INTRODUÇÃO: O intervalo PR longo, em conjunto com a duração e a morfologia do QRS gerado pela estimulação cardíaca artificial, associam-se com dessincronia e disfunção cardíaca em diferentes níveis. Na doença do nó sinusal, durante a programação do marca-passo, podemos optar por duas estratégias: PR longo com QRS estreito (quando se busca evitar a ativação ventricular em detrimento do sincronismo atrioventricular) ou PR otimizado e QRS largo estimulado pelo marca-passo (quando se busca corrigir o intervalo atrioventricular em detrimento da sincronia ventricular). Neste estudo, buscamos comparar a evolução clínica e estrutural cardíaca destas estratégias. MÉTODOS: Acompanhou-se por 1 ano uma coorte com doença do nó sinusal, bloqueio atrioventricular de 1º grau (doença binodal) e marca-passo DDD. Através da ecocardiografia Doppler de fluxo transmitral avaliou-se a duração do enchimento diastólico ventricular e sincronia atrioventricular (? ondas E+A>=40% do ciclo cardíaco). Os pacientes dessincrônicos (DAV) tiveram o intervalo atrioventricular otimizado (intervenção) ao melhor rendimento hemodinâmico, porém com QRS estimulado. Estes retornavam ao PR basal após 6 meses (cross-over). Os sincrônicos (SAV) foram mantidos sob PR longo e QRS intrínseco durante todo o seguimento (controles). RESULTADOS: Quarenta e três pacientes foram incluídos e 41 completaram o estudo (idade média= 71,5 anos). Confirmou-se a existência dos 2 grupos (p= <0.001): os SAV (n=19), distintos daqueles com dessincronia atrioventricular (DAV, n=24). PR>=263ms mostrou especificidade de 78,9% para diagnóstico de dessincronia AV, e a maior duração do PR mostrou relação direta com pior função sistólica ventricular basal. Os DAV eram predominantemente homens, tinham PR mais longos (média= 283,5ms) e menor duração da diástole (p= 0.032). Um subgrupo dos DAV com PR >300ms mostrou pior qualidade de vida, maior duração do QRS quando estimulado, e dessincronia não corrigível por otimização. De modo notável, em 6 meses, o grupo DAV mostrou tendência a melhora da FEVE apesar do QRS alargado, e decréscimo ao retornar ao basal. O grupo SAV apresentava PR longo antifisiológico e evolutivamente piora da regurgitação mitral (p= 0.008) e também registros de fibrilação atrial de aparição mais precoce. Foram preditores independentes de dessincronia atrioventricular o PR >263ms (RR= 1,84; p= 0.024) e a duração da diástole inferior a 40% do ciclo cardíaco (RR= 0,99; p<0.001). CONCLUSÕES: Em pacientes com doença binodal e marca-passo DDD, a mera intenção de evitar o QRS largo da estimulação ventricular artificial não resolve todos os problemas. Intervalos PR longos (>263ms) associados ao decréscimo do enchimento diastólico ventricular caracterizariam outro prejuízo eletromecânico cardíaco: a dessincronia atrioventricular, disfunção que tem repercussão hemodinâmica, clínica e estrutural. / BACKGROUND: Long PR interval and wide QRS duration duo to ectopic morphology generated by artificial cardiac pacing are associated with cardiac dysfunction and dyssynchrony at different levels. When programming a permanent pacemaker in sinus node disease, two strategies can be considered: long PR with narrow QRS (avoiding ventricular pacing despite the risk of losing atrioventricular syncrony) or optimized PR interval with pacemaker-induced wide QRS (aiming to correct the atrioventricular delay despite loss of the ventricular synchrony). In this study, we aimed to compare the clinical and cardiac structural outcomes of these two strategies. METHODS: Sudy a cohort of patients with sinus node disease, first-degree AV block (binodal disease) and DDD pacemaker was followed for 1 year follow-up. atrioventrucular synchrony (AVS) was assessed echocardiographically by the ventricular diastolic filling time on Doppler transmitral flow: sum of the duration of E and A waves >=40% of the cardiac cycle. Patients with AV dyssynchrony (AVD) had the AV delay optimized (intervention