Compliance Of Left Ventricle Research Articles

Heart-Lung Interactions.

The pulmonary and cardiovascular systems have profound effects on each other. Overall cardiac function is determined by heart rate, preload, contractility, and afterload. Changes in lung volume, intrathoracic pressure (ITP), and hypoxemia can simultaneously change all of these four hemodynamic determinants for both ventricles and can even lead to cardiovascular collapse. Intubation using sedation depresses vasomotor tone. Also, the interdependence between right and left ventricles can be affected by lung volume-induced changes in pulmonary vascular resistance and the rise in ITP. An increase in venous return due to negative ITP during spontaneous inspiration can shift the septum to the left and cause a decrease in left ventricle compliance. During positive pressure ventilation, the increase in ITP causes a decrease in venous return (preload), minimizing ventricular interdependence and will decrease left ventricle afterload augmenting cardiac output. Thus, positive pressure ventilation is beneficial in acute heart failure patients and detrimental in hypovolemic patients where it can cause a significant decrease in venous return and cardiac output. Recently, this phenomenon has been used to assess patient's volume responsiveness to fluid by measuring pulse pressure variation and stroke volume variation. Heart-lung interaction is very dynamic and changes in lung volume, ITP, and oxygen level can have various effects on the cardiovascular system depending on preexisting cardiovascular function and volume status. Heart failure and either hypo or hypervolemia predispose to greater effects of ventilation of cardiovascular function and gas exchange. This review is an overview of the basics of heart-lung interaction.

Sex differences in heart failure patients assessed by combined echocardiographic and cardiopulmonary exercise testing.

We aimed to test the differences in peak VO2 between males and females in patients diagnosed with heart failure (HF), using combined stress echocardiography (SE) and cardiopulmonary exercise testing (CPET). Patients who underwent CPET and SE for evaluation of dyspnea or exertional intolerance at our institution, between January 2013 and December 2017, were included and retrospectively assessed. Patients were divided into three groups: HF with preserved ejection fraction (HFpEF), HF with mildly reduced or reduced ejection fraction (HFmrEF/HFrEF), and patients without HF (control). These groups were further stratified by sex. One hundred seventy-eight patients underwent CPET-SE testing, of which 40% were females. Females diagnosed with HFpEF showed attenuated increases in end diastolic volume index (P = 0.040 for sex × time interaction), significantly elevated E/e' (P < 0.001), significantly decreased left ventricle (LV) end diastolic volume:E/e ratio (P = 0.040 for sex × time interaction), and lesser increases in A-VO2 difference (P = 0.003 for sex × time interaction), comparing to males with HFpEF. Females diagnosed with HFmrEF/HFrEF showed diminished increases in end diastolic volume index (P = 0.050 for sex × time interaction), mostly after anaerobic threshold was met, comparing to males with HFmrEF/HFrEF. This resulted in reduced increases in peak stroke volume index (P = 0.010 for sex × time interaction) and cardiac output (P = 0.050 for sex × time interaction). Combined CPET-SE testing allows for individualized non-invasive evaluation of exercise physiology stratified by sex. Female patients with HF have lower exercise capacity compared to men with HF. For females diagnosed with HFpEF, this was due to poorer LV compliance and attenuated peripheral oxygen extraction, while for females diagnosed with HFmrEF/HFrEF, this was due to attenuated increase in peak stroke volume and cardiac output. As past studies have shown differences in clinical outcomes between females and males, this study provides an essential understanding of the differences in exercise physiology in HF patients, which may improve patient selection for targeted therapeutics.

Right Ventricle Response to Major Lung Resection (the RIVER Study).

