Ventricular Ejection Performance Research Articles

Associations of increased arterial stiffness with left ventricular ejection performance and right ventricular systolic pressure in mitral regurgitation before and after surgery: Wave intensity analysis

BackgroundThe effect of increased arterial stiffness on mitral regurgitation (MR) is not clear. Using wave intensity (WI) analysis, which is useful for analyzing ventriculo-arterial interaction, we aimed to elucidate associations of increased arterial stiffness with left ventricular (LV) ejection performance and right ventricular systolic pressure (RVSP) in MR. Methods and ResultsWe noninvasively measured carotid arterial WI and stiffness parameter (β) in 98 patients with non-ischemic chronic MR before and after surgery, and 98 age-and-gender matched healthy subjects by ultrasonography. WI is defined as WI=(dP/dt)(dU/dt) [P: blood pressure, U: velocity, t: time]. The peak value of WI (W1) increases with LV peak dP/dt. The temporal WI index (Q-W1)st, which is the standardized interval between the Q wave of the ECG and W1, is a surrogate for preejection period. Ejection fraction (EF), left atrial volume index (LAVI), effective regurgitant orifice area (ERO), RVSP, and other echocardiographic data were also obtained. W1 was enhanced in the MR group before surgery compared with the normal group (10.7±5.7 vs 8.5±3.6×103 mmHg m/s3, p<0.05). However, the results of two-way ANOVA showed this enhancement of W1 was observed only in the subgroup of MR before surgery with lower arterial stiffness (β<13, p<0.0001). ERO, β and LAVI were predictor variables before surgery to determine RVSP. EF and (Q-W1)st before surgery were predictor variables for EF after surgery. ConclusionsIn the MR group before surgery, increased arterial stiffness suppresses compensatory enhancement of W1, and increases RVSP. Prolonged (Q-W1)st has the potential for predicting low EF after surgery.

Influence of antenatal physical exercise on haemodynamics in pregnant women: a flexible randomisation approach.

BackgroundNormal pregnancy is associated with marked changes in haemodynamic function, however the influence and potential benefits of antenatal physical exercise at different stages of pregnancy and postpartum remain unclear. The aim of this study was therefore to characterise the influence of regular physical exercise on haemodynamic variables at different stages of pregnancy and also in the postpartum period.MethodsFifity healthy pregnant women were recruited and randomly assigned (2 × 2 × 2 design) to a land or water-based exercise group or a control group. Exercising groups attended weekly classes from the 20th week of pregnancy onwards. Haemodynamic assessments (heart rate, cardiac output, stroke volume, total peripheral resistance, systolic and diastolic blood pressure and end diastolic index) were performed using the Task Force haemodynamic monitor at 12–16, 26–28, 34–36 and 12 weeks following birth, during a protocol including postural manoeurvres (supine and standing) and light exercise.ResultsIn response to an acute bout of exercise in the postpartum period, stroke volume and end diastolic index were greater in the exercise group than the non-exercising control group (p = 0.041 and p = 0.028 respectively). Total peripheral resistance and diastolic blood pressure were also lower (p = 0.015 and p = 0.007, respectively) in the exercise group. Diastolic blood pressure was lower in the exercise group during the second trimester (p = 0.030).ConclusionsAntenatal exercise does not appear to substantially alter maternal physiology with advancing gestation, speculating that the already vast changes in maternal physiology mask the influences of antenatal exercise, however it does appear to result in an improvement in a woman’s haemodynamic function (enhanced ventricular ejection performance and reduced blood pressure) following the end of pregnancy.Trial registrationClinicalTrials.gov NCT02503995. Registered 20 July 2015.

Interdependence of Parkin-Mediated Mitophagy and Mitochondrial Fission in Adult Mouse Hearts.

