Cardiovascular disease remains the leading cause of death in the developed world. In this thesis computational modelling techniques were used to study the mechanisms and genesis of atrial arrhythmias. It is separated into 2 parts: (1) The mechanistic links between mutations of the fast Na+ channel (INa) and the ability of the sinoatrial node to pace the surrounding atrial muscle were investigated. The mutations were separated into two groups, one for the mutations affecting the steady-state activation, and the other for those affecting steady-state inactivation. On the single cell level it was found that all mutations slowed the pacing rate of the sinoatrial node in a similar way, but at the 2D level the two mutation groups modulated the excitation of the tissue differently. One caused a conduction block between the sinoatrial node and atrium, where the other abolished pacemaking all together. (2) A new set of mathematical models were then developed for the sheep atria. This was incorporated into an anatomically detailed 3D geometry of the whole sheep atria to form a platform suitable for the study of clinical atrial fibrillation, and other atrial arrhythmias. Due to the lack of single cell electrophysiology data available, a method of cross-species modelling was utilised. A biophysically detailed model of the 3D sheep atria was created, and used in a preliminary study into the susceptibility of tissue to atrial fibrillation from the rapid pacing of the pulmonary vein area. It was found that both electrical heterogeneity and the complex fibre structure of the atria need to be considered for sustained atrial fibrillation to be seen.

Submitted by Isaac Francisco de Souza Dias (isaac.souzadias@ufpe.br) on 2016-04-14T17:15:59Z No. of bitstreams: 2 license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) DISSERTAÇÃO Vanessa Pereira da Silva.pdf: 747912 bytes, checksum: d6cd4bafe4a97e4af064c701c490f583 (MD5) / Made available in DSpace on 2016-04-14T17:15:59Z (GMT). No. of bitstreams: 2 license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) DISSERTAÇÃO Vanessa Pereira da Silva.pdf: 747912 bytes, checksum: d6cd4bafe4a97e4af064c701c490f583 (MD5) Previous issue date: 2014-02-25 / CAPES / Introdução: A carbamazepina é uma dos principais fármacos, utilizado no tratamento de epilepsia, transtorno bipolar e várias formas de neuropatias. Também atua como antidiurético interferindo na liberação do hormônio antidiurético. A vasopressina e a ocitocina são hormônios antidiuréticos sintetizados no hipotálamo e armazenados na neurohipófise. Esses hormônios são liberados em resposta à hiperosmolaridade e à hipovolemia, atuam aumentando o volume sanguíneo e diminuindo a concentração do sódio extracelular. O peptídeo natiurético atrial é um hormônio antidiurético sintetizado no átrio direito e liberado em resposta a expansão do volume sanguíneo, possui efeito natriurético. A liberação desses hormônios pode causar um desequilíbrio na osmolalidade de fluidos corporais fundamentais para a sobrevivência, já que uma expansão do volume hídrico pode levar a crises epilépticas. O objetivo deste estudo foi investigar in vitro vasopressina, ocitocina e peptídeo natriurético atrial na presença da droga carbamazepina. Já que até o momento não existe estudos sobre a ação deste fármaco sobre o sistema neuroendócrino in vitro e estudos in vivo são controversos Método: No experimento foi empregado um total de 28 ratos, sacrificados por decapitação. Hipotálamo, neurohipófise e coração foram removidos cirurgicamente e incubados em Krebs contendo carbamazepina nas concentrações 10-4M, 10-6M e10-8M. O meio de incubação foi extraído para dosagem de vasopressina, ocitocina e peptídeo natriurético atrial, sendo utilizado radioimunoensaio. Resultado: No hipotálamo, os níveis de vasopressina, ocitocina e peptídeo natriurético atrial no meio de incubação contendo carbamazepina diminuíram significativamente (p<0,05); no coração, diminuiu significativamente (p<0,05) a liberação de peptídeo natriurético atrial; e na neurohipófise, os níveis de vasopressina e ocitocina não tiveram diferença significativa. Conclusão: A presença da carbamazepina diminuiu os níveis de hormônios liberados in vitro. / Introduction: Carbamazepine is one of the main drugs used to treat epilepsy, bipolar disorder and various forms of neuropathy. Also acts as antidiuretic interfering in the release of antidiuretic hormone. Vasopressin and oxytocin are antidiuretic hormone synthesized in the hypothalamus and stored in the neurohypophysis. These hormones are released by hyperosmolarity and hypovolemia response, work