Major lung resection is associated with high postoperative morbidity and mortality, especially due to cardiorespiratory complications. Right ventricle (RV) ejection, pulmonary artery (PA) pressure, and tone are tightly coupled. Since the RV is exquisitely sensitive to changes in afterload, an acute increase in RV outflow resistance (i.e., acute pulmonary embolism [PE]) will cause acute RV dilatation and, a reduction of left ventricle compliance too, rapidly spiraling to acute cardiogenic shock and death. We investigated the changing in RV performance after major lung resection. We carried out transthoracic echocardiography (TTE) aiming at searching for the incidence of early RV systolic dysfunction (defined as tricuspid annulus plane systolic excursion [TAPSE] <17 cm, S'-tissue Doppler imaging <10 cm/s) and estimate the RV-PA coupling by the TAPSE/pulmonary artery pressures (PAPs) ratio after major lung resection. The TTE has been performed before and immediately after surgery. After the end of the operation the echocardiographic parameters of the RV function worsened. TAPSE decreased from 24 (21 ÷ 28) to 18 (16 ÷ 22) mm (P = 0.015) and PAPs increased from 26 (25 ÷ 30) to 30 (25 ÷ 39) mmHg (P = 0.013). TAPSE/PAPs ratio decreased from 0.85 (0.80 ÷ 0.90) to 0.64 (0.54 ÷ 0.79) mm/mmHg (P = 0.002). In line with previous reports, after major lung resection the increase in afterload reduces the RV function, but the impairment remains clinically not relevant. The different clinical picture of an acute cor pulmonale due to PE implies that the pathogenesis of cardiac failure involves more pathways than the mere mechanic occlusion of the blood flow.

Abstract 13543: Impaired Stroke Volume Response During Exercise in Patients With Heart Failure With Preserved Ejection Fraction (HFpEF): The Role of Dynamic Starling Mechanisms

Introduction: Impaired stroke volume (SV) response during exercise is common in HFpEF. The regulation of SV during low intensity exercise is dependent on end-diastolic volume (EDV) reserve from a compliant left ventricle (LV). The Dynamic Starling Mechanism (DSM) quantifies beat-by-beat modulation of SV by respiratory-mediated changes in LV filling pressure and provides insight into the relationship between changes in LV compliance and SV response during exercise. We hypothesized low SV reserve during exercise would track with greater impairments in DSM gain in HFpEF patients. Methods: 11 HFpEF patients (68 ± 6 years; 7 females) were studied at rest and during 20 Watts of upright cycling and separated into higher or lower SV reserve (direct Fick) groups based on median SV response (&gt; vs ≤ 20% increase). DSM was quantified by transfer function (input/output frequency) analyses of beat-by-beat changes in pulmonary artery diastolic pressure (PAD, right heart catheterization) and SV (modelflow from radial arterial line waveform). Due to the small group size, magnitude of differences (i.e. effect size) between conditions and groups is assessed via Hedges’ g . Results: HFpEF patients with low SV reserve had blunted increases in SV compared to higher SV group patients (Δ 2 vs 31 ml, g = -2.0; Table). Compared to higher SV reserve, the lower SV reserve group exhibited a moderately greater increase in the power spectral density (PSD) of PAD ( g = 0.4) and decrease in PSD-SV ( g = 0.5) from rest to 20W. While both groups decreased DSM gain from rest to exercise, the lower SV reserve group had a greater decline (Δ -1.37 vs -0.61 ml/mmHg, g = -1.2). Conclusion: Lower SV reserve in patients with HFpEF is associated with impaired DSM gain during exercise. The lower gain was a function of increases in PAD PSD and decreases in SV PSD suggesting lower LV compliance and lower EDV reserve during exercise. Impaired DSM may explain low SV response and contribute to exercise limitations in patients with HFpEF.

Enhancing respiratory sinus arrhythmia increases cardiac output in rats with left ventricular dysfunction.

Respiratory sinus arrhythmia is physiological pacing of the heart that disappears in cardiovascular disease and is associated with poor cardiac prognosis. In heart failure, cardiac pacing has little, if any, variation in rate at rest. We proposed that reinstatement of respiratory sinus arrhythmia would improve cardiac function in rats with heart failure. Heart failure rats were paced daily for 2weeks with either respiratory sinus arrhythmia or paced monotonically at a matched heart rate; cardiac function was measured using non-invasive echocardiography. Cardiac output and stroke volume were increased in rats paced with respiratory sinus arrhythmia compared to monotonic pacing, via improvement in systolic function that persisted beyond the pacing treatment period. We propose that respiratory sinus arrhythmia pacing reverse-remodels the heart in heart failure and is worth considering as a new form of cardiac pacemaking. Natural pacing of the heart results in heart rate variability, an indicator of good health and cardiac function. A contributor to heart rate variability is respiratory sinus arrhythmia or RSA - an intrinsic respiratory modulated pacing of heart rate. The loss of RSA is associated with poor cardiac prognosis and sudden cardiac death. We tested if reinstatement of respiratory-modulated heart rate (RMH) would improve cardiac performance in heart failure. Heart failure was induced in Wistar rats by ligation of the left anterior descending coronary artery. Rats were unpaced, monotonically paced and RMH paced; the latter had the same average heart rate as the monotonically paced animals. Cardiac function was assessed non-invasively using echocardiography before and after 2weeks of daily pacing at a time when pacing was turned off. RMH increased cardiac output by 20±8% compared to monotonic pacing (-3±5%; P<0.05). This improvement in cardiac output was associated with an increase in stroke volume compared to monotonic pacing (P=0.03) and improvement in circumferential strain (P=0.02). Improvements in ejection fraction (P=0.08) and surrogate measures of left ventricle compliance did not reach significance. Increases in contractility (P<0.05) and coronary blood flow (P<0.05) were seen in vitro during variable pacing to mimic RMH. Thus, in rats with left ventricular dysfunction, chronic RMH pacing improved cardiac function through improvements in systolic function. As these improvements were made with pacing switched off, we propose the novel idea that RMH pacing causes reverse-remodelling.

