Volume atrial esquerdo como índice de função diastólica
Universidade Federal de Sergipe e Hospital São Lucas de Aracajú - Aracajú, SE
A insuficiência cardíaca congestiva (ICC) constitui uma das principais causas de morte e internações hospitalares em nosso meio, segundo dados do Datasus1. Essa síndrome clínica é progressiva e caracterizada por adaptações cardíacas e sistêmicas complexas que variam ao longo da evolução da doença2.
Verificou-se, todavia, que em aproximadamente 30% a 50% dos indivíduos que desenvolvem ICC a função sistólica, estimada pela fração de ejeção (FE) do ventrículo esquerdo (VE), apresenta-se normal ou relativamente normal3. Portanto, a razão da descompensação cardíaca desses pacientes é a disfunção diastólica do VE, justificando o termo "insuficiência cardíaca diastólica"4.
Ainda se conhece pouco sobre a história natural dessa doença, particularmente no que se refere aos mecanismos causadores de morte nos pacientes afetados5, embora seja reconhecida sua prevalência em certas populações como idosos e mulheres, e que usualmente antecede a disfunção sistólica na maioria das afecções cardíacas, inclusive na miocardiopatia chagásica6-9.
Existem poucas publicações concernentes à incidência de ICC em portadores de disfunção diastólica evidenciada pela ecocardiografia Doppler. Foi demonstrado, numa população de indivíduos maiores de 65 anos sem evidências clínicas de doença cardíaca, que a detecção desse tipo de disfunção através da ecocardiografia Doppler tem valor preditivo para o desenvolvimento de ICC em 11% a 15 %, num período de cinco anos10.
Na conceituação clínica mais usualmente empregada11, a fase diastólica do ciclo cardíaco, inicia-se com o fechamento das valvas semilunares, compreende a maior parte do relaxamento ventricular ativo, com os períodos de relaxamento isovolumétrico e de enchimento ventricular rápido, assim como a diástase ou enchimento passivo e, finalmente, o período que envolve a contração atrial. A ilustração gráfica desse conceito pode ser apreciada na
Apesar de inúmeros fatores independentes afetarem as propriedades diastólicas do VE, suas ações convergem para o gradiente de pressão transmitral que, em última análise, é o determinante físico do enchimento ventricular esquerdo12.
No período de relaxamento isovolumétrico, o VE comporta-se como uma câmara isolada, uma vez que as valvas aórtica e mitral encontram-se fechadas; portanto, o seu volume não se modifica enquanto se registra queda progressiva da pressão intracavitária. O relaxamento do coração também é o determinante fundamental do enchimento ventricular rápido, que decorre da abertura da valva mitral conseqüente à queda da pressão no interior do VE, abaixo da verificada no átrio esquerdo (AE)13. Trata-se de um processo dependente de energia, que corresponde à seqüestração ativa, contragradiente, do íon cálcio liberado da troponina durante a ativação contrátil14.
O enchimento ventricular rápido que, em circunstâncias normais, é responsável por 80% do enchimento ventricular, deve-se ainda à pressão no átrio esquerdo no momento da abertura da valva mitral (pré-carga) e ao recolhimento elástico (sucção) do VE. Esse fenômeno ocorre porque as fibras musculares encurtadas no final da sístole, juntamente com a matriz colágena, funcionam como uma mola comprimida para gerar forças de recolhimento na fase inicial da diástole14, proporcionando queda da pressão do VE, a despeito do progressivo incremento do seu volume. O esvaziamento do AE proporciona a equalização manométrica entre as câmaras esquerdas, constituindo-se a fase de diástase.
Nessa fase, que é influenciada pela complacência (relação pressão/volume) do VE, o enchimento ventricular decorre, basicamente, do fluxo venoso pulmonar, uma vez que o AE se comporta como um "conduto passivo", possibilitando a passagem direta do sangue das veias pulmonares até o VE15. A contração atrial, que acontece no final do período diastólico, contribui para 15% a 20% do enchimento ventricular, em pessoas normais16, e depende de interações do VE com o pericárdio e com o ventrículo direito (VD), do sincronismo atrioventricular (intervalo PR do eletrocardiograma), do ritmo cardíaco (perda da contração atrial na presença de arritmias como a fibrilação atrial) e das pressões no AE e VE14,17,18.
O VE normal deve ser capaz de acomodar um volume significativo de sangue sem provocar elevação na pressão diastólica. Desse modo, a proporção do enchimento ventricular durante as fases inicial e final da diástole é dependente do relaxamento miocárdico, do recolhimento elástico, da complacência do VE e da pressão do AE, que derivam da interação entre o processo de enfermidade cardíaca e a volemia14.
