Load Dependent Diastolic Dysfunction in Heart Failure

Congestive heart failure may result from cardiovascular overload, from systolic or from diastolic dysfunction. Diastolic left ventricular dysfunction may result from structural resistance to filling such as induced by pericardial constraint, right ventricular compression, increased chamber stiffness (hypertrophy) and increased myocardial stiffness (fibrosis). A distinct and functional etiology of diastolic dysfunction is slow and incomplete myocardial relaxation. Relaxation may be slowed by pathological processess such as hypertrophy, ischemia and by asynchronous left ventricular function. The present contribution analyses the occurrence of slow and incomplete myocardial relaxation in response to changes in systolic pressure and in response to changes in venous return. The regulation of myocardial relaxation by load is critically dependent on the transition from myocardial contraction to relaxation, which occurs in dogs when 82% of peak isovolumetric pressure has developed or at a relative load of 0.82. This corresponds to early ejection in normal hearts, but is situated even before aortic valve opening in severely diseased hearts. When load is developed beyond this transition, relaxation becomes slow and even incomplete. This is load dependent diastolic dysfunction. Load dependent diastolic dysfunction occurs in normal hearts facing heavy afterload and in severely diseased hearts even with normal hemodynamic parameters. This dysfunction should contribute to elevating filling pressures in most patients with severe congestive heart failure. This dysfunction can be reverted by decreasing systolic pressures or by decreasing venous return. Load dependent diastolic dysfunction gives us an additional reason to agressively treat CHF patients with diuretics and vasodilators.     

Right atrium enlargement is related to increased heart damage and mortality in well-controlled hypertension

Background and aimLeft heart remodeling is a well-known pathophysiological effect of arterial hypertension. Right Heart status is not considered in its evaluation. No data are available on right atrium (RA) and its impact on the outcome in hypertension.We wondering to understand whether RA may play a role as a marker of an increased risk for organ damage in well-controlled hypertensives, to probe the clinical significance and whether it could indicate an increased risk.Methods and resultsWe studied well-controlled hypertensive patients. Heart damage was assessed by echocardiography. Patients were subdivided into those with RA area ≤18 cm² (normal RA - Group 1) (554 pts, 227 M, aged 60.35 ± 10.48 years) and those >18 cm² (Increased RA - Group 2) (101 pts, 71 M, age 61.65 ± 9.46 years). Group 2 had a higher left ventricle mass (LVM) and left atrium volume (LAV) both as absolute value (both p < 0.0001) and indexed for body surface area (LVMi p < 0.013; LAVi p = 0.0013). Group 2 showed an increased vascular stiffness (p < 0.0001) and carotid stenosis percentage (p = 0.011). TAPSE (p < 0.0001) resulted significantly increased. In The RA area was significantly correlated directly to LVM and LAV in both groups, but these correlations persisted in indexed values only in Group 2. Moreover, in this group there was a significant direct correlation between RA area and Tricuspid s'wave at echocardiography TDI analysis. Finally, Group 2 had an increased mortality rate compared to Group 1 (Log-Rank p = 0.0006).ConclusionGroup 2 hypertensive patients showed more alterations in dimensional and volumetric left heart parameters, and an increased mortality.     

Single-beat estimation of the left ventricular end-systolic pressure–volume relationship in patients with heart failure

