terça-feira, 15 de novembro de 2011

My name is TEP!! - by Fábio Soares

Dia 09 de novembro de 2011, às 1:30h da manhã, o dia começaria cedo...Sobreaviso acionado!

Caso 1: Pcte masc, 58 anos, em 1PO de prostatectomia radical por neoplasia maligna. Encaminhado a UTI por hipotensão sintomática, posterior evolução para choque e 10 PCRs. Solicitado Eco a beira do leito:

Ok, amanhece e a rotina corre normalmente até a tarde, quando...

Caso 2: Paciente feminina, 78 anos em 4PO de histerectomia e anexectomia por neoplasia maligna de endométrio. Cursando com dispnéia e hipoxemia em unidade aberta.

Pergunta: O que fazer nestes 2 casos?
Trombólise (2 cirurgias de grandeporte recentíssima)?
Heparinização plena apenas?
Trombólise in situ (via hemodinämica)?
Nada a fazer?

domingo, 13 de novembro de 2011

PARTNER B - by theheart.org

San Francisco, CA - Two-year outcomes in the PARTNER B trial, testing transcatheter aortic-valve replacement (TAVR) using the Sapien device (Edwards Lifesciences) against best medical care, show that survival curves are continuing to separate and the number needed to treat to save one life dropped from five at one year to four patients at two.

"Two-year data continue to support the role of TAVR as the standard of care for symptomatic patients with aortic stenosis who are not surgical candidates," said Dr Raj R Makkar (Cedars-Sinai Medical Center, Los Angeles, CA), who presented the results here at TCT 2011.
The FDA approved the Sapien valve for the US market last week, based on PARTNER B results.
By two years, 67.6% of patients in the medical group had died, compared with 43.3% in the TAVR group, a difference of 24.3%, Makkar noted. In a landmark analysis looking only at deaths between the one- and two-year mark, 35% of patients randomized to medical management who survived one year were dead within two, whereas half that amount, just 18% of the TAVR group, died in this period.
A similar separation of curves was seen for cardiovascular mortality and repeat hospitalizations. In fact, said Makkar, "there was half the number of repeat hospitalizations in the TAVR group as in the standard-therapy group, despite the fact that there were many more patients alive in the TAVR group at one year." The difference in median days alive out of hospital between the two groups added up to a full year.
Two-year outcomes: PARTNER B
End pointStandard therapy (%)TAVR (%)Absolute differenceLog rank p
All-cause mortalitya67.643.324.3< 0.0001
Cardiovascular mortalityb62.431.031.4< 0.0001
Repeat hospitalizations72.53537.5< 0.0001

a. Intention-to-treat analysis; crossover patients followed

b. Intention-to-treat analysis; crossover patients censured

A low number of cerebrovascular events continued to accrue in the TAVR arm, but not the standard-therapy arm, after the one-year mark. By two years, the "all-strokes" rate was twice as high in the TAVR group, at 11.2%, compared with 5.5% in the standard group.
Showing slides that used 30 days as the cut point—to separate periprocedural stroke from other stroke causes—Makkar showed that four hemorrhagic strokes and five ischemic strokes occurred between 30 days and two years in the TAVR group, compared with one hemorrhagic stroke and four ischemic strokes in the standard group.

"Beyond 30 days, the reason for strokes is multifactorial," he said, including things like medication use and falls.
Of note, an analysis looking at patients with mild or no paravalvular leaks and moderate or severe leaks found no mortality difference at two years.
Commenting on the study during a morning press conference, Dr Michael Mack observed, "This is absolutely a dramatic result that bolsters the one-year results. An extremely positive trial. You don't have to do anything more than look at the lines of survival between TAVR and control: there was a dramatic difference, with a 20% absolute improvement at one year, and the question is how long is the improvement going to be sustained? And the answer from this is two years . . . and hopefully longer than that."

sábado, 12 de novembro de 2011

First-of-kind HCM diagnosis, treatment recommendations published - by theheart.org

Dallas, TX and Washington, DC - "It still has the reputation of something that's hard to treat, and what we've done here, not only in the guidelines, but in the research leading up to the guidelines, is to try to change that perception," said Dr Barry J Maron (Minneapolis Heart Institute, MN), referring to a landmark set of society-sponsored recommendations for the diagnosis and management of patients with hypertrophic cardiomyopathy (HCM) [1].
Medicine's perception of the disorder, "the most common cause of sudden death in young people," Maron told heartwire, has evolved from something a bit mysterious with a generally poor outcome to "a complex but highly treatable genetic heart disease. The guidelines are an accurate recognition of not only the change in our perception of the disease and its treatment, but also of what hypertrophic cardiomyopathy is today."
Treatment follows several, sometimes overlapping, pathways that address the heightened sudden-death risk and development and progression of heart failure; atrial fibrillation is another possible manifestation that can be directly addressed.
In particular, "the defibrillator, translated to patients with hypertrophic cardiomyopathy, has altered the clinical course of the disease for many patients and is in fact the only treatment available in HCM that is proven to prolong life," Maron said.