Muitos pacientes com ICC e função sistólica preservada têm, predominantemente, mecanismos diastólicos que determinam os sintomas de dispnéia e fadiga. Nesses indivíduos, o VE não é dilatado e contrai normalmente, entretanto a função diastólica é comprometida19. Na insuficiência cardíaca diastólica, o VE tem complacência diminuída e é incapaz de encher adequadamente com pressões normais. Essa condição resulta na redução do volume diastólico final, que causa queda no volume sistólico e sintomas de baixo débito cardíaco, e/ou elevação da pressão diastólica final que, por sua vez, determina o surgimento de sintomas de congestão pulmonar20. Assim, as características da ICC (inabilidade do coração em bombear sangue para manter as necessidades metabólicas teciduais, preservando as pressões de enchimento) podem decorrer, primariamente, por anormalidades lusitrópicas9.
Existem três tipos básicos de disfunção diastólica: a) aumento da rigidez ventricular, comum na doença isquêmica do coração, no idoso, na amiloidose cardíaca e na endomiocardiofibrose; b) hipertrofia ventricular, cujo principal responsável é a HAS; c) interferências mecânicas, causadas pela estenose mitral, mixoma de AE, pericardite constrictiva e tamponamento cardíaco19.
Parte da dificuldade em se estudar a função diastólica do VE deve-se ao fato de que os seus principais determinantes (o relaxamento e a complacência) atuam em diferentes fases da diástole, com sobreposição no tempo de ação. Além de sofrerem interação mútua, são, também, influenciados, conforme exposto acima, pela função sistólica do VE, pela freqüência cardíaca (FC) e pelo sistema de condução cardíaco.
A análise do padrão de enchimento ventricular promove informações valiosas sobre o desempenho diastólico do VE. Historicamente, o estudo hemodinâmico através do cateterismo cardíaco tem sido o padrão de referência para a aquisição dessas informações21. Todavia, seu caráter invasivo torna essa metodologia inviável para a prática clínica rotineira. Avaliações da função diastólica podem, também, ser obtidas, de forma não-invasiva, pela determinação do volume ou dimensões do VE durante o ciclo cardíaco, pela angiografia radioisotópica22, ou mediante a ecocardiografia Doppler12,23.
O emprego da ecocardiografia Doppler na avaliação da função diastólica iniciou-se na década de 1970 com Gibson & Brown24, os quais desenvolveram método de análise da variação contínua da dimensão ventricular esquerda, utilizando um sistema computadorizado de aproveitamento de traçado ecocardiográfico. Em nosso meio, essa técnica foi padronizada por Marin-Neto e Sousa25 e utilizada na demonstração da disfunção diastólica precoce da doença de Chagas6, mostrando-se reprodutível, porém laboriosa, o que de certa forma limita a sua utilização corriqueira.
Conforme visto anteriormente, alterações no relaxamento e na complacência do VE secundários a defeito na interação actina/miosina e aumento na deposição de colágeno ou das propriedades viscoelásticas do coração promovem elevação da PD2VE e, conseqüentemente, elevação da pressão no AE para manter o enchimento ventricular26. O aumento da tensão parietal leva à dilatação da câmara atrial, que, portanto, reflete a disfunção diastólica do VE27,28. O AE se comporta como um reservatório durante a sístole ventricular, como um conduto que permite a passagem do sangue procedente das veias pulmonares para o VE no início da diástole e como uma câmara contrátil, ativa, no final da diástole.
Durante o período diastólico, essa câmara atrial está diretamente exposta às pressões do VE, através da valva mitral aberta28, conforme ilustrado na
Os métodos corriqueiramente disponíveis para a determinação do tamanho do AE, mediante a ecocardiografia Doppler, são a medida da dimensão ântero-posterior obtida na projeção paraesternal em eixo maior e cálculo do volume utilizando, também, as projeções apicais em duas ou quatro câmaras34. A medida uniplanar da dimensão ântero-posterior tem acurácia reduzida e baixa reprodutibilidade, para a quantificação da dimensão atrial esquerda, em virtude de limitações técnicas, tais como a angulação do feixe de ultra-som, a geometria irregular do AE e pelo fato de que o crescimento dessa câmara não é uniforme em razão da limitação física imposta pelo esterno e pela coluna vertebral35.
Isso pode, em parte, explicar os resultados conflitantes descritos na literatura especializada quando o tamanho do AE avaliado pela dimensão ântero-posterior é utilizado, como variável, para estabelecer prognóstico em certas situações clínicas; em portadores de FA crônica, que participaram do estudo AFASAK36, a dimensão ântero-posterior não teve valor em predizer tromboembolismo, enquanto em outra investigação (SPAF)37, utilizando população semelhante, essa variável foi o melhor preditor de AVC.