group) for the best hemodynamic performance, but under wide artificially paced QRS. These returned to baseline PR interval after 6 months (cross-over). Those with AVS were kept under intrinsic QRS throughout the follow-up period despiste long PR interval (control group). RESULTS: Forty-three patients were included (mean age = 71.5 years), and 41 completed the 1-year follow-up. The existence of the 2 groups was confirmed (p<=0.001): patients with AVS (n=19), differed from those with AVD (n=24). Within a homogeneous sample (mean age= 71.5 years), PR >=263 ms had a specificity of 78.9% for the diagnosis of AVD, and longer PR intervals were associated with worse baseline ventricular systolic function. Most patients with AVD were men, had longer PR intervals (mean= 283.5 ms), and had significantly lower diastole duration (p= 0.032). A subgroup of AVD patients with PR >300 ms had poorer quality of life, significantly greater use of ?-blockers (p= 0.011), longer paced QRS width, and AV dyssynchrony that is non-correctable by optimization. Notably, at 6 months, the AVD group lean towards to have better LVEF values despite the wide QRS and a decrease when returning to baseline. Patients with AVS also had PR intervals different from the physiological condition (157.9 to 330 ms) and, over time, had worsening of mitral regurgitation (p=0.008) and earlier atrial fibrillation. PR>263 ms (RR= 1.84; p= 0.024) and diastole duration <40% of the cardiac cycle (RR= 0.99; p<0.001) were independent predictors of AVD. CONCLUSIONS: For patients with binodal disease and DDD pacemaker, the strategy of avoiding the wide QRS, usually applied by modern algorithms for minimizing ventricular pacing, is not enough to solve all problems. Long PR intervals (>=263 ms) may be associated with decreased ventricular diastolic filling time and characterize another cardiac electromechanical impairment: AV dyssynchrony, with hemodynamic, clinical and structural repercussions by itself.

INTRODUÇÃO: O intervalo PR longo, em conjunto com a duração e a morfologia do QRS gerado pela estimulação cardíaca artificial, associam-se com dessincronia e disfunção cardíaca em diferentes níveis. Na doença do nó sinusal, durante a programação do marca-passo, podemos optar por duas estratégias: PR longo com QRS estreito (quando se busca evitar a ativação ventricular em detrimento do sincronismo atrioventricular) ou PR otimizado e QRS largo estimulado pelo marca-passo (quando se busca corrigir o intervalo atrioventricular em detrimento da sincronia ventricular). Neste estudo, buscamos comparar a evolução clínica e estrutural cardíaca destas estratégias. MÉTODOS: Acompanhou-se por 1 ano uma coorte com doença do nó sinusal, bloqueio atrioventricular de 1º grau (doença binodal) e marca-passo DDD. Através da ecocardiografia Doppler de fluxo transmitral avaliou-se a duração do enchimento diastólico ventricular e sincronia atrioventricular (? ondas E+A>=40% do ciclo cardíaco). Os pacientes dessincrônicos (DAV) tiveram o intervalo atrioventricular otimizado (intervenção) ao melhor rendimento hemodinâmico, porém com QRS estimulado. Estes retornavam ao PR basal após 6 meses (cross-over). Os sincrônicos (SAV) foram mantidos sob PR longo e QRS intrínseco durante todo o seguimento (controles). RESULTADOS: Quarenta e três pacientes foram incluídos e 41 completaram o estudo (idade média= 71,5 anos). Confirmou-se a existência dos 2 grupos (p= <0.001): os SAV (n=19), distintos daqueles com dessincronia atrioventricular (DAV, n=24). PR>=263ms mostrou especificidade de 78,9% para diagnóstico de dessincronia AV, e a maior duração do PR mostrou relação direta com pior função sistólica ventricular basal. Os DAV eram predominantemente homens, tinham PR mais longos (média= 283,5ms) e menor duração da diástole (p= 0.032). Um subgrupo dos DAV com PR >300ms mostrou pior qualidade de vida, maior duração do QRS quando estimulado, e dessincronia não corrigível por otimização. De