Constrictive pericarditis arises as a result of the fibrous thickening of the pericardium due to chronic inflammatory changes from various injuries. Increased pulmonary and systemic venous pressures manifest clinical features of left and right heart failure. Idiopathic or post-viral pericarditis is the most common cause followed by postpericardiotomy, radiation-induced causes. Right-sided heart failure symptoms predominate over left-sided heart failure symptoms due to the equalization of pressures. No single diagnostic test can provide a definitive diagnosis or evidence of constrictive pericarditis. Medical management is difficult for constrictive pericarditis. The treatment of choice for constrictive pericarditis is pericardiectomy.

Hintergrund: Bei etwa der Hälfte aller Patienten mit Herzinsuffizienz kann die Symptomatik auf eine Herzinsuffizienz bei erhaltener Ejektionsfraktion (HFPEF) zurückgeführt werden. Lange Zeit wurde der Herzinsuffizienz bei erhaltener Ejektionsfraktion eine bessere Prognose nachgesagt als der systolischen Herzinsuffizienz. Neuere Untersuchungen zeigen allerdings, dass die Prognose vergleichbar schlecht und gegenüber der Allgemeinbevölkerung deutlich herabgesetzt ist. Trotz großer klinischer Relevanz gibt es weder eine allgemeingültige Leitlinie zur Diagnostik der HFPEF noch eine überzeugende Therapie, die Morbidität und Mortalität reduziert. Auch ist bislang nicht geklärt, inwieweit sich demographische und klinische Faktoren auf die den Empfehlungen zugrunde liegenden Zielparameter auswirken. Ebenfalls ungeklärt ist, ob und wie diese krankheitstypischen, für die Diagnose wegweisenden Schlüsselparameter wie Leistungsfähigkeit, diastolische Funktion, neurohumorale Aktivierung und linksatriales und linksventrikuläres Remodeling auch unabhängig von demographischen und klinischen Faktoren untereinander assoziiert sind. Dieses ist von großem Interesse, da man die Parameter, anhand derer man eine Krankheit diagnostizieren und den Effekt einer Therapie messen will, gut kennen sollte und die Einflüsse, denen sie unterliegen, bekannt sein sollten. Material und Methoden: In der vorliegenden Arbeit werden Baselinedaten der Aldo-DHF-Studie präsentiert, die 422 ambulante Patienten mit einer symptomatischen Herzinsuffizienz bei erhaltener Ejektionsfraktion einschloss (mittleres Alter 67 Jahre, 48% männlich). Anhand dieser Daten wurden die Zusammenhänge zwischen zahlreichen demographischen und klinischen Charakteristika und Werten der Leistungsfähigkeit (peak VO 2), Werten der diastolischen Dysfunktion ( E/e‘), Höhe der neurohumoralen Aktivität (NT-proBNP) und Werten des kardialen Remodelings (linksatrialer Volumenindex und linksventrikulärer Massenindex) ermittelt sowie ihre Assoziation untereinander geprüft. Dazu wurden die Patienten nach ihrem jeweiligen NYHA-Stadium in zwei Gruppen unterteilt (NYHA-Stadium II, n= 363 Patienten; NYHA-Stadium III, n= 59 Patienten). Beziehungen zwischen Basischarakteristika und dem jeweiligen Zielparameter wurden zunächst mit einfacher Regression und anschließend mit multipler Regression untersucht. Beziehungen der Zielparameter untereinander wurden zum einen durch den Pearson-Korrelationskoeffizienten 5 Zusammenfassung 61 und zum anderen nach Adjustierung durch einen partiellen Korrelationskoeffizienten dargestellt. Ergebnisse: Wir stellten fest, dass das Alter der einzige Faktor ist, der sich auch unabhängig von demographischen und klinischen Faktoren signifikant negativ auf alle fünf untersuchten Schlüsselparameter auswirkt: die peak VO2 (p= < 0.001), das E/e‘ (p= 0,009), das NT-proBNP (p= < 0.001), den LAVI (p= 0.003) und den LVMI (p= 0.02). Die Leistungsfähigkeit (peak VO2) wird negativ durch ein weibliches Geschlecht (p= <0.001), chronotrope Inkompetenz (p= 0.002) und einzelne Begleiterkrankungen wie KHK (p= 0.002), DM (p= 0.05) und das Schlafapnoe-Syndrom(p= 0.02) beeinflusst. Außerdem wird die diastolische Funktion (E/e‘) durch weibliches Geschlecht (p= 0.008), durch einen höheren Pulsdruck (p= 0.04), eine niedrigere Ruheherzfrequenz (p= 0.03) und die Behandlung mit Betablockern (p= 0.001) herabgesetzt. Bei der Untersuchung des Zusammenhangs von Charakteristika des Patientenkollektivs und der neurohumoralen Aktivität zeigte sich, dass ein höherer BMI (p= 0.03) mit einem niedrigeren NT-proBNP-Spiegel assoziiert ist. Vorhofflimmern (p= < 0.001), eine niedrige Ruheherzfrequenz (p= 0.05), chronotrope Inkompetenz (p= 0.02), eine schlechte Nierenfunktion (p= 0.05), niedrige Hämoglobinspiegel (p= < 0.001), die Einnahme von Diuretika (p= 0.05) und Betablockern (p= < 0.001) sind hingegen mit einem erhöhten NT-proBNP-Spiegel assoziiert. Obgleich signifikant, korrelieren die peak VO2, E/e‘ und NT-proBNP unadjustiert lediglich moderat miteinander, während LAVI und LVMI gar nicht mit der Leistungsfähigkeit assoziiert sind. Nach Adjustierung entfällt die Signifikanz des zuvor genannten Zusammenhangs von peak VO2 mit E/e‘ und NT-proBNP. Das bedeutet, dass die Leistungsfähigkeit mit keinem der anderen Schüsselparameter in Zusammenhang steht, wenn man sie unabhängig von demographischen und anderen klinischen Faktoren betrachtet. Der Zusammenhang von E/e‘, NT-proBNP und LAVI sowie LVMI und LAVI bleibt auch nach Adjustierung bestehen. Patienten mit einem entsprechend den vorgegebenen Grenzwerten niedrigen NT-proBNP-Spiegel (NT-proBNP ≤ 220 ng/l) und niedrigen E/e‘-Werten (E/e‘ ≤ 15) hatten signifikant bessere peak VO2- und AT VO2-Werte als Patienten, bei denen auch nur einer dieser beiden Werte erhöht war. Schlussfolgerung: Wir untersuchten, welche demographischen und klinischen Faktoren mit der körperlichen Leistungsfähigkeit, der diastolischen Funktion, der neurohumoralen 5 Zusammenfassung 62 Aktivierung und dem linksatrialen sowie linksventrikulären Remodeling bei Patienten mit Herzinsuffizienz und erhaltener systolischer Funktion assoziiert sind. Besonders interessant war, dass die maximale Leistungsfähigkeit mit keinem der anderen diagnostischen Schlüsselparameter, unabhängig von demographischen und klinischen Faktoren, in Zusammenhang steht. Dennoch scheinen empfohlene Grenzwerte bei NT-proBNP und E/e‘ zur Diagnose einer HFPEF sinnvoll, da sie grundsätzlich Patienten mit einer niedrigeren peak VO2 selektieren. Die Herzinsuffizienz mit erhaltener EF ist ein multifaktoriell beeinflusstes klinisches Syndrom. Da die eingeschränkte Leistungsfähigkeit nicht unabhängig von anderen Faktoren mit den diagnostischen Parametern assoziiert ist, ist die individuelle Bewertung von Faktoren, die zu den Symptomen der Patienten beitragen, obligatorisch für die klinische Beurteilung und Therapie bei Patienten mit HFPEF.

