Chronic Volume Overload Research Articles

A patient with Fontan physiology for laparoscopic cholecystectomy: A challenge for an anesthesiologist

Patients with a congenital single ventricular chamber, survives only because the systemic and pulmonary venous blood mixes. However such an arrangement has two major disadvantages of arterial desaturation and chronic volume overload to the single ventricle. In 1971, Francis Fontan from France, reported a new approach to the operative treatment of these malformations, separating the systemic and pulmonary circulations. The advancement of surgical techniques and medical management have resulted in greater than 90% survival rate of about 10 years after Fontan palliation. As a result, patients with Fontan physiology are increasingly presenting in the adult perioperative setting for various noncardiac surgeries. Understanding the Fontan physiology is essential for the successful anaesthetic management of these patients. We report a case of 22 year female with fontan physiology posted for elective laparoscopic cholecystectomy.

TRPC3 channel inhibitor pyrazole-3 suppresses atrial fibrillation in rats with aorto-venocaval shunt as a pathological condition of chronic volume overload

TRPC3 channel inhibitor pyrazole-3 suppresses atrial fibrillation in rats with aorto-venocaval shunt as a pathological condition of chronic volume overload

The effect of dialysis type on left atrial functions in patients with end-stage renal failure: A propensity score-matched analysis.

Despite the widespread use of both hemodialysis (HD) and peritoneal dialysis (PD), there is no study comparing the effects of these dialysis methods on the left atrial (LA) volume and functions. In this study, we investigated the impact of different dialysis methods on the LA volume and function in the patients exposed to chronic pressure overload and volume overload. This study was carried out on the patients who received dialysis treatment at our healthcare center between March, 2015 and January, 2016. Twenty-eight patients receiving hemodialysis (HD) treatment and 24 patients under PD treatment were enrolled into the study. Patients were divided into 2 groups according to the dialysis therapy, and the atrial volumetric and mechanical functions were investigated. As the basal demographical characteristics of patients in the PD and HD groups were significantly different, 44 patients matched on a 1:1 basis were taken for final analysis (22 HD, 22 PD, and the average age of 42.4±4.8; 73% was male). After propensity score matching analysis, it was determined that left atrial volume index (LAVi) was higher in the HD group while peak LA strain and LA contraction strain were higher in the PD group. Additionally, both strain parameters showed a good negative correlation with LAVi. We demonstrated that the left atrial structure and functions were better in the PD group suggesting that PD may be a relatively better option for the preservation and maintenance of the left atrial functions as compared to HD.

Association of interdialytic weight gain and glycosylated hemoglobin in chronic hemodialysis patients

Introduction: The most common cause of mortality among chronic hemodialysis (HD) patients is cardiovascular disease. Hypervolemia is an important risk factor for hypertension and cardiovascular mortality in HD patients that include chronic volume overload and interdialytic weight gain (IDWG). Objectives: The objective of this study is to assess the role of blood glucose in IDWG. Patients and Methods: In this cross-sectional study we enrolled 231 adult chronic HD patients. Patients with congestive heart failure, hypoalbuminemia, cirrhosis, hypothyroidism and recent blood transfusion were excluded. We weighted patients at the end of dialysis and before initiation the next dialysis in midweek dialysis sessions. Glycosylated hemoglobin (HbA1C) was measured in all patients. Patients were divided into three groups according HbA1C levels ( 7%). Additionally IDWG of three groups was compared using analysis of variance (ANOVA) method. Results: HbA1C was <6% in 158 (68%) patients (group A), 6-7% in 40 (17%) patients (group B) and >7% in 33 (14%) patients (group C). Mean IDWG was 2.44 kg in group A, 2.25 kg in group B and 2.71 kg in group C. In this study, no significant difference of IDWG in patients with different values of HbA1C was detected (P=0.206). Conclusion: Our study showed that blood glucose level had no significant role in IDWG in chronic HD patients.