modo notável, em 6 meses, o grupo DAV mostrou tendência a melhora da FEVE apesar do QRS alargado, e decréscimo ao retornar ao basal. O grupo SAV apresentava PR longo antifisiológico e evolutivamente piora da regurgitação mitral (p= 0.008) e também registros de fibrilação atrial de aparição mais precoce. Foram preditores independentes de dessincronia atrioventricular o PR >263ms (RR= 1,84; p= 0.024) e a duração da diástole inferior a 40% do ciclo cardíaco (RR= 0,99; p<0.001). CONCLUSÕES: Em pacientes com doença binodal e marca-passo DDD, a mera intenção de evitar o QRS largo da estimulação ventricular artificial não resolve todos os problemas. Intervalos PR longos (>263ms) associados ao decréscimo do enchimento diastólico ventricular caracterizariam outro prejuízo eletromecânico cardíaco: a dessincronia atrioventricular, disfunção que tem repercussão hemodinâmica, clínica e estrutural. / BACKGROUND: Long PR interval and wide QRS duration duo to ectopic morphology generated by artificial cardiac pacing are associated with cardiac dysfunction and dyssynchrony at different levels. When programming a permanent pacemaker in sinus node disease, two strategies can be considered: long PR with narrow QRS (avoiding ventricular pacing despite the risk of losing atrioventricular syncrony) or optimized PR interval with pacemaker-induced wide QRS (aiming to correct the atrioventricular delay despite loss of the ventricular synchrony). In this study, we aimed to compare the clinical and cardiac structural outcomes of these two strategies. METHODS: Sudy a cohort of patients with sinus node disease, first-degree AV block (binodal disease) and DDD pacemaker was followed for 1 year follow-up. atrioventrucular synchrony (AVS) was assessed echocardiographically by the ventricular diastolic filling time on Doppler transmitral flow: sum of the duration of E and A waves >=40% of the cardiac cycle. Patients with AV dyssynchrony (AVD) had the AV delay optimized (intervention group) for the best hemodynamic performance, but under wide artificially paced QRS. These returned to baseline PR interval after 6 months (cross-over). Those with AVS were kept under intrinsic QRS throughout the follow-up period despiste long PR interval (control group). RESULTS: Forty-three patients were included (mean age = 71.5 years), and 41 completed the 1-year follow-up. The existence of the 2 groups was confirmed (p<=0.001): patients with AVS (n=19), differed from those with AVD (n=24). Within a homogeneous sample (mean age= 71.5 years), PR >=263 ms had a specificity of 78.9% for the diagnosis of AVD, and longer PR intervals were associated with worse baseline ventricular systolic function. Most patients with AVD were men, had longer PR intervals (mean= 283.5 ms), and had significantly lower diastole duration (p= 0.032). A subgroup of AVD patients with PR >300 ms had poorer quality of life, significantly greater use of ?-blockers (p= 0.011), longer paced QRS width, and AV dyssynchrony that is non-correctable by optimization. Notably, at 6 months, the AVD group lean towards to have better LVEF values despite the wide QRS and a decrease when returning to baseline. Patients with AVS also had PR intervals different from the physiological condition (157.9 to 330 ms) and, over time, had worsening of mitral regurgitation (p=0.008) and earlier atrial fibrillation. PR>263 ms (RR= 1.84; p= 0.024) and diastole duration <40% of the cardiac cycle (RR= 0.99; p<0.001) were independent predictors of AVD. CONCLUSIONS: For patients with binodal disease and DDD pacemaker, the strategy of avoiding the wide QRS, usually applied by modern algorithms for minimizing ventricular pacing, is not enough to solve all problems. Long PR intervals (>=263 ms) may be associated with decreased ventricular diastolic filling time and characterize another cardiac electromechanical impairment: AV dyssynchrony, with hemodynamic, clinical and structural repercussions by itself.