P5250Diastolic strain rate ratio as determined on MRI on detecting left ventricle stiffness and predict heart failure in post-STEMI patients

Abstract Background ST-elevation myocardial infarction (STEMI) Patients suffered from progressive heart failure, for which progressive and aggravated Left ventricle stiffness was one of the major culprit. Myocardial deformation in the early diastole is largely affected by the left ventricle compliance which could partly reflect chamber stiffness and potentially predict left ventricular remodeling for post-STEMI patients. Purpose To determine the value of diastolic strain rate in detecting left ventricle stiffness and early heart failure in post-STEMI patients. Methods A number of 52 (M/F: 46/6, age: 54.27 [46.8–62.3]yrs) patients with STEMI three months ago were prospectively recruited from 2016 to 2017. Follow-up was done until 2018. The primary end points were the symptoms of heart failure (NYHA II-IV). Consent was acquired from each patient and 3.0 T MRI was arranged. Imaging analysis was performed on Cvi 42 (V5.9.3 Canada). Peak radial strain (PS) and strain rate (SR) were extracted both from 2D short- and long-axis cine images, while peak circumferential parameters only from the short axis slices and longitudinal the long axis slices. The diastolic strain rate ratios (DSRRs) were calculated as the peak early diastolic SR divided by the peak late diastolic SR, which were derived from the two peak points on the corresponding curve of time-to-SR curve in the diastole (Figure 1a). Receiver-operating characteristics curve analysis and Logistic regression test were done for statistical analysis on R project and P&lt;0.05 was considered as significant. Results Three patients were excluded due to unsatisfied cine images. Among the 52 patients, none of the patients died or had congestive heart failure. 23/52 (44.2%) patients complained of heart failure symptoms at the one-year follow-up. No significant difference was found in LVEF and three directional peak strain values or systolic peak strain rates between the patients with and without heart failure. Patients with symptoms had lower Longitudinal PS (P=0.049), early diastolic radial SR (P=0.01798), longitudinal SR (P=0.0042), and decreased DSRR in all directions (Figure 1b). Multivariate Logistic regression test showed that only DSRR in the radial direction on the short axis (DSRR-SR) was the independent predictor of the heart failure symptoms (6.59; range, 6.71–3.68; P=0.026). ROC analysis demonstrated that the DSRR-SR of 2.35 had sensitivity 91.3% and specificity 58.6% for the prediction of heart failure (Figure 1c). Figure 1 Conclusion DSRR especially DSRR-SR was more sensitive to left ventricle stiffness change and help predict the progression of heart failure for Post-STEMI patients. Further studies were needed to verify the its association with other cardiovascular clinical events. Acknowledgement/Funding the National Natural Science Foundation of China (81600299,81471721, 81471722, 81771887, and 81771897,);

Trabecular cutting: a novel surgical therapy to increase diastolic compliance.