A prospective study examining the role of myocardial Fibrosis in outcome following mitral valve repair IN DEgenerative mitral Regurgitation: rationale and design of the mitral FINDER study

BackgroundThe optimal management of chronic severe primary degenerative mitral regurgitation (MR) is to repair the valve but identification of the optimal timing of surgery remains challenging. Current guidelines suggest ‘watchful waiting’ until the onset of symptoms or left ventricular (LV) dysfunction but these have been challenged as promoting ‘rescue surgery’. Better predictors are required to inform decision-making in relation to the necessity and timing of surgery. Chronic volume overload is a stimulus for adverse adaptive LV remodelling. Subclinical reduction in LV strain before mitral repair predicts a fall in LV ejection fraction following surgery and is thought to reflect the development of myocardial fibrosis in response to chronic volume overload. Myocardial fibrosis can be detected non-invasively using cardiac magnetic resonance (CMR) imaging techniques as an expansion of the extracellular volume (ECV).Methods/designThis study investigates whether: 1) patients with above median ECV will have smaller reduction in end-systolic volume index (as a measure of the degree of reverse LV remodelling) on CMR following mitral valve repair, compared to those with below median ECV; and 2) higher ECV on CMR, validated through histology, adversely impacts upon post-operative complications and symptomatic improvement following surgery.This is a multi-centre, prospective, cross-sectional comparison of patients prior to and 9 months following surgery for chronic severe primary degenerative MR. To establish the natural history of ECV in MR, an additional cohort of patients with asymptomatic MR who do not wish to consider early repair will be followed. Investigations include CMR, cardiopulmonary exercise test, stress echocardiography, signal-averaged electrocardiogram, 24-h electrocardiogram monitoring, laboratory tests and patient-reported outcome measures. Patients undergoing surgery will have cardiac biopsies performed at the time of mitral valve repair for histological quantification of fibrosis.DiscussionThis study will advance our understanding of ventricular remodelling in MR, its impact on patient symptoms and ventricular response following surgery. Establishing the link between myocardial fibrosis (measured on CMR and validated through histology), with early ventricular dysfunction, will offer physicians a novel non-invasive biomarker that can further inform the timing of surgery.Trial registrationThis trial was registered at ClinicalTrials.gov (NCT02355418) on 30th November 2015.

Management of Cardiovascular Disease in Dialysis Patients

Cardiovascular disease is a common cause of death and disease in patients with end-stage renal disease (ESRD). Registry data show that 41% of deaths in ESRD patients are due to a variety of cardiovascular causes, such as acute myocardial infarction, congestive heart failure, arrhythmia/sudden cardiac death, and stroke. In the general population, each of these disease entities in isolation can be effectively managed according to evidence from large clinical trials and evidence-based guidelines. However, many of these trials did not include patients with ESRD, limiting the transferability of this evidence to the care of patients on dialysis. To complicate matters, cardiovascular events in ESRD patients are likely augmented from a unique interplay of cardiac risk due to both reduced kidney function and the necessity for artificial renal replacement therapies. In this light, the patient on dialysis is subjected to a series of unique factors: the continued presence of the metabolic perturbations of uremia and the peculiar environment of the dialysis treatment itself. Since the ESRD heart is under a considerable amount of strain due to chronic volume overload, rapid electrolyte and fluid shifts, and accelerated vascular calcification, management can be complex and outcomes multifactorial. In this review, we summarize the current evidence regarding management of acute myocardial infarction, heart failure, sudden cardiac death, and atrial fibrillation. We also address modifiable risk factors related to the dialysis procedure itself and highlight recent randomized controlled trials that included dialysis patients and measured important cardiovascular outcomes.

Intrinsic Wave Propagation of Myocardial Stretch, A New Tool to Evaluate Myocardial Stiffness: A Pilot Study in Patients with Aortic Stenosis and Mitral Regurgitation

Left ventricular (LV) filling following atrial contraction generates LV myocardial stretch that propagates from base to apex with a speed proportional to myocardial elasticity. The aim of this study was to test the hypothesis that intrinsic velocity propagation of myocardial stretch (iVP) would be altered in patients with valvular disease and chronic LV pressure overload or volume overload, which may adversely affect mechanical properties of the LV tissue. A second aim was to compare iVP with flow propagation velocity in the chamber. Sixty subjects were prospectively recruited: 20 with severe aortic stenosis (AS), 20 with severe degenerative mitral regurgitation (MR), and 20 normal control subjects. LV iVP was measured using ultrahigh-frame rate tissue Doppler (350-460frames/sec) and flow propagation velocity by color flow M-mode imaging. Follow-up data (up to 2years) were retrieved from medical records. iVP was highest in patients with AS (2.2±0.7m/sec), intermediate in those with MR (1.6±0.5m/sec), and lowest in control subjects (1.4±0.2m/sec; P<.0001). Fourteen patients with AS and eight withMR had iVP>1.8m/sec. Overall, iVP correlated with age, LV morphology, severity of aortic valve obstruction, and measures of LV preload and afterload. At follow-up, patients with high iVP had lower survival free of major adverse cardiac events (P=.002). Flow propagation velocity was similar between groups and correlated poorly with iVP (r=0.26, P=.10). A significant number of patients with severe AS and severe MR had rapid transmission of myocardial stretch, indicating increased myocardial stiffness. This information was not conveyed by measurement of flow propagation. Larger studies are needed to investigate the clinical utility of this novel measurement.