Background: Pulmonary arterial hypertension (PAH) is a condition with severe morbidity and mortality. It is associated with an increase in incidence of all forms of arrhythmias which further increase morbidity and mortality. The monocrotaline (MCT) model of pulmonary hypertension (PH) in the rat is analogous to PAH in humans and was used to study how PH causes arrhythmias. Methods: A single injection of MCT or a volume matched saline injection (control) was given to the rats on day 0 of the protocol. The hearts of both groups of rats were studied in vivo with echocardiography (echo) and electrocardiogram (ECG). The rat’s condition was monitored and they were electively sacrificed when they showed symptoms or on day 28. Live cardiac tissue was studied using the Langendorff preparation and a right atrial preparation that incorporated the sinoatrial (SA) and atrioventricular (AV) nodes. Molecular biology techniques including reverse transcription quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry were used identify changes in the heart caused by PH. The effects of macitentan, an endothelin receptor antagonist used in the treatment of PAH, on the MCT injected rats was assessed using echo and ECGResults: Echo demonstrated that the MCT treated rats developed severe pulmonary hypertension with a decreased pulmonary artery acceleration time (P<0.005) and an increased pulmonary artery deceleration (P<0.005). The MCT treated rats also developed right ventricular hypertrophy (P<0.05) and dilation (P<0.005). The in vivo ECG demonstrated QT prolongation (P<0.005). Ex vivo functional experiments demonstrated QT prolongation (P<0.005) and prolonged ventricular effective refractory period (P<0.005). AV node dysfunction was also seen in the ex vivo experiments with an increased AV effective refractory period (P<0.05), AV functional refractory period (P<0.05) and incidence of complete heart block (P<0.05). RT-qPCR demonstrated significant changes in the mRNA expression of several ion channels and exchanges, Ca2+ handling proteins and autonomic receptors including a downregulation of HCN4 and CaV1.2 in the AV nodal tissues (P<0.05). Treatment of established pulmonary hypertension led to a reduction in the prolongation of the QT interval caused by MCT administration at day 21 (P<0.05).Conclusions: PH causes arrhythmogenic changes including prolonged repolarisation in the working myocardium and AV node dysfunction. These changes may be caused by dysregulation of ion channels and Ca2+ handling proteins. These ion channels and Ca2+handling proteins may play a key role in both physiological and pathological processes within the AV node.

Congenital heart defects (CHDs) constitute a major proportion of clinically significant birth defects and are an important component of pediatric cardiovascular disease. Atrioventricular septal defects (AVSDs) include a range of anomalies characterized by atrial, ventricular, and atrioventricular (AV) valve defects. AVSDs commonly occur in the presence of a syndrome, most frequently Down syndrome; they also occur in isolation and are referred to as non-syndromic AVSDs (NSAVSDs). These studies were performed to evaluate for presence of an intermediate phenotype in parents and siblings of a child with a NSAVSD, risk factors associated with NSAVSDs, and prognostic risk factors for left AV valve replacement following primary repair of an AVSD. It was shown that the mean body surface area-standardized AV septal length (AVSL) was significantly shorter in the NSAVSD parents and siblings than in parents and siblings of syndromic AVSD case and control children. Using age- and gender-adjusted body surface area-standardized AVSL, it was determined that there was evidence for two component distributions in parents and siblings of NSAVSD children, suggesting the presence of an intermediate. Broadening the definition of AVSD to include those with a shortened AVSL may increase the power of genetic association and mapping studies to identify susceptibility genes. Risk factors associated with NSAVSD were examined using the 1997-2005 National Birth Defects Prevention Study database. Mothers who actively smoked or were exposed to passive smoke anytime from one month prior to pregnancy through the end of the first trimester were more likely to have an infant with a NSAVSD. There was a suggestive association between AVSDs and use of antibacterial, antifungal, and antiviral medications. Additional investigations are warranted to investigate associations with specific medications as well as to uncover possible gene-environment interaction effects that may modify these risks in order to develop improved primary prevention strategies. Using the Pediatric Cardiac Care Consortium database, factors associated with time to first reoperation and time to replacement following primary AVSD repair were evaluated. Type of AVSD repair, closure of the mitral valve cleft, moderate to severe postoperative left AV valve regurgitation, and presence of postoperative complete heart block were associated with earlier time to reoperation after adjusting for age and weight at AVSD repair. Down syndrome and presence of postoperative mitral stenosis were associated with earlier time to replacement. Prognostic risk factors following left AV valve replacement in children who had previously undergone AVSD repair were also identified. A prosthetic valve size to body weight ratio of greater than 3 and the presence of Down syndrome were identified as predictors of in-hospital death following left AV valve replacement. By adding to our knowledge of the AVSD familial and environmental risk factors from these studies, we will be able to (1) improve genetic counseling, (2) identify other family members for genetic testing, (3) begin to devise primary prevention strategies, and (4) improve treatment modalities. By recognizing prognostic factors which influence survival, optimal patient care can be devised which will not only improve treatment modalities, but also long-term survival.

