Volume Overload Of Left Ventricle Research Articles

Role of chest radiographs and electrocardiograms in predicting the hemodynamics of congenital heart disease

Aim: This study aimed to evaluate the role of chest radiographs and electrocardiograms in predicting the hemodynamics of congenital heart disease (CHD). Methods: This retrospective study included 50 patients with a diagnosis of CHD who had undergone any form of cardiac intervention, either surgical or nonsurgical between September 2019 and September 2020. Chest radiographs and electrocardiograms were evaluated and compared with the diagnostic gold standard echocardiography. Results: Chest radiographs had the highest sensitivity, specificity, and accuracy, with all being 100%, in detecting situs and cardiac position. There was a very good agreement between chest radiographs and echocardiography in the detection of both situs and cardiac position (κ = 1.00, P < 0.001), while moderate agreement was observed for the detection of cardiomegaly, position of the aortic knuckle, main pulmonary artery dilation, and right pulmonary artery dilation. Electrocardiograms had a high sensitivity (100.00%), but modest specificity and accuracy for the detection of left ventricle pressure overload. For the detection of left atrial enlargement and left ventricle volume overload, electrocardiograms had high specificity (94.12% and 94.29%, respectively) but low sensitivity and modest accuracy. There was a moderate agreement between electrocardiograms and echocardiography in the detection of right ventricle pressure overload (κ = 0.43, P = 0.002) and left ventricle volume overload (κ = 0.46, P < 0.001). Conclusions: The study findings indicate that chest radiographs and electrocardiograms alone are not adequate for the assessment of hemodynamics of CHD and reinstates the recommendation that in addition to routine chest radiographs and electrocardiograms, echocardiography should be performed.

Comprehensive assessment of the aortic valve in critically ill patients for the non-cardiologist. Part II: Chronic aortic regurgitation of the native valve.

Inadequate diastolic closure of the aortic valve causes aortic regurgitation (AR). Diastolic regurgitation towards the left ventricle (LV) causes LV volume overload, resulting in eccentric LV remodelling. Transthoracic echocardiography (TTE) is the first line examination in the work-up of AR. TTE allows quantification of left ventricular end-diastolic diameter and volume and left ventricular ejection fraction, which are key elements in the clinical decision making regarding the timing of valve surgery. The qualitative echocardiographic features contributing to the AR severity grading are discussed: fluttering of the anterior mitral valve leaflet, density and shape of the continuous wave Doppler signal of the AR jet, colour flow imaging of the AR jet width, and holodiastolic flow reversal in the descending thoracic aorta and abdominal aorta. Volumetric assessment of the AR is performed by measuring the velocity time integral of the left ventricular outflow tract (LVOT) and transmitral valve (MV) plane, and diameters of LVOT and MV. We explain how the regurgitant fraction and effective regurgitant orifice area (EROA) can be calculated. Alternatively, the proximal isovelocity surface area can be used to determine the EROA. We overview the utility of pressure half time and vena contracta width to assess AR severity. Further, we discuss the role of transoesophageal echocardiography, echocardiography speckle tracking strain imaging, cardiac magnetic resonance imaging and computed tomography of the thoracic aorta in the work-up of AR. Finally, we overview the criteria for valve surgery in AR.

Effects of the loss of estrogen on the heart's hypertrophic response to chronic left ventricle volume overload in rats.