Blood volume-monitored regulation of ultrafiltration to decrease the dry weight in fluid-overloaded hemodialysis patients: a randomized controlled trial

BackgroundBecause chronic fluid volume overload is associated with higher mortality, we tested whether blood-volume monitored regulation of ultrafiltration and dialysate conductivity (UCR) and/or regulation of ultrafiltration and temperature (UTR) would facilitate dry weight reduction, in comparison to conventional dialysis (CONV).MethodsWe carried out a multicenter, 4-week, randomized controlled trial in hemodialysis patients ≥15% above normal extracellular fluid volume (ECV), per bioimpedance spectroscopy, who were randomized 1:1:1. Applying UCR (Nikkiso), UTR (Fresenius) and CONV, initial dry weight was reduced rapidly to target. Dry weight reduction was attenuated and eventually stopped at the occurrence of dialysis complications. The primary outcome was defined as intra- and postdialytic complications. Secondary outcomes were magnitudes of dry weight and blood pressure reduction.ResultsOf 244 patients assessed, N = 95 had volume overload ≥15% above normal ECV. Fifty patients received the allocated interventions (N = 16 UCR, N = 18 UTR, N = 16 CONV) and completed the trial. The rate of complications was significantly lower in UTR compared to CONV (21 ± 21% vs 34 ± 20%, p = 0.022), and also compared to UCR (vs 39 ± 27%, p = 0.028), but not statistically different between UCR and CONV (p = 0.93). Dry weight reduction was significantly higher in UTR compared to UCR (5.0 ± 3.4% vs 2.0 ± 2.7% body weight, p = 0.013), but not compared to CONV (vs 3.9 ± 2.1% body weight, p = 0.31). Systolic blood pressure reduction throughout the intervention phase was 17 ± 22 mmHg overall, but not significantly different between the three groups. Average maximum ultrafiltration rates were significantly higher in UTR than in UCR and CONV, at statistically similar dialysis times. Retrospective examination of randomly selected hemodialysis sessions in the UCR group identified technical mistakes in 36% of the dialysis sessions, despite considerable training efforts.ConclusionsEven in patients with volume overload, fluid removal was challenging. Despite the relative advantage of UTR, which must be interpreted with caution in view of the poor technical execution of UCR, this study renders clear that fluid removal must not be reinforced rapidly. Apprehension of this obstacle is imperative for future clinical and academic endeavors aimed at improving dialysis outcomes by correcting volume status.Trial registrationClinicalTrials.gov (NCT01416753), trial registration date: August 12, 2011.

The Role of Cardiopulmonary Exercise Testing for Decision Making in Patients with Repaired Tetralogy of Fallot.

Tetralogy of Fallot is the most common form of cyanotic congenital heart disease. As a result of the surgical strategies employed at the time of initial repair, chronic pulmonary regurgitation (PR) is prevalent in this population. Despite sustained research efforts, patient selection and timing of pulmonary valve replacement (PVR) to address PR in young asymptomatic patients with repaired tetralogy of Fallot (rToF) remain a fundamental but as yet unanswered question in the field of congenital heart disease. The ability of the heart to compensate for the chronic volume overload imposed by PR is critical in the evaluation of the risks and benefits of PVR. The difficulty in clarifying the functional impact of PR on the cardiovascular capacity may be in part responsible for the uncertainty surrounding the timing of PVR. Cardiopulmonary exercise testing (CPET) may be used to assess abnormal cardiovascular response to increased physiologic demands. However, its use as a tool for risk stratification in asymptomatic adolescents and young adults with rToF is still ill-defined. In this paper, we review the role of CPET as a potentially valuable adjunct to current risk stratification strategies with a focus on asymptomatic rToF adolescents and young adults being considered for PVR. The role of maximal and submaximal exercise measurements to identify young patients with a decreased or borderline low peak VO2 resulting from impaired ventricular function is explored. Current knowledge gaps and research perspectives are highlighted.

