759–1764.

Heart

2009;95:1711–1718

2008;94:1497–1502

Heart

Boa Páscoa a todos... "Você sabe com quem está falando?"

Dica de Dra Janine Magalhães

Aterosclerose e Estenose Aórtica... Espectros de uma mesma doença?

- Este artigo não trata do velho assunto Estatina x Estenose aórtica, mas sim da presença de hemorragia intravalvular podendo contribuir para rápida progressão da estenose aórtica degenerativa, tal qual ocorre em placas ateroscleróticas em coronárias, aorta e carótidas.

Intraleaflet haemorrhage is associated with rapid progression of degenerative aortic valve stenosis

Hirokuni Akahori1, Takeshi Tsujino2*, Yoshiro Naito1, Mika Matsumoto1, Masaaki Lee-Kawabata1, Mitsumasa Ohyanagi3, Masataka Mitsuno4, Yuji Miyamoto4, Takashi Daimon5, Hiroyuki Hao6, Seiichi Hirota6, and Tohru Masuyama1

Aims - The haemorrhage in the plaque (intraplaque haemorrhage) plays a critical role in the progression of atherosclerosis. The purpose of this study is to clarify whether the haemorrhage in the aortic valve leaflet (intraleaflet haemorrhage) accelerates the progression of aortic valve stenosis (AS).

Methods and results - We examined specimens of aortic valve leaflets obtained from 36 patients who had undergone aortic valve replacement for degenerative AS and in whom echocardiographic data were available just before the operation and at least 180 days before the last study. The stenotic valves were examined by immunohistochemistry to detect intraleaflet haemorrhage with antibody against glycophorin A, an erythrocyte-specific protein. The progression of AS was assessed by annualized change in the aortic valve area (DAVA: cm2/year). The patients were divided into two groups, namely the rapid progression group (DAVA ≥ 0.1 cm2/year) and the slow progression group (DAVA , 0.1 cm2/year), according to the reported average progression rate of AS. Intraleaflet haemorrhage was observed in 78 % of the specimens. Intraleaflet haemorrhage was associated with neovascularization and macrophage infiltration. The areas of intraleaflet haemorrhage and macrophage infiltration were greater in the rapid progression group than in the slow progression group. Multivariate analysis has shown that the area of intraleaflet haemorrhage was the sole independent factor that positively correlated with DAVA.

Conclusions Intraleaflet haemorrhage was frequently observed in the valve leaflets of degenerative AS and associated with a rapid progression of AS.

Insuficiência mitral após IAM anterior





Só uma dor de cabeça... - by Fábio Soares

Adendo do Post anterior - Takotsubo reverso

Ennezat PV, Pesenti-Rossi D, Aubert JM, Rachenne V, Bauchart JJ, Auffray JL, Logeart D, Cohen-Solal A, Asseman P. Transient left ventricular basal dysfunction without coronary stenosis in acute cerebral disorders: a novel heart syndrome (inverted Takotsubo). Echocardiography. 2005 Aug;22(7):599-602.

Sanchez-Recalde A, Costero O, Oliver JM, Iborra C, Ruiz E, Sobrino JA. Images in cardiovascular medicine. Pheochromocytoma-related cardiomyopathy: inverted Takotsubo contractile pattern. Circulation. 2006 May 2;113(17):e738-9.

Recomendo a leitura

http://ejechocard.oxfordjournals.org/content/10/2/332.full.pdf

http://www.mayoclinicproceedings.com/content/81/11/1499.full.pdf+html

Síndrome de Takotsubo - by Fábio Soares

- A Cardiomiopatia de Takotsubo (MTC) é uma síndrome cardíaca transitória que envolve acinesia apical do ventrículo esquerdo e simula a síndrome coronária aguda (SCA). Foi descrita pela primeira vez no Japão em 1990 por Sato et al. Os pacientes geralmente apresentam dor precordial, elevação do segmento ST, elevação dos marcadores de necrose miocárdica compatíveis com infarto do miocárdio. Caracteristicamente, a coronariografia não evidencia doença aterosclerótica significativa.