by increasing blood volume and decreasing the concentration of extracellular sodium. The atrial natiuretic peptide is a antidiuretic hormone synthesized in the right atrium and released in response to expansion of blood volume, has natriuretic effect . The release of these hormones can cause an imbalance in the body fluid osmolality fundamental to the survival, since a volume expansion of water may lead to seizures. The aim of this study was to investigate in vitro vasopressin, oxytocin and atrial natriuretic peptide in the presence of the drug carbamazepine . Since so far there are no studies on the action of this drug on the neuroendocrine system in vitro and in vivo studies are controversial. Methods: The experiment was employed a total of 28 mice were sacrificed by decapitation. Hypothalamus , neurohypophysis and heart were surgically removed and incubated in Krebs containing carbamazepine in concentrations of 10-4M , 10-6M and 10-8M . The incubation medium was extracted for determination of vasopressin, oxytocin and atrial natriuretic peptide, being used radioimmunoassay. Result: In the hypothalamus, the levels of vasopressin, oxytocin and atrial natriuretic peptide in the incubation medium containing carbamazepine decreased significantly (p <0,05); in the heart , decreased significantly (p < 0,05) release of atrial natriuretic peptide ; neurohypophysis and the levels of oxytocin and vasopressin had no significant difference. Conclusion: The presence of carbamazepine decreased levels of hormones released in vitro.

Cardiac conduction abnormalities can often lead to heart failure, stroke and sudden cardiac death. Heart disease stands as the leading cause of mortality and morbidity in the United States, accounting for 30% of all deaths. Early detection of malfunctions such as arrhythmias and systolic heart failure, the two heart conditions studied in this dissertation, would definitely help reduce the burden cardiovascular diseases have on public health and overcome the current clinical challenges. The imaging techniques currently available to doctors for cardiac activation sequence mapping are invasive, ionizing, time-consuming and costly. Thus, there is an undeniable urgent need for a non-invasive and reliable imaging tool, which could play a crucial role in the early diagnosis of conduction diseases and allow physicians to choose the best course of action. The 12-lead electrocardiogram (ECG) is the current non-invasive clinical tool routinely used to diagnose and localize cardiac arrhythmias prior to intracardiac catheter ablation. However, it has limited accuracy and can be subject to operator bias. Besides, QRS complex narrowing on the clinical ECG after pacing device implantation is also used for response assessment in patients undergoing Cardiac Resynchronization Therapy (CRT). The latter is an established treatment for systolic heart failure patients who have Left Bundle Branch Block as well as a reduced ejection fraction and prolonged QRS duration. Yet, it is still not well understood why 30 to 40 % of CRT recipients do not respond. Echocardiography, due to its portability and ease-of-use, is the most frequently used imaging modality in clinical cardiology. In this dissertation, we assess the clinical performance of Electromechanical Wave Imaging (EWI) as a high frame rate ultrasound-based functional modality that can non-invasively map the electromechanical activation of the heart, i.e., the transient deformations immediately following the electrical activation. The objective of this dissertation is to demonstrate the potential clinical value of EWI for both arrhythmia detection and CRT characterization applications. The first step in translating EWI to the clinic was ensuring that the technique could reli- ably and reproducibly measure the electromechanical activation sequence independently of the probe angle and imaging view in healthy human volunteers (n=7). This dissertation then demonstrated the accuracy of EWI for localizing a variety of ventricular and atrial arrhythmias (accessory pathways in Wolff-Parkinson-White (WPW) syndrome, premature ventricular contractions, focal atrial tachycardia and macro-reentrant atrial flutter) in pediatric (n=14) and adult (n=55) patients prior to catheter ablation more accurately than 12-lead ECG predictions, as validated against electroanatomical mapping. Additionally, 3D-rendered EWI isochrones were illustrated to be capable of significantly distinguishing different biventricular pacing conditions (p≤0.05) with the RWAT and LWAT metrics, assessing the ventricular dyssynchrony change in heart