Ventricular dysfunction remains a hallmark of most cardiac disease. The mouse has become an essential model system for cardiovascular biology, and echocardiography an established tool in the study of normal and genetically altered mice. This review describes the measurement of ventricular function, most often left ventricular function, by echocardiographic methods in mice. Technical limitations related to the small size and rapid heart rate in the mouse initially argued for the performance of echocardiography under anesthesia. More recently, higher frame rates and smaller probes operating at higher frequencies have facilitated imaging of conscious mice in some, but not all, experimental protocols and conditions. Ventricular function may be qualitatively and quantitatively evaluated under both conditions. Particular detail is provided for measurement under conscious conditions, and measurement under conscious and sedated or anesthestized conditions are contrasted. Normal values for echocardiographic indices for the common C57BL/6 strain are provided. Diastolic dysfunction is a critical pathophysiologic component of many disease states, and progress in the echocardiographic evaluation of diastolic function is discussed. Finally, echocardiography exists among several competing imaging technologies, and these alternatives are compared.

Although great strides have been made in the areas of ventricular pacing, it is still appreciated that dyssynchrony can be malignant, and that appropriately placed pacing leads may ameliorate mechanical dyssynchrony. However, the unknowns at present include: 1. The mechanisms by which ventricular pacing itself can induce dyssynchrony; 2. Whether or not various pacing locations can decrease the deleterious effects caused by ventricular pacing; 3. The impact of novel methods of pacing, such as atrioventricular septal, lead-less, and far-field surface stimulation; 4. The utility of ECG and echocardiography in predicting response to therapy and/or development of dyssynchrony in the setting of cardiac resynchronization therapy (CRT) lead placement; 5. The impact of ventricular pacing-induced dyssynchrony on valvular function, and how lead position correlates to potential improvement. This review examines the existing literature to put these issues into context, to provide a basis for understanding how electrical, mechanical, and functional aspects of the heart can be distorted with ventricular pacing. We highlight the central role of the mitral valve and its function as it relates to pacing strategies, especially in the setting of CRT. We also provide future directions for improved pacing modalities via alternative pacing sites and speculate over mechanisms on how lead position may affect the critical function of the mitral valve and thus overall efficacy of CRT.

Men with congestive heart failure (CHF) have relatively low testosterone levels. Several studies demonstrated that testosterone treatment increases cardiac output and reduces peripheral vascular resistance. However, the effects of testosterone on heart function, cardiomyocyte apoptosis and ventricular remodeling have not been fully elucidated. This study was conducted to investigate the effects of testosterone on heart function, cardiomyocyte apoptosis and ventricular remodeling in male rats post-myocardial infarction. A total of 86 male rats were randomly assigned to undergo ligation of the coronary artery (n=70) or pseudosurgery (n=16). After 6 weeks, a left ventricular ejection fraction (LVEF) of ≤45% was defined as a successful model of CHF. The model rats were randomly assigned to 3 groups, namely low-dose testosterone (TU), high-dose TU and placebo (PL) groups. After treatment for 12 weeks, the expression of several mRNA transcripts in myocardial tissue was measured by quantitative polymerase chain reaction. Immunofluorescence was used to measure myocardial caspase-3 expression. Compared to the PL group, LVEF was significantly improved in the TU treatment groups. Moreover, the mRNA expression of atrial natriuretic peptide, brain natriuretic peptide, matrix metalloproteinase-2 and sarcoendoplasmic reticulum Ca2+-ATPase 2a was significantly reduced, while the mRNA expression of glycogen synthase kinase 3β and tissue inhibitor of metalloproteinase-2 was markedly increased in the TU groups. TU treatment also significantly reduced caspase-3 expression. Therefore, different doses of TU suppressed ventricular remodeling and improved left ventricular function, reduced apoptosis and prevented mortality in a CHF rat model.

Reduced left ventricular (LV) ejection fraction increases the risk of ventricular arrhythmias; however, LV ejection fraction has a low sensitivity to predict ventricular arrhythmias. LV dilatation and mass may be useful to further risk-stratify for ventricular arrhythmias.

The mitral annulus (MA) is a crucial structure that is in constant motion throughout the cardiac cycle. The main purpose of this study was to determine if M-mode evaluation of the longitudinal motion of the MA could be useful to examine atrio-ventricular interactions.

Heart failure (HF) is a major cause of cardiovascular admissions and hypertensive heart failure (HHF) is the most common cause of HF admissions in sub-Saharan Africa, Nigeria inclusive. Right ventricular (RV) dysfunction is being increasingly recognized in HF and found to be an independent predictor of adverse outcomes in HF. This study aimed to determine the prevalence of RV systolic dysfunction in HHF by several echocardiographic parameters.