Desmin loss and mitochondrial damage precede left ventricular systolic failure in volume overload heart failure.

Heart failure due to chronic volume overload (VO) in rats and humans is characterized by disorganization of the cardiomyocyte desmin/mitochondrial network. Here, we tested the hypothesis that desmin breakdown is an early and continuous process throughout VO. Male Sprague-Dawley rats had aortocaval fistula (ACF) or sham surgery and were examined 24 h and 4 and 12 wk later. Desmin/mitochondrial ultrastructure was examined by transmission electron microscopy (TEM) and immunohistochemistry (IHC). Protein and kinome analysis were performed in isolated cardiomyocytes, and desmin cleavage was assessed by mass spectrometry in left ventricular (LV) tissue. Echocardiography demonstrated a 40% decrease in the LV mass-to-volume ratio with spherical remodeling at 4 wk with ACF and LV systolic dysfunction at 12 wk. Starting at 24 h and continuing to 4 and 12 wk, with ACF there is TEM evidence of extensive mitochondrial clustering, IHC evidence of disorganization associated with desmin breakdown, and desmin protein cleavage verified by Western blot analysis and mass spectrometry. IHC results revealed that ACF cardiomyocytes at 4 and 12 wk had perinuclear translocation of αB-crystallin from the Z disk with increased α, β-unsaturated aldehyde 4-hydroxynonelal. Use of protein markers with verification by TUNEL staining and kinome analysis revealed an absence of cardiomyocyte apoptosis at 4 and 12 wk of ACF. Significant increases in protein indicators of mitophagy were countered by a sixfold increase in p62/sequestosome-1, which is indicative of an inability to complete autophagy. An early and continuous disruption of the desmin/mitochondrial architecture, accompanied by oxidative stress and inhibition of apoptosis and mitophagy, suggests its causal role in LV dilatation and systolic dysfunction in VO.NEW & NOTEWORTHY This study provides new evidence of early onset (24 h) and continuous (4-12 wk) desmin misarrangement and disruption of the normal sarcomeric and mitochondrial architecture throughout the progression of volume overload heart failure, suggesting a causal link between desmin cleavage and mitochondrial disorganization and damage.

Management of Cardiovascular Disease in Dialysis Patients

Cardiovascular disease is a common cause of death and disease in patients with end-stage renal disease (ESRD). Registry data show that 41% of deaths in ESRD patients are due to a variety of cardiovascular causes, such as acute myocardial infarction, congestive heart failure, arrhythmia/sudden cardiac death, and stroke. In the general population, each of these disease entities in isolation can be effectively managed according to evidence from large clinical trials and evidence-based guidelines. However, many of these trials did not include patients with ESRD, limiting the transferability of this evidence to the care of patients on dialysis. To complicate matters, cardiovascular events in ESRD patients are likely augmented from a unique interplay of cardiac risk due to both reduced kidney function and the necessity for artificial renal replacement therapies. In this light, the patient on dialysis is subjected to a series of unique factors: the continued presence of the metabolic perturbations of uremia and the peculiar environment of the dialysis treatment itself. Since the ESRD heart is under a considerable amount of strain due to chronic volume overload, rapid electrolyte and fluid shifts, and accelerated vascular calcification, management can be complex and outcomes multifactorial. In this review, we summarize the current evidence regarding management of acute myocardial infarction, heart failure, sudden cardiac death, and atrial fibrillation. We also address modifiable risk factors related to the dialysis procedure itself and highlight recent randomized controlled trials that included dialysis patients and measured important cardiovascular outcomes.

Pulmonary hypertension: a long-term risk stratifier in primary mitral regurgitation.