Aim: The end-systolic pressure–volume relationship (ESPVR) constructed from multiple pressure–volume (PV) loops acquired during load intervention is an established method to asses left ventricular (LV) contractility. We tested the accuracy of simplified single-beat (SB) ESPVR estimation in patients with severe heart failure. Methods: Nineteen heart failure patients (NYHA III-IV) scheduled for surgical ventricular restoration and/or restrictive mitral annuloplasty and 12 patients with normal LV function scheduled for coronary artery bypass grafting were included. PV signals were obtained before and after cardiac surgery by pressure-conductance catheters and gradual pre-load reductions by vena cava occlusion (VCO). The SB method was applied to the first beat of the VCO run. Accuracy was quantified by the root-mean-square-error (RMSE) between ESPVR_SB and gold-standard ESPVR_VCO. In addition, we compared slopes (E_ES) and intercepts (end-systolic volume at multiple pressure levels (70–100 mmHg: ESV₇₀–ESV₁₀₀) of ESPVR_SB vs. ESPVR_VCO by Bland–Altman analyses. Results: RMSE was 1.7 ± 1.0 mmHg and was not significantly different between groups and not dependent on end-diastolic volume, indicating equal, high accuracy over a wide volume range. SB-predicted E_ES had a bias of −0.39 mmHg mL⁻¹ and limits of agreement (LoA) −2.0 to +1.2 mmHg mL⁻¹. SB-predicted ESVs at each pressure level showed small bias (range: −10.8 to +9.4 mL) and narrow LoA. Two-way anova indicated that differences between groups were not dependent on the method. Conclusion: Our findings, obtained in hearts spanning a wide range of sizes and conditions, support the use of the SB method. This method ultimately facilitates less invasive ESPVR estimation, particularly when coupled with emerging noninvasive techniques to measure LV pressures and volumes.     

心肌桥对冠状动脉血流量的影响

目的研究心肌桥对壁冠状动脉血流量的影响。方法利用心肌桥模拟装置,建立壁冠状动脉受压迫状态的圆形收缩模型,并进行心肌桥在收缩期到舒张期影响壁冠状动脉血流量的数值模拟,用有限元软件CFD对数值进行模拟分析。结果在血管狭窄部位血流主要为高速层流,随压迫程度增大,高速层流区流速加快。在同一心率、同一血压范围内,流速随着收缩程度的增大而加快。结论心肌桥对冠状动脉压力和流量的影响与其对冠状动脉的压迫程度和频率有关。     

Dyssynchrony of segment shortening in the anterior wall of the feline left ventricle

Non-uniformity of regional contraction may be both spatial and temporal. This study was undertaken to deal with the temporal aspects of shortening and to quantify non-uniformity with regard to timing. Nine cats were anaesthetized and artificially ventilated. Two pairs of ultrasonic crystals were situated in the anterior midwall of the left ventricle to measure regional shortening. One pair, longitudinal segment, was oriented to align with midwall fibres. The other pair, transverse segment, was placed perpendicular to the first one. Registrations in control state, during caval occlusion, and during aortic constriction were carried out with and without isoprenaline infusion. Cyclic events were analysed in terms of phase angle, 0–2π representing one heart cycle. Transverse segments showed marked shift of duration of shortening, from 1.19π± 0.06π (meanæM) in the control state to 0.40π± 0.14π during caval occlusion with isoprenaline infusion. Duration of shortening of longitudinal segments showed less prominent shift with mean values between 1.38π and 1.11π. Regional uniformity of timing, expressed as synchronization index, varied markedly with interventions (P < 0.0005). Dyssynchrony was most prominent during caval occlusion with mean values less than 0.6. A simple model of force generation for the two segments visualizes that segment shortening of the transverse segment is of shorter duration than the longitudinal segment and a common mechanism for temporal and spatial non-uniformity within a region could be elaborated. This study quantifies both the time course of shortening and temporal non-uniformity of two cross-oriented segments within the same myocardial region.     

Left ventricular systolic time intervals. A comparison between the conventional carotid pulse curve method and the doppler ultrasound method

From amplitude registration of the doppler ultrasound signal,timing of cardiac valve opening and closure may be achievedand used for the registration of the time intervals of the cardiaccycle. In 42 normal subjects and unselected patients with heartdisease a comparison was made of the simultaneously derivedleft ventricular systolic time intervals (LVSTI) from the conventionalnoninvasive method of electrocardiogram, phonocardiogram andcarotid pulse curve tracing and from an alternative more directnoninvasive method by use of the amplitude tracing of the dopplerultrasound signal. There was a strong correlation between thetwo methods for each of the different periods of the LVSTI.Differences between the pulse transmission times of curve upstrokeand incisura, and possible limitations of both methods are discussed.     