Heart failure with preserved ejection fraction (HFpEF) is a common cause of hospital admission in patients over 65 yr old and has high mortality. HFpEF is characterized by left ventricular (LV) hypertrophy that reduces compliance. Current HFpEF therapies control symptoms, but no existing medications or therapies can sustainably increase LV compliance. LV trabeculae develop hypertrophy and fibrosis that contribute to reduced LV compliance. This study expands our previous results in ex vivo human hearts to show that severing LV trabeculae increases diastolic compliance in an ex vivo working rabbit heart model. Trabecular cutting was performed in ex vivo rabbit hearts set up in a working heart perfusion system perfused with oxygenated Krebs-Henseleit buffer. A hook was inserted in the LV to cut trabeculae. End-systolic and end-diastolic pressure-volume relationships during transient preload reduction were recorded using an admittance catheter in the following three groups: control (no cutting; n = 9), mild cutting (15 cuts; n = 5), and aggressive cutting (30 cuts; n = 5). In a second experiment, each heart served as its own control. Hemodynamic data were recorded before and after trabecular cutting (n = 10) or sham cutting (n = 5) within the same heart. In the first experiments, trabecular cutting did not affect systolic function (P > 0.05) but significantly increased overall diastolic compliance (P = 0.009). Greater compliance was seen as trabecular cutting increased (P = 0.002, r2 = 0.435). In the second experiment, significant increases in systolic function (P = 0.048) and diastolic compliance (P = 0.002) were seen after trabecular cutting compared with baseline. In conclusion, trabecular cutting significantly increases diastolic compliance without reducing systolic function.NEW & NOTEWORTHY We postulate that, in mammalian hearts, free-running trabeculae carneae exist to provide tensile support to the left ventricle and minimize diastolic wall stress. Because of hypertrophy and fibrosis of trabeculae in patients with left ventricular hypertrophy, this supportive role can become pathologic, worsening diastolic compliance. We demonstrate a novel operation involving cutting trabeculae as a method to acutely increase diastolic compliance in patients presenting with heart failure and diastolic dysfunction to improve their left ventricle compliance.

Microstructure-based finite element model of left ventricle passive inflation

Isolating the role(s) of microstructural pathological features in affecting diastolic filling is important in developing targeted treatments for heart diseases. We developed a microstructure-based constitutive model of the myocardium and implemented it in an efficient open-source finite element modeling framework to simulate passive inflation of the left ventricle (LV) in a representative 3D geometry based on experimentally measured muscle fiber architecture. The constitutive model was calibrated using previous tissue-level biaxial mechanical test data derived from the canine heart and validated with independent sets of measurements made at both the isolated constituent and organ level. Using the validated model, we investigated the load taken up by each tissue constituent and their effects on LV passive inflation. The model predicts that the LV compliance is sensitive to the collagen ultrastructure, specifically, the collagen fiber azimuthal angle with respect to the local muscle fiber direction and its waviness. The model also predicts that most of the load in the sub-epicardial and sub-endocardial regions is taken up, respectively, by the muscle fibers and collagen fiber network. This result suggests that normalizing LV passive stiffness by altering the collagen fiber network and myocyte stiffness is most effective when applied to the sub-endocardial and sub-epicardial regions, respectively. This finding may have implication for the development of new pharmaceutical treatments targeting individual cardiac tissue constituents to normalize LV filling function in heart diseases. Statement of SignificanceCurrent constitutive models describing the tissue mechanical behavior of the myocardium are largely phenomenological. While able to represent the bulk tissue mechanical behavior, these models cannot distinguish the contribution of the tissue constituents and their ultrastructure to heart function. Although microstructure-based constitutive models can be used to isolate the role of tissue ultrastructure, they have not been implemented in a computational framework that can accommodate realistic 3D organ geometry. The present study addresses these issues by developing and validating a microstructure-based computational modeling framework, which is used to investigate the role of tissue constituents and their ultrastructure in affecting heart function.

Modeling left ventricular dynamics using a switched system approach based on a modified atrioventricular piston unit

The contribution of the longitudinal atrioventricular plane displacement to ventricular pumping has drawn more and more attentions. In this paper, differential equations of the left ventricle (LV) are derived via the atrioventricular piston concept. The contribution of left ventricular radial function to blood flow was converted to an equivalent coefficient. A systemic circulatory model incorporating the modified atrioventricular piston unit was developed on a switched system form by adding some state-dependent switching planes. Simulation results prove that the end-systolic pressure volume relationship of the model with a changing systemic arterial resistance is approximately linear and insensitive to perturbations in afterload. Then the LV model was validated using a data fitting method. A pressure–volume loop from a patient undergoing routine diagnostic cardiac catheterization with LV angiography was used as measurements. Model parameters and the trapezoidal profile of contraction forces were adjusted by a trial method. The root mean squared error between the measured and estimated LV pressure is 2.99 mmHg. The LV compliance is 0.34 ml/mmHg. The ratio between left ventricular and left atrial cross-section is 1.8. Therefore, parameter values used in the modified LV model match physiological data. The model can reproduce the realistic pressure-flow relationship in the LV chamber.

