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Homeostasis, also known as adaptation, refers to the ability of a system to counteract persistent external disturbances and tightly control the output of a key observable. Existing studies on homeostasis in network dynamics have mainly focused on 'perfect adaptation' in deterministic single-input single-output networks where the disturbances are scalar and affect the network dynamics via a pre-specified input node. In this paper we provide a full classification of all possible network topologies capable of generating infinitesimal homeostasis in arbitrarily large and complex multiple inputs networks. Working in the framework of 'infinitesimal homeostasis' allows us to make no assumption about how the components are interconnected and the functional form of the associated differential equations, apart from being compatible with the network architecture. Remarkably, we show that there are just three distinct 'mechanisms' that generate infinitesimal homeostasis. Each of these three mechanisms generates a rich class of well-defined network topologies-called homeostasis subnetworks. More importantly, we show that these classes of homeostasis subnetworks provides a topological basis for the classification of 'homeostasis types': the full set of all possible multiple inputs networks can be uniquely decomposed into these special homeostasis subnetworks. We illustrate our results with some simple abstract examples and a biologically realistic model for the co-regulation of calcium ( Ca ) and phosphate ( PO 4 ) in the rat. Furthermore, we identify a new phenomenon that occurs in the multiple input setting, that we call homeostasis mode interaction, in analogy with the well-known characteristic of multiparameter bifurcation theory.

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Context: Congenital hypopituitarism is a genetically heterogeneous condition. Whole exome sequencing (WES) is a promising approach for molecular diagnosis of patients with this condition. Objectives: The aim of this study is to conduct WES in a patient with congenital hypopituitarism born to consanguineous parents, CDH2 screening in a cohort of patients with congenital hypopituitarism, and functional testing of a novel CDH2 variant. Design: Genomic DNA from a proband and her consanguineous parents was analyzed by WES. Copy number variants were evaluated. The genetic variants were filtered for population frequency (ExAC, 1000 genomes, gnomAD, and ABraOM), in silico prediction of pathogenicity, and gene expression in the pituitary and/or hypothalamus. Genomic DNA from 145 patients was screened for CDH2 by Sanger sequencing. Results: One female patient with deficiencies in growth hormone, thyroid-stimulating hormone, adrenocorticotropic hormone, luteinizing hormone, and follicle-stimulating hormone and ectopic posterior pituitary gland contained a rare homozygous c.865G>A (p.Val289Ile) variant in CDH2. To determine whether the p.Val289Ile variant in CDH2 affects cell adhesion properties, we stably transfected L1 fibroblast lines, labeled the cells with lipophilic dyes, and quantified aggregation. Large aggregates formed in cells expressing wildtype CDH2, but aggregation was impaired in cells transfected with variant CDH2 or non-transfected. Conclusion: A homozygous CDH2 allelic variant was found in one hypopituitarism patient, and the variant impaired cell aggregation function in vitro. No disease-causing variants were found in 145 other patients screened for CDH2 variants. Thus, CDH2 is a candidate gene for hypopituitarism that needs to be tested in different populations. Significance statement: A female patient with hypopituitarism was born from consanguineous parents and had a homozygous, likely pathogenic, CDH2 variant that impairs cell aggregation in vitro. No other likely pathogenic variants in CDH2 were identified in 145 hypopituitarism patients.

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Studies suggest that the dose of the standard benznidazole (BNZ) treatment regimen might be too high. We investigated the efficacy of BNZ 20 and 40 mg/kg/day compared with standard dose (100 mg/kg/day) to induce cure in mice infected with Trypanosoma cruzi Y strain in the acute and chronic phases of Chagas' disease. Our findings indicate that an experimental treatment with a BNZ low-dose (40 mg/kg/day) is similarly effective as the usual dose in the chronic mice model (100% of cure). In addition, the treatment in the chronic model of Chagas' disease presented better results than the acute model and colon appears to be a key tissue when it comes to evaluating treatment efficacy compared to blood and heart. Therefore, our data suggest the reconsideration of the current therapy, mainly in the chronic phase of the disease.