- Os critérios modificados da MayoClinic para o diagnóstico de miocardiopatia de Takotsubo pode ser aplicado a um paciente no momento da apresentação e devem conter todas as quatro aspectos:

     • Hipocinesia transitória, discinesia ou acinesia dos segmentos médios do ventrículo esquerdo com ou sem envolvimento apical; as anormalidades de movimento regional de parede se estendem além de uma distribuição epicárdica vascular único, um gatilho, muitas vezes é estressante, mas nem sempre presentes.
     • Ausência de doença coronária obstrutiva ou evidência angiográfica de ruptura aguda de placa
     • Anormalidades eletrocardiográficas nova (elevação do segmento ST e / ou inversão de onda T) ou modesta elevação ndos níveis de troponina
    • Ausência de feocromocitoma ou miocardite

Kawai S, Kitabatake A, Tomoike H. Guidelines for diagnosis of takotsubo (ampulla) cardiomyopathy. Circ J. Jun 2007;71(6):990-2.

- A exata etiologia da cardiomiopatia de Takotsubo  ainda é desconhecida, mas várias teorias têm sido propostas e estão sendo investigadas. Estas incluem o espasmo de múltiplos vasos da árvore coronária, disfunção microvascular, ineficiência no metabolismo dos ácidos graxos do miocárdio, síndrome coronariana aguda com injúia de reperfusão, e microinfartos ou stunning miocárdico induzido por catecolaminas endógenas.

- As porções apicais do VE têm as maiores concentrações da inervação simpática encontradas no coração e pode explicar o motivo pelo qual o excesso de catecolaminas determina as alterações da contratilidade segmentar.

Dorfman TA, Iskandrian AE. Takotsubo cardiomyopathy: State-of-the-art review. J Nucl Cardiol. Jan-Feb 2009;16(1):122-34.



- Estudos têm relatado que 1,7-2,2% dos pacientes que tinham suspeita de síndrome coronariana aguda foram posteriormente diagnosticados com cardiomiopatia de Takotsubo.

- As complicações agudas ocorrem em aproximadamente 20% dos pacientes, incluindo choque cardiogênico, insuficiência cardíaca, edema pulmonar, arritmias, formação de trombo ventricular, ruptura da parede livre do ventrículo esquerdo, e morte. Estimativas das taxas de mortalidade variaram 1-3,2%.

- Os pacientes são tipicamente asiáticas ou do Cáucaso. Em uma revisão de literatura de casos em que a raça foi referida 57,2% eram asiáticos, 40% eram brancos e 2,8% eram de outras raças. Quase 90% dos casos relatados envolvem mulheres na pós-menopausa. Revisão da literatura relatam uma média de idade do paciente de 67 anos, embora os casos ocorreram em crianças e adultos jovens

Donohue D, Movahed MR. Clinical characteristics, demographics and prognosis of transient left ventricular apical ballooning syndrome. Heart Fail Rev. Dec 2005;10(4):311-6

Gianni M, Dentali F, Grandi AM, Sumner G, Hiralal R, Lonn E. Apical ballooning syndrome takotsubo cardiomyopathy: a systematic review. Eur Heart J. Jul 2006;27(13):1523-9.

Fenômeno da Cavitação - by Fábio Soares

O fenômeno de cavitação é a rápida formação de microbolhas em meio líquido devido a uma redução local da pressão a níveis abaixo da pressão de vapor sendo bastante similar a ebulição. A 1 atmosfera, a água entra em ebulição a 100oC. Quando a pressão cai, o ponto de ebulição também cai. Assim, a cavitação é o processo no meio líquido onde o ponto de ebulição é alcançado não por aumento da temperatura, mas por diminuição da pressão.

Em uma prótese metálica, por um momento, quando os discos se aproximam, o sangue é "espremido" gerando uma zona de baixa pressão enrtre a superfície oclusora e a superfície de sustentação, favorecendo a ocorrência da cavitação.

Uma outra hipótese para queda  da pressão e possibilitar a cavitação está no núcleo do vórtice. A pressão cai porque a velocidade aumenta para o centro do vórtice do fluxo transprotético.

Se os eventos envolvidos no fechamento da prótese valvar podem gerar zonas de baixa pressão suficientes para haver a cavitação, é provável que isso pode danificar a estrutura da prótese e as céluas sangüíneas circunvizinhas, aumentando o risco de eventos tromboembólicos.