No abstract available

The right ventricle and left ventricle are physically coupled through the interventricular septum. Therefore, changes in the geometry and mechanics of one ventricle can directly affect the function of the other. In treatment of pediatric pulmonary arterial hypertension, the left ventricle is often overlooked, with clinical focus primarily on improving right ventricular function. Pediatric pulmonary arterial hypertension represents a disease distinct from adult pulmonary arterial hypertension based on etiology and survival rates. We aimed to assess left ventricular torsion rate in pediatric pulmonary arterial hypertension and its role in right ventricular dysfunction. Cardiac magnetic resonance images with tissue tagging were prospectively acquired for 18 pediatric pulmonary arterial hypertension (WHO class I) patients and 17 control subjects with no known cardiopulmonary disease. The pulmonary arterial hypertension cohort underwent cardiac magnetic resonance within 48 hours of clinically indicated right heart catheterization. Using right heart catheterization data, we computed single beat estimation of right ventricular end-systolic elastance (as a measure of right ventricular contractility) and ventricular vascular coupling ratio (end-systolic elastance/arterial afterload). Left ventricular torsion rate was quantified from harmonic phase analysis of tagged cardiac magnetic resonance images. Ventricular and pulmonary pressures and pulmonary vascular resistance were derived from right heart catheterization data. Right ventricular ejection fraction and interventricular septum curvature were derived from cardiac magnetic resonance. Left ventricular torsion rate was significantly reduced in pulmonary arterial hypertension patients compared to control subjects (1.40 ± 0.61° vs. 3.02 ± 1.47°, P < 0.001). A decrease in left ventricular torsion rate was significantly correlated with a decrease in right ventricular contractility (end-systolic elastance) ( r = 0.61, P = 0.007), and an increase in right ventricular systolic pressure in pulmonary arterial hypertension kids ( r = -0.54, P = 0.021). In both pulmonary arterial hypertension and control subjects, left ventricular torsion rate correlated with right ventricular ejection fraction (controls r = 0.45, P = 0.034) (pulmonary arterial hypertension r = 0.57, P = 0.032). In the pulmonary arterial hypertension group, interventricular septum curvature demonstrated a strong direct relationship with right ventricular systolic pressure ( r = 0.7, P = 0.001) and inversely with left ventricular torsion rate ( r = -0.57, P = 0.013). Left ventricular torsion rate showed a direct relationship with ventricular vascular coupling ratio ( r = 0.54, P = 0.021), and an inverse relationship with mean pulmonary arterial pressure ( r = -0.60, P = 0.008), and pulmonary vascular resistance ( r = -0.47, P = 0.049). We conclude that in pediatric pulmonary arterial hypertension, reduced right ventricular contractility is associated with decreased left ventricular torsion rate.

Vagal nerve stimulation (VNS) ameliorates pulmonary vascular remodeling and improves survival in a rat model of pulmonary hypertension (PH). However, the direct impact of VNS on right ventricular (RV) function, which is the key predictor of PH patients, remains unknown. We evaluated the effect of VNS among the three groups: pulmonary artery banding (PAB) with sham stimulation (SS), PAB with VNS, and control (no PAB). We stimulated the right cervical vagal nerve with an implantable pulse generator, initiated VNS 2 weeks after PAB, and stimulated for 2 weeks. Compared to SS, VNS increased cardiac index (VNS: 130 ± 10 vs. SS: 93 ± 7 ml/min/kg; p < 0.05) and end-systolic elastance assessed by RV pressure-volume analysis (VNS: 1.1 ± 0.1 vs. SS: 0.7 ± 0.1 mmHg/μl; p < 0.01), but decreased RV end-diastolic pressure (VNS: 4.5 ± 0.7 vs. SS: 7.7 ± 1.0 mmHg; p < 0.05). Furthermore, VNS significantly attenuated RV fibrosis and CD68-positive cell migration. In PAB rats, VNS improved RV function, and attenuated fibrosis, and migration of inflammatory cells. These results provide a rationale for VNS therapy as a novel approach for RV dysfunction in PH patients.