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Multi-Input, Multi-Output (MIMO) techniques are seeing widespread usage in wireless communication systems due to their large capacity gains. On the other hand, security is a concern of any wireless system, which can make schemes that implement physical layer security key in assuring secure communications. In this paper, we study the physical layer security issues of MIMO with Singular Value Decomposition (SVD) schemes, employed along with Single-Carrier with Frequency-Domain Equalization (SC-FDE) techniques. More concretely. the security potential against an unintended eavesdropper is analysed, and it is shown that the higher the distance between the eavesdropper and the transmitter or receiver, the higher the secrecy rate. In addition, in a scenario where there is Line of Sight (LOS) between all users, it is shown that the secrecy rate can be even higher than in the previous scenario. Therefore, MIMO-SVD schemes combined with SC-FDE can be an efficient option for highly secure MIMO communications.

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The first description of patients with combined pituitary hormone deficiencies (CPHD) caused by PROP1 mutations was made 20 years ago. Here we updated the clinical and genetic characteristics of patients with PROP1 mutations and summarized the phenotypes of 14 patients with 7 different pathogenic PROP1 mutations followed at the Hospital das Clínicas of the University of Sao Paulo. In addition to deficiencies in GH, TSH, PRL and gonadotropins some patients develop late ACTH deficiency. Therefore, patients with PROP1 mutations require permanent surveillance. On magnetic resonance imaging, the pituitary stalk is normal, and the posterior lobe is in the normal position. The anterior lobe in patients with PROP1 mutations is usually hypoplastic but may be normal or even enlarged. Bi-allelic PROP1 mutations are currently the most frequently recognized genetic cause of CPHD worldwide. PROP1 defects occur more frequently among offspring of consanguineous parents and familial cases, but they also occur in sporadic cases, especially in countries in which the prevalence of PROP1 mutations is relatively high. We classified all reported PROP1 variants described to date according to the American College of Medical Genetics and Genomics and the Association for Molecular Pathology (ACMG-AMP) guidelines: 29 were pathogenic, 2 were likely pathogenic, and 2 were of unknown significance. An expansion of the phenotype of patients with PROP1 mutations was observed since the first description 20 years ago: variable anterior pituitary size, different pathogenic mutations, and late development of ACTH deficiency. PROP1 mutations are the most common cause of autosomal recessive CPHD with a topic posterior pituitary lobe. Arch Endocrinol Metab. 2019;63(2):167-74.

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ABSTRACT The first description of patients with combined pituitary hormone deficiencies (CPHD) caused by PROP1 mutations was made 20 years ago. Here we updated the clinical and genetic characteristics of patients with PROP1 mutations and summarized the phenotypes of 14 patients with 7 different pathogenic PROP1 mutations followed at the Hospital das Clínicas of the University of Sao Paulo. In addition to deficiencies in GH, TSH, PRL and gonadotropins some patients develop late ACTH deficiency. Therefore, patients with PROP1 mutations require permanent surveillance. On magnetic resonance imaging, the pituitary stalk is normal, and the posterior lobe is in the normal position. The anterior lobe in patients with PROP1 mutations is usually hypoplastic but may be normal or even enlarged. Bi-allelic PROP1 mutations are currently the most frequently recognized genetic cause of CPHD worldwide. PROP1 defects occur more frequently among offspring of consanguineous parents and familial cases, but they also occur in sporadic cases, especially in countries in which the prevalence of PROP1 mutations is relatively high. We classified all reported PROP1 variants described to date according to the American College of Medical Genetics and Genomics and the Association for Molecular Pathology (ACMG-AMP) guidelines: 29 were pathogenic, 2 were likely pathogenic, and 2 were of unknown significance. An expansion of the phenotype of patients with PROP1 mutations was observed since the first description 20 years ago: variable anterior pituitary size, different pathogenic mutations, and late development of ACTH deficiency. PROP1 mutations are the most common cause of autosomal recessive CPHD with a topic posterior pituitary lobe. Arch Endocrinol Metab. 2019;63(2):167-74