ECG warning system is established for real time monitoring of a patient's electrocardiogram (ECG) and automatic detection of certainement cardiac diseases, namely myocardial infarction, hyperkalemia and atrioventricular block. A distinctive research work related on the assimilation of modern technologies: software, computer and information technologies. ECG early warning system's algorithm is developed in accordance to measuring the average of the ECG signatures and Interprets the data with simulated healthy curve. The prototype system INITIALLY classifies the data and Evaluated it with natural healthy simulated curve. Meanwhile the system discards f healthy curve exists otherwise the system stores the distinguished abnormalities in the curve then transfers Warning to the doctor and patient. Cardiac patients can be assisted by this warning system by detecting abnormalities at the very early stage. Consequently, doctors Provide better tools to identify cardiac diseases resulting things more accurate medical advice

Introduction: Factors that influence atrioventricular (AV) nodal conduction are complex and not well understood. Multiple studies have been performed to explain the mechanisms responsible for AV nodal conduction but the AV node (AVN) remains a "riddle". With ageing there is an increase in the incidence of AV nodal dysfunction leading to AV block. Methodology: I have performed electrophysiological (EP) and immunohistochemistry experiments on male Wistar-Hanover rats aged 3 months (equivalent to 20 year old humans; n=24) and 2 years (equivalent to 70 year old humans; n=15). AH interval, Wenkebach cycle length (WCL) and AV node effective refractory period (AVNERP) were measured. I used cesium (Cs+ = 2 mM) to block HCN channels responsible for the funny current "If " (and therefore the membrane clock), and ryanodine (2 μM) to block RyR2 channels responsible for Ca2+ release from the sarcoplasmic reticulum (and therefore the Ca2+ clock) in the two age groups. Protein expression in each group (from n=9 young and n=8 old rats) from different regions of the AV conduction axis: inferior nodal extension (INE), compact node (CN), proximal penetrating bundle (PPB) and distal penetrating or His bundle (His) were studied using immunofluorescence and confocal microscopy. The expression of the gap junction channels Cx43 and Cx40 and ion channel’s including HCN4 (responsible for If current), Nav1.5 (major cardiac Na+ channel responsible for INa) and Cav1.3 (L-type Ca2+ channel), and calcium handling proteins, RyR2 and SERCA 2a (involved in Ca2+ release and reuptake from cardiac sarcoplasmic reticulum, SR) were studied. Semi-quantitative signal intensity of these channels was measured using Volocity software. Structural characteristics of the tissue were studied using histology (Masson’s trichome stain and picrosirius red stain for collagen). Statistical analysis was performed with Prism 6.0. Electrophysiological measurements were performed using Spike2.Results: Without drugs to block the If current and Ca2+ release from the SR, there was a significant prolongation of the AH interval (P<0.005), WCL (P<0.005) and AVNERP (P<0.001) with ageing. In young rats (but not old rats), Cs+ prolonged the AH interval (P<0.001), WCL (P<0.01) and AVNERP (P<0.01). Ryanodine prolonged the AH interval (P<0.01) and WCL (P<0.01) in young and old rats. Immunofluorescence revealed that with ageing: Cx43 is downregulated in the PPB and His (P<0.05); Cx40 is upregulated in the INE and CN (P<0.05); HCN4 is downregulated in the His bundle (P=0.05); Nav1.5 is downregulated in the CN and PB (P<0.05); RyR2 is downregulated in the CN and PPB (P<0.05); SERCA2a and Cav1.3 is upregulated in the PPB (P<0.05). Histology confirmed that with ageing that the cells of CN, PPB and His are more loosely packed and irregularly arranged. There is cellular hypertrophy, decrease in the number of nuclei and increase in the collagen content with ageing. The clinical study has shown that elderly patients with syncope and cardiac conduction system disease are at risk of high mortality and recurrent transient loss of consciousness. Conclusion: For the first time, we have shown that both HCN and RyR2 channels play an important role in AV nodal conduction. With ageing the expression of HCN4 and the role of If in AV nodal conduction decreases, whereas the role of Ca2+ clock in AV nodal conduction was unchanged, although the expression of RyR2 and SERCA2a changes. The clinical study suggests that AV nodal disease is associated with significant morbidity and higher mortality among elderly patients who present with transient loss of consciousness.