Pausa no blog...Até segunda!!!

Operação Tapa Buracos! - Forame oval patente

Migraine Intervention With STARFlex Technology (MIST)

From: http://heartdisease-alaircastro.blogspot.com/2008/03/migraine-intervention-with-starflex.html

Writer: Anthony A. Bavry, M.D., M.P.H.


Description


The goal of this trial was to evaluate closure of patent foramen ovale (PFO) compared with a sham procedure in patients with refractory migraine headache.
Hypothesis


Closure of a PFO with the STARFlex device will be more effective in reducing migraine headache.


Drugs/Procedures Used


After general anesthesia, patients underwent transesophageal echocardiography to assess the interatrial septal anatomy. Patients were then randomized to PFO closure (n = 74) or a sham procedure that consisted of a skin incision (n = 73).


Concomitant Medications


Patients received aspirin (300 mg) and clopidogrel (300 mg) 24 hours prior to the procedure and for 90 days after the procedure at a dose of 75 mg daily for both medications. Patients continued any prophylactic medication that they were on at the start of the trial.


Principal Findings


Of the migraine patients referred for potential study enrollment, a right-to-left shunt from a moderate-to-large PFO was documented by transthoracic echocardiography in 38%. Any type of shunt, including atrial septal defect, was present in 60%. The mean number of migraine attacks in the 30 days prior to the procedure was 4.82 in the closure group and 4.51 in the sham group. No PFO was identifiable in 7% of the closure group. Residual moderate-to-large right-to-left shunt was present in four patients at 6 months. There were more serious procedural-related adverse events in the closure group (atrial fibrillation, n = 2; pericardial tamponade, n = 2; retroperitoneal hemorrhage, n = 1; and chest pain, n = 2).
Three patients in each group reported migraine cessation (p = 1.0). Similarly, for closure versus sham, there was no difference in any of the secondary endpoints; frequency of migraine attacks per month (3.23 vs. 3.52, p = 0.14), total MIDAS headache score (17 vs. 18, p = 0.88), or headache days per 3 months (18 vs. 21, p = 0.79).
No difference in treatment effect was noted, regardless of whether a residual shunt was present at follow-up. Two patient outliers accounted for one-third of the study headache burden. When these patients were removed from analysis, there was a reduction of 2.2 headache days per month in the closure group versus 1.3 days per month in the sham group (p = 0.027).


Interpretation


This was the first randomized sham-controlled trial to study the effect of PFO closure in patients with refractory migraine. An important finding was that among migraine patients referred for analysis, some type of right-to-left shunt was documented in 60% (in 38% due to PFO). The primary outcome, cessation of migraine, occurred in three patients in each group. Secondary outcomes such as frequency of migraines and headache scores were also similar between the two groups.When the two patient outliers were excluded from analysis, a difference was noted in the reduction of headache days favoring PFO closure; however, this finding should only be hypothesis generating since it was a post-hoc analysis.
Failure to detect a difference between treatment groups may have been at least partly explained by lack of adequate power. It is unknown if a longer duration of follow-up to allow for more complete healing of the defect would have also been beneficial. Additionally, patients continued prophylactic medications throughout the trial, which may have made it more difficult for the PFO device to show benefit. Additional trials on the topic are forthcoming.


References:


Dowson A, Mullen MJ, Peatfield R, et al. Migraine Intervention With STARFlex Technology (MIST) Trial. A Prospective, Multicenter, Double-Blind, Sham-Controlled Trial to Evaluate the Effectiveness of Patent Foramen Ovale Closure With STARFlex Septal Repair Implant to Resolve Refractory Migraine Headache. Circulation 2008;Mar 3:[Epub ahead of print].

O Estranho Caso do Fechamento do Foramen Oval Patente em AVC Criptogênico

From: http://medicinabaseadaemevidencias.blogspot.com/2010/11/o-estranho-caso-do-fechamento-do.html

Segundo o dicionário Wiktionary, criptogênico significa “de causa desconhecida”. Pois bem, é uma prática comum o fechamento de forâmen oval patente (FOP) em pacientes com acidente vascular cerebral (AVC) criptogênico. Isso é baseado na seguinte premissa: se não sabemos a causa do AVC e o paciente tem um FOP, este pode ser a causa (embolia paradoxal), então vamos fechar este buraco que o paciente não mais terá o AVC. No entanto, não há ensaios clínicos que demonstrem este procedimento ser eficaz na prevenção de AVC recorrente.