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BACKGROUND: Mutations in PROP1, HESX1 and LHX3 are associated with combined pituitary hormone deficiency (CPHD) and orthotopic posterior pituitary lobe (OPP). OBJECTIVE: To identify mutations in PROP1, HESX1 and LHX3 in a large cohort of patients with CPHD and OPP (35 Brazilian, two Argentinian). DESIGN AND METHODS: We studied 23 index patients with CPHD and OPP (six familial and 17 sporadic) as well as 14 relatives. PROP1 was sequenced by the Sanger method in all except one sporadic case studied using a candidate gene panel. Multiplex ligation-dependent probe amplification (MLPA) was applied to one familial case in whom PROP1 failed to amplify by PCR. In the 13 patients without PROP1 mutations, HESX1 and LHX3 were sequenced by the Sanger method. RESULTS: We identified PROP1 mutations in 10 index cases. Three mutations were novel: one affecting the initiation codon (c.1A>G) and two affecting splicing sites, c.109+1G>A and c.342+1G>C. The known mutations, c.150delA (p.Arg53Aspfs*112), c.218G>A (p.Arg73His), c.263T>C (p.Phe88Ser) and c.301_302delAG (p.Leu102Cysfs*8), were also detected. MLPA confirmed complete PROP1 deletion in one family. We did not identify HESX1 and LHX3 mutations by Sanger. CONCLUSION: PROP1 mutations are a prevalent cause of congenital CPHD with OPP, and therefore, PROP1 sequencing must be the first step of molecular investigation in patients with CPHD and OPP, especially in populations with a high frequency of PROP1 mutations. In the absence of mutations, massively parallel sequencing is a promising approach. The high prevalence and diversity of PROP1 mutations is associated with the ethnic background of this cohort.

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CONTEXT: Mutations in the GH1 promoter are a rare cause of isolated growth hormone deficiency (IGHD). OBJECTIVE: To identify the molecular aetiology of a family with IGHD. DESIGN: DNA sequencing, electromobility shift (EMSA) and luciferase reporter assays. SETTING: University Hospital. PATIENTS: Three siblings (2M) born to consanguineous parents presented with IGHD with normal pituitary on MRI. METHODS: The GH1 proximal promoter, locus control region, five exons and four introns as well as GHRHR gene were sequenced in genomic DNA by Sanger method. DNA-protein interaction was evaluated by EMSA in nuclear extracts of GH3 pituitary cells. Dual-luciferase reporter assays were performed in cells transiently transfected with plasmids containing four different combinations of GH1 allelic variants (AV). RESULTS: The patients harboured two homozygous variants (c.-185T>C and c.-223C>T) in the GH1 promoter within a highly conserved region and predicted binding sites for POU1F1/SP1 and SP1 respectively. The parents and brother were carriers and these variants were absent in 100 controls. EMSA demonstrated absent binding of GH3 nuclear extract to the c.-223C>T variant and normal binding of both POU1F1 protein and GH3 nuclear extract to the c.-185T>C variant. In contrast to GH1 promoter with AV only at c.-185, the GH1 promoter containing the AV only at c.-223 and at both positions drove significantly less expression of luciferase compared with the promoter containing either positions wild type in luciferase reporter assays. CONCLUSION: To our knowledge, c.-223C>T is the first homozygous point mutation in the GH1 promoter that leads to short stature due to IGHD.

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OBJECTIVE: Our aim was to correlate 11-deoxycortisol levels obtained by two currently available techniques for 11-deoxycortisol measurement: radioimmunoassay, and high performance liquid chromatography followed by tandem mass spectrometry (MS/MS). The latter is the gold standard method for steroid hormone measurement. MATERIALS AND METHODS: We selected 88 samples and the results of these two methods were compared by Deming regression. RESULTS: The analytical sensitivity of the RIA was 0.30 ng/mL, with inadequate linearity and inadequate precision profile (34% of the samples had a CV ≥ 20%). From the selected samples, 54 had measurable levels of 11-deoxycortisol in both methods and were used in the comparison. The comparison of RIA with LC-MS/MS showed an overestimation of the results by RIA. The correlation coefficient was 0.610; linear regression slope was 3.751; and the intercept was 0.145, indicating a poor correlation between the two methods. CONCLUSION: We concluded that 11-deoxycortisol measured by radioimmunoassay, despite a good analytical sensitivity, showed very low specificity, precluding its use as a reliable method for 11-deoxycortisol measurement.

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Objetivo : Nosso objetivo foi comparar duas técnicas de dosagem do 11-desoxicortisol: a técnica de radioimunoensaio iodado, a qual foi validada neste trabalho, e a cromatografia líquida de alta performance seguida por espectrometria de massa em tandem (LC-MS/MS), sendo a última considerada o padrão-ouro para dosagem dos hormônios esteroides. Materiais e métodos : Para a comparação entre os resultados de 11-desoxicortisol, foram selecionadas 88 amostras. Resultados : A sensibilidade analítica do radioimunoensaio foi de 0,30 ng/mL, com linearidade e perfil de precisão inadequado (34% das amostras com CV ≥ 20%). Das 88 amostras selecionadas, apenas 54 apresentaram resultados mensuráveis em ambos os métodos. A comparação desses resultados, por meio da regressão de Deming, resultou em um coeficiente de correlação de 0,610, inclinação de 3,751, intercepção de 0,145, evidenciando a pobre correlação entre os resultados e a superestimação dos resultados pelo RIA. Conclusão : Concluímos que o método de dosagem de 11-desoxicortisol por radioimunoensaio iodado apresentou resultados inadequados nos diversos parâmetros avaliados, inviabilizando sua utilização como método de dosagem do 11-desoxicortisol. Arq Bras Endocrinol Metab. 2014;58(3):232-6 .