failure patients (n=16) undergoing CRT, and visualizing it in 3D. EWI also provided quantification of %𝘙𝘔𝘓𝘝 in CRT patients (n=38): the amount of left-ventricular resynchronized myocardium, which was found to be a reliable response predictor at 3-, 6-, or 9-month clinical follow-up through its post-CRT values by significantly identifying super-responders from non-responders within 24 hours of implantation (p≤0.05). Furthermore, 3D-rendered isochrones successfully characterized the ventricular activation resulting from His Bundle pacing for the first time (n=4), which was undistinguishable from true physiological activation in sinus rhythm healthy volunteers with the EWI-based activation time distribution dispersion metric. The dispersion was, however, reported to significantly discriminate novel His pacing from other more conventional biventricular pacing schemes (p≤0.01). Finally, we developed and optimized a fully automated zero-crossing algorithm towards a faster, more robust and less observer dependent EWI isochrone generation process. The support vector machine (SVM) and Random Forest machine learning models were both shown capable of successfully identifying the accessory pathway in WPW patients and the pacing electrode location in paced canines. Nevertheless, the best performing algorithm was hereby proven to be the Random Forest classifier with n=200 trees with a precision rising to 97%, and a predictivity that was not impacted by the type of testing dataset it was applied to (human or canine). Overall, in this dissertation, we established the clinical potential of EWI as a viable assisting visual feedback tool, that could not only be used for diagnosis and treatment planning prior to surgical procedures, but also for monitoring during, and assessing long-term resolution of arrhythmia after catheter ablation or heart failure after a CRT implant.

A variety of cardiomyopathies are due to familial disease. Most are primarily associated with cardiac involvement and can lead to hypertrophic, dilated, or restrictive cardiomyopathy. Myotonic dystrophy (MD) is a multisystem disease with autosomal dominant inheritance and variable penetrance. Cardiac diseases are important causes of morbidity and mortality in MD patients. Patients with primary MD should be carefully investigated with an electrocardiogram, stress test, and an echocardiogram to identify preclinical cardiac involvement and to prevent life-threatening complications. Any new onset of atrial flutter or atrial fibrillation in a young patient without any underlying cardiac abnormality should be investigated for underlying myopathy. The authors report on a male adolescent with MD who presented with atrial flutter. The patient had been diagnosed with MD at birth. He had an impaired ejection fraction of 38% to 45%. The patient described sharp chest pain in the retrosternal area, with no radiation, that was induced by exercise.

No description available.

No description available.

Intensive training is associated with hemodynamic changes that typically induce an enlargement of cardiac chamber. Despite LA dilatation in athletes has been interpreted as a benign adaptation, little evidence is available. The aim of this thesis is to demonstrate that LA size changes in response to alterations in loading conditions and to analyse atrial myocardial function in athletes through the application of novel echocardiographic techniques. We found that top-level athletes exhibit a dynamic morphological and functional LA remodelling, induced by training, with an increase in reservoir and conduit volumes, but stable active volume. Training causes an increase in biatrial volumes which is accompanied by normal filling pressures and stiffness. These changes in atrial morphology are not associated with respective electrical changes. Extending the evidence from adult athletes to children, we found that training-induced atrial remodelling can occur in the early phases of the sports career and is associated with a preserved biatrial function. Finally, in a meta-analysis study of the available evidence we demonstrated that atrial function and size are not affected by aging. In conclusions, athlete’s heart is characterized by a physiological biatrial enlargement. This adaptation occurs in close association with LV cavity enlargement, is dynamic and reversible. This increase in biatrial size is not intrinsically an expression of atrial dysfunction. Indeed, in athletes the atria are characterized by a preserved reservoir function, normal myocardial stiffness, and dynamic changes in response to different loading conditions.

