Left Ventricular Filling Pressure in Chronic Thromboembolic Pulmonary Hypertension

BackgroundChronic thromboembolic pulmonary hypertension (CTEPH) is characterized by obstruction of major pulmonary arteries with organized thrombi. Clinical risk factors for pulmonary hypertension due to left heart disease including metabolic syndrome, left-sided valvular heart disease, and ischemic heart disease are common in CTEPH patients.ObjectivesThe authors sought to investigate prevalence and prognostic implications of elevated left ventricular filling pressures (LVFP) in CTEPH.MethodsA total of 593 consecutive CTEPH patients undergoing a first diagnostic right and left heart catheterization were included in this study. Mean pulmonary arterial wedge pressure (mPAWP) and left ventricular end-diastolic pressure (LVEDP) were utilized for assessment of LVFP. Two cutoffs were applied to identify patients with elevated LVFP: 1) for the primary analysis mPAWP and/or LVEDP >15 mm Hg, as recommended by the current pulmonary hypertension guidelines; and 2) for the secondary analysis mPAWP and/or LVEDP >11 mm Hg, representing the upper limit of normal. Clinical and echocardiographic features, and long-term mortality were assessed.ResultsLVFP was >15 mm Hg in 63 (10.6%) and >11 mm Hg in 222 patients (37.4%). Univariable logistic regression analysis identified age, systemic hypertension, diabetes, atrial fibrillation, calcific aortic valve stenosis, mitral regurgitation, and left atrial volume as significant predictors of elevated LVFP. Atrial fibrillation, calcific aortic valve stenosis, mitral regurgitation, and left atrial volume remained independent determinants of LVFP in adjusted analysis. At follow-up, higher LVFPs were measured in patients who had meanwhile undergone pulmonary endarterectomy (P = 0.002). LVFP >15 mm Hg (P = 0.021) and >11 mm Hg (P = 0.006) were both associated with worse long-term survival.ConclusionsElevated LVFP is common, appears to be due to comorbid left heart disease, and predicts prognosis in CTEPH.     

Determination of Left Ventricular Filling Pressure by Doppler Echocardiography in Patients With Coronary Artery Disease: Critical Role of Left Ventricular Systolic Function

Objectives. This study was designed to determine the usefulness of transthoracic Doppler measurements in detecting increased left ventricular (LV) end-diastolic pressure in patients with coronary artery disease, specifically examining the influence of systolic function on the accuracy of these methods.

Background. Studies that have correlated Doppler indexes with LV filling pressures primarily involved patients with LV systolic dysfunction. The reliability of Doppler indexes in estimating filling pressures in patients with coronary artery disease and preserved systolic function is unclear.

Methods. Pulsed wave Doppler transmitral and pulmonary venous flow velocity curves and LV pressure were recorded in 83 patients with coronary artery disease.

Results. Conventional Doppler indexes (deceleration time of mitral E wave velocity, ratio of peak mitral E to A wave velocities and pulmonary venous systolic fraction) correlated with LV filling pressure in patients with an ejection fraction (EF) ≤50% but not in those with an EF >50%. Previously published regression analysis for prediction of LV filling pressure was accurate in patients with an EF ≤50% but not in those with an EF >50%. The difference between flow duration with atrial contraction in the pulmonary veins and transmitral flow duration with atrial contraction correlated with LV filling pressure in both groups.

Conclusions. Analysis of the early diastolic portion of the transmitral or pulmonary venous flow velocity curves can be used to predict LV filling pressures in patients with systolic dysfunction, but are inaccurate in patients with preserved systolic function. The combined analysis of both flow velocity curves at atrial contraction is a reliable, feasible predictor of increased LV filling pressure, irrespective of systolic function.     