The role of Parkin in hearts is unclear. Germ-line Parkin knockout mice have normal hearts, but Parkin is protective in cardiac ischemia. Parkin-mediated mitophagy is reportedly either irrelevant, or a major factor, in the lethal cardiomyopathy evoked by cardiac myocyte-specific interruption of dynamin-related protein 1 (Drp1)-mediated mitochondrial fission. To understand the role of Parkin-mediated mitophagy in normal and mitochondrial fission-defective adult mouse hearts. Parkin mRNA and protein were present at low levels in normal mouse hearts, but were upregulated after cardiac myocyte-directed Drp1 gene deletion in adult mice. Alone, forced cardiac myocyte Parkin overexpression activated mitophagy without adverse effects. Likewise, cardiac myocyte-specific Parkin deletion evoked no adult cardiac phenotype, revealing no essential function for, and tolerance of, Parkin-mediated mitophagy in normal hearts. Concomitant conditional Parkin deletion with Drp1 ablation in adult mouse hearts prevented Parkin upregulation in mitochondria of fission-defective hearts, also increasing 6-week survival, improving ventricular ejection performance, mitigating adverse cardiac remodeling, and decreasing cardiac myocyte necrosis and replacement fibrosis. Underlying the Parkin knockout rescue was suppression of Drp1-induced hyper-mitophagy, assessed as ubiquitination of mitochondrial proteins and mitochondrial association of autophagosomal p62/sequestosome 1 (SQSTM1) and processed microtubule-associated protein 1 light chain 3 (LC3-II). Consequently, mitochondrial content of Drp1-deficient hearts was preserved. Parkin deletion did not alter characteristic mitochondrial enlargement of Drp1-deficient cardiac myocytes. Parkin is rare in normal hearts and dispensable for constitutive mitophagic quality control. Ablating Drp1 in adult mouse cardiac myocytes not only interrupts mitochondrial fission, but also markedly upregulates Parkin, thus provoking mitophagic mitochondrial depletion that contributes to the lethal cardiomyopathy.

Containing Hypertrophy With a PICOT Fence

See related article, pages 307–314 Cardiac hypertrophy is the common myocardial response to chronic hemodynamic overload. It currently affects nearly 5 million Americans and is responsible for &50 000 deaths annually. From the perspective of cardiac mechanics, it seems surprising that cardiac hypertrophy is a killer. The physics of reactive hypertrophy date to the 19th century1 and predict that hypertrophy will compensate for increased hemodynamic loading through normalization of ventricular wall stress, the phylogenetically conserved set point for cardiac load.2 The Laplace relationship (stress=½ pr/h), describes wall stress increasing in direct proportion with intraluminal pressure (p) and chamber radius (r), but decreasing as wall thickness (h) grows. Accordingly, whether the ventricle dilates or is subjected to increased pressure, hypertrophic thickening of its walls should compensate.3 And it does. However, long-term functional compensation relies on the quality of hypertrophied myocardium being invariant as quantity increases, which is not the case. Multiple studies have defined molecular, cellular, and functional characteristics of reactive hypertrophy that differentiate it from normal myocardium and from cardiac enlargement caused by physiological conditioning.4–6 Such findings gave rise to the notions of pathological and physiological hypertrophies7 and provide a mechanistic framework for why reactive hypertrophy ultimately fails,8 whereas physiological conditioning of the heart does not. Cardiac hypertrophy also has effects unrelated to contractility and ventricular ejection performance. To quote Joseph Stalin out of context, “Quantity has a quality all its own”, meaning that a steady quantitative change can create a sudden qualitative shift. The heart aptly demonstrates this principle because reactive hypertrophy and wall thickening increase ventricular stiffness, which leads to diastolic dysfunction and heart failure with preserved ejection fraction.9 Moreover, a number of studies have suggested that cardiac hypertrophy is not essential to …

Synergistic Effects of Atorvastatin and Sildenafil in Cardioprotection—Role of NO