Abstract Cardiac hypertrophy provides an adaptive mechanism to maintain cardiac output in response to increased workload, and although initially beneficial, hypertrophy eventually leads to heart failure, a major cause of morbidity and mortality in Western countries. The hypertrophic response in cardiac myocytes is accompanied by e.g. activation of signal transduction pathways, such as mitogen-activated protein kinases (MAPKs), and complex changes in gene programming. The purpose of this study was to characterize gene expression patterns in experimental models of cardiac load by using high-throughput DNA microarray technologies. In the present study, changes in gene expression were evaluated in response to acute pressure overload and prolonged hypertension as well as during the development of left ventricular hypertrophy (LVH) and the transition to diastolic heart failure in an animal model of genetic hypertension, the spontaneously hypertensive rat (SHR). Increased expression of several immediate early genes was seen in response to acute hemodynamic overload in vivo. The transition from LVH to diastolic hypertensive heart failure was almost exclusively associated with changes in genes encoding extracellular matrix proteins and their regulatory processes showing the importance of progressive extracellular matrix remodeling. The effect of p38 MAPK activation on gene expression patterns in vivo was elucidated. Cardiac-specific overexpression of p38 MAPK resulted in upregulation of genes controlling cell division and inflammation as well as cell signaling and adhesion. Accordingly, the functional role of p38 MAPK was related to myocardial cell proliferation, inflammation and fibrosis. Finally, temporal analysis of mechanical stretch induced gene expression changes in neonatal rat cardiomyocyte cultures in vitro indicated that mechanical stretch induced complex gene expression profiles, demonstrating that both positive and negative regulators are involved in the hypertrophic process. Many novel stretch responsive genes were identified, and a subset of them may be putative downstream targets of p38 MAPK. In conclusion, in the present study a number of well-established gene expression changes of cardiac hypertrophy were observed and novel modulators associated with increased cardiac load, such as thrombospondin-4, were identified. The study provides a better understanding of molecular mechanisms associated with increased cardiac load, and may indicate potential targets for novel therapeutic interventions.

Orientador: Heitor Moreno Junior / Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas / Made available in DSpace on 2018-08-22T03:24:36Z (GMT). No. of bitstreams: 1 Santos_RodrigoCardoso_D.pdf: 1300897 bytes, checksum: 316736a36c07e5e655cecc5c8f664bdd (MD5) Previous issue date: 2013 / Resumo: Introdução: A disfunção diastólica do ventrículo esquerdo (DDVE) e a hipertrofia ventricular são consideradas marcadores frequentes para lesão cardíaca e fatores de risco de progressão para insuficiência cardíaca congestiva (ICC), especialmente em pacientes com hipertensão arterial resistente (HAR). A redução dos níveis pressóricos arteriais pode melhorar a disfunção diastólica do ventrículo esquerdo e os sintomas de insuficiência cardíaca. Entretanto, frequentemente esta redução não é atingida nos pacientes com HAR. Inibidores da fosfodiesterase 5 (PDE5) apresentam efeitos vasodilatadores discretos e, recentemente, se demonstrou que a administração de sildenafil a ratos hipertensos melhorou a disfunção diastólica do ventrículo esquerdo, através de ação direta sobre os miócitos cardíacos, evidenciando a presença de PDE5 neste tecido. Objetivo: Avaliar se o uso de um inibidor de PDE5 de longa duração (tadalafil) melhora a DDVE em pacientes com HAR de maneira independente de outros mecanismos secundários. Casuística e Métodos: Realizou-se um estudo intervencionista, cego, controlado por placebo, cruzado de uma via, incluindo 19 pacientes com HAR e DDVE. Inicialmente, receberam por via oral uma dose diária de placebo por 14 dias, com realização de medidas da pressão arterial de consultório e MAPA, avaliação da função endotelial (técnica de FMD), ecocardiograma e medidas de concentrações sanguíneas de BNP-32, GMPc e nitrito, antes e após o período de administração. Posteriormente, repetimos o mesmo procedimento, mas substituindo o placebo por tadalafil 20mg por dia. Ao final, as variáveis obtidas foram comparadas antes e após os usos de tadalafil e placebo, utilizando-se o método t de student pareado, com ?