Doppler Markers of Elevated Left Atrial and Ventricular Filling Pressure in a Critically Ill Patient

Accurate assessment of intracardiac flows by Doppler echocardiography may add important hemodynamic information in the critically ill patient. Detailed analysis of flow gradients through different sites and their correlation with timing of cardiac events may help us in better understanding the pathophysiology of the underlying disease. We report the clinical case of a 78‐year‐old patient with septic shock, in whom an A‐dip of aortic regurgitation, shortening of diastolic filling, and diastolic mitral regurgitation were detected by Doppler analysis. Pathophysiologic explanation of these phenomena and their evolution after inotropic drug infusion are reported.     

Evaluation of Right and Left Ventricular Diastolic Filling

A conceptual fluid–dynamics framework for diastolic filling is developed. The convective deceleration load (CDL) is identified as an important determinant of ventricular inflow during the E wave (A wave) upstroke. Convective deceleration occurs as blood moves from the inflow anulus through larger-area cross-sections toward the expanding walls. Chamber dilatation underlies previously unrecognized alterations in intraventricular flow dynamics. The larger the chamber, the larger becomes the endocardial surface and the CDL. CDL magnitude affects strongly the attainable E wave (A wave) peak. This underlies the concept of diastolic ventriculoannular disproportion. Large vortices, whose strength decreases with chamber dilatation, ensue after the E wave peak and impound inflow kinetic energy, averting an inflow-impeding, convective Bernoulli pressure rise. This reduces the CDL by a variable extent depending on vortical intensity. Accordingly, the filling vortex facilitates filling to varying degrees, depending on chamber volume. The new framework provides stimulus for functional genomics research, aimed at new insights into ventricular remodeling.     

Impaired Left Ventricular Filling in Young Female Diabetics

ABSTRACT To assess left ventricular (LV) function in diabetes mellitus, M-mode echocardiograms were recorded in 36 insulin-treated diabetic women, mean age 25±6 (SD) years, and 13 healthy women of the same age. Echocardiographic tracings of the septum and LV posterior wall were digitized and continuous plots were made of LV dimension and its rate of change. The pattern of LV filling was abnormal in 19 diabetics, when the mean value ±2 SD in the healthy women was taken as the normal range of the indices. The most common abnormality was a prolonged rapid filling period. The LV systolic function was normal in all diabetics. Diabetics with severe microvascular complications had thicker LV walls (p<0.05) and smaller LV end-diastolic diameters and stroke volumes (p<0.01) than the healthy women. The electrocardiographic voltage was lower in the diabetic group (p<0.05). These studies suggest that minor abnormalities in LV function reflecting stiffness of the myocardium are common in young female diabetics, a patient group with a relatively low prevalence of coronary artery disease.     

Left Ventricular Untwisting in Restrictive and Pseudorestrictive Left Ventricular Filling: Novel Insights into Diastology

Background: Conceptually, an ideal therapeutic agent should target the underlying mechanisms that cause left ventricular (LV) diastolic dysfunction. The objective of our study was to gain further insight into the mechanics of diastology by comparison of LV untwisting measured by speckle tracking echocardiography (STE) in young healthy adults with normal and “pseudorestrictive” LV filling, and dilated cardiomyopathy (DCM) patients with “true restrictive” LV filling. Methods: The study comprised 20 healthy volunteers with a Doppler LV‐inflow pattern compatible with restrictive LV filling but a diastolic early phase filling velocity/early diastolic velocity of the mitral annulus (E/Em) ratio <8 (“pseudorestrictive”), 20 for age and gender‐matched healthy volunteers with normal LV filling and an E/Em ratio <8, and 10 DCM patients with “true restrictive” LV filling and an E/Em ratio >15. LV untwisting parameters were determined by STE. Results: Compared to healthy subjects, DCM patients had decreased peak diastolic untwisting velocity (−62 ± 33 degrees/s vs −113 ± 25 degrees/s, P < 0.01) and untwisting rate (−15 ± 9 degrees/s vs −51 ± 24 degrees/s, P < 0.01). Compared to healthy subjects with normal LV filling, healthy subjects with “pseudorestrictive” LV filling had increased peak diastolic untwisting velocity (−123 ± 25 degrees/s vs −104 ± 30 degrees/s, P < 0.05) and untwisting rate (−59 ± 23 degrees/s vs −44 ± 22 degrees/s, P < 0.05). Conclusion: Faster LV untwisting plays a pivotal role in the rapid early diastolic filling occasionally seen in young healthy individuals. In contrast, in DCM patients untwisting is severely delayed and this impairment to utilize suction may reduce LV filling. (Echocardiography 2010;27:269‐274)     