Humans have a lower risk of death from myocardial infarction (MI) living at low elevations (<2500 m), which are not high enough to induce hypoxia. Both chronic hypoxia pre-MI, achieved by altitude simulation >5000 m, and intermittent hypobaric hypoxia post-MI can reduce MI size in rodents, and it is believed that hypoxia is the key stimulus. To explore mechanisms beyond hypoxia we studied whether altitude simulation <2500 m would also be associated with reduced infarct size. We performed left-anterior descending artery ligation on C57BL6 mice. Control mice (n = 12) recovered at 754 mmHg (atmospheric pressure, control), and treatment group mice (n = 13) were placed in a hypobaric chamber to recover 3-hours daily at 714 mmHg for 1 week. Echocardiographic evaluation of left ventricular function was performed on Day 0, Day 1 and Day 8. Intermittent hypobaric treatment was associated with a 14.2±5.3% improvement in ejection fraction for treatment group mice (p<0.01 vs. Day 1), with no change observed in control mice. Cardiac output, stroke volume, and infarct size were also improved in treated mice, but no changes were observed in HIF-1 activation or neovascularization. Next, we studied the acute hemodynamic effects of low altitude stimulation in intact mice breathing 100% oxygen using left ventricular catheterization and recording of pressure-volume loops. Acute reductions in barometric pressure from 754 mmHg to 714 mmHg and 674 mmHg were associated with reduced systemic vascular resistance, increased stroke volume and cardiac output, and no change in blood pressure or heart rate. Ex-vivo vascular function was studied using murine mesenteric artery segments. Acute reductions in barometric pressure were associated with greater vascular distensibility. We conclude that intermittent hypobaric treatment using simulated altitudes <2500 m reduces infarct size and increases ventricular function post-MI, and that these changes are related to altered arterial function and not hypoxia-associated neovascularization.

To investigate the changes in ventricular function that occur during continuous positive-pressure ventilation, we studied the effects of separate increases in lung volume, pleural pressure, and right ventricular afterload in 15 dogs. Isovolume increases of pleural pressure caused changes in right and left ventricular hemodynamics indistinguishable from those induced by preload reduction. Lung distension with the chest open to atmosphere caused both right and left atrial intracavitary pressures to rise as cardiac output fell, suggesting altered function of both ventricles. Raising right ventricular afterload by pulmonary artery constriction did not reproduce the hemodynamic changes observed during increases of lung volume. These data indicate that the apparent alteration of ventricular function that occurs during continuous positive-pressure ventilation is produced by the associated increase in lung volume and that a right ventricular afterload-ventricular interdependence effect is not the responsible mechanism.

Echocardiographic assessment of the left ventricular diastolic function (LVDF), an integrated part of evaluation of left ventricular function is still a delicate task and is performed with substantial inter-rater variability. Therefore, we aimed to create and evaluate a guidelines-based automated decision support. An algorithm was created for a hierarchical analysis of LVDF based on variables as recommended by the latest guidelines. Age-adjusted normal ranges were pooled from previously published studies into an integrated reference table. For proof-of-concept, 20 echocardiographic examinations were analyzed offline by four experienced physicians with more than 10 years of echocardiographic experience. The first assessments were to be performed as they would be in the clinical practice. Six months later, the assessments were repeated based on the 2017 ASE/EACVI guidelines. The overall inter-rater agreement for the first clinical assessments was moderate, while the guidelines-based assessments had only fair inter-rater agreement. Both kinds of manual assessment had poor agreement with the standardized automated assessment algorithm of LVDF. In conclusion, the presented automated decision support for evaluation of diastolic LV function by Doppler echocardiography is mainly based on current guidelines involving multiple parameters in combination. Incorporating age dependency aspects in our program (available for use at https://liu.se/en/research/left-ventricular-diastolic-function-decision-support) enhances the accuracy of the evaluation and reduces variability in evaluation of LVDF. The large inter-rater variation in classification in this study also underscores the usefulness of tools to support a standardized evaluation.

Pulmonic stenosis (PS) is the most common congenital heart disease in dogs. This condition causes right ventricle (RV) overload and disrupts overall systolic function. The aim of this study was to examine the alterations of cardiac electrical activity and mechanical function in dogs with PS compared to normal healthy dogs.

Left ventricle myocardium has a complex micro-architecture, which was revealed to consist of myocyte bundles arranged in a series of laminar sheetlets. Recent imaging studies demonstrated that these sheetlets re-orientated and likely slided over each other during the deformations between systole and diastole, and that sheetlet dynamics were altered during cardiomyopathy. However, the biomechanical effect of sheetlet sliding is not well-understood, which is the focus here. We conducted finite element simulations of the left ventricle (LV) coupled with a windkessel lumped parameter model to study sheetlet sliding, based on cardiac MRI of a healthy human subject, and modifications to account for hypertrophic and dilated geometric changes during cardiomyopathy remodeling. We modeled sheetlet sliding as a reduced shear stiffness in the sheet-normal direction and observed that (1) the diastolic sheetlet orientations must depart from alignment with the LV wall plane in order for sheetlet sliding to have an effect on cardiac function, that (2) sheetlet sliding modestly aided cardiac function of the healthy and dilated hearts, in terms of ejection fraction, stroke volume, and systolic pressure generation, but its effects were amplified during hypertrophic cardiomyopathy and diminished during dilated cardiomyopathy due to both sheetlet angle configuration and geometry, and that (3) where sheetlet sliding aided cardiac function, it increased tissue stresses, particularly in the myofibre direction. We speculate that sheetlet sliding is a tissue architectural adaptation to allow easier deformations of the LV walls so that LV wall stiffness will not hinder function, and to provide a balance between function and tissue stresses. A limitation here is that sheetlet sliding is modeled as a simple reduction in shear stiffness, without consideration of micro-scale sheetlet mechanics and dynamics.