Na verdade, nem sabemos se FOP realmente causa AVC. Para começar, FOP está presente em 25% da população geral. Sendo uma condição tão comum, pode muito bem estar presente em quem teve um AVC, sem necessariamente ter causado o AVC. Em segundo lugar, estudos de coorte prospectiva demonstram que a associação de FOP e risco de AVC desaparece após ajuste para os demais fatores de risco. Em terceiro lugar, há duas semanas foi apresentado no congresso do AHA o estudo CLOSURE I, o primeiro ensaio clínico randomizado que testa a hipótese de que fechar FOP reduz o risco de um novo AVC. Neste trabalho, 909 pacientes foram randomizados para fechamento percutâneo do FOP associado a AAS e Clopidogrel versus tratamento conservador com AAS e anticoagulante oral. Não houve diferença na incidência de AVC recorrente entre os dois grupos. Ou seja, o primeiro ensaio clínico randomizado foi negativo, reforçando a idéia de que é inadequado indicar procedimentos na ausência de evidências científicas. Vale salientar que alguns pacientes do grupo intervencionista apresentaram AVC decorrente do próprio procedimento, além da ocorrência de complicações vasculares.

O critério de inclusão deste estudo foi descrito como AVC criptogênico e a média de idade da amostra (45 anos, relativamente jovem) reforça a idéia de que era uma população com características criptogênicas. Mas precisamos esperar a publicação do artigo na íntegra, para conhecer melhor a população que foi estudada. Outro detalhe importante é que este ainda é um estudo relativamente pequeno e pode carecer de poder estatístico para detectar diferenças que não sejam de grande magnitude. De acordo com meus cálculos, seriam necessários 5000 pacientes randomizados para gerar um poder de 80% para detectar uma diferença absoluta de 2%.

Outro aspecto é que este estudo não avalia exatamente se o procedimento reduz AVC, pois o tratamento medicamentoso foi diferente entre os grupos. Para testar essa hipótese, o tratamento medicamentoso deveria ser igual nos dois grupos. Não sabemos se não houve benefício porque o fechamento do FOP não vale nada ou porque vale alguma coisa semelhante à anticoagulação. De qualquer forma, sendo igual a anticoagulação, não justifica um procedimento mais complexo e de altíssimo custo (a prótese custa mais que R$ 50.000). Finalmente, fica a questão se em subgrupos específicos, “mais criptogênicos”, pode haver benefício.

Realmente não podemos considerar esta uma questão fechada, mas o conjunto de evidências (FOP como fator de risco e o primeiro ensaio clínico) existentes fala contra o benefício do procedimento. Para agravar a questão da realização de um procedimento sem evidências, temos presenciado a indicação de fechamento de FOP em pacientes que não se encaixam na definição de criptogênico, mas que tiveram um ecocardiograma transesofágico indicando a presença de FOP.

Ontem mesmo, uma amiga me contou o caso de sua tia idosa, que cursou com acidente isquêmico transitório, sendo diagnosticado um FOP no ecocardiograma transecofágico e prontamente tratada com o fechamento do FOP. “Graças a Deus, a causa do problema foi identificada e tratada, agora está resolvido”. Naquela conversa informal, acessando como quem não quer nada os fatores de risco da tia idosa, percebi que clinicamente o quadro era de um AIT de origem aterotrombótica. Isso ainda levanta a questão do uso apropriado de ecocardiograma transesofágico em pacientes com AVC. Indicações indiscriminadas podem levar a fechamento desnecessários de FOP. Assim como cateterismo desnecessário leva a angioplastia desnecessária, ecocardiograma transesofágico desnecessário pode levar a fechamento de FOP desnecessário.

Esse é mais um exemplo do paradigma mecanicista (fechar buraco) prevalecendo sobre o paradigma da medicina baseada em evidências. Esperemos as evidências futuras, há maiores ensaios clínicos em andamento.

Qual o diagnóstico? - by Fábio Soares

Você reconhece este fenômeno? Existe repercussão clínica?