HMG-CoA (3-hydroxy-3-methylflutaryl coenzyme A) reductase inhibitors, or statins, were originally designed to reduce serum cholesterol levels and the development of cardiovascular disease. Statins prevent the formation of cholesterol as well as other products in the biosynthetic pathway, which include isoprenoid intermediates such as farnesyl pyrophosphate and geranylgeranyl pyrophosphate [1]. Over the years, it has become clear that use of statins extend well beyond their lipid lowering actions, and the unexpected pleiotropic effects have a major role in protecting the myocardium against ischemic injury. A number of studies have shown that statins improve cardiac function, reduce infarct size and infiltration of polymorphonuclear neutrophils following ischemia/reperfusion injury [2,3]. The myocardial protective effect of statins is mediated by increasing eNOS protein expression due to stabilizing eNOS mRNA [4,5]. However, others suggested that statins may increase the activity of eNOS not by altering its absolute concentration, but by increasing eNOS phosphorylation at serine-1177 through the phosphatidyl-inositol-3-kinase and protein kinase Akt signaling cascade [6]. Atorvastatin added at the onset of reperfusion, increased eNOS phosphorylation at serine-1177 in isolated mice hearts subjected to ischemia [7]. Furthermore, these protective effects of statins are dependent on eNOS because mice deficient in eNOS were completely resistant to the cardioprotective actions of statin treatment [3]. We recently showed that atorvastatin induced both acute and delayed myocardial preconditioning effect in-vivo resulting in marked reduction in infarct size. The preconditioning in the delayed phase was mediated by iNOS and involves opening of mitochondrial KATP channels [8]. Because delayed preconditioning can be maintained by intermittent stimuli, our results suggest that atorvastatin may be able to produce a chronically preconditioned state which might render the myocardium more resistant to prolonged episodes of ischemia. Recent work suggests that statins activate protein kinase G (PKG) to elicit further activations of MAPK pathways, induce hemeoxygenase-1 gene expression, which provides a novel anti-inflammatory mechanism in the therapeutic validity [9]. Statins have also been shown to attenuate the myocardial dysfunction associated with heart failure and significant increases in the survival rate following the induction of myocardial infarction [10,11]. Furthermore, statins reduced cardiac myocyte hypertrophy, interstitial fibrosis, as well as preserved left ventricular ejection performance [10‐12]. Interestingly, the ability of statins to exert its beneficial effects in models of heart failure also appears to be eNOS dependent [11]. Clinical studies suggest that statins reduce mortality in patients with severe heart failure [13]. The statin treated patients experienced a reduction in mortality that was demonstrated as early as 30 days post intervention and statins remained a predictor for survival at six months [14].

Pathophysiology of valvular heart disease: Implications for nuclear imaging

In general, the echocardiogram has become the mainstay of diagnosis in patients with valvular heart disease. Its strength is that it provides information about valve pathoanatomy and about the severity of stenosis and regurgitation not available by other techniques. However, radionuclide studies offer a more precise gauge of left and right ventricular ejection performance, which is useful in the timing of surgery. Because, at present, most cardiac catheterization procedures in patients with valve disease are performed to evaluate coronary anatomy, a noninvasive technique for detecting coronary disease could obviate the need for invasive studies prior to surgery. The presence of left ventricular hypertrophy especially in aortic stenosis has made myocardial imaging less than perfect in this preoperative evaluation, but clearly this is an area of potential fruitfulness in the use of radionuclide techniques. Additional studies regarding the utility of exercise RNA seem warranted and might be of particular interest in mitral regurgitation, in which little is known about the ability of such studies to help time mitral valve surgery. The addition of estimates of loading during exercise studies is an attractive pathophysiologic adjunct and should be helpful in the interpretation of such studies. The potential role for targeted “hot spot” imaging of ischemia, apoptosis, and necrosis in patients with valvular heart disease remains undefined, although such imaging represents another potential area of investigation that warrants further evaluation.

Improvement of Left Ventricular Ejection Performance After Partial Left Ventriculectomy: A Consequence of Changed Left Ventricular Geometry?

Improvement of Left Ventricular Ejection Performance After Partial Left Ventriculectomy: A Consequence of Changed Left Ventricular Geometry?

Improvement of left ventricular ejection performance after partial left ventriculectomy: a consequence of changed left ventricular geometry?

Improvement of left ventricular ejection performance after partial left ventriculectomy: a consequence of changed left ventricular geometry?

