Change In Diastolic Volume Research Articles

Assessment of Diastolic Function in Hypertrophic Cardiomyopathy by Computed Tomography-Derived Analysis of Left Ventricular Filling.

Hypertrophic cardiomyopathy (HCM) is characterized by diastolic dysfunction, which is difficult to assess by noninvasive methods. We hypothesized that measurement of simultaneous left ventricular (LV) and left atrial (LA) volume changes by cardiac computed tomography would be useful in the assessment of diastolic function in HCM. We studied 21 patients with HCM and 21 age-matched controls. The LA and LV volumes were calculated and early and late diastolic volume changes derived. The HCM patients had significantly larger LA volumes and reduced LA total emptying fraction (30 ± 7% vs 42 ± 6%; P < 0.0001). Conduit volume was increased (30 ± 6 vs 22 ± 4 mL/m; P < 0.0001) and contributed a significantly higher proportion of total LV diastolic filling, suggesting that passive filling of the LV compensates for LA dysfunction, but at the expense of increased pulmonary filling pressure. This study suggests that simultaneous depiction of computed tomography-derived LV and LA volume changes can characterize diastolic dysfunction in HCM.

CONTEMPORARY METHODS FOR MYOCARDIAL FUNCTION EVALUATION IN PATIENTS WITH HYPERTROPHIC CARDIOMYOPATHY BEFORE AND AFTER SURGICAL TREATMENT

Aim. To invent and qualify a diagnostic algorhythm for systolic and diastolic myocardium function evaluation in the left ventricle in patients with hypertrophic cardiomyopathy before and after surgical treatment. Material and methods. Totally 88 patients included, 54 with hypertrophic cardiomyopathy (27 male, 27 female) with median age 59±13 y.o. Obstructive type of HCMP was found in 41 pt. Transluminal ethanol-based septal ablation was done for 17 pts. Myoectomy/myotomy was done for 11 pts. The control consisted of 34 healthy volunteers with medial age 36,7±8,3 y.o.: 24 men (70%) and 10 women (30%). To everyone included the echocardiography was performed using the Vivid E9 machine (GE, USA) with multifrequent sensor 3,5-5,0 MHz. The data was then processed by computer-based Multivox program. The "flow-volume" loop of the single cardiac cycle was reconstructed using numeric data for everyone of patients; also the data on myocardium segment shift were used. Results. The parameters of volume change rapidity (dVol/dt (s, d)) and the parameters of systolic and diastolic summes of normal velocities (I Vr (s, d)) serve as strict independent predictors of the impaired systolic and diastolic function of LV myocardium and also as early markers of LV disordered function recovery in HCMP after surgical treatment. The markers of long axis diastolic shift (dL/dt (d)) and diastolic volume changes (dVol/dt (d)) are the most accurate in prediction of left ventricle changes after surgical treatment in HCMP Conclusion. We have invented a novel and original approach to the evaluation of systolic and diastolic myocardial function in patients with obstructive type hypertrophic cardiomyopathy before and after surgical treatment using our own algorhythm based on echocardiographical measurements of myocardium shift rapidity.

Cardiac Dysfunction in Pneumovirus-Induced Lung Injury in Mice

To determine biventricular cardiac function in pneumovirus-induced acute lung injury in spontaneously breathing mice. Experimental animal study. Animal laboratory. C57Bl/6 mice. Mice were inoculated with the rodent pneumovirus, pneumonia virus of mice. Pneumonia virus of mice-infected mice were studied for right and left ventricular function variables by high-field strength (7 Tesla) cardiac MRI at specific time points during the course of disease compared with baseline. One day before and at peak disease severity, pneumonia virus of mice-infected mice showed significant right and left ventricular systolic and diastolic volume changes, with a progressive decrease in stroke volume and ejection fraction. No evidence for viral myocarditis or viral presence in heart tissue was found. These findings show adverse pulmonary-cardiac interaction in pneumovirus-induced acute lung injury, unrelated to direct virus-mediated effects on the heart.