Por sua vez, o volume do AE (VAE) geralmente pode ser obtido de várias maneiras: a) método do cubo38, segundo o qual a câmara atrial tem um formato esférico, através da seguinte fórmula: AE=4/3 Ø7 x (dimensão ântero-posterior/2)3; b) método elipsóide39, assumindo forma elíptica do AE, mediante a fórmula: 4/3 Ø7 x dimensão ântero-posterior/2 x comprimento/2 x dimensão médio-lateral/2, em que o comprimento é a distância entre o ponto de coaptação das cúspides da valva mitral e a parede superior do AE e dimensão médio-lateral é a dimensão transversa, obtidos na posição apical de quatro câmaras. Todos os cálculos devem ser realizados ao final da sístole; c) método biplanar área-comprimento40, usando a fórmula: 0,85 x área em 4 câmaras x área em 2 câmaras/eixo perpendicular, na qual as áreas são obtidas nas posições apicais, excluindo-se o apêndice atrial esquerdo e a confluência das veias pulmonares; o comprimento perpendicular é medido entre o plano do anel da VM e a porção superior do AE; d) método dos discos de Simpson uniplanar ou biplanar41, no qual o operador procede ao traçado do endocárdio atrial esquerdo nas projeções apicais em 2 e 4 câmaras, conforme exemplificado na
As metodologias de medidas do VAE que melhor se aplicam à pratica clínica são as que utilizam a técnica de Simpson, quer seja uniplanar34 ou biplanar42. Lester e cols.34 observaram que a técnica uniplanar, derivada da posição apical em 4 câmaras, representa medida acurada do verdadeiro tamanho do AE. Segundo Schiller & Foster43, o volume do AE, normalizado para a superfície corporal, é um índice da dimensão atrial esquerda que parece ser melhor indicador do verdadeiro tamanho dessa cavidade, e concluíram, com base em experiência pessoal, que o valor normal para o índice de volume do AE, em ambos os sexos, é de 21 ml/m2, sendo 32 ml/m2 o limite superior de normalidade (com intervalo de confiança de 90% do percentil 95). O método de Simpson para obtenção do VAE já foi validado em estudos clínicos, utilizando-se técnica de angiografia biplanar44 e de cinetomografia computadorizada45. Mais recentemente, Khankirawatana e cols.42, comparando vários modos de aferição do volume do AE, demonstraram, também, a grande acurácia da técnica de Simpson.
Alguns estudos46,47 reportaram que o tamanho do AE naturalmente aumentaria com a idade. Essas observações ganham reforço com a constatação de que 70% dos pacientes com FA apresentam mais de 65 anos de idade48. Assim, a senescência pode proporcionar alterações que culminariam com a dilatação e a disfunção do AE, aumentando, assim, a predisposição para arritmias atriais49. Entretanto, nesses estudos foram utilizados parâmetros derivados do modo-M para a avaliação da dimensão atrial, técnica que, de modo comprovado, é geometricamente menos rigorosa. Thomas e cols.50 não encontraram variações significativas no VAE produzidas pelo envelhecimento, mediante o método de Simpson, sugerindo, portanto, que a constatação de aumento do AE traduz manifestação patológica, e não um processo fisiológico de envelhecimento. Ainda nessa investigação, os autores constataram que, para compensar a diminuição do enchimento ventricular que ocorre nas fases iniciais da diástole (dependentes do relaxamento), o idoso aumenta o volume de esvaziamento ativo (contração atrial), de modo que o volume total de esvaziamento permanece inalterado. O aumento da velocidade da onda A do fluxograma mitral, observado nos idosos (vide abaixo), reflete esse fenômeno.
O VAE tem sido considerado índice independente de variações agudas de pré-carga e, portanto, proporciona avaliação mais acurada da disfunção ventricular18,34. Todavia, Barberato e cols.51, em publicação recente, demonstraram pela primeira vez que o índice de volume do AE é afetado por modificações agudas da pré-carga, utilizando um modelo clínico de variação de volume oferecido pela hemodiálise. Vale ressaltar, entretanto, que essa dependência da pré-carga observada foi menor do que a sofrida pelos índices derivados do Doppler.
Vários estudos clínicos têm atestado a utilidade do VAE no prognóstico de diversas patologias. Tsang e cols.52, avaliando um grupo de pacientes sem história de valvopatias, demonstraram que essa variável traduz uma sensível expressão morfofisiológica do grau de disfunção diastólica do VE e, ainda, se constitui em útil marcador de risco cardiovascular. Cioffi e cols.53, estudando a relação entre a geometria ventricular esquerda e a dimensão do AE em pacientes com hipertensão arterial sistêmica, constataram que a hipertrofia concêntrica do VE se associa a maior VAE, traduzindo, portanto, maior grau de comprometimento da função diastólica, avaliada, também, pelo fluxograma mitral, do que a hipertrofia excêntrica. Nesse estudo, o grau de incremento da câmara atrial se correlacionou, similarmente, com a massa do VE, nos dois padrões de geometria ventricular. O mesmo grupo, em publicação anterior, havia demonstrado, todavia, que, em portadores de doença valvar aórtica crônica, o aumento volumétrico do AE está diretamente associado à massa do VE, no contexto da geometria concêntrica.