Primary MR is a degenerative disease whose rates are continuously increasing within the elderly population. It is a progressive disease in which chronic volume overloading causes myocardial damage, heart failure and even death; however, the correction of MR is curative (1). The ideal timing of surgical intervention in primary MR is critical but still challenging. The degree of dyspnoea, amount of regurgitant volume, signs of left ventricular (LV) decompensation, and complications of atrial fibrillation and PH are considered when deciding the timing of the intervention. PH is a negative prognostic factor in various heart diseases, including primary MR (2). With PH in primary MR, more severe dyspnoea, higher operation-related and long-term mortality and more frequent persistent PH after surgery are associated (3-6).

Abstract 13289: Reduction in Extracellular Volume Fraction After Mitral Valve Repair of Chronic Mitral Regurgitation: A Cardiac MRI Pilot Study

Background: Global extracellular volume fraction (ECV) assessed with cardiac magnetic resonance (CMR) has been shown to be elevated in patients with chronic mitral regurgitation compared with healthy controls. Limited work has been published on ECV changes following reduction in chronic volume overload with mitral valve intervention. We examined changes in ECV in patients with chronic mitral valve regurgitation after surgical mitral valve repair (SMVR). Methods: All patients underwent CMR studies before and after SMVR. CMR studies were performed with cine, phase contrast, T1 maps, and late gadolinium enhancement (LGE) imaging. Mid, short axis T1 maps were divided into 6 cardiac segments, each classified as LGE absent or present. ECV was derived from T1 maps using area-weighted averages of only segments where LGE was absent, by a reader blinded to study date, clinical history and valve status. Results: Fifteen patients underwent SMVR a median of 1.4 (interquartile range [IQR] 0.8, 2.3) months after an initial CMR study (Table). Repeat CMR was performed a median 12.4 (IQR 7.2, 19.2) months after SMVR. None were on calcium channel blockers, nitrates, or direct arterial vasodilators. Following SMVR, significant reverse remodeling was seen with reductions in indexed left atrial volume and left ventricular parameters except end systolic volume (Table). ECV decreased from a mean 28.3% to 26.0% (p=0.01) (Table). No significant correlation was seen between changes in left sided CMR parameters and ECV (p=NS). Conclusion: In this pilot study of patients with significant chronic mitral regurgitation undergoing valve repair, a reduction in extracellular volume fraction was seen after 6 months or more, suggesting a decrease in myocardial fibrosis alongside reverse structural remodeling. Larger studies are needed to substantiate these findings and evaluate the clinical significance of ECV changes beyond cardiac reverse remodeling in patients undergoing mitral valve repair.

Estrogen receptor antagonism exacerbates cardiac structural and functional remodeling in female rats.

We assessed the estrogen receptor (ER) dependence of female-specific cardioprotection using a rat model of chronic volume-overload stress. ER antagonism worsened ventricular wall stress, ventricular dilation, and cardiac dysfunction induced by volume overload. Further, blocking ERs resulted in cardiac remodeling and functional changes similar to that previously found in ovariectomized rats.

The Electrophysiologic Effects of Acute Mitral Regurgitation in a Canine Model

Atrial fibrillation (AF) occurs in 30% of patients with mitral regurgitation referred for surgical intervention. However, the underlying mechanisms in this population are poorly understood. This study examined the effects of acute left atrial volume overload on atrial electrophysiology and the inducibility of AF. Ten canines underwent insertion of an atrioventricular shunt between the left ventricle and left atrium. Shunt and aortic flows were calculated, and the shunt was titrated to a shunt fraction to 40% to 50% of cardiac output. An epicardial plaque with 250 bipolar electrodes was used to determine activation and refractory periods. Biatrial pressures and volumes, conduction times, and atrial fibrillation inducibility were recorded. Data were collected at baseline and 20 minutes after shunt opening and closure. Mean shunt flow was 1.3 ± 0.5 L/min with a shunt fraction of 43% ± 6% simulating moderate to severe mitral regurgitation. Compared with baseline, left atrial volumes and maximum pressures increased by 27% and 29%, respectively, after shunt opening. Biatrial effective refractory periods did not change significantly after shunt opening or closure. Conduction times increased by 9% with shunt opening and returned to baseline after closure. AF duration or inducibility did not change with shunt opening. This canine model of mitral regurgitation demonstrated that acute left atrial volume overload did not increase the inducibility of atrial arrhythmias in contrast with experimental and clinical findings of chronic left atrial volume overload. This suggests that the substrates for AF in patients with mitral regurgitation are a result of chronic remodeling.