<0,05. Resultados: os pacientes apresentaram melhora da DDVE, demonstrada pela velocidade da onda E de 67,8±18,3cm/s para 77,8±16,0cm/s (p=0,025); relação E/A de 0,9±0,3 para 1,08±0,3 (p=0,01); tempo de desaceleração da onda E de 234,1±46,0ms para 194,4±43,3ms (p<0,01); tempo de relaxamento isovolumétrico de 128,7±17,6ms para 96,8±26,9ms (p<0,01); velocidade de onda E' lateral de 7,7±2,1cm/s para 8,8±2,8cm/s (p=0,025); velocidade de onda S' septal de 6,3±1,4cm/s para 7,7±1,7cm/s (p<0,01) e velocidade de onda S' lateral de 7,5±2,3cm/s para 8,3±2,2cm/s (p=0,014) (todas as variáveis expressas como em média e desvio-padrão). Houve, também, redução nos níveis de BNP-32 de 143±33,3 para 119,3±31,3 pg/mL e aumento no GMPc de 62,4±32,2 para 112,6±75,3pmol/mL. A concentração de nitrito foi semelhante com o uso de placebo e tadalafil. Em relação às medidas de pressão arterial, independentemente do método, também apresentam valores semelhantes antes e após o uso do fármaco, assim como a função endotelial. Os pacientes sob ação do placebo, não mostraram alterações em nenhuma das variáveis avaliadas. Conclusões: Os resultados sugerem que o uso de tadalafil melhora o relaxamento do ventrículo esquerdo em pacientes com HAR, independente da pressão arterial e da função endotelial, podendo constituir um importante tratamento adjunto em pacientes hipertensos sintomáticos com DDVE / Abstract: Introduction: Left ventricular hypertrophy and diastolic dysfunction (LVDD) remain frequent markers of cardiac damage and risk of progression to symptomatic heart failure (HF), especially in resistant hypertension (RHTN). Lowering BP may improve diastolic function and relieve HF symptoms; however, very often this target is not achieved in RHTN subjects. PDE-5 inhibitors have mild systemic vasodilatory effects, and recently, we demonstrated that administration of sildenafil in hypertensive rats improves LVDD, acting in cardiac myocytes with PDE5 expression in this tissue. Objective: To analyze if a long-acting PDE-5 inhibitor (tadalafil) may be clinically useful for improving LVDD in RHTN patients. Methods: We developed a single- blinded, placebo-controlled, one-way crossover, interventional study that enrolled 19 patients with RHTN and LVDD. At first, subjects were given a placebo daily oral dosage, for 2 weeks and they were submitted to blood pressure measurements (both ABPM and office), endothelial function (FMD) assessment, echocardiographic study and plasmatic BNP-32, cGMP and nitrite levels, before and after this 2-week period. Next, subjects were submitted to the same protocol receiving tadalafil (20 mg) orally instead of placebo. Variables were compared before and after placebo and tadalafil administration, using the paired student's t-test. The level of significance (?) accepted was less than 0.05. Results: Patients had an improvement in LVDD represented by changes in E-wave peak velocity from 67.8±18.3cm/s to 77.8±16.0cm/s (p=0.025), E/A ration from 0.9±0.3 to 1.08±0.3 (p=0.01), E wave deceleration time from 234.1±46.0ms to 194.4±43.3ms (p<0.001), isovolumic relaxation time from 128.7±17.6ms to 96.8±26.9ms (p<0.001), lateral E' wave velocity from 7.7±2.1cm/s to 8.8±2.8cm/s (p=0.025), septal S' wave velocity from 6.3±1.4cm/s to 7.7±1.7cm/s (p<0.01) and lateral S' wave velocity from 7.5±2.3cm/s to 8.3±2.2cm/s (p=0.014) (Values are expressed as mean ± standard deviation). We also noticed a decrease in BNP-32 levels from 143±33.3 to 119.3±31.3 pg/mL and an increase in cGMP levels from 62.4±32.2 to 112.6±75.3pmol/mL. No significant differences were detected in office and ABPM measurements, in endothelial function and nitrite levels. Conclusion: The current findings suggest that tadalafil enhances LV relaxation in resistant hypertensive patients and, despite its mild antihypertensive effect, may serve as an important adjunct to treat symptomatic hypertensive patients with evident LVDD / Doutorado / Farmacologia / Doutor em Farmacologia

No description available.