Introdução: Na última década, desde a descrição inicial da ablação das veias pulmonares, a ablação por cateter da fibrilação atrial (FA) tem evoluído consideravelmente em eficácia e segurança, consolidando-se como opção terapêutica em pacientes selecionados com FA. No entanto, a ablação da FA é um procedimento complexo e não isento de riscos. Ainda que seja uma complicação rara, o desenvolvimento de fístulas átrio-esofágicas (FAE) é a segunda complicação responsável por morte relacionada ao procedimento e responde por 16% dos casos de morte após ablação de FA. Consensos atuais não orientam recomendações definitivas para prevenção de lesões esofágicas, consideradas lesões precursoras de FAE. O objetivo deste trabalho foi comparar a incidência de lesões esofageanas e periesofageanas por ecoendoscopia após ablação de fibrilação atrial, utilizando diferentes estratégias de proteção esofágica durante as aplicações de radiofrequência na parede posterior do átrio esquerdo. Método: No período de outubro/2012 a julho/2014, foram estudados 45 pacientes submetidos à ablação percutânea de FA, portadores de FA paroxística ou persistente há menos de um ano. Todos os pacientes foram submetidos a ablação circunferencial com isolamento elétrico das veias pulmonares, com cateter de ablação 8 mm. Antes do procedimento, os pacientes foram randomizados para uma de três estratégias de proteção esofágica durante as aplicações de radiofrequência na parede posterior do átrio esquerdo para ablação da FA: Grupo I - aplicações limite fixo e de baixa energia, 30 W; Grupo II - aplicações com energia limitada pela temperatura esofágica; GIII - aplicações com limite fixo de energia durante resfriamento esofágico contínuo. A pesquisa de lesões esofágicas/periesofágicas foi feita por ecoendoscopia realizada em até 48 horas após a ablação. Resultados: As características basais foram similares nos três grupos, não sendo encontradas diferenças significativas entre as variáveis clínicas, laboratoriais, ecocardiográficas ou ecoendoscópicas prévias, com exceção da distância átrio-esofágica pré-ablação medida pela ecoendoscopia, que foi menor no Grupo III (GI = 3,9 mm +- 0,4; GII = 3,9 mm +- 0,5; GIII = 3,4 mm +- 0,4, p = 0.002). Nas ecoendoscopias pós-ablação de FA, foram encontradas 04 lesões esofágicas/periesofágicas: duas úlceras de parede esofágica e dois casos de edemas de mediastino periesofágico. Todos os casos de lesões esofágicas/periesofágicas ocorreram no grupo de resfriamento esofágico, G III (p= 0,008). A comparação das características clínicas dos pacientes que apresentaram lesões esofágicas/periesofágicas com os que não apresentaram essas alterações, pela análise bivariada, mostrou que foram similares nos dois grupos, exceto pelos valores médios de proteína C reativa (PCR) após a ablação de fibrilação atrial, que foram significativamente maiores no grupo com lesões (Grupo sem lesões: PCR = 0,82 mg/dl; Grupo com lesões: PCR = 2,12 mg/dl, p < 0,001). A comparação dos parâmetros das ablações por regiões das veias abordadas, quanto ao tempo das aplicações de radiofrequência, a potência e a temperatura do cateter de ablação, identificou que os pacientes que apresentaram lesões esofágicas/periesofágicas tiveram maiores valores de média de potência nas aplicações realizadas na parede posterior das veias pulmonares esquerdas, que os pacientes que não tiveram lesões (Grupo sem lesões esofágicas: potência média cateter = 37,7 w; Grupo com lesões esofágicas: potência média do cateter = 48,8 w, p = 0.013). A incidência de recorrência de arritmia após um único procedimento de ablação de Fibrilação Atrial, em seguimento clínico de 11 +- 5 meses, foi de 7 casos (15.6%), sem diferença significativa entre os grupos (GI = 26,7%, GII = 13,3% e GIII = 6,7%, p = 0,305). A incidência de complicações maiores relacionadas aos procedimentos de ablação realizados foi de 2,2% (um caso de congestão pulmonar no segundo dia após o procedimento, resolvido com uso de diuréticos). Conclusão: O uso da estratégia de resfriamento esofágico durante ablação de FA foi ineficaz como estratégia preventiva de lesões esofágicas/periesofágicas na população estudada, quando comparada às estratégias