Jornada do Hospital Santa Izabel - Estimulação Cardíaca

Teremos um tópico sobre o Ecocardiograma no papel da terapia de ressincronização ventricular. Estamos todos convidados.

Colchicine halves incidence of postpericardiotomy syndrome - from Heartwire

Stockholm, Sweden - The first large-scale double-blind, placebo-controlled trial to test the efficacy of colchicine to prevent the development of postpericardiotomy syndrome (PPS) after heart surgery has shown that the drug is very effective, with only eight people needing to be treated to prevent one from developing the syndrome.

"Colchicine halves the risk of postpericardiotomy syndrome following cardiac surgery, and not only is it efficacious but it is safe," said lead author of the study, Dr Massimo Imazio (Maria Vittoria Hospital, Turin, Italy), who presented the findings at the European Society of Cardiology 2010 Congress today. The results were also published simultaneously in the European Heart Journal.

Discussant for the study, Dr Andre Keren (Hadassah University Hospital, Jerusalem, Israel), concurred. He said this was "a carefully performed trial in which colchicine proved an effective and safe treatment modality—it halved the risk of developing postpericardiotomy syndrome without major side effects, and I would like to congratulate the study authors."

Impressive reduction of primary end point with colchicine

 

Imazio explained that PPS is a relatively common and troublesome complication following cardiac surgery, occurring a few days to several weeks after the surgical operation in 10% to 40% of patients. PPS can have a difficult course and complicate the postoperative period with life-threatening events such as cardiac tamponade; moreover, it may prolong the hospital stay and increase management costs, he said. Treatment is based on aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs), with steroids being considered in the case of contraindications to or failure of NSAIDs. At present, no pharmacological strategies have been proven to be efficacious in the prevention of the syndrome, he noted. Anecdotal reports have suggested that colchicine may be useful for the treatment of patients with PPS, and it has also been proposed for the primary prevention of the condition on the basis of a preliminary report from Israel. However, this study was insufficiently powered to show a benefit of colchicine in this indication, Imazio explained. The new trial, Colchicine for the Prevention of the Postpericardiotomy Syndrome (COPPS), is the first prospective, randomized, multicenter trial to test colchicine for the primary prevention of PPS using intention-to-treat analysis, he added.  In the study, 360 cardiac-surgery patients were randomized to colchicine or placebo on the third postoperative day, with those receiving the active drug taking 1.0 mg twice daily for the first day followed by a maintenance dose of 0.5 mg twice daily for one month in those >70 kg; doses were halved for those <70 kg or intolerant to the higher dose. The primary efficacy end point was the incidence of PPS at 12 months. The secondary end point was the combined rate of disease-related hospitalization, cardiac tamponade, constrictive pericarditis, and relapses. There was an "impressive" relative risk reduction with colchicine of 57.9% for the primary end point, Imazio said. Colchicine also significantly reduced the rate of the secondary end point, although Keren observed in his discussion that this was not as great a reduction as that seen with the primary end point.

The rate of side effects (mainly related to gastrointestinal intolerance) was similar in the colchicine and placebo groups (respectively, 8.9% vs 5.0%; p=0.212). The relative lack of side effects seen in this trial could be due to the fact that Imazio and colleagues used a much lower dose of colchicine, around a third of that used in the earlier preliminary Israeli trial, Keren said. In their paper, the Italian researchers say the exact mechanism of colchicine action is not fully understood. Most of the pharmacological effects of the drug on inflammation appear to be related to its capacity to disrupt microtubules, and by this mechanism, colchicine is able to inhibit various leukocyte functions, they note, adding that this effect is likely the most significant for the anti-inflammatory action.

Definition of PPS still problematic

Imazio added that the major limitation of the study relates to the definition of PPS, "because there is no general agreement on how to diagnose the syndrome," with the only published criteria having been proposed in the preliminary study from Israel.

"We adopted the same diagnostic criteria for PPS. They can be criticized and considered weak," he and his colleagues state in the paper. "Nevertheless, they represent the first attempt to have an objective approach to the diagnosis."

Massimo Imazio M, Trinchero R, Brucato A, et al. Colchicine for the Prevention of the Post-pericardiotomy Syndrome (COPPS): A multicentre, randomized, double-blind, placebo-controlled trial. Eur Heart J 2010; DOI:10.1093/eurheartj/ehq319. Available at: http://eurheartj.oxfordjournals.org.