L'insuffisance cardiaque à fraction d’éjection préservée (IC/FEp) constitue un problème de santé croissant. Elle pourrait devenir la principale cause d'IC d'ici une décennie. C’est une pathologie associée à un taux élevé de morbidité et de mortalité. La prise en charge thérapeutique de l’IC/FEp reste limitée en raison de sa physiopathologie encore mal élucidée. Dans le présent travail, après avoir mis au point un modèle d’IC/FEp sur le rat adulte mâle et l’avoir caractérisé, nous avons évalué le phénotype fonctionnel et l’homéostasie calcique des cardiomyocytes. Les cœurs de ces animaux ont montré une fraction d’éjection supérieure à 50%, associée à une congestion pulmonaire, une hypertrophie concentrique avec une augmentation de la masse du ventricule gauche, une rigidité myocardique, une relaxation et un remplissage ventriculaire passif altérés et une dilatation auriculaire. Au niveau cellulaire, la contraction mesurée sur des cardiomyocytes isolés ainsi que le transitoire calcique sont augmentées. On note, de même, une surcharge en Ca2+ diastolique favorisée par une fuite à travers les canaux Ryanodine 2 et par un dysfonctionnement de l’échangeur Na+ /Ca2+ qui contribuent à générer des événements calciques spontanés. La phosphorylation du phospholamban, régulateur de l’activité de la SERCA2a, a également augmenté, laissant suggérer une compensation adaptative du cycle de Ca2+. Enfin, en présence de Ranolazine, inhibiteur du courant sodique soutenu, les évènements calciques spontanés ont été réprimés. En conclusion, le remodelage cardiaque dans l’IC/FEp semble être diffèrent de celui observé dans l’IC/FEr et ouvre la voie vers de nouveaux acteurs physiopathologiques et thérapeutiques. / Heart failure with preserved ejection fraction (HFpEF) is a growing health problem. It could become the leading cause of HF within a decade. It is a pathology associated with high morbidity and mortality. Therapeutic options are limited due to a lack of knowledge of the pathology and its evolution. In this work, we investigated the cellular phenotype and Ca2+ handling in hearts recapitulating HFpEF criteria. HFpEF was induced in a portion of male Wistar rats four weeks after abdominal aortic banding. These animals had nearly normal ejection fraction and presented elevated blood pressure, lung congestion, concentric hypertrophy, increased LV mass, wall stiffness, impaired active relaxation and passive filling of the left ventricle, enlarged left atrium, and cardiomyocyte hypertrophy. Left ventricular cell contraction was stronger and the Ca2+ transient larger. Ca2+ cycling was modified with a RyR2 mediated Ca2+ leak from the sarcoplasmic reticulum and impaired Ca2+ extrusion through the Na+ /Ca2+ (NCX), which promoted an increase in diastolic Ca2+ and spontaneous Ca2+ waves. PLN phosphorylation which promotes SERCA2a activity, was increased, suggesting an adaptive compensation of Ca2+ cycling. In the presence of Ranolazine, a sustained sodium current inhibitor, spontaneous Ca2+ events were suppressed. Cardiac remodeling in hearts with a HFpEF status differs from that known for HFrEF and opens the way to new pathophysiological and therapeutic actors.