Pulmonary Vein Flow Impedance: An Early Predictor of Cardiac Dysfunction in Intrauterine Growth Restriction

Introduction: In intrauterine growth restriction (IUGR), increased uteroplacental vascular impedance contributes to preferential flow to left ventricle (LV), with consequent alteration of its compliance and increased left atrial (LA) pressure. Pulmonary vein pulsatility index (PVPI) reflects the increased impedance to LA filling and could be used as a cardiac monitoring parameter in IUGR. Material and Methods: A total of 27 IUGR fetuses (group 1), 28 fetuses with appropriate growth for gestational age from hypertensive mothers (group 2), and 28 controls (group 3) were studied. Pulsatility indices (PIs) of pulmonary veins and ductus venosus were calculated by Doppler echocardiography. Obstetric ultrasound was used to assess the PIs of uterine, umbilical, and middle cerebral arteries. Statistical analysis used analysis of variance, post-hoc Tukey, and Pearson’s tests. Results: Mean PVPI was higher in IUGR group (1.27 ± 0.39) when compared to groups 2 (1.02 ± 0.37; p = 0.01) and 3 (0.75 ± 0.12; p < 0.001). In group 2, moderate correlation between PVPI and ductus venosus pulsatility index (DVPI) was found but not between PVPI and cerebroplacental ratio (CPR). Discussion: Higher PVPI in IUGR reflects decreased LV compliance and altered LA dynamics. As LV dysfunction precedes right ventricle, our results suggest that PVPI could be an early echocardiographic parameter of fetal diastolic function in IUGR.

Heart rate-induced modifications of concentric left ventricular hypertrophy: exploration of a novel therapeutic concept.

Lowering the heart rate is considered to be beneficial in heart failure (HF) with reduced ejection fraction (HFrEF). In a dilated left ventricle (LV), pharmacological heart rate lowering is associated with a reduction in LV chamber size. In patients with HFrEF, this structural change is associated with better survival. HF with preserved ejection fraction (HFpEF) is increasingly prevalent but, so far, without any evidence-based treatment. HFpEF is typically associated with LV concentric remodeling and hypertrophy. The effects of heart rate on this structural phenotype are not known. Analogous with the benefits of a low heart rate on a dilated heart, we hypothesized that increased heart rates could lead to potentially beneficial remodeling of a concentrically hypertrophied LV. This was explored in an established porcine model of concentric LV hypertrophy and fibrosis. Our results suggest that a moderate increase in heart rate can be used to reduce wall thickness, normalize LV chamber volumes, decrease myocardial fibrosis, and improve LV compliance. Our results also indicate that the effects of heart rate can be titrated, are reversible, and do not induce HF. These findings may provide the rationale for a novel therapeutic approach for HFpEF and its antecedent disease substrate.

Low-flow, low-gradient severe aortic stenosis in patients with normal ejection fraction

The occurrence of low-flow low-gradient severe aortic stenosis in patients with normal left ventricle (LV) ejection fraction has only been recently described. The purpose of this review is to highlight the diagnostic and management specificities of this entity. In the American College of Cardiology/American Heart Association guidelines, the criteria for severe aortic stenosis are an effective orifice area less than1.0 cm or less than 0.6 cm/m, a transvalvular mean gradient greater than 40 mmHg and a peak aortic jet velocity greater than 4.0 m/s. The guidelines also acknowledge that lower gradients may be observed in patients with depressed ejection fraction, with the implication that such an occurrence is not expected in patients with normal ejection fraction. However, recent studies confirm that a bona fide low-flow, low-gradient (LFLG) state may nonetheless be observed in 10-25% of patients with severe aortic stenosis and normal left ventricular ejection fraction (LVEF). This entity bears analogy with normal LVEF heart failure and is due to a restrictive physiology in relation with more pronounced LV concentric remodeling, a smaller LV cavity size and reductions in LV compliance and filling. The clinical relevance of LFLG severe aortic stenosis is now recognized in the most recent European (European Society of Cardiology/European Association for Cardio-Thoracic Surgery) guidelines, which also emphasize that it should be confirmed as being due to low-flow conditions. In particular, patients with bona fide paradoxical LFLG aortic stenosis should be distinguished from patients with normal flow and low gradient because of inconsistent cutoff criteria because, among patients with severe aortic stenosis, the former have the worst prognosis, whereas the latter have the best.