Alguns aspectos funcionais do aparelho circulatório da baleia têm sido objeto de importantes relatos na literatura, destacando a acentuada bradicardia que ocorre durante o mergulho. Entretanto, existem poucas informações relativas à morfologia dos seus órgãos circulatórios, principalmente os componentes do complexo valvar cardíaco. Este trabalho tem como objetivo, abordar a morfologia macroscópica da valva atrioventricular esquerda da Baleia Minke, abrangendo também, os músculos papilares e as cordas tendíneas. Foram estudados os componentes anatômicos do complexo valvar atrioventricular esquerdo em onze corações de Baleias Minke (Balaenoptera acutorostrata). Esses órgãos foram obtidos no ano de 1980, quando ainda era permitida a caça desses animais no Brasil, no Porto de Cabedelo, Estado da Paraíba. Desde então são mantidos em solução aquosa de formol a 10%, no Laboratório de Anatomia da FMVZ/USP. Fez-se uma abordagem da valva atrioventricular esquerda pelo afastamento, após incisão, da parede direita do ventrículo esquerdo, verificando-se que o coração da baleia Minke se assemelha em sua morfologia ao coração de mamíferos terrestres, apresentando um mínimo de quatro cúspides. A cúspide septal é maior que a parietal. Como nas demais espécies, as cúspides permitem o balonamento durante a sístole ventricular. A cúspide com maior área por corda tendínea é a septal. O complexo valvar atrioventricular esquerdo apresenta feixes compactos de cordas tendíneas, reduzindo o volume de componentes dentro da cavidade ventricular. Caracterizaram-se quatro tipos morfológicos de cordas tendíneas, caracterizadas como dos tipos I, II, III, IV e comissurais. O músculo papilar subatrial é o mais proeminente. A baleia pode apresentar, além dos músculos papilares subatrial e subauricular, um músculo papilar acessório. / A few information exist in the literature relative to the morphology of the circulatory organs of the whale, especially concerning the valvar complex of the heart. It tried to approach in this work, the macroscopic anatomy of the left atrioventricular valve of the whale Minke, as well as the musculi papillaris and Chordae tendineae. It was studied the anatomical components of eleven hearts of the Minke whales. Those organs were obtained in 1980, in the port of Cabedelo - Paraíba - Brazil, when the hunt of those animals was still allowed in Brazil. Those hearts are maintained in aqueous solution of formol at 10%, in the laboratory of Veterinary Anatomy of FMVZ/USP. Do Made himself then the access for the left atrioventricular valve, moving away the wall right ventricular of the cardiac wall by means of magnet incision in \" V \". The analysis of those hearts demonstrated that : the morphology of heart of the Minke whales is similar to the other terrestrial mammals, presenting a minimum of four leaflets. The septal leaflet is larger than to the parietal leaflet. As in the other species, the leaflets balloons during the ventricular systole. The leaflet with larger area for Chordae tendineae is the septal leaflet. The left atrioventricular valvar complex of the whale, presents bunches of strings compact tendineae, reducing the volume of components inside of the cavity ventricular. There is also, strings tendíneas classifieds as I, II, III IV and comissural types. The subatrial papilar muscle is the most prominent. The whale can present, besides the subatrial and subauricular muscles, one accessory papilar muscle.