INTRODUÇÃO: Endomiocardiofibrose (EMF) é uma cardiomiopatia restritiva (CMR), caracterizada por uma disfunção diastólica, mas com a função sistólica e a fração de ejeção preservadas ou, em fases avançadas da doença, pouco prejudicadas. O consumo máximo de oxigênio (VO2) é um marcador de mortalidade na insuficiência cardíaca sistólica (ICS). Apesar da mortalidade ser semelhante entre a CMR e ICS, ainda não é conhecido se o treinamento físico pode melhorar o VO2 pico em pacientes com EMF. O objetivo deste estudo foi verificar se 4 meses de treinamento combinado podem melhorar a capacidade funcional e qualidade de vida em pacientes com EMF. MÉTODOS: Vinte e um pacientes com EMF (classe funcional II e III, NYHA) foram divididos em 2 grupos: treinamento físico (EMF-TF, n = 9) e sedentários (EMF-Sed, n = 12). Foram avaliados: VO2 pico, pulso de O2, relação deltaFC/deltaVO2 e relação deltaVO2/deltaW, pelo teste cardiopulmonar (TECP); volume diastólico final (VDF), volume sistólico (VS) e volume diastólico do átrio esquerdo (AE), pela ecocardiografia (Simpson); e qualidade de vida, pelo questionário Minnesota Living With Heart Failure Questionnaire (MLWHFQ). Os resultados do TECP dos pacientes com EMF foram comparados com os resultados de indivíduos controle saudáveis sedentários (CSS). Foi considerado significativo P < 0,05. RESULTADOS: Idade não foi diferente entre EMF-Sed, EMF-TF e CSS (58±9 vs. 55±8 vs. 53±6 anos, P = 0,31; respectivamente). O grupo EMF-TF apresentou um aumento do VO2 pico pós-intervenção, comparado com o momento pré e comparado com o grupo EMF-Sed, mas esse valor foi menor, comparado ao CSS (17,4 ± 3,0 para 19,7 ± 4,4 vs. 15,3 ± 3,0 para 15,0±2.0 vs. 24,5 ± 4,6 ml/kg/min, P < 0,001; respectivamente). O pulso de O2 do grupo EMF-TF no momento pós-intervenção foi maior, comparado ao momento pré e ao grupo EMF-Sed, mas foi semelhante, quando comparado ao grupo CSS (9,3 ± 2,6 para 11,1 ± 2,8 vs. 8,6 ± 2,2 para 8,6 ± 1 vs. 11,2 ± 2,9 ml/batimentos; P < 0,05; respectivamente). A relação deltaFC/deltaVO2 diminuiu no momento pós-intervenção no grupo EMF-TF, comparado ao momento pré e ao grupo EMF-Sed, igualando-se ao grupo CSS (75 ± 36 para 57 ± 14 vs. 68 ± 18 para 73 ± 14 vs. 56±17 bpm/L; P < 0,05; respectivamente). O grupo EMF-TF reduziu significativamente a relação deltaVO2/deltaW, após o período de treinemento, comparado ao momento pré e ao grupo EMF-Sed, igualando-se ao grupo CSS (12,3 ± 2.8 para 10,2 ± 1.9 vs. 12,6±1.7 para 12,4 ± 1.7 vs. 10,0 ± 0,9 ml/min/Watts; P = 0,002; respectivamente). O treinamento físico também aumentou o VDF do grupo EMF-TF, quando comparado ao grupo EMF-Sed (102,1 ± 64,6 para 136,2 ± 75,8 vs. 114,4 ± 55,0 para 100,4 ± 49,9 ml; P < 0,001; respectivamente) e o VS (57,5±31,9 para 72,2 ± 27,4 vs. 60,1 ± 25,2 para 52,1 ± 18,1 ml; P = 0,01; respectivamente), e diminuiu o volume diastólico do AE [69,0 (33,3- 92,7) para 34,9 (41,1-60,9) vs. 44,6 (35,8-73,3) para 45,6 (27,0-61,7) ml; P < 0,001; respectivamente). A qualidade de vida dos pacientes EMF-TF, quando comparados com o grupo EMF-Sed também melhorou após o período de treinamento físico (45±17 para 27±15 vs. 47±20 para 45 ± 23 pontos; P < 0,05; respectivamente). CONCLUSÃO: Esses resultados esclarecem que os pacientes com EMF se beneficiaram com o treinamento físico combinado, enfatizando a importância dessa ferramenta não farmacológica no tratamento clínico habitual desses pacientes / BACKGROUND: Endomyocardial fibrosis (EMF) is a restrictive cardiomyopathy (RCM), characterized by a diastolic dysfunction, but with preserved systolic function and preserved ejection fraction, except in severe cases, in which these two present mild reduction. Maximal