Tem sido revelado, também, o seu valor como preditor de FA. Tsang e cols.54, estudando uma população de idosos, de ambos os sexos, que se encontravam, no início da investigação, em ritmo sinusal e sem doenças cardíacas significativas, observaram que um aumento de 30% do VAE se acompanhava de incremento de 43% no risco de apresentar FA. Os autores verificaram, ainda, que o valor preditivo dessa variável para o surgimento de FA em idosos aparentemente sadios é superior ao obtido mediante a combinação de fatores clínicos e medida do AE ao modo-M. Moller e cols.55 concluíram que o índice de VAE é um robusto preditor de mortalidade precoce após infarto agudo do miocárdio e que também adicionava informações prognósticas aos parâmetros clínicos e às medidas convencionais de função sistólica e diastólica do VE. Nessa investigação foi ainda observado que quando esse índice se encontrava normal, o prognóstico do paciente era favorável, mesmo que a sua função sistólica estivesse comprometida. Beinart e cols.56 observaram, em população semelhante, que esse índice, obtido nas primeiras 48 horas da admissão, é também um preditor independente de mortalidade tardia, incorporando informações adicionais às obtidas clinicas e ecocardiográficas. Recentemente, Sabharwal e cols.57 relataram que, na miocardiopatia isquêmica (FE
Estudando uma população de idosos, Barnes e cols.59 demonstraram a importância do VAE como preditor independente do primeiro AVC isquêmico e de morte, em indivíduos sem FA prévia. Apesar de ser atrativa a concepção de que o aumento da dimensão do AE propiciaria maior aparecimento de FA e, conseqüentemente, maior incidência de AVC, os investigadores especulam a existência de outro mecanismo para explicar tal associação, já que apenas 15% de todos os acidentes isquêmicos cerebrais são atribuídos à FA60. Em estudo populacional, recentemente publicado, Prichett e cols.61 verificaram que a disfunção diastólica está associada ao aumento do índice de VAE, independentemente da presença de doença cardiovascular, de disfunção sistólica do VE e de hipertrofia ventricular, e, ainda, que esse índice é um indicador fidedigno da presença de disfunção lusitrópica de grau importante.
A avaliação do VAE, mediante a ecocardiografia Doppler, se constitui em índice sensível que expressa a severidade da disfunção diastólica do VE, além de fornecer informações prognósticas em diversas cardiopatias. Aos poucos essa metodologia vai se incorporando à prática cotidiana, graças à sua relativa facilidade técnica e ao potencial de informações relevantes que podem gerar, facilitando o manuseio dos pacientes que a utilizam.
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51. Barberato SH, Mantilla DEV, Misocami M, Gonçalves SM, Bignelli AT, Riella MC, Pecoits-Filho R. Effect of preload reduction by hemodialysis on left atrial volume and echocardiographic Doppler parameters in patients with end-stage renal disease. Am J Cardiol 2004; 94: 1208-10.
52. Tsang TSM, Gersh BJ, Appleton CP, Tajik AJ, Barnes ME, Bailey KR, Seward JB. Left atrial volume as a morphophysiologic expression of left ventricular diastolic dysfunction and relation to cardiovascular risk burden. Am J Cardiol 2002; 90: 1284-9.
53. Cioffi G, Mureddu GF, Stefenelli C, Simine G. Relationship between left ventricular geometry and left atrial size anf function in patients with systemic hypertension. J hypertens 2004; 22: 1589-96.
54. Tsang TSM, Barnes ME, Gersh BJ, Bailey KR, Oh JK, Leibson C, Montgomery SC, Seward JB. Left ventricular diastolic dysfunction as a predictor of the first diagnosed nonvalvular atrial fibrillation in 840 elderly men and women. J Am Coll Cardiol 2002; 40: 1636-44.
55. Moller JE, Hillis GS, Oh JK, Seward JB, Reeder GS, Wright S, Park SW, Bailey KR, Pellika PA. Left atrial volume. A powerful predictor of survival after acute myocardial infarction. Circulation 2003; 107: 2207-12.
56. Beinart R, Boyko V, Schwammenthal E, Kuperstein R, Sagie A, Hod H, Matetzky S, Behar S, Eldar M, Feinberg MS. Long-term prognostic significance of left atrial volume in acute myocardial infarction. J Am Coll Cardiol 2004; 44: 327-34.