Objective : Our aim was to correlate 11-deoxycortisol levels obtained by two currently available techniques for 11-deoxycortisol measurement: radioimmunoassay, and high performance liquid chromatography followed by tandem mass spectrometry (MS/MS). The latter is the gold standard method for steroid hormone measurement. Materials and methods : We selected 88 samples and the results of these two methods were compared by Deming regression. Results : The analytical sensitivity of the RIA was 0.30 ng/mL, with inadequate linearity and inadequate precision profile (34% of the samples had a CV ≥ 20%). From the selected samples, 54 had measurable levels of 11-deoxycortisol in both methods and were used in the comparison. The comparison of RIA with LC-MS/MS showed an overestimation of the results by RIA. The correlation coefficient was 0.610; linear regression slope was 3.751; and the intercept was 0.145, indicating a poor correlation between the two methods. Conclusion : We concluded that 11-deoxycortisol measured by radioimmunoassay, despite a good analytical sensitivity, showed very low specificity, precluding its use as a reliable method for 11-deoxycortisol measurement. Arq Bras Endocrinol Metab. 2014;58(3):232-6 .

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Lipoid pneumonia is an underdiagnosed disease that is caused by the aspiration of lipid particles into the lungs. Although most of the reported cases have been associated with the use of mineral oil as a laxative, other lipid substances can also cause the disease. We report the case of a 50-year-old female patient with a complaint of productive cough who was initially diagnosed with bronchial hyperresponsiveness and gastroesophageal reflux disease (GERD). The patient was treated for GERD. Because the productive cough persisted, the patient underwent chest CT, fiberoptic bronchoscopy, and open lung biopsy. She was diagnosed with lipoid pneumonia. The patient was questioned regarding the use of lipid substances, and she reported the chronic use of evening primrose oil. After the discontinuation of the substance and the maintenance of GERD treatment, her condition improved.

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A pneumonia lipoide é uma doença pouco diagnosticada, causada pela aspiração de partículas oleosas para dentro dos pulmões. Os casos relatados têm sido relacionados ao uso de óleo mineral como laxativo, mas outras soluções oleosas também podem causar a doença. Relatamos o caso de uma paciente de 50 anos com queixa de tosse produtiva, sendo diagnosticada inicialmente com hiper-reatividade brônquica e doença do refluxo gastroesofágico (DRGE). A paciente foi submetida a tratamento para DRGE. Devido à persistência da tosse, a paciente foi submetida a TC de tórax, fibrobroncoscopia e biópsia pulmonar a céu aberto, sendo diagnosticada com pneumonia lipoide. A paciente foi questionada quanto ao uso de substâncias oleosas, relatando o uso crônico de óleo de prímula. Com a suspensão do uso da substância e a continuidade do tratamento para DRGE, houve melhora do quadro.

Lipoid pneumonia is an underdiagnosed disease that is caused by the aspiration of lipid particles into the lungs. Although most of the reported cases have been associated with the use of mineral oil as a laxative, other lipid substances can also cause the disease. We report the case of a 50-year-old female patient with a complaint of productive cough who was initially diagnosed with bronchial hyperresponsiveness and gastroesophageal reflux disease (GERD). The patient was treated for GERD. Because the productive cough persisted, the patient underwent chest CT, fiberoptic bronchoscopy, and open lung biopsy. She was diagnosed with lipoid pneumonia. The patient was questioned regarding the use of lipid substances, and she reported the chronic use of evening primrose oil. After the discontinuation of the substance and the maintenance of GERD treatment, her condition improved.

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O aneurisma de apêndice atrial esquerdo é uma entidade extremamente rara e diagnosticada, na maioria das vezes, a partir da segunda década de vida, sendo patologia geralmente oligossintomática e diagnóstico de caráter ocasional. Este caso refere-se a um paciente de 21 anos, com quadro de taquicardia supraventricular sustentada sintomática. O diagnóstico foi feito a partir do ecocardiograma transtorácico, após o achado de aumento de área cardíaca em radiografia do tórax. O tratamento cirúrgico é mandadório e o paciente foi submetido à cirurgia para ressecção do apêndice atrial.