Effects of Atrial Fibrillation on Left Ventricular Function and Geometry in Mitral Stenosis

This study shows that patients with mitral stenosis have depressed left ventricular ejection performance and spherical remodeling of the left ventricular cavity, which is more marked in those with atrial fibrillation. These changes have important clinical implications regarding treatment strategy in patients with mitral stenosis and chronic atrial fibrillation.

Left Ventricular Ejection Performance Before and Following Percutaneous Mitral Valvuloplasty in Mitral Stenosis

Background:In cases of pure mitral stenosis, it is known that the impairment of left ventricular (LV ejection performance is frequently accompanied, but long term follow up studies on the LV ejection performance after successful percutaneous mitral valvuloplasty are rare so far. Methods:An prospective investigation was performed on 32 cases of patients, 10 being male and 22 female, who have been maintained after successful percutaneous mitral valvuloplasty of pure mitral stenosis. The LV ejection performances have been measured with cardiomechanography and echocardiography before and following the procedure, and the follow-up periods were 24 months in average, in the range of 12 to 35 months. Results:The stroke volume, cardiac output, cardiac index, ejection fraction, mean velocity of circumferential shortening and fractional shortening(FS, which are indices of LV ejection performance, all increased in follow-up than before procedure. In addition, LV end-diastolic dimension and LV end-diastolic dimension index, which are indices of LV preload, increased, and the end-systolic LV wall stress which is an index of afterload, decreased. And the ratio of measured FS to expected FS, which is an index of myocardial contractility, increased in follow-up. Conclusion:The successful percutaneous mitral valvuloplasty of pure mitral stenosis is found to improve LV ejection performance in long term by increasing preload, decreasing afterload, and incr- easing myocardial contractility of left ventricle.

Changes of left ventricular function after percutaneous balloon mitral valvuloplasty in mitral stenosis with impaired left ventricular performance

The pathophysiological role of mechanical and myocardial factors for impairment of left ventricular performance in mitral stenosis is still not clear. To investigate this controversy, 27 patients of mitral stenosis with left ventricular ejection fraction <50% were studied. Patients were divided into two groups: Group 1: 20 patients, left ventricular ejection fraction improved to >50% after valvuloplasty, and Group 2: 7 patients, left ventricular ejection fraction still <50% after valvuloplasty. The clinical and hemodynamic characteristics were comparable for the two groups before valvuloplasty. Follow-up catheterization done one week later showed similar changes in mitral valve area, cardiac index, pulmonary pressure, left ventricular end-diastolic volume index and systemic vascular resistance between the two groups. However, left ventricular end-systolic volume was significantly decreased after valvuloplasty in Group 1 but not in Group 2, resulting in significantly higher ejection fraction in Group 1 than in Group 2. Postoperatively, regional wall motion scores were lower in Group 1 than in Group 2 (2.0 ± 0.6 vs. 2.7 ± 0.5 at the anterolateral wall, P = 0.002; 1.9 ± 0.6 vs. 2.9 ± 0.4 at the posterobasal wall, P = 0.0003). Most of our mitral stenosis patients with impaired left ventricular ejection fraction showed improvement after mitral valvuloplasty had released the mechanical obstruction. However, in some patients, impaired ejection fraction persisted after valvuloplasty, suggesting the mechanism of myocardial failure. Thus, both myocardial and mechanical factors play important roles in the pathogenesis of left ventricular ejection performance impairment.

Effects of exercise on left ventricular performance determined by echocardiography in chronic, severe mitral regurgitation secondary to mitral valve prolapse