Aortic valve regurgitation (AR) can result in heart failure from chronic overloading of the left ventricle (LV). Little is known of the role of estrogens in the LV responses to this condition. The aim of the study was to compare LV remodeling in female rats with severe AR in absence of estrogens by ovariectomy (Ovx). In a first study, we investigated over 6 months the development of hypertrophy in four groups of female Wistar rats: AR or sham-operated (sham) and Ovx or not. Ovx reduced normal heart growth. As expected, volume overload (VO) from AR resulted in significant LV dilation (42% and 32% increase LV end-diastolic diameter in intact and Ovx groups vs. their respective sham group; p < 0.0001). LV weight was also significantly and similarly increased in both AR groups (non-Ovx and Ovx). Increase in stroke volume or cardiac output and loss of systolic function were similar between AR intact and AR Ovx groups compared to sham. We then investigated what were the effects of 17beta-estradiol (E2; 0.03 mg/kg/day) treatment on the parameters studied in Ovx rats. Ovx reduced uterus weight by 85% and E2 treatment restored up to 65% of the normal weight. E2 also helped normalize heart size to normal values. On the other hand, it did not influence the extent of the hypertrophic response to AR. In fact, E2 treatment further reduced LV hypertrophy in AR Ovx rats (41% over Sham Ovx + E2). Systolic and diastolic functions parameters in AR Ovx + E2 were similar to intact AR animals. Ovx in sham rats had a significant effect on the LV gene expression of several hypertrophy markers. Atrial natriuretic peptide (Nppa) gene expression was reduced by Ovx in sham-operated females whereas brain natriuretic peptide (Nppb) expression was increased. Alpha (Myh6) and beta (Myh7) myosin heavy chain genes were also significantly modulated by Ovx in sham females. In AR rats, LV expression of both Nppa and Nppb genes were increased as expected. Ovx further increased it of AR rats for Nppa and did the opposite for Nppb. Interestingly, AR in Ovx rats had only minimal effects on Myh6 and Myh7 genes whereas they were modulated as expected for intact AR animals. In summary, loss of estrogens by Ovx in AR rats was not accompanied by a worsening of hypertrophy or cardiac function. Normal cardiac growth was reduced by Ovx in sham females but not the hypertrophic response to AR. On the other hand, Ovx had important effects on LV gene expression both in sham and AR female rats.

Testosterone deficiency reduces cardiac hypertrophy in a rat model of severe volume overload.

The aim of the study was to characterize if the development of cardiac hypertrophy (CH) caused by severe left ventricle (LV) volume overload (VO) from chronic aortic valve regurgitation (AR) in male rats was influenced by androgens. We studied Wistar rats with/without orchiectomy (Ocx) either sham‐operated (S) or with severe AR for 26 weeks. Loss of testosterone induced by Ocx decreased general body growth. Cardiac hypertrophy resulting from AR was relatively more important in intact (non‐Ocx) animals than in Ocx ones compared to their respective S group (60% vs. 40%; P = 0.019). The intact AR group had more LV dilation, end‐diastolic LV diameter being increased by 37% over S group and by 17% in AROcx rats (P < 0.0001). Fractional shortening (an index of systolic function) decreased only by 15% in AROcx compared to 26% for intact AR animals (P = 0.029). Changes in LV gene expression resulting from CH were more marked in intact rats than in AROcx animals, especially for genes linked to extracellular matrix remodeling and energy metabolism. The ratio of hydroxyacyl‐Coenzyme A dehydrogenase activity over hexokinase activity, an index of the shift of myocardial substrate use toward glucose from the preferred fatty acids, was significantly decreased in the AR group but not in AROcx. Finally, pJnk2 LV protein content was more abundant in AR than in AROcx rats, indicating decreased activation of this stress pathway in the absence of androgens. In summary, testosterone deficiency in rats with severe LV VO resulted in less CH and a normalization of the LV gene expression profile.

[Phenomenological Regularities of Assessment of Left Ventricle Function in Mitral Valve Insufficiency].

to examine relationship between anatomical changes of the left ventricle (LV), dynamics of velocity of its volume modification, and blood flows in the LV in patients with mitral regurgitation (MR) before and after surgical treatment. We included into this study 58 patients with severe 3-4 degree MR (38 men, 20 women aged 24-69 [mean age 51±9] years) in sinus rhythm (96 %) or atrial fibrillation (4 %). The control group included 86 healthy volunteers, mean age 39±7 years. Transthoracic echocardiographic studies were performed in both groups by standard technique at rest using a high-quality echocardiograph Vivid E9, equipped with a 3.5-4.6 MHz multi frequency transducer (in patients before and after surgical repair - mitral valve [MV] replacement and MV reconstruction with annuloplasty ring). The analysis of files recorded was performed off-line by vector analysis technique including estimation of myocardial deformation velocities and dynamics of LV volume modification, construction of "flow-volume" diagram, calculation of the expended kinetic energy, and registration of intraventricular blood flows. End diastolic volume (EDV), end systolic volume (ESV) and total stroke volume (TSV) (effective + retrograde) were significantly increased in patients with severe LV volume overload before surgery in comparison with the control group (p.