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Acute heart failure (AHF) is a serious clinical condition associated with high morbidity and mortality. The authors present the case of a 61-year-old man, with a past history of idiopathic dilated cardiomyopathy with heart failure, who came to the emergency room due to acute decompensation. During hospital stay he developed cardiogenic shock and inotropic support was initiated, followed by mechanical circulatory assistance with intra-aortic balloon counterpulsation, as a bridge to heart transplantation. The authors discuss theoretical considerations concerning subtypes and etiology of AHF, and indications for the use of mechanical support and heart transplantation.

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BACKGROUND: Cardiac resynchronization therapy (CRT) is currently used in selected patients with dilated cardiomyopathy and heart failure. However, 30% of patients do not respond to CRT when selection is based on clinical and electrocardiographic criteria. Left ventricular dyssynchrony can be evaluated by tissue Doppler imaging and it has been described as a useful precdictor of response to CRT. OBJECTIVE: To evaluate whether left ventricular dyssynchrony, as measured by tissue Doppler imaging, can be used to predict response to CRT. METHODS: 23 consecutive patients (age 67 +/- 10 years, 13 male) with heart failure refractory to medical therapy and who underwent CRT were studied. Before and six months after the procedure, various characteristics - clinical (including NYHA functional class), electrocardiographic (QRS interval) and echocardiographic (left ventricular ejection fraction [EF] and respective volumes)--were evaluated. In addition, pulsed wave tissue Doppler imaging was used to assess the time interval (QS) between the beginning of the QRS complex and the beginning of the systolic wave on the Doppler signal, in the basal segments of the septal, lateral, anterior and inferior walls. Left ventricular dyssynchrony was quantified as the difference between the maximum and minimum QS interval (QS(max-min)). The patients were divide into two groups: responders, if functional class improved by at least one and EF increased by more than 10%, and non-responders for the remainder. Differences between groups were assessed and predictors of response to CRT were determined. RESULTS: CRT improved functional class by at least one in 87% of patients and EF improved from 21 +/- 6 to 33 +/- 9% (p < 0.001). QS(max-min) was reduced from 80 +/- 38 to 38 +/- 14 ms (p < 0.001). In 15 patients (65%), classified as responders, there was an improvement in functional class and an increase in EF of more than 10%. There were no differences between groups, except for QS(max-min). Patients in the responder group had greater left ventricular dyssynchrony (QS(max-min) 94 +/- 39 vs. 54 +/- 16 ms, p = 0.002). QSmix-min was an independent predictor of response to CRT and a cut-off of 60 ms identified responders with a sensitivity of 87% and specificity of 75%. CONCLUSION: Despite the good results achieved with CRT, about one third of patients do not benefit from it. Left ventricular dyssynchrony can be quantified by tissue Doppler imaging using QS(max-min) and values greater than 60 ms can identify responders to CRT.

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BACKGROUND: Cardiac resynchronization therapy (CRT) improves left ventricular synchrony as evaluated by tissue Doppler imaging (TDI), leading to improved left ventricular performance and reverse remodeling. New CRT devices enable programming of left and right VV delay. The aim of this study was to determine whether sequential biventricular (BiV) pacing by echo-guided programming of VV delay would enhance the response to CRT. METHODS: 15 consecutive patients with severe heart failure and left bundle branch block underwent CRT by BiV device implantation. They were studied with conventional and TDI echo the day before implantation. Left ventricular ejection fraction (LVEF) was determined, and the electromechanical delay (QS), defined as the time interval from the beginning of the QRS to the S wave in pulsed TDI, was assessed in each of the four left ventricular basal segments. The dyssynchrony index was calculated as the difference between the longest and shortest electromechanical delay (QS(max-min)). The parameters were re-evaluated the day after implantation during simultaneous BiV pacing and with seven different VV delays. The optimal VV delay was determined by finding the VV interval corresponding to the maximum aortic velocity time interval (VTI). RESULTS: QS(max-min) decreased from 85.3 +/- 27.0 msec to 46.7 +/- 23.0 msec (p = 0.0002), LVEF increased from 21.7 +/- 7.3% to 30.0 +/- 7.7% (p = 0.0001) and aortic VTI increased from 12.7 +/- 3.6 cm to 15.2 +/- 4.0 cm (p < 0.0001), with simultaneous BiV pacing. The VV intervals were programmed as follows: LV pre-excitation by 10 msec in five patients, 20 msec in three, 30 msec in two, and 40 msec in three; and RV pre-excitation by 10 msec in one and by 20 msec in one. The maximal aortic VTI obtained with VV delay programming increased from 15.2 +/- 4.0 cm to 17.7 +/- 4.0 cm (p = 0.0005). During optimized sequential BiV pacing, QS(max-min) further decreased from 46.7 +/- 23.0 msec to 30.6 +/- 21.0 msec (p = 0.02) and LVEF further increased from 30.0 +/- 7.7% to 35.0 +/- 7.7% (p = 0.0003). CONCLUSIONS: Sequential BiV pacing with VV delay optimized by evaluation of aortic VTI enhanced the response to CRT with additional improvements in left ventricular synchrony and left ventricular function compared to simultaneous CRT.