"The idea that you can effectively prevent sudden death in this disease is a major innovation for the patient population. These are young, otherwise-healthy people, generally, who—if they are high risk—can now have the expectation that it's possible to prevent sudden cardiac death and achieve normal longevity."

The new recommendations are published online today in Circulation and copublished in the Journal of the American College of Cardiology and the Journal of Thoracic and Cardiovascular Surgery, with Maron and Dr Bernard Gersh (Mayo Clinic, Rochester, MN) as the first two authors and noted as cochairs of the writing committee.

With the American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) as its marquis sponsoring organizations, the document, it says, was developed in collaboration with the American Association for Thoracic Surgery, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons.

The writing committee acknowledged that their recommendations (aimed mainly at cardiologists, Maron noted) are rooted primarily in expert consensus (level of evidence C) given a "lack of high levels of evidence regarding HCM provided by clinical trials." But that in itself may represent something of an achievement, given the broad subspecialty spectrum of the organizations that signed off on the recommendations and their sometimes-contrasting takes on diagnostic and therapeutic approaches.

Septal reduction therapy: Two strategies
For example, the document's class I position on invasive correction of left ventricular outflow tract (LVOT) obstruction, a hallmark of HCM, says "septal-reduction therapy should be performed only by experienced operators in the context of a comprehensive HCM clinical program and only for the treatment of eligible patients with severe drug-refractory symptoms and LVOT obstruction."
But how septal reduction is carried out has sometimes been a touchy issue, one on which different subspecialties—and their representing organizations, to some extent—have historically had different takes. Although the guidelines favor a long tried-and-true surgical approach as first line and define a catheter-based technique as second tier, in clinical practice the latter is performed more broadly than that.
"The guidelines say that for patients with progressive heart failure refractory to drug treatment who are severely symptomatic, the preferred and gold-standard treatment for most of those patients is surgical septal myectomy," Maron said, adding that the percutaneous strategy, alcohol septal ablation, is an effective alternative in selected patients.
"When surgery is contraindicated or the risk is considered unacceptable because of serious comorbidities or advanced age," the guidelines state, "alcohol septal ablation, when performed in experienced centers, can be beneficial in eligible adult patients with HCM."

Gene testing most powerful for relatives
Genetic testing, another issue that has evolved over the years and been crystallized in the new guidelines, should be reserved for HCM patients and their families and only in some circumstances; it isn't specific enough for broad population screening.
The guidelines, Maron said, point out that tests for known HCM-related gene variants can't usefully predict outcomes "but have proved to be most powerful in family screening and early detection of relatives without left ventricular hypertrophy."
In class I recommendations, the guidelines state that "screening (clinical, with or without genetic testing) is recommended in first-degree relatives of patients with HCM" and that "genetic testing for HCM and other genetic causes of unexplained cardiac hypertrophy is recommended in patients with an atypical clinical presentation of HCM or when another genetic condition is suspected to be the cause" (level of evidence B for both).
Otherwise, a class IIa recommendation states, genetic testing of the HCM patient is "reasonable . . . to facilitate the identification of first-degree family members at risk for developing HCM" (level of evidence B).

Exercising caution
The guidelines document is much further reaching, however, covering risk-stratification techniques; the roles and relative value of different imaging modalities, including transthoracic echocardiography (TTE), angiography, and cardiac magnetic resonance (CMR); drug therapy, with beta blockade a cornerstone and positive inotropic agents generally persona non grata; and recommendations on engaging in sports and other physical activities.
Almost any sport at an advanced competitive level should be off-limits for patients with HCM, according to the document, but it makes room for engagement in light competitive sports such as golf and in a range of recreational sports, including cycling, "modest hiking," lap swimming, doubles tennis, and bowling.
But "patients with HCM should avoid recreational sports in which participation is intense and simulates competitive organized athletics." Sports that entail "burst exertion" are less suitable than those with more consistent exertion, such as lap swimming or cycling.
"General recommendations for recreational exercise in patients with HCM should be tailored to the individual's desires and abilities," the document states.

quinta-feira, 10 de novembro de 2011

Onda L - by Fábio Soares

E alguém ainda lembra da onda L?