Data on the effects of exercise on left ventricular (LV) volumes and ejection performance in patients with severe mitral regurgitation (MR) are limited. With use of a matched-pairs design, 10 asymptomatic patients with chronic, severe MR and normal LV systolic function who were not receiving vasodilator therapy (group 1) and 10 matched normal control subjects with no structural heart disease (group 2) performed symptom-limited upright bicycle ergometry with quantitative echocardiographic analysis. An additional 8 patients with severe, chronic MR and normal LV systolic function who were receiving vasodilator therapy at the time of testing (group 3) were studied for comparison. The 3 cohorts exercised for similar periods of time. Group 1 and 3 patients had similar end-diastolic volumes at rest, both of which were significantly greater than those of normal controls. Although resting LV end-systolic volume was greater in groups 1 and 3 than in normal controls, the 3 groups had similar relative percent reductions in end-systolic volume during exercise (30 ± 12%, 32 ± 13%, and 30 ± 24%; p = NS). A similar percent increase in LV ejection fraction was also observed in all 3 cohorts (18 ± 9%, 15 ± 9%, and 14 ± 6%; p = NS). Forward stroke volume increased significantly in group 1 (59 ±21 and 71 ± 18 ml; p < 0.001) and in group 3 (59 ± 17 and 68 ± 13 ml; p < 0.05). Thus, in asymptomatic patients with chronic, severe MR and normal LV ejection fraction at rest, there is an improvement in LV ejection fraction and an increase in forward stroke volume during exercise. These effects are comparable to those observed in normal controls. Directional differences in the cohort receiving no active therapy were indistinguishable from either patients receiving vasodilator therapy or normal control subjects.

Changes of left ventricular function after percutaneous balloon mitral valvuloplasty in mitral stenosis with impaired left ventricular performance

<h2>Abstract</h2> The pathophysiological role of mechanical and myocardial factors for impairment of left ventricular performance in mitral stenosis is still not clear. To investigate this controversy, 27 patients of mitral stenosis with left ventricular ejection fraction <50% were studied. Patients were divided into two groups: Group 1: 20 patients, left ventricular ejection fraction improved to >50% after valvuloplasty, and Group 2: 7 patients, left ventricular ejection fraction still <50% after valvuloplasty. The clinical and hemodynamic characteristics were comparable for the two groups before valvuloplasty. Follow-up catheterization done one week later showed similar changes in mitral valve area, cardiac index, pulmonary pressure, left ventricular end-diastolic volume index and systemic vascular resistance between the two groups. However, left ventricular end-systolic volume was significantly decreased after valvuloplasty in Group 1 but not in Group 2, resulting in significantly higher ejection fraction in Group 1 than in Group 2. Postoperatively, regional wall motion scores were lower in Group 1 than in Group 2 (2.0 ± 0.6 vs. 2.7 ± 0.5 at the anterolateral wall, <i>P</i> = 0.002; 1.9 ± 0.6 vs. 2.9 ± 0.4 at the posterobasal wall, <i>P</i> = 0.0003). Most of our mitral stenosis patients with impaired left ventricular ejection fraction showed improvement after mitral valvuloplasty had released the mechanical obstruction. However, in some patients, impaired ejection fraction persisted after valvuloplasty, suggesting the mechanism of myocardial failure. Thus, both myocardial and mechanical factors play important roles in the pathogenesis of left ventricular ejection performance impairment.

952-30 Left Ventricular Ejection Performance Improves Late After Aortic Valve Replacement in Patients with Aortic Stenosis and Reduced Ejection Fraction

To assess the time course and magnitude of change in left ventricular (LV) wall stress and ejection performance indices, 24 patients undergoing aortic valve replacement (AVR) for aortic stenosis were prospectively evaluated. Each patient underwent resting radionuclide angiography (RNA), echocardiography, and cardiac catheterization (high fidelity pressure) before AVR, then RNA and echocardiogram at one week and six months after AVR. Patients were stratified by preoperative ejection fraction (EF) into reduced EF (&lt;50%) and normal EF (≥50%) groups. Pre-operatively, peak positive dp/dt was lower in the reduced EF group (1300 vs 1700 mmHg/sec, p = 0.035), and wall stress was elevated similarly in both groups (p = NS). Temporal Relationships of EF and Wall Stress Pre-op 1 Week 6 Mos Normal EF (n = 14) Mean Ejection Fraction (%) 66 64 68 Mean Wall Stress (dyne/cm 2 × 10 3 ) 62 34 44 Reduced EF (n = 10) Mean Ejection Fraction (%) 38 37 57 Mean Wall Stress (dyne/cm 2 × 10 3 ) 78 52 61 Wall stress was reduced at one week post-operatively (p &lt; 0.005) in both groups. Ejection fraction remained depressed in the reduced EF group. By six months, however, EF had dramatically improved in the reduced EF group (p = 0.002). In patients with LV dysfunction, EF remains low one week after AVR despite rectification of afterload mismatch. At six months, however, ejection performance improves. Therefore, when measured by ejection phase indices, the surgical benefit from AVR is not evident until late post-operatively.