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INTRODUCTION AND OBJECTIVE: In patients (pts) with dilated cardiomyopathy and intraventricular conduction disturbances, resynchronization therapy improves cardiac function and functional capacity. Determination of the optimal AV interval is essential to optimize the therapy results and various methods have been used in daily practice to obtain such an interval. The aim of this work is to assess optimal AV determined by impedance cardiography and compare it to the interval previously obtained by transmitral flow Doppler echocardiography. PATIENTS: Seven pts were evaluated, five men, mean age of 61 +/- 10 years, with dilated cardiomyopathy, intra-ventricular conduction disturbances and heart failure, New York Heart Association functional class III or IV. Four pts had ischemic cardiomyopathy and three idiopathic. All pts had an implanted cardioverter-defibrillator with cardiac resynchronization. METHODS: The optimal AV delay was estimated by transmitral flow pulsed Doppler using the method previously described by Ritter. Subsequently, cardiac output (CO) was determined by impedance cardiography. CO was estimated for different AV delays, beginning with 80 ms until occurrence of fusion QRS. The optimal AV delay was defined as the value corresponding to the highest measured CO. The ideal AV interval was compared between the two methods used. RESULTS: The AV delay determined by echocardiography varied between 120 and 170 ms (134 +/- 17 ms). The optimum AV delay based on CO estimation varied between 110 and 190 ms (137 +/- 26 ms). There was a correlation between the delays determined by the two methods (r = 0.844; p = 0.017). CONCLUSIONS: In pts undergoing ventricular resynchronization therapy, AV delay optimization based on CO determined by impedance cardiography is comparable to that measured by transmitral flow pulsed Doppler. However, impedance cardiography seems a more objective and simpler technique.

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INTRODUCTION AND OBJECTIVE: Ventricular resynchronization therapy improves cardiac function in patients (pts) with dilated cardiomyopathy and intraventricular conduction disturbances. The effects of ventricular resynchronization on right ventricular function have been poorly studied. Tricuspid annular motion can be studied with tissue Doppler echocardiography, which enables quantitative assessment of right ventricular function. The aim of this study was to evaluate the effects of ventricular resynchronization on right ventricular function with pulsed tissue Doppler. PATIENTS: We studied ten pts, eight male, mean age 65 +/- 10 years, with dilated cardiomyopathy, intraventricular conduction disturbances and heart failure, New York Heart Association functional class III or IV. Five pts had coronary artery disease and the others idiopathic dilated cardiomyopathy. All pts had an implanted cardioverter-defibrillator with ventricular resynchronization. METHODS: Before and one month after device implantation right ventricular function was evaluated with pulsed wave tissue Doppler study of tricuspid annular motion. The maximum velocity of the S wave (MV-S), E wave (MV-E), and A wave (MV-A), E/A ratio, isovolumetric contraction time (IVCT) and ejection time (ET) were determined. Right ventricular size and left ventricular ejection fraction (EF) were measured. Functional class before and after implantation was assessed. RESULTS: MV-S, MV-E and MV-A did not change significantly. The E/A ratio decreased significantly (p = 0.017). There were no differences in IVCT and ET, nor in right ventricular size before and after resynchronization. EF improved in all but one patient (p = 0.003). All pts had an improvement in functional class, except the one without increased EF. CONCLUSIONS: Ventricular resynchronization therapy does not appear to have a deleterious effect on right ventricular function in pts with dilated cardiomyopathy and intraventricular conduction disturbances. The main beneficial effect of this type of therapy appears to be improvement in left ventricular function.

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