Intravenous contrast echocardiography after myocardial infarction: relationship among residual myocardial perfusion, contractile reserve and long-term remodelling

Previous studies have shown the potential role played by intracoronary myocardial contrast echocardiography (MCE) in predicting long-term remodelling and function after myocardial infarction (MI). Scanty data, however, are available on the role of intravenous MCE in this regard. The aim of this study was to assess the role of residual myocardial blood volume in the asynergic region in modulating ventricular volume changes over time post-MI. Thirty-two consecutive patients with anterior MI were studied predischarge using low-dose dobutamine echocardiography (Dob) and intravenous triggered MCE. Videointensity plots were generated from the apical approach and fitted exponentially. Volumes were assessed at baseline, during Dob and at 8 months. Baseline volumes, which appeared related to the extent of the asynergic region (P < 0.01) but showed no relation with videointensity in that area, did not change at follow-up, although Dob had elicited significant contractile reserve. However, videointensity in the asynergic region showed a significant interaction (P = 0.044) with the change in diastolic volume over time, with patients with the highest videointensity reverting remodelling (n = 11, from 69 +/- 16 to 65 +/- 16 ml/m) as compared with the remaining population (n = 21, from 68 +/- 16 to 73 +/- 21 ml/m). This was not seen when Dob-derived parameters were used. Multivariate analysis ranked videointensity second (P = 0.066), after baseline stroke volume (P = 0.005), in predicting changes in volumes over time. Unlike inotropic reserve, residual myocardial blood volume in the dysfunctioning muscle, as assessed by predischarge quantitative intravenous MCE, has the potential to modulate remodelling in patients who suffered an anterior MI.

New concepts in diastolic dysfunction and diastolic heart failure: Part II: causal mechanisms and treatment.

As described in Part I of this 2-part article,1 diastolic heart failure is common and causes significant alterations in prognosis. In Part II, experimental studies that have provided insight into the mechanisms that cause diastolic heart failure will be described.2–19⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓ In addition, current treatment strategies and the design of future clinical trials of diastolic heart failure will be discussed. The development of truly effective therapy for diastolic heart failure depends on gaining a clear understanding of the basic mechanisms that alter diastolic function and the ability to efficiently target these mechanisms to correct these abnormalities in diastolic function. Conceptually, the mechanisms that cause abnormalities in diastolic function that lead to the development of diastolic heart failure can be divided into factors intrinsic to the myocardium itself (myocardial) and factors that are extrinsic to the myocardium (extramyocardial; Table 1). Myocardial factors can be divided into structures and processes within the cardiac muscle cell (cardiomyocyte), within the extracellular matrix (ECM) that surrounds the cardiac muscle cell, and that activate the autocrine or paracrine production of neurohormones. Each of these mechanisms are active in the major pathological processes that result in diastolic dysfunction and heart failure. Myocardial and extramyocardial mechanisms, cellular and extracellular mechanisms, and neurohumoral activation each play a role in the development of diastolic heart failure caused by ischemia, pressure-overload hypertrophy, and restrictive and hypertrophic cardiomyopathy. View this table: Table 1105290. Diastolic Heart Failure: Mechanisms ### Cardiomyocyte Diastolic dysfunction can be caused by mechanisms that are intrinsic to the cardiac muscle cells themselves. These include changes in calcium homeostasis caused by (1) abnormalities in the sarcolemmal channels responsible for short- and long-term extrusion of calcium from the cytosol, such as the sodium calcium exchanger and the calcium pump; (2) …

Left ventricular diastolic suction with zero left atrial pressure in open-chest dogs.

We investigated left ventricular (LV) diastolic volume changes (suction inflows) with left atrial pressure (LAP) clamped to ambient pressure in six open-chest, anesthetized dogs. The left atrium was cannulated and connected to a servo pump, and LAP was clamped to a set point near 0 mmHg for four beats by withdrawing blood. LAP averaged 5.88 +/- 1.44 mmHg before the clamp and fell to 0.74 +/- 0.61 mmHg (P < 0.0001) after the clamp. During the first clamped beat a transmitral pressure gradient of 1.0 +/- 0.6 mmHg was observed, resulting in LV filling of 2.6 +/- 1.8 ml. Subsequent beats developed suction-driven (mean negative LV pressure: -1.5 +/- 1.3 mmHg; P < 0.005 vs. zero) LV filling of 4.5 +/- 2.8 ml/beat with a peak transmitral pressure gradient of 1.7 +/- 0.6 mmHg. These data are consistent with the hypothesis that LV suction can be an important filling mechanism under condition in which LV end-systolic volume is reduced, e.g., reduced filling pressures, high heart rates, exercise, or increased inotropic drive.