de aplicações de radiofrequência com baixa energia ou de energia limitada pela temperatura esofágica / Introduction: In the last decade, since the initial description of the ablation of pulmonary veins, the atrial fibrillation (AF) catheter ablation has evolved significantly in terms of efficacy and safety, consolidating itself as the therapeutic choice for AF selected patients. However, AF ablation is a complex procedure not without risks. Despite being a rare complication, the development of atrialesophageal fistulas (AEFs) ranks second in terms of procedure-related deaths, accounting for 16% of all post-AF ablation losses of life. Current consensus is not dispositive with regards to directives for the prevention of esophageal lesions, which come first and lead to AEFs. The objective of this work is to compare the incidence of esophageal and periesophageal lesions post-AF ablation, given use of different esophageal protection strategies during the radiofrequency applications on the left-atrium posterior wall. Method: From October 2012 through July 2014, 45 patients submitted to AF percutaneous ablation were studied. All of them were bearers of paroxistic or persistent AF for less than one year, and all of them were submitted to 8mm-catheter, pulmonary vein electric-shielding circumferential ablation. Before the procedure, patients were randomly assigned to one of three esophageal lesion protection strategies: Group I - 30w, low energy, fixed limited applications; Group II - energy applications limited by esophageal temperature; and Group III - fixed limit energy applications during continuous esophageal cooling. The survey for esophageal/periesophageal lesions was carried by means of esophageal endoscopy combined with radial ultrasound performed within 48 hours post ablation. Results: Baseline characteristics were even across groups; no significant differences in clinical, laboratorial, ecocardiographic or endoscopic variables were found, except for pre-ablation distance between posterior left atrium wall and the esophagus as measured by radial ultrasound endoscopic, smaller in Group III (GI = 3,9 mm +- 0,4; GII = 3,9 mm +- 0,5; GIII = 3,4 mm +- 0,4, p = 0.002). Post FA-ablation endoscopies revealed the existence of 4 counts of esophageal/periesophageal lesions: 2 esophageal wall ulcer and 2 periesophageal mediastin edema. All cases of esophageal/periesophageal lesions occurred in the esophageal cooling group (GIII) (p=0.008). Bivariate analysis on the clinical characteristics of patients that presented esophageal/periesophageal lesions showed no significant difference from those in the lesion-free group, except for average values for post ablation reactive-C protein (RCP), significantly greater in the lesion group (2.12 mg/dl vs. 0.82 mg/dl for the lesion-free group, p < 0.001). Ablation parameter comparison by approached vein region revealed that patients with post ablation lesions had received higher-powered applications in their posterior wall left pulmonary veins (average catheter power = 48.8 w vs. 37.7 w for lesion-free group, p=0.013). After a 11 +- 5 month clinical following, arrhythmia recurrence post a single AF ablation procedure added to 7 cases (15.6%), and no significant difference among the three different groups was found (GI = 26.7%, GII = 13.3% e GIII = 6.7%, p = 0.305). Incidence of major complications related to the ablation procedures reached 2.2% (one case of pulmonary congestion occurring in the second day post procedure, and resolved with the use of diuretics). Conclusion: The use of esophageal cooling during AF ablation was an ineffective strategy to prevent esophageal/periesophageal lesions in the studied population when compared to low-energy radiofrequency or energy limited by esophageal temperature lesion prevention strategies