A new diagnostic feasibility for cardiomyopathy utilizing acoustic microscopy

Aims: Dilated cardiomyopathy often shows left ventricular systolic dysfunction, although histologically it always exhibits non-specific abnormality. We hypothesized that myocyte sound speed might be altered due to incomplete protein accumulation in cells. Methods and Results: Ninety eight biopsied samples were obtained from 49 patients comprising 43 with clinical dilated cardiomyopathy and 6 with hypertrophic cardiomyopathy. Sound speed was evaluated in deparaffinized 10 μm thick sections using an acoustic microscope (frequency range: 50 - 105 MHz). Conventional histology revealed 7 cases of persistent myocarditis derived from clinical dilated cardio- myopathy samples. Histology of the remaining dilated cardiomyopathy patients indicated non-specific abnormality. All hypertrophic cardiomyopathy cases exhibited myocardial disarray. Ten normal autopsied hearts were compared as controls. The sound speed of controls was 1627 ± 30m/sec. The sound speed in dilated cardiomyopathy samples (1700 ±51m/sec) was 1.045-fold faster compared to controls. The sound speed in hypertrophic cardiomyopathy samples (1734 ±51m/sec, 1.066-fold compared to controls) was faster than that of the myocarditis group (1672 ±30m/sec, 1.028-fold) (P = 0.0218). Furtheremore, desmin expression was evaluated as extent of emergence (grading 0 - 4). The desmin expression score in hypertrophic cardiomyopathy samples (2.7 ± 0.8) was significantly higher than in other groups (dilated 2.0 ± 1.4, myocarditis 1.6 ± 1.5 vs., controls 0, P ≤ 0.0001, 0.0001, 0.0129, respectively). Conclusion: Cardio-myopathy enhanced the sound speed, which correlated with the elasticity of myocytes, following the impaired compliance of left ventricle, despite the absence of histological changes. The elevation of sound speed of myocytes may be linked to cytoskeletal changes. Myocyte sound speed may be a new diagnostic tool for diagnosis of idiopathic cardiomyopathy independently of conventional histological diagnosis.

MicroRNAs 29 are involved in the improvement of ventricular compliance promoted by aerobic exercise training in rats

MiRNAs regulate cardiac development, hypertrophy, and angiogenesis, but their role in cardiac hypertrophy (CH) induced by aerobic training has not previously been studied. Aerobic training promotes physiological CH preserving cardiac function. This study assessed involvement of miRNAs-29 in CH of trained rats. Female Wistar rats (n=7/group) were randomized into three groups: sedentary (S), training 1 (T1), training 2 (T2). T1: swimming sessions of 60 min/5 days/wk/10 wk. T2: similar to T1 until 8th wk. On the 9th wk rats swam 2×/day, and on the 10th wk 3×/day. MiRNAs analysis was performed by miRNA microarray and confirmed by real-time PCR. We assessed: markers of training, CH by ratio of left ventricle (LV) weight/body wt and cardiomyocytes diameter, pathological markers of CH (ANF, skeletal α-actin, α/β-MHC), collagen I and III (COLIAI and COLIIIAI) by real-time PCR, protein collagen by hydroxyproline (OH-proline) concentration, CF and CH by echocardiography. Training improved aerobic capacity and induced CH. MiRNAs-1, 133a, and 133b were downregulated as observed in pathological CH, however, without pathological markers. MiRNA-29c expression increased in T1 (52%) and T2 (123%), correlated with a decrease in COLIAI and COLIIIAI expression in T1 (27%, 38%) and T2 (33%, 48%), respectively. MiRNA-29c was inversely correlated to OH-proline concentration (r=0.61, P<0.05). The E/A ratio increased in T2, indicating improved LV compliance. Thus, these results show that aerobic training increase miR-29 expression and decreased collagen gene expression and concentration in the heart, which is relevant to the improved LV compliance and beneficial cardiac effects, associated with aerobic high performance training.