 

Trombose de Prótese Mecânica - by Fábio Soares

Há exatos alguns minutos atrás estávamos discutindo um caso na UTI. Tratava-se de uma paciente feminina, 56 anos, com passado de trova valvar mitral há 18 anos (3 trocas prévias por por disfunção), evoluindo há 30 dias com dispnéia aos esforços. Quando do início dos sintomas, realizou ECO transtorácico que evidenciou prótese mecânica normofuncionante (gradiente médio AE/VE 6mmHg e PSAP estimada em 30mmHg). Os sintomas agravaram-se, sendo admitida na UTI há 48h com franca insuficiência respiratória devido a edema agudo de pulmão. Realizou ecocardiograma transtorácico e transesofágico que evidenciou disfunção de prótese, com restrição da mobilidade de um de seus folhetos, com diferença de velocidade na abertura dos discos, determinando gradiente AE/VE máximo 34mmHg e médio 16mmHg, com PSAP estimada em 90mmHg. Não foram visuaizados trombos. A paciente encontra-se em VM, em uso de baixas drogas de vasoativas, com edema agudo de pulmão refratário. O que fazer? Este foi o motivo de muita discussão entre Ecocardiografistas, Cardiologistas clínicos e Cirurgião Cardiovascular.

Pontos a lembrar

- Idade 56 anos

- Fibrilação atrial permanente

- HP grave

- 4 cirurgias prévias para troca de próteses em posição mitral

- Edema agudo de pulmão refratário /IC CF IV

- TP fora da faixa terapêutica

- Ecocardiograma há 30 dias, sem evidências de disfunção de prótese

O que fazer? Trombolítico? Cirurgia Cardíaca?

Conforme a literatura...

The Thrombosed Prosthetic Valve Current Recommendations Based on Evidence From the Literature

Joseph S. Alpert, MD, FACC
 
1. All patients with suspected TPVs should undergo echocardiographic study. If adequate visualization of the

prosthetic valve is not obtained by a transthoracic study, then a transesophageal echocardiographic study should be undertaken (level of evidence I).

2. Patients with right-sided TPVs should be treated with intravenous rtPA (100 mg administered as 10 mg immediate intravenous bolus followed by 90 mg infused over 90 min) or SK (500,000 IU over 20 min followed by 1.5 million IU infused over 10 h). Reduced doses should be employed in children and very small adults (level of evidence IIa).

3. Patients who are critically ill on presentation with TPV (pulmonary edema, hypotension, NYHA class III/IV symptoms) should receive immediate intravenous thrombolytic therapy as outlined earlier following appropriate echocardiographic confirmation of TPV (level of evidence IIa).

a. Serial echocardiographic studies should be performed in these individuals, and repeated infusions of trombolytic therapy should be administered if complete resolution of prosthetic valve thrombus is not achieved (level of evidence IIa).

b. Concomitant intravenous unfractionated heparin should be administered along with thrombolytic therapy to achieve an activated partial thromboplastin time that is 1.5 to 2.0 times control (level of evidence IIb).

c. Cardiac surgical consultation should be sought urgently. Valve replacement should be seriously considered

if repeated infusions of thrombolytic therapy fail to adequately dissolve the thrombus on the prosthetic valve (level of evidence IIa).

4. Patients with TPV who are clinically stable, that is, in NYHA clinical class I or II, may be managed medically with thrombolytic/antithrombotic therapy or surgically with valve replacement depending on physician/patient preference (level of evidence IIa).

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Echocardiographic signs of obstructive prosthetic valve thrombosis

 

• Reduced valve mobility
• Presence of thrombus
• Abnormal transprosthetic flow
• Central prosthetic regurgitation
• Elevated transprosthetic gradients
• Reduced effective prosthetic area

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 THROMBOSIS OF PROSTHETIC HEART VALVES: DIAGNOSIS AND THERAPEUTIC CONSIDERATIONS
Raymond Roudaut, Karim Serri, Stephane Lafitte

Heart 2007;93:137–142. doi: 10.1136/hrt.2005.071183

Para descontrair...

Já tinha visto este vídeo antes, mas tinha esquecido até rever no site Cardiopapers.