Foi definido que elementos regulatórios da expressão atrial-específica do promotor da SMyHC3 estão contidos em um elemento complexo de resposta a receptores nucleares (ECRRN). Ensaios de transativação celular indicam que alguns receptores nucleares se ligam nesta região. A partir destes ensaios verificamos a ativação do promotor por um receptor nuclear, o COUP-TFII. Ele regula muitos processos biológicos, como angiogênese e o próprio desenvolvimento atrial. Através da deleção do ECRRN observamos que o promotor não era ativado por COUP-TFII, indicando a sua ligação nessa região. Verificamos ainda que somente o domínio de ligação ao ligante do COUP-TFII é capaz de ativar o promotor, sugerindo a necessidade de uma interação com outros RNs para ativar o promotor. Uma análise proteômica indica que a maioria dos interactores de COUP-TFII está relacionada com complexos reguladores da transcrição e com a via de sinalização do receptor de andrógenos (AR). Ensaios de transativação celular mostram que juntos, COUP-TFII e AR, são capazes de aumentar a ativação do promotor. / It was determined that regulatory elements of the atrial-specific expression of the promoter SMyHC3 are contained in a complex nuclear receptor response element (CNRRE). Cellular transactivation assays indicated certain nuclear receptors (NR) can bind in this region. From these trials, was observed the promoter activation by a nuclear receptor, COUP-TFII. It regulates many biological processes such as angiogenesis and atrial development. Deletion of CNRRE resulted in no activation of the promoter by COUP-TFII, indicating their connection in this region. We also verified that only the ligand binding domain of COUP-TFII is able to activate the promoter, suggesting interaction with other NRs to activate it. A proteomic analysis revealed that most of COUP-TFII partners relates to complexes of transcription regulators and the androgen receptor (AR) signaling pathway. Cell transactivation assays showed that together, COUP - TFII and AR, are able to increase promoter activation.

O Yorkshire Terrier é uma das raças com maior predisposição a doenças cardíacas congênitas e, principalmente, a doenças adquiridas como é o caso da doença mixomatosa da valva mitral (DMVM). Na literatura há apenas um trabalho estabelecendo para a raça os valores de referência ecocardiográficos de estudo de ventrículo esquerdo e de mensuração de aorta (Ao) e de átrio esquerdo (AE) por um método. É frequente observar que animais hígidos (sem doença cardiovascular) da raça em questão apresentem valores de relação átrio esquerdo/aorta (AE/Ao) aumentados, não sendo condizente com a avaliação subjetiva do exame ecocardiográfico realizado. A hipótese é de que os animais da raça Yorkshire Terrier apresentem valores ecocardiográficos diferenciados de mensuração do átrio esquerdo do que é considerado normal para as demais raças de pequeno porte e também para as escalas alométricas atualmente disponíveis para utilização na rotina clínica. Os objetivos do trabalho foram: determinar e padronizar valores de mensuração de AE, utilizando a relação AE/Ao, por meio da ecocardiografia, utilizando quatro métodos bidimensionais relatados na literatura e determinar e padronizar os valores de função atrial e volume atrial esquerdo, pelo método biplanar área-comprimento, em cães sadios da raça Yorkshire Terrier. Realizou-se estudo observacional e transversal com 50 cães adultos (acima de 15 meses e até sete anos) e clinicamente sadios da raça Yorkshire Terrier. Os animais foram submetidos à seguinte avaliação: mensuração de pressão arterial pelo método Doppler, exame físico, exame ecocardiográfico, exame eletrocardiográfico, exames laboratoriais (hematológico e bioquímico) e radiografias torácicas. Foram excluídos 13 animais diagnosticados com DMVM estágio B1. A mensuração da Ao foi feita por três métodos distintos, descritos pelos autores Rishniw, Hansson (método sueco) e Chetboul. O AE foi avaliado pelos três métodos e pela largura septo-lateral no corte longitudinal direito (método longitudinal). A determinação da área e do volume (máximo, pré-contração atrial e mínimo) do AE foi realizada no corte apical duas (2C) e quatro (4C) câmaras. Foram realizadas três determinações de cada parâmetro, avaliados nas diferentes fases do ciclo cardíaco, considerando-se a média dos valores obtidos. Os resultados principais da área e do volume atrial, com a média e o desvio padrão, foram: Vmáx 2185&#177;690 mm3, Vpré 1390&#177;431 mm3, Vmin 728&#177;255 mm3, AAEmáx 4C 58,4&#177;15 mm2/kg, AAEmáx 2C 53,4&#177;12,2 