Assessment of Left Ventricular Filling Pressure in Myocardial Infarction Using the First Derivative of the Apexcardiogram

ABSTRACT We recorded the apexcardiogram (ACG) and its first derivative (dA/dt) in 24 patients with acute or recent myocardial infarction. From dA/dt, an index I = × 10 dRFW/dS was defined (dRFW and dS = peaks of dA/dt corresponding to the rapid filling wave and to the systolic upstroke of the ACG). A significant correlation was found between I and pulmonary capillary wedge pressure (PCW, mmHg). PCW = 2.3 × I+6.5 (r=0.80, p<0.001). Normal PCW was found in 15 patients who all had an I<2.8. Elevated PCW was found in 9 patients who all had an I>2.8. Thus the ability of I to predict elevated PCW was 100% (95% confidence limit > 66.4%). The ability to predict normal PCW was 100% (95% confidence limit > 76.2%). No significant correlation was found between I and cardiac index (r=0.29, p>0.1).     

Hemodynamic Determinants of Echocardiographically-Derived Indices of Left Ventricular Filling

Noninvasive techniques have made it easy to detect abnormalities in the pattern of left ventricular diastolic filling. Abnormalities in diastolic filling patterns have been identified in a wide variety of cardiac disorders and are sensitive, early indicators of myocardial disease. However, changes in noninvasive indices of left ventricular diastolic filling are caused not only by pathological processes but also by several physiological determinants. The purpose of this review is to describe the measurements used to quantitate diastolic function, define the physiological and pathological determinants of these measurements, and discuss the use of these measurements in the diagnosis and treatment of cardiac disease.     

Modulation of Left Atrial Function by Ventricular Filling Impairment

Left atrial function is an important determinant of ventricular filling. Assessment of the complex role that the atrial cavity exerts in the ventricular filling process can be made noninvasively. Computing the net instantaneous difference between mitral and pulmonary venous flow is an approach which permits the construction of the left atrial volume curve throughout the cardiac cycle (as well as the left ventricular volume curve during diastole), and to quantify the 3 different functions that the cavity performs. In particular, increasing degrees of ventricular filling impairment are met by mechanical left atrial adaptations which basically rely on the Starling mechanism, with the reservoir/pump complex activated to the limit of the preload reserve of the cavity. At end-stage left ventricular dysfunction, however, the atrial reservoir and the booster pump function decline and conduit takes precedence, suggesting afterload mismatch, impaired atrial compliance and, perhaps, depressed atrial contractility. Increased wall stiffening and reduced elastic recoil induced by chronic atrial distension might explain the additional power of atrial size in stratifying prognostically patients with left ventricular dysfunction.     

Left Ventricular Pressure Responses in Post-Angiographic Angina

Alterations in left ventricular end-diastolic pressure and in dp/dt observed in ten patients with coronary heart disease who developed angina pectoris following left ventricular cineangiography were compared with those of six other patients who developed angina spontaneously and with patients who underwent left ventricular cineangiography without experiencing angina. In the patients with post-angiographic angina there was a greater increase in end-diastolic pressure than that seen in the other patients, but there was no significant change in dp/dt. Changes in left ventricular pressure associated with post-angiographic angina would appear to reflect the combined effects of increased preload provided by the contrast material and of ventricular dysfunction including diminished compliance associated with angina. A rise in end-diastolic pressure greater than 20 mmHg following left ventricular cineangiography should alert the physician that the patient may be having myocardial ischemia.     