Female rats with severe left ventricle volume overload exhibit more cardiac hypertrophy but fewer myocardial transcriptional changes than males

Aortic valve regurgitation (AR) imposes a volume overload (VO) to the left ventricle (LV). Male rats with a pathological heart overload usually progress more quickly towards heart failure than females. We examined whether a sexual dimorphism exists in the myocardial transcriptional adaptations to AR. Adult Wistar male and female rats either underwent a sham operation or were induced with AR and then followed for 26 weeks. Female AR rats gained relatively more LV mass than males (75 vs. 42%). They had a similar increase in LV chamber dimensions compared to males but more wall thickening. On the other hand, fatty acid oxidation (FAO)-related LV enzyme activity was only decreased in AR males. The expression of genes encoding FAO-related enzymes was only reduced in AR males and not in females. A similar situation was observed for the expression of genes involved in mitochondrial biogenesis or function as well as for genes encoding for transcription factors implicated in the control of bioenergetics and mitochondrial function (Errα, Errγ or Pgc1α). Although females develop more LV hypertrophy from severe VO, their myocardial gene expression remains closer to normal. This could provide survival benefits for females with severe VO.

Aortic regurgitation and heart valve disease in mice.

Heart valve disease, in both congenital and acquired forms, is an important and growing public health problem. Epidemiologic studies in the United States have revealed an overall prevalence of 2.5%, and the incidence increases with age. Heart valve disease has a growing clinical impact and significant economic burden (1,2). In patients with aortic stenosis (AS) or aortic regurgitation (AR), morbidity and mortality is increased because of heart failure from chronic left ventricle (LV) disfunction (3,4). An analysis of the mechanism by which chronic LV volume overload leads to heart failure due to AR or AS is important and a useful mice model is timely.

Transcriptional Changes Associated with Long-Term Left Ventricle Volume Overload in Rats: Impact on Enzymes Related to Myocardial Energy Metabolism.

Patients with left ventricle (LV) volume overload (VO) remain in a compensated state for many years although severe dilation is present. The myocardial capacity to fulfill its energetic demand may delay decompensation. We performed a gene expression profile, a model of chronic VO in rat LV with severe aortic valve regurgitation (AR) for 9 months, and focused on the study of genes associated with myocardial energetics. Methods. LV gene expression profile was performed in rats after 9 months of AR and compared to sham-operated controls. LV glucose and fatty acid (FA) uptake was also evaluated in vivo by positron emission tomography in 8-week AR rats treated or not with fenofibrate, an activator of FA oxidation (FAO). Results. Many LV genes associated with mitochondrial function and metabolism were downregulated in AR rats. FA β-oxidation capacity was significantly impaired as early as two weeks after AR. Treatment with fenofibrate, a PPARα agonist, normalized both FA and glucose uptake while reducing LV dilation caused by AR. Conclusion. Myocardial energy substrate preference is affected early in the evolution of LV-VO cardiomyopathy. Maintaining a relatively normal FA utilization in the myocardium could translate into less glucose uptake and possibly lesser LV remodeling.

Endurance training or beta-blockade can partially block the energy metabolism remodeling taking place in experimental chronic left ventricle volume overload.

BackgroundPatients with chronic aortic valve regurgitation (AR) causing left ventricular (LV) volume overload can remain asymptomatic for many years despite having a severely dilated heart. The sudden development of heart failure is not well understood but alterations of myocardial energy metabolism may be contributive. We studied the evolution of LV energy metabolism in experimental AR.MethodsLV glucose utilization was evaluated in vivo by positron emission tomography (microPET) scanning of 6-month AR rats. Sham-operated or AR rats (n = 10-30 animals/group) were evaluated 3, 6 or 9 months post-surgery. We also tested treatment intervention in order to evaluate their impact on metabolism. AR rats (20 animals) were trained on a treadmill 5 times a week for 9 months and another group of rats received a beta-blockade treatment (carvedilol) for 6 months.ResultsMicroPET revealed an abnormal increase in glucose consumption in the LV free wall of AR rats at 6 months. On the other hand, fatty acid beta-oxidation was significantly reduced compared to sham control rats 6 months post AR induction. A significant decrease in citrate synthase and complex 1 activity suggested that mitochondrial oxidative phosphorylation was also affected maybe as soon as 3 months post-AR.Moderate intensity endurance training starting 2 weeks post-AR was able to partially normalize the activity of various myocardial enzymes implicated in energy metabolism. The same was true for the AR rats treated with carvedilol (30 mg/kg/d). Responses to these interventions were different at the level of gene expression. We measured mRNA levels of a number of genes implicated in the transport of energy substrates and we observed that training did not reverse the general down-regulation of these genes in AR rats whereas carvedilol normalized the expression of most of them.ConclusionThis study shows that myocardial energy metabolism remodeling taking place in the dilated left ventricle submitted to severe volume overload from AR can be partially avoided by exercise or beta-blockade in rats.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2261-14-190) contains supplementary material, which is available to authorized users.