mm2/kg, AAEpré 4C 141&#177;35,2 mm2/kg, AAEpré 2C 38,9&#177;9,6 mm2/kg, AAEmín 4C 27,2&#177;5,82 mm2/kg, AAEmín 2C 26,2&#177;6,63 mm2/kg. As relações AE/Ao encontradas foram: Rishniw 1,55&#177;0,12, Chetboul 1,15&#177;0,10 e longitudinal 1,75&#177;0,15, que são semelhantes aos valores obtidos na literatura, e sueco 1,51&#177;0,16, que é maior do que o relatado, sugerindo que a raça em questão apresente valores de mensuração de AE superiores quando utilizado este método na avaliação. A única variável de função atrial que não apresentou diferença estatística quando comparada às faixas de peso foi a AAEpré. O método sueco apresentou concordância e melhor correlação positiva quando comparado aos demais. Não houve diferença estatística na comparação das relações AE/Ao com relação às faixas de peso previamente estabelecidas (&lt;3kg, 3-4kg, &gt;4kg). / The Yorkshire Terrier is one of the breeds with a greater predisposition to congenital heart disease and, mainly, to acquired diseases such as myxomatous mitral valve disease (MMVD). There is only one study establishing echocardiographic reference values for this breed, including left ventricle, aortic (Ao) and left atrial (LA) measurements (using a single method). It is often observed that healthy Yorkshire dogs (with no cardiovascular disease) have increased left atrial/aortic ratio (LA/Ao) values which are not consistent with the subjective evaluation of the echocardiographic examination performed. The hypothesis is that Yorkshire Terrier dogs have different echocardiographic values for left atrial measurement from what is considered normal for other small breed dogs and also for the allometric scales currently available for use in clinical routine. The objectives of this study were: to determine and standardize LA measurement values, using LA/Ao ratio, employing four two-dimensional echocardiographic methods reported in the literature, and to determine and standardize atrial function and left atrial volume values by the biplane area-length method in Yorkshire Terrier dogs. An observational and cross-sectional study was performed with 50 adult dogs (between 15 months and seven years) and clinically healthy Yorkshire Terrier dogs. The animals were submitted to the following evaluation: measurement of blood pressure by the Doppler method, physical examination, echocardiographic and electrocardiographic examination, laboratory tests (hematological and biochemical) and chest radiographs. 13 animals diagnosed with MMVD stage B1 were excluded. Ao measurement was done by three different methods, described by the authors Rishniw, Hansson (\"Swedish\" method) and Chetboul. LA was evaluated by these three methods and by the septum-lateral width in the right paraesternal axis view (\"longitudinal\" method). The determination of LA area and volume (maximum, pre-atrial contraction and minimum) was performed in the apical two (2C) and four (4C) chambers view. Three determinations of each parameter were performed, evaluated in different phases of the cardiac cycle, considering the average of the obtained values. The main results of the area and atrial volume, with mean and standard deviation, were: Vmax 2185 &#177; 690 mm3, Vpre 1390 &#177;431 mm3, Vmin 728 &#177 255 mm3, AAEmax 4C 58,4 &#177 15 mm2/kg, AAEmax 2C 53,4 &#177 12,2 mm2/kg, AAEpre 4C 141 &#177 35,2 mm2/kg, AAEpre 2C 38,9 &#177 9,6 mm2/kg, AAEmin 4C 27,2 &#177 5,82 mm2/kg, AAEmin 2C 26,2 &#177 6,63 mm2/kg. The only atrial function parameter that did not present statistical difference when compared to the weight ranges was AAEpre. The LA/Ao ratios found were: \"Rishniw\" 1,55 &#177 0,12, \"Chetboul\" 1,15 &#177 0,10 and \"longitudinal\" 1,75 &#177 0,15, which are similar to the values obtained on te literature, and \"Swedish\" 1,51 &#177 0,16, which is higher then what is demonstrated on the literature, suggesting that this breed have highers values of LA measurement when this technique is used on evaluation. The Swedish method presented a better positive correlation when compared to the others. There was no statistically significant difference in LA/Ao ratios when compared to previously established weight ranges (&lt;3kg, 3-4kg,&gt; 4kg).