Sequential echocardiographic-Doppler assessment of left ventricular remodelling and mitral regurgitation during evolving experimental heart failure

The aim was to study the nature, magnitude, and time course of left ventricular structural adaptations to evolving heart failure. 17 male mongrel dogs, weight 24.9(SD 3.7) kg, underwent rapid ventricular pacing (250 beats.min-1) until severe heart failure developed. Two dimensional echocardiographic and Doppler studies were performed at control, then weekly to severe heart failure. Haemodynamic measurements were made at control and severe heart failure. All studies were performed with the animals conscious during temporary sinus rhythm. Left ventricular diastolic volume gradually increased and the left ventricle assumed a more globular shape associated with significant wall thinning. Both the change in diastolic volume after one week of pacing and at the time of severe heart failure correlated with the time to peak heart failure. Mitral regurgitation was mild after one week of pacing, became moderate in most animals at severe heart failure, and lagged temporarily behind the increase in cardiac dimensions. The percentage increase in mitral annular size was significantly less than the increase in left ventricular cross sectional area. In pacing induced heart failure (1) marked left ventricular remodelling occurs, (2) the extent of left ventricular dilatation, both early and late, correlates directly with the time required for the development of severe heart failure, (3) mitral regurgitation is an epiphenomenon and is most likely to be caused by the increase in left ventricular cross sectional area.

Clinical and hemodynamic significance of left ventricular diastolic volume changes by exercise radionuclide ventriculography in coronary artery disease

Recent studies have suggested that left ventricular (LV) dilatation during exercise radionuclide ventriculography may identify coronary artery disease (CAD). Coronary anatomy and LV end-diastolic pressure at catheterization were compared with results of supine exercise radionuclide ventriculography in 66 patients evaluated for chest pain. Forty-six patients had significant CAD (>75% diameter stenosis) and 20 patients were normal. Radionuclide ventriculography was performed within 18 hours of catheterization, at rest and at peak exercise. Relative LV end-diastolic volumes were extrapolated from end-diastolic counts. LV end-diastolic counts increased during exercise in 19 of 20 normal subjects. In patients with CAD, LV end-diastolic counts increased in 35 (group A) and decreased in 11 (group B). The percent change in LV end-diastolic counts from rest to exercise, rest ejection fraction, exercise ejection fraction and rest LV end-diastolic pressure for each group were 20 ± 23%, 60 ± 13%, 67 ± 13% and 8 ± 3 mm Hg in normal subjects; 20 ± 20%, 50 ± 12%, 47 ± 13% and 12 ± 4 mm Hg in group A; and −9 ± 8%, 54 ± 21%, 49 ± 18% and 21 ± 7 mm Hg in group B (mean ± standard deviation). An increase in LV end-diastolic counts was unrelated to ejection fraction response or presence of underlying CAD but only correlated to rest LV end-diastolic pressure (p < 0.01). Both normal subjects and group A patients with CAD increased LV end-diastolic counts in the setting of a normal LV end-diastolic pressure, whereas group B patients with CAD and high LV end-diastolic pressure decreased LV end-diastolic counts. Thus, supine exercise-induced left ventricular dilatation is the expected response in normal subjects and patients with CAD and normal filling pressure.

End-systolic pressure-volume relations of isolated ejecting rabbit left ventricles after quick diastolic volume changes.