Alguns aspectos funcionais do aparelho circulatório da baleia têm sido objeto de importantes relatos na literatura, destacando a acentuada bradicardia que ocorre durante o mergulho. Entretanto, existem poucas informações relativas à morfologia dos seus órgãos circulatórios, principalmente os componentes do complexo valvar cardíaco. Este trabalho tem como objetivo, abordar a morfologia macroscópica da valva atrioventricular esquerda da Baleia Minke, abrangendo também, os músculos papilares e as cordas tendíneas. Foram estudados os componentes anatômicos do complexo valvar atrioventricular esquerdo em onze corações de Baleias Minke (Balaenoptera acutorostrata). Esses órgãos foram obtidos no ano de 1980, quando ainda era permitida a caça desses animais no Brasil, no Porto de Cabedelo, Estado da Paraíba. Desde então são mantidos em solução aquosa de formol a 10%, no Laboratório de Anatomia da FMVZ/USP. Fez-se uma abordagem da valva atrioventricular esquerda pelo afastamento, após incisão, da parede direita do ventrículo esquerdo, verificando-se que o coração da baleia Minke se assemelha em sua morfologia ao coração de mamíferos terrestres, apresentando um mínimo de quatro cúspides. A cúspide septal é maior que a parietal. Como nas demais espécies, as cúspides permitem o balonamento durante a sístole ventricular. A cúspide com maior área por corda tendínea é a septal. O complexo valvar atrioventricular esquerdo apresenta feixes compactos de cordas tendíneas, reduzindo o volume de componentes dentro da cavidade ventricular. Caracterizaram-se quatro tipos morfológicos de cordas tendíneas, caracterizadas como dos tipos I, II, III, IV e comissurais. O músculo papilar subatrial é o mais proeminente. A baleia pode apresentar, além dos músculos papilares subatrial e subauricular, um músculo papilar acessório. / A few information exist in the literature relative to the morphology of the circulatory organs of the whale, especially concerning the valvar complex of the heart. It tried to approach in this work, the macroscopic anatomy of the left atrioventricular valve of the whale Minke, as well as the musculi papillaris and Chordae tendineae. It was studied the anatomical components of eleven hearts of the Minke whales. Those organs were obtained in 1980, in the port of Cabedelo - Paraíba - Brazil, when the hunt of those animals was still allowed in Brazil. Those hearts are maintained in aqueous solution of formol at 10%, in the laboratory of Veterinary Anatomy of FMVZ/USP. Do Made himself then the access for the left atrioventricular valve, moving away the wall right ventricular of the cardiac wall by means of magnet incision in \" V \". The analysis of those hearts demonstrated that : the morphology of heart of the Minke whales is similar to the other terrestrial mammals, presenting a minimum of four leaflets. The septal leaflet is larger than to the parietal leaflet. As in the other species, the leaflets balloons during the ventricular systole. The leaflet with larger area for Chordae tendineae is the septal leaflet. The left atrioventricular valvar complex of the whale, presents bunches of strings compact tendineae, reducing the volume of components inside of the cavity ventricular. There is also, strings tendíneas classifieds as I, II, III IV and comissural types. The subatrial papilar muscle is the most prominent. The whale can present, besides the subatrial and subauricular muscles, one accessory papilar muscle.

The atrioventricular junction (AVJ) is a complex anatomical structure. It has an important role in maintaining synchronised atrioventricular conduction and protects from ventricular tachycardia, as well as bradycardia. Its embryological development and function is under tight transcription factor control. Heart failure is a chronic systemic condition, affecting one million people in the UK alone. Slowing of atrioventricular conduction in heart failure is associated with increased morbidity and mortality. The molecular and anatomical basis of abnormal atrioventricular conduction was studied in a rabbit model of heart failure due to aortic insufficiency and abdominal aortic constriction. The PR interval was significantly prolonged in heart failure animals. Using laser-assisted microdissection, the tiny tissues of the AVJ were collected for RT-PCR analysis. HCN1, Cav1.3, Cx40 and Cx43 transcripts were significantly downregulated by heart failure, with a compensatory increase in CLCN2, Nav1.1, Navβ1, SUR2A and PAK1. Immunolabelling for Cx43 showed reduction in protein level and longitudinal dissociation not only in the inferior nodal extension but also in the His bundle in heart failure animals. Anatomical studies of the AVJ have previously been limited by its small size and inaccessible location. Contrast-enhanced micro-CT scanning allowed non-destructive imaging of the AVJ anatomy. AVJ length and volume were increased in the rabbit model of heart failure, which is expected to contribute to atrioventricular conduction abnormalities. Micro-CT additionally resolved the anatomy of the canine AVJ and atria, including fibre orientation in the pulmonary vein sleeves and Bachmann’s bundle. The physiological effects of loss of T-box transcription factor 5 (Tbx5) in the AVJ were studied in a transgenic inducible Tbx5 knockout mouse model using optical mapping. Tbx5-deficient mice had a prolonged PR interval in vivo and a higher incidence of atrioventricular block and ventricular conduction abnormalities in Langendorff-perfused hearts.

No description available.