Sex differences in volume overload in skinned fibers.

BackgroundThe impact of sex on cardiac morphology and function in chronic volume overload has been described in detail. However, the relation between sex and contractile properties at the actin-myosin level has not been well defined. Therefore, we evaluated the influence of sex on the contractile capacities of patients with chronic volume overload.MethodsIn 36 patients (18 males, 65 ± 9 years; 18 females, 65 ± 13 years) scheduled for elective mitral valve surgery due to severe mitral regurgitation (MR) with preserved left ventricular function, right auricle samples were obtained prior to extracorporal circulation. The fibers were prepared and skinned and exposed to a gradual increase in the calcium concentration (from pCa of 6.5–4.0) for calcium-induced force-developing measurements. Calcium sensitivity was also measured and recorded.ResultsThe pCa-force relationship of the fibers obtained from males and females was significantly different, with the force values of the female fibers greater than those of male fibers at maximum calcium concentrations (pCa of 4.0: 3.6 ± 0.3 mN versus 3.2 ± 0.4 mN, p 0.02) and pCa of 4.5 2.6 ± 0.6 versus 2.0 ± 0.5, p 0.002). In contrast, the force values of female fibers were lower at mean calcium concentrations compared to those of male fibers (at 5.5 and pCa of 6.0: 1.0 ± 0.3 mN versus 1.2 ± 0.5 mN, p 0.04; 0.61 ± 0.05 versus 0.88 ± 0.09, p 0.04).Calcium sensitivity was observed at pCa of 5.0 in females and pCa of 4.5 in males.ConclusionThis study demonstrated that female fibers from patients exposed to chronic volume overload developed higher force values at a given calcium concentration compared to fibers from male patients. We assume that female patients might tap the full force potential, which is required when exposed to the highest calcium concentrations in our experimental cycle. The calcium sensitivity among genders was significantly different, with the results suggesting that males have higher calcium sensitivity and might compensate for lower force values at maximal calcium concentrations by a higher affinity for calcium. Hence, female patients with MR seem to work more “energy efficient”.

Changes in Myocardial Composition and Conduction Properties in Rat Heart Failure Model Induced by Chronic Volume Overload.

Volume overload leads to development of eccentric cardiac hypertrophy and heart failure. In our previous report, we have shown myocyte hypertrophy with no fibrosis and decrease in gap junctional coupling via connexin43 in a rat model of aorto-caval fistula at 21 weeks. Here we set to analyze the electrophysiological and protein expression changes in the left ventricle and correlate them with phenotypic severity based upon ventricles to body weight ratio. ECG analysis showed increased amplitude and duration of the P wave, prolongation of PR and QRS interval, ST segment elevation and decreased T wave amplitude in the fistula group. Optical mapping showed a prolongation of action potential duration in the hypertrophied hearts. Minimal conduction velocity (CV) showed a bell-shaped curve, with a significant increase in the mild cases and there was a negative correlation of both minimal and maximal CV with heart to body weight ratio. Since the CV is influenced by gap junctional coupling as well as the autonomic nervous system, we measured the amounts of tyrosine hydroxylase (TH) and choline acetyl transferase (ChAT) as a proxy for sympathetic and parasympathetic innervation, respectively. At the protein level, we confirmed a significant decrease in total and phosphorylated connexin43 that was proportional to the level of hypertrophy, and similarly decreased levels of TH and ChAT. Even at a single time-point, severity of morphological phenotype correlates with progression of molecular and electrophysiological changes, with the most hypertrophied hearts showing the most severe changes that might be related to arrhythmogenesis.