Gordura Epicárdica - by Fábio Soares

Epicardial Fat: An Additional Measurement for Subclinical Atherosclerosis and Cardiovascular Risk Stratification?

Matthew R. Nelson, MD, Farouk Mookadam, MD, FACC, MSc(HRM), Venkata Thota, MD, Usha Emani, MD, Mohsen Al Harthi, MD, FACC, Steven J. Lester, MD, FACC, FRCPC, FASE, Stephen Cha, MSc, Jan Stepanek, MD, MPH, and R. Todd Hurst, MD, FACC, FASE, Scottsdale, Arizona; Rochester, Minnesota

Background: The value of epicardial adipose tissue (EAT) thickness as determined by echocardiography in cardiovascular risk assessment is not well understood. The aim of this study was to determine the associations between EAT thickness and Framingham risk score, carotid intima media thickness, carotid artery plaque, and computed tomographic coronary calcium score in a primary prevention population.

Methods: Patients presenting for cardiovascular preventive care (n = 356) who underwent echocardiography

as well as carotid artery ultrasound and/or coronary calcium scoring were included.

Results: EAT thickness was weakly correlated with Framingham risk score. The prevalence of carotid plaque

was significantly greater in those with EAT thickness >5.0 mm who either had low Framingham risk scores or had body mass indexes >25 kg/m2, compared with those with EAT thickness <;5.0 mm. No significant association between EAT thickness and carotid intima-media thickness or coronary calcium score existed.

Conclusion: EAT thickness >5.0 mm may identify an individual with a higher likelihood of having detectable carotid atherosclerosis. (J Am Soc Echocardiogr 2011;24:339-45.)

Resposta do caso clínico da semana - by Fábio Soares

Megaesôfago Chagásico + Cardiomiopatia Dilatada Grave (MCC) + Trombo móvel em VE

Abaixo, um relato de caso semelhante, porém com acalásia ao invés de megaesôfago, mas usando contraste.

Para todo benefício, há um preço... - by Fábio Soares

Background—Permanent pacemaker (PPM) requirement is a recognized complication of transcatheter aortic valve implantation. We assessed the UK incidence of permanent pacing within 30 days of CoreValve implantation and formulated an anatomic and electrophysiological model.

Methods and Results—Data from 270 patients at 10 centers in the United Kingdom were examined. Twenty-five patients (8%) had preexisting PPMs; 2 patients had incomplete data. The remaining 243 were 81.3 6.7 years of age; 50.6% were male. QRS duration increased from 105 23 to 135 29 milliseconds (P 0.01). Left bundle-branch block incidence was 13% at baseline and 61% after the procedure (P 0.001). Eighty-one patients (33.3%) required a PPM within 30 days. Rates of pacing according to preexisting ECG abnormalities were as follows: right bundle-branch block, 65.2%; left bundle-branch block, 43.75%; normal QRS, 27.6%. Among patients who required PPM implantation, the median time to insertion was 4.0 days (interquartile range, 2.0 to 7.75 days). Multivariable analysis revealed that periprocedural atrioventricular block (odds ratio, 6.29; 95% confidence interval, 3.55 to 11.15), balloon predilatation (odds ratio, 2.68; 95% confidence interval, 2.00 to 3.47), use of the larger (29 mm) CoreValve prosthesis (odds ratio, 2.50; 95% confidence interval, 1.22 to 5.11), interventricular septum diameter (odds ratio, 1.18; 95% confidence interval, 1.10 to 3.06), and prolonged QRS duration (odds ratio, 3.45; 95% confidence interval, 1.61 to 7.40) were independently associated with the need for PPM.

 

Conclusion—One third of patients undergoing a CoreValve transcatheter aortic valve implantation procedure require a PPM within 30 days. Periprocedural atrioventricular block, balloon predilatation, use of the larger CoreValve prosthesis, increased interventricular septum diameter and prolonged QRS duration were associated with the need for PPM. (Circulation. 2011;123:951-960.)

Caso Clínico da Semana - by Fábio Soares

Alguém arrisca o diagnóstico somente baseado nas imagens, sem a história clínica?
Uma dica, não é um cisto pericárdico (como o do post anterior), nem um aneurisma da aorta torácica.