Acute Change in Left Ventricle End-diastolic Pressure after Primary Percutaneous Coronary Intervention in Patients with ST Segment Elevation Myocardial Infarction

ST segment elevation myocardial infarction (STEMI) causes decreasing left ventricle compliance, increasing left ventricle end-diastolic pressure (LVEDP), and diastolic dysfunctioning. It is known that primary percutaneous coronary intervention (PCI) has an acute effect on left ventricle compliance. This study aims to determine whether left ventricle diastolic function improves and LVEDP decreases post-PCI in patients with STEMI. Twenty-nine patients (21 male, mean age 62 ± 12) diagnosed with a first anterior or inferior STEMI and hospitalized in the first six hours were enrolled. Coronary angiography (CAG) showed occlusion of the right coronary artery (RCA), circumflex (Cx), or left anterior descending (LAD) coronary artery. Aortic pressure and LVEDP were measured and compared before and after PCI. After successful reperfusion, left ventricle diastolic function improved and LVEDP decreased significantly. Decrease in mean LVEDP was 5.7 ± 2.9 mmHg (p=0.0005) and 4.9 ± 6.5 mmHg (p=0.026) in inferior and anterior MI, respectively. Clinical and electrocardiographic (ECG) findings improved quickly. Primary PCA provides rapid improvement of LVEDP and diastolic functions in both anterior and inferior MI. Left ventricular pressure (before and after PCI) can be measured during the procedure without any complication, so it can be used for quick evaluation of left ventricular diastolic function improvement.

The Influence of Left Ventricle Diastolic Function on Natriuretic Peptides Levels in Patients with Atrial Fibrillation

The diagnosis of the impaired left ventricle (LV) diastolic function during atrial fibrillation (AF) using traditional methods is very difficult. Natriuretic peptides seem to be useful for assessment of diastolic function in patients with AF. To evaluate the influence of LV diastolic dysfunction on natriuretic peptides concentrations and to assess the diagnostic value of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in patients with AF and impaired LV diastolic function. The study included 42 patients (23 males, 19 females), aged 58.6 +/- 8.2 years with nonvalvular persistent AF with preserved LV systolic function who were converted into sinus rhythm by DC cardioversion (CV) and maintained sinus rhythm for at least 30 days. Echocardiography (ECG), ANP, and BNP level measurements were taken at baseline 24 hours before CV and 24 hours and 30 days after CV. On the 30th day following CV in patients with sinus rhythm, Doppler ECG was performed to assess LV diastolic function. Thirty days after CV, normal LV diastolic function in 15 patients and impaired diastolic function in 27 patients was diagnosed: 20 with impaired LV relaxation and seven with impaired LV compliance. During AF and 24 hours, and 30 days after sinus rhythm restoration, significantly higher ANP and BNP levels were observed in patients with LV diastolic dysfunction as compared to the subgroup with normal LV diastolic function. The average values of ANP during AF in patients with normal and impaired diastolic function were 167.3 +/- 70.1 pg/mL and 298.7 +/- 83.6 pg/mL, respectively (P < 0.001), and the average values of BNP in the above mentioned subgroups were 49.5 +/- 14.7 pg/mL and 145.6 +/- 49.6 pg/mL respectively (P < 0.001). While comparing the diagnostic value of both natriuretic peptides it was noted that BNP was a more specific and sensitive marker of impaired LV diastolic function. ANP value >220.7 pg/mL measured during AF identified patients with impaired LV diastolic function with 85% sensitivity and 90% specificity. BNP value >74.7 pg/mL proved 95% sensitive and 100% specific in the diagnosing of such a group. The increase of ANP/BNP concentration in patients with AF results not only from the presence of AF, but also reflects the impaired LV diastolic function. Natriuretic peptides, especially BNP, may be useful in diagnosing LV diastolic dysfunction in patients with AF.

Study of Lamb wave dispersion in porcine myocardium.

Diastolic dysfunction is the impaired ability of the left ventricle (LV) to passively fill during diastole and maintain its stroke volume at physiologic filling pressures and is associated with impaired relaxation and reduced compliance of LV. Knowledge of the quantitative values of the myocardial viscoelastic properties would improve the clinician’s ability to evaluate diastolic dysfunction in patients. To gain better understanding of the viscoelastic properties of the LV as a function of geometry, we studied Lamb wave propagation in different directions in excised porcine free‐wall myocardium. The phantom consisting of a dissected porcine LV free‐wall embedded in gelatin was fixed in a water tank. A mechanical shaker was used for harmonic excitation over a range of 40–500 Hz and a 7.5 MHz ultrasound transducer was used for motion measurements. Motion amplitude and phase at different depths of the sample were analyzed to obtain dispersion curves in four orthogonal directions. The data were fitted to the Lamb wave equations and shear elasticity and viscosity coefficients were estimated. The values of μ1 and μ2 were 13.75 ± 0.96 and 5.86 ± 0.75 Pa s. Our results suggest that the viscoelastic characteristics of the porcine LV free‐wall in orthogonal directions were similar.