oxygen consumption (VO2) is a marker of mortality in systolic heart failure (SHF). Although mortality in RCM can be similar to SHF, it is still unknown if physical training can improve peak VO2 in patients with EMF. The aim of the present study was to evaluate if 4 months of combined physical training could improve functional capacity and quality of life in patients with EMF. METHODS: Twenty one EMF patients (functional class II and III, NYHA) were divided into 2 groups: physical training (EMF-PT, n = 9) and sedentary (EMF-Sed, n = 12). Peak VO2, O2 pulse, deltaFC/deltaVO2 relation and deltaVO2/deltaW relation were evaluated by cardiopulmonary exercise test (CPX); end diastolic volume (EDV), stroke volume (SV) and left atrium diastolic volume were evaluated by echocardiography (Simpson); and quality of life was evaluated by Minnesota Living With Heart Failure Questionnaire (MLWHFQ). CPX results from EMF patients were compared to a healthy sedentary (HS) control group. Significance was considered P < 0,05. RESULTS: Age was not different between EMF-PT, EMF-Sed and HS (58 ± 9 vs. 55±8 vs. 53 ± 6 years, P = 0,31; respectively). EMF-PT group presented an increase in peak VO2 after training compared to EMF-Sed group, but was lower compared to HS (17,4 ± 3,0 to 19,7 ± 4,4 vs. 15,3 ± 3,0 to 15,0 ± 2.0 vs. 24,5 ± 4,6 ml/kg/min, P < 0,001; respectively). O2 pulse in EMF-PT group increased after training compared to EMFSed group, and was similar compared to HS (9,3 ± 2,6 to 11,1±2,8 vs. 8,6±2,2 to 8,6 ± 1 vs. 11,2±2,9 ml/betas; P < 0,05; respectively). deltaFC/deltaVO2 relation decreased after training in EMF-PT group compared to EMF-Sed group, and was similar compared to HS (75 ± 36 to 57 ± 14 vs. 68 ± 18 to 73 ± 14 vs. 56 ± 17 bpm/L; P < 0,05; respectively). deltaVO2/deltaW relation decreased after training in EMF-PT group compared to EMF-Sed group, and was similar compared to HS (12,3 ± 2.8 to 10,2 ± 1.9 vs. 12,6 ± 1.7 to 12,4 ± 1.7 vs. 10,0 ± 0,9 ml/min/Watts; P = 0,002; respectively). Physical training also increased EDV in EMF-PT compared to EMFSed (102,1±64,6 to 136,2±75,8 vs. 114,4±55,0 to 100,4±49,9 ml; P < 0,001; respectively) and SV (57,5±31,9 to 72,2±27,4 vs. 60,1±25,2 to 52,1±18,1 ml; P = 0,01; respectively), and decreased left atrium diastolic volume [69,0 (33,3-92,7) to 34,9 (41,1-60,9) vs. 44,6 (35,8- 73,3) to 45,6 (27,0-61,7) ml; P < 0,001; respectively). Quality of life in EMF-PT group improved after training when compared to EMF-Sed group (45±17 to 27±15 vs. 47 ± 20 to 45 ± 23 points; P < 0,05; respectively). CONCLUSION: These results point out that patients with EMF benefit from combined physical training emphasizing the importance of this nonpharmacological tool in the clinical treatment of these patients

A doença arterial coronária é importante e prevalente manifestação da aterosclerose. A avaliação da função diastólica pelos parâmetros mitrais obtidos com Doppler ecocardiográfico possui limitações nos coronariopatas com fração de ejeção do ventrículo esquerdo (FEVE) preservada. Nestes, a disfunção diastólica, independentemente da FEVE, associa-se a maior incidência de desfechos desfavoráveis. A elevação da pressão diastólica final (PD2) do ventrículo esquerdo (VE) é a principal consequência fisiológica da disfunção diastólica. A pesquisa por melhores formas de determinação da PD2 do VE estendeu-se às modernas técnicas ecocardiográficas de quantificação da mecânica cardíaca. O objetivo deste estudo é correlacionar as medidas de deformação miocárdica, obtidas pelo speckle-tracking ecocardiográfico bidimensional, com a medida invasiva da PD2 do VE em pacientes com insuficiência coronariana e FEVE preservada. Métodos: foram avaliados 81 coronariopatas (idade: 61 ±8 anos) com FEVE >50%, encaminhados para cineangiocoronariografia eletiva, 40 destes com PD2 elevada (>16 mm Hg). Todos os indivíduos foram submetidos à avaliação ecocardiográfica convencional imediatamente antes do cateterismo e subsequente avaliação offline, com ecocardiografia speckle tracking (EST) para obtenção de medidas sistólicas e diastólicas de strain e strain rate circunferenciais e longitudinais, e estudo rotacional do VE. Foram analisadas as variáveis diastólicas da EST, tanto de forma isolada, quanto combinada com a velocidade da onda E ao Doppler. Resultados: Comparativamente, os pacientes do grupo com PD2 do VE elevada (n=40) mostraram aumento do volume indexado do átrio esquerdo (22 ±6 mL vs 26 ±8,26 mL p=0,04), velocidade da onda E (65 ±15 cm/s vs 78 ±20 cm/s p=0,02), relação E/e\' médio (8,14 ±2,0 vs 11,54 ±2,7 p=0,03) e relação E/strain rate global circunferencial (SRGC) pico E (39 cm vs 46 cm p <0,01). Nos 81 pacientes a correlação de Spearman com a medida invasiva da PD2 do VE foi de 0,56 para a relação E/e\' (p=0,03) e de 0,43 para a relação E/ESRGC pico E (p<0,01). A área sob a curva ROC foi significativa em ambas, sendo 0,83 e 0,73 respectivamente (p<0,05). Conclusão: A relação E/SRGC pico E é capaz de identificar elevação da PD2 do VE em coronariopatas com FEVE preservada, com menor desempenho que a relação E/e\'. / Introduction: Coronary artery disease (CAD) is important and prevalent manifestation of atherosclerosis. The assessment of diastolic function by mitral Doppler echocardiographic parameters has limitations in patients with CAD and preserved left ventricular ejection fraction (LVEF). Diastolic dysfunction is associated with higher incidence of unfavorable outcomes in these patients, regardless of LVEF. The increase in left ventricle end-diastolic pressure (LVEDP) is the main physiological consequence of diastolic dysfunction. The search for better ways of determining the LVEDP extended to the quantitative evaluation of cardiac mechanics with the modern echocardiographic techniques. The aim of this study is to correlate the invasive mesures of LVEDP and myocardial deformation measurements obtained by the two-dimensional speckle-tracking echocardiography in patients with coronary artery disease and preserved LVEF. Methods: 81 CAD patients (age: 61 ± 8 years) with LVEF >50%, scheduled for elective coronary angiography were evaluated, 40 of these with high LVEDP (>16 mm Hg). All subjects underwent conventional echocardiography immediately before catheterization and subsequent offline assessment with speckletracking echocardiography (STE) to obtain systolic and diastolic values of circumferential and longitudinal strain and strain rate, and rotational LV study. Diastolic variables of EST were analyzed both isolated and combined with the speed of the transmitral Doppler E wave. Results: Patients in the group with the high LVEDP (n =40) showed increased left atrial volume index (22 ± 6 mL vs 26 ± 8.26 mL p =0.04), E wave velocity (65 ± 15 cm/s vs 78 ±20 cm/s p = 0.02), E/e\' (average) ratio ( 8.14 ± 2.0 vs 11.54 ± 2.7 p = 0.03) and E/global circumferential strain rate (GCSR) peak E (39 cm vs 46 cm p <0.01). In 81 patients, Spearman\'s correlation with the invasive measurement of LVEDP was 0,56 (p =0.03) for the E/e\' ratio and 0.43 for the E/GCSR peak E (p <0.01). The area under the ROC curve was significant for both (p < 0.05): 0.83 and 0.73 respectively. Conclusion: The E/GCSR peak E ratio is able to identify elevated LVEDP in CAD patients with preserved LVEF, with less performance than the E/e\' ratio.

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