- A diástase compreende o período da diástole entre as fases de enchimento precoce e tardia, sendo muitas vezes assumida como quiescente. Em alguns casos, um  gradiente transmitral positivo está presente durante a diástase, freqüentemente observadas durante a análise do Doppler mitral como onda"L". Graficamente, corresponde a uma curva positiva ocorrendo entre as ondas E e A,  determinando um padrão trifásico ("fluxo da médio diástole" - FMD).

- A diástole é um processo complexo e incompletamente compreendida  envolvendo elementos ativos e passivos. Didaticamente é dividida em fases: relaxamento isovolumétrico, enchimento ventricular esquerdo precoce,  diástase e enchimento ventricular esquerdo tardio (devido à contração atrial esquerda). Seguindo a fase de enchimento inicial, as pressões do AE e VE se equilibram, e praticamente cessa o fluxo mitral. Em alguns indivíduos jovens normais, o relaxamento ativo do VE é determinado por um recoil pronunciado  (untwist) que cria uma "avenida" para a sucção do VE levando ao início de enchimento do VE. Este fenômeno , determina uma rápida queda dapressão do AE e aumeto da pressão do VE, com uma inversão transitória do gradiente AE/VE. Quando o átrio recebe o fluxo dasveias pulmonares, ocorre reestabelecimento do gradiente AE/VE e o fluxo mitral é reacelerado na médio-diástole.

- Na presença de alguma patologia miocárdica, essa aspiração vigorosa deixaria de ocorrer e não seria suficiente para ocorrência deste fluxo na médio-diástole, e portanto da onda L. Uma hipótese seria que o retardo acentuado do relaxamento ativo do VE pode promover o FMD, diminuindo a pressão diastólica do VE durante a diástase. Mas a maioria dos trabalhos, relaciona o FMD com as pressões de enchimento do VE elevadas e sobrecarga volumétrica, determinando mais um efeito "push" (aumento da rigidez atrial) que um efeito "pull"(sucção do VE).

Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography
Journal of the American Society of Echocardiography February 2009

Middiastolic flow is an important signal to recognize. Low velocities can occur in normal subjects, but when increased (20 cm/s), they often represent markedly delayed LV relaxation and elevated filling pressures.

Ha JW, Oh JK, Redfield MM, Ujino K, Seward JB, Tajik AJ. Triphasic mitral inflow velocity with middiastolic filling: clinical implications and associated echocardiographic findings. J Am Soc Echocardiogr 2004;17: 428-31.

segunda-feira, 7 de novembro de 2011

Resposta do Caso Clínico - by Fábio Soares

Paciente fora admitido na enfermaria, proveniente de unidade básica de saúde. à chegada, evoluiu com rebaixamento do nível de consciência e choque. Realizado intubação orotraqueal, e encaminhado à UTI. Realizado ressuscitação volêmica e introduzido drogas vasoativas.
Ao exame físico, chamava a atenção pulso em martelo d´água, discrepância da PAS e PAD, com precordio bastante ativo. À ausculta, ritmo cardíaco regular em 3 tempos, às custas de B3, com SD 6/6 em FAo e SS 3/6 em FAo.

Ecocardiograma realizado a beira do leito: Aumento grave de câmaras esquerdas. Função sisitólica do VE preservada (em uso de DVA). Grande quantidade de vegetações aderidas à ambas as faces da valva aórtica, determinando desabamento da cúspide não coronariana determinando insuficiência de grau grave. Observa-se ainda, vegetações aderidas à porção basal do septo interventricular, bem como aderida à junção sinotubular. Valva mitral apresenta insuficiência de grau moderado, com vegetações em ambas as faces da valva mitral.

Após estabilização clínica inicial, fora encaminhado à TAC de crânio, que não evidenciou sangramento. Introduzido ATBterapia empírica (Penicilina + Gentamicina + Ampicilina) após coleta das culturas. Chamada a equipe cirúrgica, que preferiu aguardar 24 horas de ATB para realizar a cirurgia.
Paciente mantendo quadro de choque séptico em uso de doses elevadas de drogas vasoativas, sendo encaminhado para cirurgia. Relato do intra-operatório:
- Valva aórtica bastante distorcida com grande quantidade de grumos aderida à face ventricular e aórtica, com extensão para o septo interventricular e aorta ascendente. Observavam-se vegetações aderidas à face atrial da valva mitral.
Realizado troca da valva aórtica por bioprótese e plastia da valva mitral
Retornou à UTI, mantendo-se em quadro de choque circulatório, em doses elevadas de DVA. Passou a apresentar anúria e acidose metabólica grave, sendo iniciado CVVHDF. No 3o PO evoluiu para choque refratário e óbito

Hemoculturas positivas para S. aureus.