This investigation evaluated the effect of continuous milrinone infusion on right ventricular (RV) function during off-pump coronary artery bypass graft (OPCAB) surgery in patients with reduced RV function. Fifty patients scheduled for OPCAB, with thermodilution RV ejection fraction (RVEF) <35% after anesthesia induction, were randomly allocated to either milrinone (0.5 microg/kg/min) or control (saline) group. Hemodynamic variables and RV volumetric data measured by thermodilution method were collected as follows: after anesthesia induction (T1); 10 min after heart displacement for obtuse marginal artery anastomosis (T2); after pericardial closure (T3). Cardiac index and heart rate increased and systemic vascular resistance significantly decreased in milrinone group at T2. Initially lower RVEF of milrinone group was eventually comparable to control group after milrinone infusion. RVEF did not significantly change at T2 and T3 in both groups. RV end-diastolic volume in milrinone group consistently decreased from the baseline at T2 and T3. Continuous infusion of milrinone without a bolus demonstrated potentially beneficial effect on cardiac output and RV afterload in patients with reduced RV function during OPCAB. However, aggressive augmentation of intravascular volume seems to be necessary to maximize the effect of the milrinone in these patients.

Left ventricular (LV) involvement in diabetic cardiomyopathy has been reported; however, only limited data exist on right ventricular (RV) involvement. Therefore, our purpose was to investigate RV systolic dysfunction and its association with LV longitudinal myocardial dysfunction in patients with type 2 diabetes mellitus (T2DM) and preserved LV ejection fraction (LVEF).

To examine the effect of pioglitazone on myocardial insulin sensitivity and left ventricular (LV) function in patients with type 2 diabetes (T2D).

Chronic mitral regurgitation (MR) historically has been shown to primarily affect left ventricular (LV) function. The impact of increased left atrial (LA) volume in MR on morbidity and mortality has been highlighted recently, yet the LA does not feature as prominently in the current guidelines as the LV. Thus, we aimed to study LA and LV function in chronic rheumatic MR using traditional volumetric parameters and strain imaging.

The left atrium (LA) is exposed to left ventricular pressure during diastole. Applying the 2016 American Society of Echocardiography left ventricular diastolic function (LVDF) guidelines, this study aims to investigate whether left atrial ejection fraction (LAEF) and left atrial active emptying fraction (LAAEF) are markers of diastolic dysfunction (LVDD).

Sport-specific differences in the left ventricle (LV) of land-based athletes have been observed; however, comparisons to water-based athletes are sparse. The purpose of this study was to examine differences in LV structure and function in elite swimmers and runners. Sixteen elite swimmers [23 (2) years, 81% male, 69% white] and 16 age, sex, and race matched elite runners participated in the study. All athletes underwent resting echocardiography and indices of LV dimension, global LV systolic and diastolic function, and LV mechanics were determined. All results are presented as swimmers vs. runners. Early diastolic function was lower in swimmers including peak early transmitral filling velocity [76 (13) vs. 87 (11) cm ⋅ s-1, p = 0.02], mean mitral annular peak early velocity [16 (2) vs. 18 (2) cm ⋅ s-1, p = 0.01], and the ratio of peak early to late transmitral filling velocity [2.68 (0.59) vs. 3.29 (0.72), p = 0.005]. The diastolic mechanics index of time to peak untwisting rate also occurred later in diastole in swimmers [12 (10)% diastole vs. 5 (4)% diastole, p = 0.01]. Cardiac output was larger in swimmers [5.8 (1.5) vs. 4.7 (1.2) L ⋅ min-1, p = 0.04], which was attributed to their higher heart rates [56 (6) vs. 49 (6) bpm, p < 0.001] given stroke volumes were similar between groups. All other indices of LV systolic function and dimensions were similar between groups. Our findings suggest enhanced early diastolic function in elite runners relative to swimmers, which may be attributed to faster LV untwisting.