The aim of the study was to investigate the influence of quick diastolic volume changes on systolic performance of ejecting left ventricles. To measure left ventricular systolic performance the maximum ratio of ventricular pressure (P) and volume (V) was calculated on beat-to-beat basis when the diastolic loading conditions were varied in different ways. These end-systolic P-V (P-VES) points were obtained from both isovolumic and ejecting contractions. A deviation from the P-VES relation is thought to result from factors changing the inotropic condition of the heart. When steady state isovolumic and ejecting P-VES data were collected linear P-VES relations were found. The relations coincided when stroke volumes were not too large. When the diastolic volume was quickly changed (ie 10 to 20 ms) late in diastole, the P-VES points of the resulting contractions showed a significant deviation from the steady state relation (p less than 0.001). This deviation was dependent on the magnitude of the volume step. After quick volume infusions the heart ejected to end-systolic volume (ESV) values that were smaller than expected from the steady state P-VES relation and the end-systolic pressure (ESP) was larger. After quick volume withdrawals ESV values were larger and ESP was smaller than expected. The magnitude of the effect was not dependent on the preset basic diastolic volume if the volume changes were considered as fractions end-diastolic volumes (EDV). It is concluded that when diastolic volumes are varied just before stimulation, a significant deviation of the P-VES point from the steady state P-VES relation is found in the following contraction. This phenomenon suggests an alteration in the inotropic state of the heart.

Influence of the velocity of changes in end-diastolic volume on the starling mechanism of isolated left ventricles.

1. In this study the relationships between active developed systolic pressure, end-diastolic pressure and different diastolic volumes are studied in Tyrode perfused isolated rabbit left ventricles. Contractions were isovolumic. 2. Rapid diastolic volume changes were imposed on top of different preset basic diastolic volumes. These volume changes are shown to produce systolic and diastolic pressure values that cannot be explained by assuming a single pressure-volume relation during systole and diastole. The changes in pressure are in the same direction but higher than is expected on the basis of the increase or decrease of the ventricular end-diastolic volume alone. 3. The variation of the diastolic pressure-volume relation cannot be explained by assuming variations of the heart's passive elasticity or viscous effects within its wall. During diastole the effect is completely reversible without concomitant systolic effects. No velocity dependent effect of the quick volume change could be observed if the time duration was varied between 10 and 65 ms. The results are in keeping with the hypothesis that active force generating mechanisms may be present during the diastolic pause. 4. The effects observed during systole suggest the possibility of length dependent activation of the myocardial cells. This results in different inotropic conditions of the heart at identical volumes, depending on how these volumes were installed. These volumes may be considered to affect intrinsic properties of the muscle cells on a beat to beat basis.

Diastolic compliance and exercise-induced left ventricular diastolic volume changes by nuclear ventriculogram in patients with coronary disease

Diastolic compliance and exercise-induced left ventricular diastolic volume changes by nuclear ventriculogram in patients with coronary disease

Quantitative radionuclide angiography in assessment of hemodynamic changes during upright exercise: Observations in normal subjects, patients with coronary artery disease and patients with aortic regurgitation

Quantitative radionuclide angiography (with the first pass technique and a computerized multicrystal camera) was used to evaluate hemodynamic changes in three subject groups during symptom-limited upright exercise. The 12 normal subjects had significant increases in heart rate, stroke volume, left ventricular ejection fraction and cardiac output during exercise; changes in end-diastolic and end-systolic volumes were not significant. In the 24 patients with coronary artery disease there were significant increases in heart rate and cardiac output during exercise, but insignificant changes in end-diastolic, end-systolic and stroke volumes and ejection fraction. The change in diastolic volume in these patients was determined by the extent of coronary artery disease, propranolol therapy, end point of exercise and presence of collateral vessels. Furthermore, patients with previous myocardial infarction had a lower ejection fraction and higher end-diastolic and end-systolic volumes during exercise than those without myocardial infarction. In the 12 patients with chronic aortic regurgitation of moderate to severe degree, there was a decrease in the end-diastolic volume during exercise. This response was distinctiy different from that of the normal subjects or the patients with coronary artery disease. All three groups had a significant decrease in pulmonary transit time during exercise. It is concluded that changes in cardiac output in normal subjects during upright exercise are related to augmentation of stroke volume and tachycardia, whereas in patients with coronary artery disease they are related mainly to tachycardia. Left ventricular dilatation during exercise occurred in some normal subjects and in patients with coronary artery disease but was not a consistent finding. However, a decrease in left ventricular end-diastolic volume is common in patients with aortic regurgitation. Such a decrease may be explained by a reduction in the regurgitant volume per beat caused by shortening of the diastolic filling period or a decrease in systemic vascular resistance, or both.