Complete revascularization surgery in patients with coronary disease with severely reduced left ventricular function. Discrepancies in the evaluation of results

Clinical data, function and compliance of left ventricle as well as regional wall motion were analysed in 17 patients with preoperatively limited left-ventricular function and signs of myocardial ischaemia after complete revascularisation surgery. Recatheterisation after 5.2 months on average after surgery showed improvement by one NYHA class, an increase of mean left-ventricular enddiastolic pressure, which was interpreted as "improved status of ischaemia", a decrease of left-ventricular compliance by 30%, of enddiastolic volume by 14% and of endsystolic volume by 20% (P less than 0.05). Loss of function occurred in 3 out of 92 bypasses. Up to the time of reporting, 22.4 months postoperatively, all patients have survived in a relatively satisfactory clinical state. All parameters of left-ventricular function as well as regional wall motion showed a tendency for improvement after surgery in the majority of patients. However, pre- and postoperative mean values were not significantly different (P greater than 0.05). Thus, despite clearcut improvement of clinical state and "ischaemia index", improvement of left-ventricular function and regional wall motion are not consistently demonstrable. The reasons of this discrepancy cannot be ascertained by this investigation. The quality of the surgical intervention and the sensitivity of parameter assessment cannot be held responsible.

Congestive heart failure in the elderly diabetic

The elderly diabetic is a potential congestive heart failure patient. Cardiac involvement is multifactorial, particularly ischemic conditions because of the accumulation at that age of vascular risk factors and therefore the frequency of coronary damages. The elderly diabetic very often has high blood pressure, with the risk of developing a hypertensive heart disease. Beyond these issues, the effects of chronic hyperglycaemia and insulin resistance on the heart specifically alter left ventricle compliance and therefore diastolic function, thus accelerating the effects proper to aging. No specific recommendation has been published on the management of the elderly diabetic with congestive heart failure. Even at an advanced age, with a clinical diagnosis of congestive heart failure that is sometimes difficult to make, the cardiological evaluation should be conducted rigorously within a global evaluation, and treatment should follow the same rules as in younger patients, with great caution given to the iatrogenic risks inherent to this population.

Na +/H + exchange inhibition and antioxidants lack additive protective effects after reperfusion injury in the working heterotopic rat heart isograft

Background The utility of combining strategies of myocardial protection was studied in intact rat hearts subjected to 1 hour of ischemia and 40 minutes blood reperfusion. Methods Lewis rats ( n = 48) were divided into 4 transplant groups. Twenty-four hearts were arrested by coronary perfusion with hypothermic Celsior solution at 60 mm Hg. The aortic valve was punctured to introduce volume into the left ventricle (LV), and the hearts were abdominally isografted. Animals were either given both the antioxidant probucol (300 mg/kg) and the sodium-hydrogen exchange inhibitor cariporide (5 mg/kg) (CP; n = 6), just cariporide (CAR; n = 6), just probucol (PROB; n = 6), or neither drug (CON; n = 6). After 40 minutes of blood reperfusion, transplanted hearts were rearrested. The control recipients’ native hearts (native; n = 6) were also arrested. Postmortem LV compliance relations and myocardial water content (MWC) were measured. Results Grafts protected by probucol were significantly more compliant than controls and significantly less compliant than grafts protected by cariporide alone and with both cariporide and probucol ( p = 0.0001, analysis of variance). Compliance relations for CP overlapped those for CAR. All grafts were less compliant than natives. MWC was significantly greater in controls and PROB than in natives. Conclusions Pretreatment with cariporide in the setting of ischemia-reperfusion injury provides greater protection against the development of diastolic abnormalities than probucol when Celsior solution is used for both arrest and preservation. In this model, there is no advantage to combining the drugs, supporting the hypothesis that there is an overlapping mechanism of protection.