Effect of isometric exercise on aortic regurgitation assessed by cardiovascular magnetic resonance

Purpose: Although the presence of aortic regurgitation (AR) may be a handicap for sport practice, the effect of isometric exercice (IE) on AR and ventricular function jointly has not been assessed previously. Cardiovascular magnetic resonance (CMR) may be useful on this purpose. Methods: We studied 20 asymptomatic patients with moderate or severe AR in the echocardiogram. We performed a CMR at rest and during the practice of a maximal IE (weight elevation with both legs). We analyzed changes in left and right ventricular function (by means of cineMR sequences) and in AR flow (by means of phase-constrast sequences). Results: During IE we noticed an increase in heart rate, systolic blood pressure and cardiac output. We observed a decrease in end-diastolic and end-systolic volume in both ventricles, without significant changes in ejection fraction. Flow analysis of ascending aorta showed a decrease in left ventricular stroke volume, whereas regurgitant volume and regurgitant fraction did not change significantly (Table 1). View this table: Table 1 Conclusions: In patients affected of AR, IE did not produce a left ventricle volume overload. CMR is useful for the evaluation of haemodynamic repercussion of IE.

Utilizing wavelet transform and support vector machine for detection of the paradoxical splitting in the second heart sound

Paradoxical splitting occurs when pulmonic valve (P2) closes before the aortic valve (A2). This causes second heart sound (S2) to be a single sound during inspiration and split during exhalation. Etiology delay in aortic closure: aortic stenosis, volume overload of left ventricle (LV), conduction defects in LV, and left bundle branch block (LBBB). In this article, a method was proposed in early detection of a reverse in the appearance of A2 and P2 within S2. This method is based on the time-frequency maps obtained with the continuous wavelet transform (CWT), namely, the Meyer wavelet. A number of patients with LBBB and others with fitted pacemakers were studied. The above method is combined with the support vector machine (SVM) and performance of this method is evaluated using classification accuracy (Ca), sensitivity (Se), specificity, positive, and negative predicted values. Results show that it is relatively easy to detect the reverse in A2 and P2 and the Ca and Se is 90.97 and 94.44%, respectively, for the sample of 42 patients whose data were collected from the Cardiology Department at Brighton and Sussex University Hospital in England.

Transcatheter closure of postsurgical residual ventricular septal defects: Early and mid‐term results

The incidence of residual ventricular septal defects (VSDs) after surgery is 5-25%. Redo surgery is associated with higher risks. Between January 2000 to December 2008, 170 patients underwent percutaneous VSD closure in our centre: 22(16M) of these had 23 closures for residual VSDs. Median age was 32.5 yrs (1.4-79). All patients had echocardiographic signs of left ventricle volume overload (Q(p)/Q(s) >or= 1.5). Nine patients had previous VSD closure, 6 tetralogy of Fallot repair, and 7, other procedures. There were 15 muscular, 6 perimembranous and 2 apical VSDs. Amplatzer VSD devices were used in all. Median VSD size was 8 mm (4.3-16). Median fluoroscopy time was 33 minutes (15-130). There were three adverse events: 1 ventricular fibrillation requiring DC cardioversion; 1 transient complete atrio-ventricular block reverting to sinus rhythm at 24-hours; one patient had transient atrial flutter during the procedure. All procedures were successful; no additional procedures were required. Trivial residual shunts were seen in 3 patients at follow-up. There were no late events. One patient experienced arrhythmic death 5-yrs after procedure. One patient was reoperated due to dehiscence of VSD patch 2-yrs after the second successful percutaneous closure. Transcatheter closure of postsurgical residual VSD is safe and efficacious management option and obviates the need for further surgery and by-pass.

Gene profiling of left ventricle eccentric hypertrophy in aortic regurgitation in rats: rationale for targeting the β-adrenergic and renin-angiotensin systems