57. Sabharwal N, Cemin R, Rajan K, Hickman M, Lahiri A, Senior R. Usefulness of left atrial volumes as a predictor of mortality in patients with ischemic cardiomyopathy. Am J Cardiol 2004; 94: 760-3.
58. Rossi A, Cicoira M, Zanolla L, Sandrini R, Golia G, Zardini P, Enriquez-Sarano M. Determinants and prognostic value of left atrial volume in patients with dilated cardiomyopathy. J Am Coll Cardiol 2002; 40: 1425-30.
59. Barnes ME, Miyasaka Y, Seward JA, Gersh BJ, Rosales AG, Bailey KR, Petty GW, Wiebers DO, Tsang TSM. Left atrial volume in the prediction of first ischemic stroke in an elderly cohort without atrial fibrillation. Mayo Clin Proc 2004; 79: 1008-14.
60. American Heart Association. Heart Disease and Stroke Statistics – 2004 Uptate. Dallas, Tex.
61. Pritchett AM, Mahoney DW, Jacobsen SJ, Rodeheffer RJ, Karon BL, Redfield MM. Diastolic dysfunction and left atrial volume. J Am Coll Cardiol 2005; 45: 87-92.
Carlos Sobral Sousa Av. Dep. Silvio Teixeira, 490/1201 49025 - 100 – Aracajú, SE Email:
Recebido em 21/06/05
Aceito em 11/11/05
Left atrial volume as an index of diastolic function
Universidade Federal de Sergipe e Hospital São Lucas de Aracajú - Aracajú, SE - Brazil
Congestive heart failure (CHF) is one of the main causes of death and hospital admissions in our country, according to data from Datasus1. This clinical syndrome is progressive and characterized by complex cardiac and systemic adaptations, which vary during disease evolution2.
It has been observed, however, that in approximately 30% to 50% of the individuals who develop CHF, the systolic function estimated through the left ventricular ejection fraction (LVEF) is normal or relatively normal3. Thus, the cause of cardiac decompensation in these patients is the left ventricular diastolic dysfunction, justifying the term "diastolic cardiac failure"4.
Little is known on the natural history of this disease, particularly regarding the mechanisms causing affected patients’ death5, although its prevalence is known among certain groups, such as the elderly and women, as well as the fact that it usually precedes the systolic dysfunction in most cardiac affections, including Chagas’ myocardiopathy6-9.
There have been few studies published in literature regarding the incidence of CHF in patients with diastolic dysfunction evidenced by Doppler echocardiography. It has been demonstrated, in a population of individuals older than 65 years with no clinical evidence of cardiac disease, that the detection of this type of dysfunction through Doppler echocardiography has a predictive value for the development of CHF in 11 a 15% of the cases within a five-year period10.
According to the most generally employed clinical concept11, the diastolic phase of the cardiac cycle, starting with the closing of the semilunar valves, comprises the largest part of the active ventricular relaxation, with periods of isovolumetric relaxation, and rapid ventricular filling, as well as diastasis or passive filling and, finally, the period that involves atrial contraction. The illustration of this concept is depicted in
Even though several independent factors affect the diastolic properties of the left ventricle (LV) its actions converge to the transmitral pressure gradient, which, in fact, is the physical determinant of the left ventricular filling12.
During the isovolumetric relaxation period, the LV behaves as an isolated chamber, as the aortic and mitral valves are closed; thus, its volume is not altered when there is a progressive decrease of intracavitary pressure. The heart relaxation is also the main determinant of the rapid ventricular filling, which is caused by the opening of the mitral valve as a result of the pressure decrease inside the LV, which is lower than that observed in the left atrium (LA)13. It is an energy-dependent process, which corresponds to the active sequestration, contragradient, of calcium ions released from troponin during the contractile activation14.
The rapid ventricular filling, which under normal circumstances is responsible for 80% of the ventricular filling, is also due to the pressure in the left atrium at the moment of the mitral valve opening (preload) and elastic recoil (suction) of the left ventricle. This phenomenon occurs because the shortened muscle fibers at the end of the systole, together with the collagen matrix, act as a compressed coil to generate recoil forces at the initial phase of the diastole14, resulting in a decrease of LV pressure, despite the progressive increment of its volume. The LA emptying provides the manometric equalization between the left chambers, comprising the diastasis phase.
In this phase, which is influenced by the LV complacency (pressure/volume ratio), ventricular filling is basically originated from the pulmonary venous flow, as the LA behaves as a "passive conduit", enabling the direct passage of blood from the pulmonary valves to the LV15. The atrial contraction, which happens at the end of the diastolic period, contributes for 15% to 20% of ventricular filling in normal individuals16, and depends on interactions of the LV with the pericardium and the right ventricle (RV), on the atrioventricular synchronism (PR interval of the electrocardiogram), on the cardiac rhythm (loss of the atrial contraction in the presence of arrhythmias such as atrial fibrillation) and on the LA and LV pressures14,17,18.