The effect of chronic digitalization on pump function in systolic heart failure

BACKGROUND: Short- and intermediate-term use of cardiac glycosides promotes inotropy and improves the ejection fraction in systolic heart failure. AIM: To determine whether chronic digitalization alters left ventricular function and performance. METHODS: Eighty patients with mild-to-moderate systolic heart failure (baseline ejection fraction < or =45%) participated from our institution in a multi-center, chronic, randomized, double-blind study of digitalis vs. placebo. Of the 40 survivors, 38 (20 allocated to the digitalis arm and 18 to the placebo arm) were evaluated at the end of follow-up (mean, 48.4 months). Left ventricular systolic function was assessed by both nuclear ventriculography and echocardiography. The ejection fraction was measured scintigraphically, while the ventricular volumes were computed echocardiographically. RESULTS: The groups did not differ, at baseline or end-of-study, with respect to the ejection fraction and the loading conditions (arterial pressure, ventricular volumes and heart rate) by either intention-to-treat or actual-treatment-received analysis. Over the course of the trial, the digitalis arm exhibited no significant increase in the use of diuretics (18%, P=0.33), in distinction from the placebo group (78%, P=0.004), and a longer stay on study drug among those patients who withdrew from double-blind treatment (28.6 vs. 11.4 months, P=0.01). CONCLUSION: Following chronic use of digitalis for mild-to-moderate heart failure, cross-sectional comparison with a control group from the same inception cohort showed no appreciable difference in systolic function or performance. Thus, the suggested clinical benefit cannot be explained by an inotropic effect.     

索他洛尔治疗右室流出道室性早搏的疗效评价

目的:观察索他洛尔治疗右室流出道室性早搏的疗效。方法:对32例右室流出道室性早搏患者,给予索他洛尔口服治疗,剂量从每天80mg开始,3天后未达有效标准者增加至每天160mg治疗,疗效及不良反应采用临床及动态心电图结果评定。结果:经索他洛尔治疗后,总有效率为75％,心室率由基础的82.5±5.5次/分降至68.3±8.2次/分;QTc由治疗前的401.52±20.28ms延长至403.44±23.85ms。无心功能恶化,不良反应轻微。结论:索他洛尔治疗右心室流出道室性早搏疗效确切,无明显致心律失常作用。     

Impact of essential hypertension and diabetes mellitus on left ventricular systolic and diastolic performance.

AIMS: To investigate left ventricular systolic and diastolic function in patients with essential hypertension and diabetes mellitus associated with hypertension by the myocardial performance index (MPI). METHODS AND RESULTS: The study included 45 patients with essential hypertension, 45 patients with diabetes mellitus and hypertension and 45 normal subjects, who underwent a complete two-dimensional and Doppler echocardiography including assessment of the isovolumetric Doppler time intervals for the estimation of the Doppler-derived MPI.The MPI was significantly higher in patients with essential hypertension and diabetes with hypertension, compared to controls (Essential hypertension=0.51+/-0.12; Diabetes=0.51+/-0.12 vs. controls 0.40+/-0.05, P=0.001). The isovolumetric contraction time was significantly prolonged in essential hypertension (56+/-26 msec vs. 40+/-17 msec, P<0.01 respectively) and among diabetes patients isovolumetric relaxation time was prolonged compared to normal subjects (100+/-20 ms vs. 87+/-16 ms, P<0.01, respectively). The index was not related to left ventricular mass, age or ejection fraction, but significantly correlated to E-wave deceleration time (rho=0.48, P<0.001). CONCLUSIONS: The MPI is increased, in both essential hypertensive patients and diabetes patients with associated hypertension, despite normal ejection fraction.