98 Evolution of cardiac remodeling associated with pregnancy in hypertensive women six months postpartum

Systemic arterial hypertension (SAH) is one of the principal risk factors for developing cardiovascular disease. When a hypertensive woman becomes pregnant, a new hemodynamic condition is installed, with transition from chronic pressure overload to chronic volume overload. This new hemodynamic condition can cause greater myocardial hypertrophy (LVH), whose postpartum evolution has been little studied in the literature. It is suspected that hypertensive women who presented LVH during pregnancy maintain this cardiac alteration, six months after delivery. to evaluate myocardial mass in hypertensive women in the third trimester of pregnancy and six months after delivery. prospective longitudinal study including 30 pregnant women beyond 35 gestational weeks and with previous SAH diagnosis, monitored at the Obstetrics Unit of the Botucatu School of Medicine – Unesp. They were submitted to clinical and echocardiographic evaluation at two moments, the gestational period and six months postpartum. LVH was defined for the left ventricular mass index as (LVMI) >45 g/m 2,7. The echocardiographic variables were compared between moments by the non-parametric test of Wilcoxon and simple linear regression models adjusted for each moment of evaluation. Significance level: p < 0.05. The median age was 29 years, the time of SAH diagnosis varied from 5 to 132 months; the majority of the women were white (83.3%) and 18 (60%) women were treated with antihypertensive medications during pregnancy. At the end of pregnancy, all except two of the women presented HVE. Six months postpartum, only four women did not present HVE. Elevated frequency of obesity and lack of ideal control of pressure levels were observed. There was a significant positive correlation between body mass index (BMI) and LVMI at the end of gestation (p = 0.001) and six months after delivery (p = 0.001). In pregnant hypertensive women, the LVH frequency is elevated at the end of pregnancy, and the recovery frequency of this hypertrophy, at the six-month follow-up after delivery, is very low. These results justify long-term follow-up with a cardiologist since persistent myocardial hypertrophy imposes a diagnosis of stage B cardiac failure, associated with greater risk of evolution to symptomatic ventricular dysfunction and death.

Mitral Valve Regurgitation in two Thoroughbred Stallions

Abstract Mitral valve (MV) disease is the most important valvular condition affecting athletic performance in horses. Twenty and 22 years old Thoroughbred Stallions used for breeding had suffered from increased respiratory and heart rate, poor performance and incomplete ejaculate release during covering, since three months ago. Cardiac examination projected irregular cardiac rhythm after a halt and an early-mid-systolic murmur. Mitral regurgitation (MR) and valvular changes were visible on echocardiography. Also volume overload of the Left Atrium (LA) and Left Ventricle (LV) were observed. Color Flow Doppler echocardiography confirmed moderate mitral valve regurgitation. A band-like fibrous and nodular degeneration of the left coronary leaflet was present. There was minimal secondary left ventricular remodeling of the apex of the left ventricle due to chronic volume overload. The therapeutic attempts included Quinapril and Furosemide. In these cases, normally no structural effect could be achieved, but clinical improvement and successful covering sessions were obtained, and when the therapy was terminated, clinical problems reappeared. In conclusion, in horses with MR, early diagnosis and appropriate therapy with Quinapril promises a reasonable performance.

The Dynamic Nature of Hypertrophic and Fibrotic Remodeling of the Fish Ventricle.

Chronic pressure or volume overload can cause the vertebrate heart to remodel. The hearts of fish remodel in response to seasonal temperature change. Here we focus on the passive properties of the fish heart. Building upon our previous work on thermal-remodeling of the rainbow trout ventricle, we hypothesized that chronic cooling would initiate fibrotic cardiac remodeling, with increased myocardial stiffness, similar to that seen with pathological hypertrophy in mammals. We hypothesized that, in contrast to pathological hypertrophy in mammals, the remodeling response in fish would be plastic and the opposite response would occur following chronic warming. Rainbow trout held at 10°C (control group) were chronically (>8 weeks) exposed to cooling (5°C) or warming (18°C). Chronic cold induced hypertrophy in the highly trabeculated inner layer of the fish heart, with a 41% increase in myocyte bundle cross-sectional area, and an up-regulation of hypertrophic marker genes. Cold acclimation also increased collagen deposition by 1.7-fold and caused an up-regulation of collagen promoting genes. In contrast, chronic warming reduced myocyte bundle cross-sectional area, expression of hypertrophic markers and collagen deposition. Functionally, the cold-induced fibrosis and hypertrophy were associated with increased passive stiffness of the whole ventricle and with increased micromechanical stiffness of tissue sections. The opposite occurred with chronic warming. These findings suggest chronic cooling in the trout heart invokes a hypertrophic phenotype with increased cardiac stiffness and fibrosis that are associated with pathological hypertrophy in the mammalian heart. The loss of collagen and increased compliance following warming is particularly interesting as it suggests fibrosis may oscillate seasonally in the fish heart, revealing a more dynamic nature than the fibrosis associated with dysfunction in mammals.