Aortic valve regurgitation (AR) imposes a severe volume overload to the left ventricle (LV), which results in dilation, eccentric hypertrophy, and eventually loss of function. Little is known about the impact of AR on LV gene expression. We, therefore, conducted a gene expression profiling study in the LV of rats with acute and severe AR. We identified 64 genes that were specifically upregulated and 29 that were downregulated out of 21,910 genes after 2 wk. Of the upregulated genes, a good proportion was related to the extracellular matrix. We subsequently studied a subset of 19 genes by quantitative RT-PCR (qRT-PCR) to see if the modulation seen in the LV after 2 wk persisted in the chronic phase (after 6 and 12 mo) and found that it did persist. Knowing that the adrenergic and renin-angiotensin systems are overactivated in our animal model, we were interested to see if blocking those systems using metoprolol (25 mg.kg(-1).day(-1)) and captopril (100 mg.kg(-1).day(-1)) would alter the expression of some upregulated LV genes in AR rats after 6 mo. By qRT-PCR, we observed that upregulations of LV mRNA levels encoding for procollagens type I and III, fibronectin, atrial natriuretic peptide, transforming growth factor-beta(2), and connective tissue growth factor were totally or partially reversed by this treatment. These observations provide a molecular rationale for a medical strategy aiming these systems in the medical treatment of AR and expand the paradigm in the study of this form of LV volume overload.

An Unusual Transesophageal Echocardiographic Finding After Surgical Correction of a Coronary Artery Fistula

A 33-YEAR-OLD MAN with a congenital right coronary artery (RCA)–left ventricle (LV) fistula was admitted because of gradually increasing heart failure. A preoperative angiogram revealed a right coronary aneurysm and LV volume overload caused by an RCA-LV shunt. The patient was scheduled for surgical closure of the fistula and reconstruction of the RCA.

Valvular Heart Disease

Aortic regurgitation (AR) is characterized by diastolic reflux of blood from the aorta into the left ventricle (LV). Acute AR typically causes severe pulmonary edema and hypotension and is a surgical emergency. Chronic severe AR causes combined LV volume and pressure overload. It is accompanied by systolic hypertension and wide pulse pressure, which account for peripheral physical findings, such as bounding pulses. The afterload excess caused by systolic hypertension leads to progressive LV dilation and systolic dysfunction. The most important diagnostic test for AR is echocardiography. It provides the ability to determine the cause of AR and to assess the severity of AR and its effect on LV size, function, and hemodynamics. Many patients with chronic severe AR may remain clinically compensated for years with normal LV function and no symptoms. These patients do not require surgery but can be followed carefully for the onset of symptoms or LV dilation/dysfunction. Surgery should be considered before the LV ejection fraction falls below 55% or the LV end-systolic [corrected] dimension reaches 55 mm. Symptomatic patients should undergo surgery unless there are excessive comorbidities or other contraindications. The primary role of medical therapy with vasodilators is to delay the need for surgery in asymptomatic patients with normal LV function or to treat patients in whom surgery is not an option. The goal of vasodilator therapy is to achieve a significant decrease in systolic arterial pressure. Future therapies may focus on molecular mechanisms to prevent adverse LV remodeling and fibrosis.

Percutaneous closure of a coronary fistula between the right coronary artery to the left atrium

We describe a case of a congenital coronary artery fistula of the right coronary artery draining into the left atrium in an eight-year-old boy. The initial diagnosis was made after the detection of a continuous cardiac murmur at the age of six years. Transthoracic echocardiography showed the right coronaric ostium dilatation, the site of drainage in the left atrium and left ventricle volume overload. Catheterization confirmed the diagnosis. The patient underwent percutaneous closure by PDA occluder device. Immediate post-closure angiograms showed complete occlusion of the fistula. The patient showed transient ischemic changes on ECG associated to an increase of plasmatic levels of the cardiac enzyme. ECG and cardiac enzyme were normal one week after the procedure.

The effect of left ventricular pressure or volume overload on ventricular dimension in children. Left ventricular volume determination from one or two ventricular dimensions.

The effect of pressure or volume overload on the geometry of the left ventricle (LV) was determined in order to examine the feasibility and accuracy of LV volume determinations from one minor axis or two dimensions (one minor axis and the longest length). The longest length (LL) and minor axis (MA) in both the anteroposterior (AP) view and lateral (LAT) view were determined from the LV cine silhouette in patients with normal LV volume and pressure (group 1), LV pressure (LVP) overload group (LVP greater than 140 mm Hg, group 2), and LV volume overload group (LV end-diastolic volume greater than 124% of normal, group 3). The ratio of the MA to the LL, which represents the spherical configuration of the LV, was less than "normal" in group 2, and higher than "normal" in group 3. In all groups the LV was less spherical at end-systole than at end-diastole. Additionally, the (MA)3 had a different relationship to true LV volume (biplane LV volume) in the three groups and from diastole to systole in each group. Left ventricular volume calculation from one minor axis was associated with a large error. In contrast, left ventricular volume can be accurately determined from two ventricular dimensions using either the anteroposterior or lateral ventricular image (r larger than or equal to 0.97).