The normal LV must be capable of accommodating a significant volume of blood without causing the diastolic pressure elevation. Hence, the proportion of ventricular filling during the initial and final phases of diastole depends on the myocardial relaxation, the elastic retraction, the LV complacency and the LA pressure, which originate from the interaction between heart disease and volemia14.
Many patients with CHF and preserved systolic function predominantly present the diastolic mechanisms that determine the symptoms of dyspnea and fatigue. In these individuals, the LV is not dilated and contracts normally; however, the diastolic function is compromised19. In diastolic heart failure, the LV has decreased complacency and it is unable to fill adequately with normal pressures. This condition results in the reduction of the final diastolic volume, which causes the decrease in the systolic volume and symptoms of low cardiac output and/or final diastolic pressure elevation, which, in turn, determines the onset of symptoms of pulmonary congestion. Thus, the characteristics of CHF (incapacity of the heart in pumping blood to maintain the tissue metabolic needs, preserving the filling pressures) can be mainly due to lusitropic abnormalities9.
There are three types of diastolic dysfunction: a) increase of ventricular rigidity, which is common in ischemic heart disease in the elderly, in cardiac amyloidosis and endomyocardiofibrosis; b) ventricular hypertrophy, of which the main cause is systemic arterial hypertension (SAH); c) mechanical obstructions, caused by mitral stenosis, LA myxoma, constrictive pericarditis and cardiac tamponade19.
Part of the difficulty in studying the diastolic function of the LV is due to the fact that its main determinants (relaxation and complacency) act in different phases of the diastole, with an overlap of the time of action. In addition to undergoing mutual interaction, they are also influenced, as mentioned above, by the LV systolic function, by the heart frequency (HF) and the heart conduction system.
The analysis of the ventricular filling pattern provides important information on the diastolic performance of the LV. Historically, the hemodynamic study through cardiac catheterism has been the reference standard for the acquisition of such information21. However, its invasive nature makes this methodology unfeasible in routine clinical practice. Diastolic function assessments can also be obtained by non-invasive techniques, such as the determination of the LV volume of dimensions during the cardiac cycle, by radioisotope angiography22, or by Doppler echocardiography12,23.
The use of Doppler echocardiography in diastolic function assessment started in the seventies with Gibson & Brown24, who developed an analysis method of the continuous variation of the LV dimension, using a computerized system of reutilization of echocardiographic tracings. In our country, this technique was standardized by Marin-Neto and Sousa25 and utilized in the demonstration of early diastolic dysfunction in Chagas disease6, showing it to be reproducible, but also time-consuming, which, in a way, limits its routine utilization.
As mentioned before, alterations in the relaxation and complacency of the LV secondary to a defect in the actin-myosin interaction and increase in collagen deposition or the viscoelastic properties of the heart cause an elevation of the left ventricular end-diastolic pressure (LVDP) and consequently, elevation of pressure in the LA to maintain the ventricular filling26. The parietal tension increase leads to the dilation of the atrial chamber, which consequently reflects the diastolic dysfunction of the LV27,28. The LA behaves as a reservoir during the ventricular systole, as a conduit that allows the passage of blood from the pulmonary veins to the LV at the beginning of the diastole, and as an active contractile chamber at the end of the diastole.
During the diastolic period, this atrial chamber is directly exposed to the pressures of the LV through the open mitral valve28, as shown in
The routinely available methods for the determination of the LA size through Doppler echocardiography are the measurement of the anteroposterior dimension obtained at the parasternal projection of its long axis and volume calculation, also utilizing the apical two-chamber and the apical four-chamber views34. The uniplane measurement of the anteroposterior dimension has decreased accuracy and low reproducibility in the quantification of the left atrial dimension, which are caused by technical limitations such as the ultrasound beam angulation, the irregular geometry of the LA and the fact that the growth of this chamber is not a uniform one, due to the physical limitation imposed by the sternum and vertebral column35.
This can, in part, explain the conflicting results described in the specialized literature regarding the size of the LA when assessed by its anteroposterior dimension, as a variable, in order to establish the prognosis in certain clinical situations; in patients with chronic AF, who took part in the AFASAK36 study, the anteroposterior dimension did not have a predictive value for thromboembolism (TE), whereas another study (SPAF)37 showed that this variable was the best predictor for stroke, when assessing a similar population.