Effect of Implantable Defibrillator Patch Electrodes on Left Ventricular Filling

Although implantation of defibrillator patch electrodes (DP) has been shown not to impair systolic function, their influence on diastolic function has not been elucidated. The aim of this study was to examine left ventricular filling sequentially in a group of patients before and after DP implantation. Doppler evaluation of mitral diastolic flow was used to assess left ventricular (LV) filling. Studies were performed preoperatively, after attaining hemodynamic stability postoperatively, and at subsequent follow-up (mean 9 weeks) in 13 patients. Patients undergoing cardiac surgery other than DP implantation and coronary artery bypass grafting were excluded, as were those with significant valvular heart disease. Immediately postoperatively, there was a reduction of deceleration time (0.26 ± 0.02 to 0.21 ± 0.01 sec, P < 0.05), consistent with mild impairment of LV filling, but the remaining parameters remained unchanged. At late follow-up, significant increases were recorded in time to peak filling (0.17 ± 0.01 to 0.25 ± 0.03 sec, P < 0.01), isovolumic relaxation time (0.07 ± 0.01 to 0.13 ± 0.02 sec, P < 0.005), while peak passive filling velocity decreased (1.02 ± 0.09 to 0.82 ± 0.07 m/sec, P < 0.05), all consistent with impairment of LV filling. We conclude that implantation of DP is associated with detectable impairment of LV filling at 2 months after surgery. (J Interven Cardiol 1989:2:3)     

Contribution of the Diastolic Vortex Ring to Left Ventricular Filling

Background

Intraventricular fluid dynamics can be assessed clinically using imaging. The contribution of vortex structures to left ventricular (LV) diastolic function has never been quantified in vivo.

Objectives

This study sought to understand the impact of intraventricular flow patterns on filling and to assess whether impaired fluid dynamics may be a source of diastolic dysfunction.

Methods

Two-dimensional flow velocity fields from color Doppler echocardiographic sequences were obtained in 20 patients with nonischemic dilated cardiomyopathy (NIDCM), 20 patients with hypertrophic cardiomyopathy (HCM), and 20 control healthy volunteers. Using a flow decomposition method, we isolated the rotational velocity generated by the vortex ring from the surrounding flow in the left ventricle.

Results

The vortex was responsible for entering 13 ± 6% of filling volume in the control group and 19 ± 8% in the NIDCM group (p = 0.004), but only 5 ± 5% in the HCM group (p < 0.0001 vs. controls). Favorable vortical effects on intraventricular pressure gradients were observed in the control and NIDCM groups but not in HCM patients. Differences in chamber sphericity explained variations in the vortex contribution to filling between groups (p < 0.005).

Conclusions

The diastolic vortex is responsible for entering a significant fraction of LV filling volume at no energetic or pressure cost. Thus, intraventricular fluid mechanics are an important determinant of global chamber LV operative stiffness. Reduced stiffness in NIDCM is partially related to enhanced vorticity. Conversely, impaired vortex generation is an unreported mechanism of diastolic dysfunction in HCM and probably other causes of concentric remodeling.     

凌晨血压增高与左心室肥厚

目的 探讨原发性高血压(EH)患者凌晨血压增高(MBPS)与左心室肥厚的关系.方法 对155例EH患者行心脏超声和动态血压测定.根据患者动态血压监测结果,EH患者155例有凌晨血压增高(MBPS组)30例与非凌晨血压增高(NMBPS组)125例,观察两组左心室质量指数(LVMI)的差别.结果 MBPS组LVMI大于NMBPS组,差异有统计学意义(P<0.05).结论 EH组人群存在早期左心室肥厚,凌晨血压增高促进高血压患者左室重构的发展.