On the other hand, the LA volume (LAV) can generally be obtained by several means: a) the cube38 method, according to which the atrial chamber has a spherical shape, through the following formula: LA=4/3 p x (anteroposterior dimension/2)3; b) ellipsoid method39, assuming an elliptical shape of the LA, according to the formula: 4/3 p x anteroposterior dimension/2 x lenght/2 x mediolateral dimension/2, in which the length is the distance between the point of coaptation of the mitral valve cuspids and the upper wall of the LA and the mediolateral dimension is the transverse dimension, obtained at the apical 4-chamber position. All calculations must be performed at the end of the systole; c) the biplane area-length measurement40, using the formula 0.85 x 4-chamber area x 2-chamber area/perpendicular axis, in which the areas are obtained at the apical positions, by excluding the left atrial appendix and the confluence of the pulmonary veins; the perpendicular length is measured between the plane of the mitral valve (MV) ring and the upper portion of the LA; d) uniplane or biplane Simpson’s disks method41, in which the technician performs the tracing of the left atrial endocardium at the apical 2- and 4-chamber positions, as shown in
The methodologies for measurement of the left atrium volume (LAV) that best apply to clinical practice are those that utilize Simpson’s technique, either uniplane34 or biplane42.
Lester and cols.34 observed that the uniplane technique, derived from the apical 4-chamber position, represents an accurate measurement of the factual size of the LA. According to Schiller & Foster43, the LA volume, normalized for the body surface, is an index of the left atrial size that seems to be a better indicator of the factual size of this cavity, and concluded, based on personal experience, that the normal value for the LA volume index in both sexes was 21 ml/m2, with 32 ml/m2 being the upper limit of normality (with a confidence interval of 90% of the 95th percentile). Simpson’s method for obtaining LAV has been validated in clinical trials utilizing the biplane angiography technique44 and cine computed tomography (CT)45. More recently, Khankirawatana e cols.42, comparing several methods of measuring LAV, also demonstrated the great accuracy of Simpson’s method.
Some studies46,47 reported that the LA size would naturally increase with age. These observations are supported by the evidence that 70% of the patients with AF are 65 years or older48. Therefore, senescence can cause alterations that would eventually culminate with LA dilation and dysfunction, thus increasing the predisposition to atrial arrhythmias49. However, these studies utilized M-mode-derived parameters to evaluate atrial dimension, which is a technique that has been shown to be geometrically less exact. Thomas and cols.50 did not find significant variations in LAV produced by aging when utilizing Simpson’s method, thus suggesting that the confirmation of LA increase indicates a pathological manifestation, and not a physiological aging process. The same authors verified that, in order to compensate for the decrease of ventricular filling that occurs in the initial phases of diastole (which depends on the relaxation), the elderly individual increases the volume of active emptying volume (atrial contraction), so that the total draining volume remains unaltered. The increased velocity of the A wave of the mitral flow chart observed in elderly individuals (see below) reflects such phenomenon.
The LAV has been considered to be an index independent from the acute variations of pre-load, and therefore, it provides a more accurate evaluation of ventricular dysfunction18,34. However, Barberato and cols.51, in a recent publication, demonstrated for the first time that the index of LAV is affected by acute pre-load modifications, by utilizing a clinical model of volume variation offered by hemodialysis. Nevertheless, it is noteworthy that this observed pre-load dependence was less than that observed in Doppler-derived indexes.
Several clinical studies have demonstrated the usefulness of LAV in the prognosis of several pathologies. Tsang and cols.52, evaluating a group of patients with no history of valvulopathies, showed that this variable translates a sensitive morphophysiological expression of the degree of LV diastolic dysfunction, and also constitutes a useful marker of cardiovascular risk. Cioffi e cols.53, studying the connection between left ventricular geometry and LA dimension in patients with systemic arterial hypertension, verified that the concentric LV hypertrophy is associated to a higher LAV, thus indicating a higher degree of diastolic function involvement, also evaluated by the mitral flow chart, than the eccentric hypertrophy. In this study, the degree of the atrial chamber increment was similarly correlated to the LV mass at the two patterns of ventricular geometry. However, the same group, in a previous study, had demonstrated that in individuals with chronic aortic valve disease, the LA volumetric increase is directly associated with LV mass, within the context of concentric geometry. Its value as an AF predictor has also been disclosed. Tsang and cols.54, by studying an elderly population of both gender who were, in the beginning of the investigation, in sinusal rhythm and did not present significant cardiac diseases, observed that an increase of 30% of the LAV was followed by an increment of 43% in the risk of presenting AF. The authors also verified that the predictive value of this variable for AF occurrence in apparently healthy elderly individuals is higher than that obtained by a combination of clinical factors and M-mode LA measurement. Moller and cols.55 concluded that the LAV index is a strong predictor of early mortality after acute myocardial infarction (AMI) and that it also added prognostic information to the clinical parameters and the conventional measurements of systolic and diastolic LV function. This investigation also showed that, if this index was normal, the patient’s prognosis was favorable, even when his or her systolic function was compromised. Beinart and cols.56 observed, in a similar population, that when this index was obtained within the first 48 hours of hospital admission, it was also an independent predictor of late mortality, incorporating additional information to the clinical and echocardiographic ones. Recently, Sabharwal57 reported that, in ischemic cardiomyopathy (EF
Barnes and cols.59, studying a population of elderly individuals, demonstrated the importance of LAV as an independent predictor of the first ischemic stroke and death, in individuals with no previous AF. Although the conception that the increase of LA dimension gives rise to a higher incidence of AF, and consequently, a higher incidence of stroke is appealing, the investigators postulate the existence of another mechanism to explain such association, as only 15% of all ischemic brain strokes are attributed to AF60. In a recently published population-based study, Prichett e cols.61 observed that the diastolic dysfunction is associated to the increase of LAV, regardless of the presence of cardiovascular disease, left ventricular systolic dysfunction and ventricular hypertrophy, and also that this index is a reliable indicator of the presence of lusitropic dysfunction of a significant degree.
The left atrial volume (LAV) evaluation by Doppler echocardiography is a sensitive index that expresses the severity of the left ventricular diastolic function, as well as providing prognostic information on several cardiopathies. This methodology is increasingly being incorporated into the routine practice, due to its relative technical simplicity and its potential for providing relevant information, making the management of the patient undergoing the technique easier for the physician.
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51. Barberato SH, Mantilla DEV, Misocami M, Gonçalves SM, Bignelli AT, Riella MC, Pecoits-Filho R. Effect of preload reduction by hemodialysis on left atrial volume and echocardiographic Doppler parameters in patients with end-stage renal disease. Am J Cardiol 2004; 94: 1208-10.
52. Tsang TSM, Gersh BJ, Appleton CP, Tajik AJ, Barnes ME, Bailey KR, Seward JB. Left atrial volume as a morphophysiologic expression of left ventricular diastolic dysfunction and relation to cardiovascular risk burden. Am J Cardiol 2002; 90: 1284-9.
53. Cioffi G, Mureddu GF, Stefenelli C, Simine G. Relationship between left ventricular geometry and left atrial size anf function in patients with systemic hypertension. J hypertens 2004; 22: 1589-96.
54. Tsang TSM, Barnes ME, Gersh BJ, Bailey KR, Oh JK, Leibson C, Montgomery SC, Seward JB. Left ventricular diastolic dysfunction as a predictor of the first diagnosed nonvalvular atrial fibrillation in 840 elderly men and women. J Am Coll Cardiol 2002; 40: 1636-44.
55. Moller JE, Hillis GS, Oh JK, Seward JB, Reeder GS, Wright S, Park SW, Bailey KR, Pellika PA. Left atrial volume. A powerful predictor of survival after acute myocardial infarction. Circulation 2003; 107: 2207-12.
56. Beinart R, Boyko V, Schwammenthal E, Kuperstein R, Sagie A, Hod H, Matetzky S, Behar S, Eldar M, Feinberg MS. Long-term prognostic significance of left atrial volume in acute myocardial infarction. J Am Coll Cardiol 2004; 44: 327-34.
57. Sabharwal N, Cemin R, Rajan K, Hickman M, Lahiri A, Senior R. Usefulness of left atrial volumes as a predictor of mortality in patients with ischemic cardiomyopathy. Am J Cardiol 2004; 94: 760-3.
58. Rossi A, Cicoira M, Zanolla L, Sandrini R, Golia G, Zardini P, Enriquez-Sarano M. Determinants and prognostic value of left atrial volume in patients with dilated cardiomyopathy. J Am Coll Cardiol 2002; 40: 1425-30.
59. Barnes ME, Miyasaka Y, Seward JA, Gersh BJ, Rosales AG, Bailey KR, Petty GW, Wiebers DO, Tsang TSM. Left atrial volume in the prediction of first ischemic stroke in an elderly cohort without atrial fibrillation. Mayo Clin Proc 2004; 79: 1008-14.
60. American Heart Association. Heart Disease and Stroke Statistics – 2004 Uptate. Dallas, Tex.
61. Pritchett AM, Mahoney DW, Jacobsen SJ, Rodeheffer RJ, Karon BL, Redfield MM. Diastolic dysfunction and left atrial volume. J Am Coll Cardiol 2005; 45: 87-9
Mailing Address: Carlos Sobral Sousa Av. Dep. Silvio Teixeira, 490/120 49025-100 – Aracajú, SE - Brazil Email:
Received in 21/06/05
Accepted in 11/11/05
13. Grossman W, McLaurin LP. Diastolic properties of the left ventricle. Ann Int Med 1976; 84: 316-26.