Regional heterogeneity of function in hypertrophic cardiomyopathy.

In patients with hypertrophic cardiomyopathy (HCM), left ventricular ejection performance may be normal while segmental myocardial function is distinctly abnormal. The advent of magnetic resonance tissue tagging has allowed the noninvasive evaluation of intramyocardial segmental shortening in vivo in a topographic and temporal manner. Ten patients with HCM documented by echocardiography and 10 healthy volunteers were studied with magnetic resonance tissue tagging by spatial modulation of magnetization. Percent circumferential myocardial shortening (%S) was compared at endocardium, midwall, and epicardial levels at four regions around the left ventricular short axis and from four short axis slices from apex to base at four or five time intervals during systole. In 8 patients and 8 control subjects, longitudinal shortening was evaluated within the septum and the lateral free wall at three levels from apex to base. Circumferential %S was less in HCM patients than in control subjects in the septal (13 +/- 5% versus 24 +/- 6%, P = .0002), inferior (13 +/- 5% versus 21 +/- 4%, P = .001), and anterior (17 +/- 5% versus 21 +/- 3%, P < .03) regions but not in the lateral region. Circumferential end-systolic %S was reduced in patients with HCM compared with control subjects at all levels from apex to base. The normal transmural gradient in circumferential end-systolic shortening was preserved with greatest %S at the endocardium. Most of the total cumulative circumferential shortening occurred earlier in systole in patients compared with control subjects, especially within the septum. Longitudinal end-systolic %S was depressed throughout the septum in patients compared with control subjects, most markedly at the base, but was normal in the lateral free wall. Circumferential myocardial segment shortening is depressed in HCM in the septum, inferior, and anterior regions and at all levels from apex to base, and much of the total cumulative shortening occurs early in systole. Longitudinal shortening is reduced in the basal septum in HCM. The heterogeneity of regional function in these patients may reflect the regional variation in the myocardial disarray and fibrosis that is characteristic of this disorder.

Ejection characteristics in primary pulmonary hypertension

Primary pulmonary hypertension (PPH) is a progressive vasculopathy of the pulmonary circulation which results in marked elevations of pulmonary artery (PA) pressure and pulmonary vascular resistance. 1–3 Cardiac output, initially preserved at rest, does not increase appropriately with exercise. 2,4,5 This combination of features explains the clinical symptoms of fatigue and dyspnea frequently present in these patients. Although considerable data exist characterizing central hemodynamics in patients with PPH, most of these studies have focused on nonpulsatile measures. Characterization of the phasic, or dynamic, nature of ejection not only provides detailed measures of instantaneous ejection performance but also can provide important insight into pathogenetic mechanisms. 6 Alterations in external vascular load will predictably affect ventricular ejection performance. The present study compares and contrasts right-sided dynamic ejection behavior at rest and during exercise in patients with PPH with an age-matched control population. Our intent was to demonstrate that phasic hemodynamics in the pulmonary circulation reflect the magnitude and nature of the PA vascular hydraulic load.

Mitral valve replacement with and without chordal preservation in patients with chronic mitral regurgitation. Mechanisms for differences in postoperative ejection performance.

Standard mitral valve replacement (MVR) in patients with chronic mitral regurgitation consistently results in a decrease in postoperative left ventricular (LV) ejection performance. This fall in ejection performance has been attributed, at least in part, to unfavorable loading conditions imposed by the elimination of the low-impedance pathway for LV emptying into the left atrium. In contrast to standard MVR in which the chordae tendineae are severed, however, MVR with chordal preservation (MVR-CP) does not usually decrease LV ejection performance despite similar removal of the low-impedance pathway. The purpose of the present study was to define the mechanisms responsible for this discordance in postoperative ejection performance between MVR with and without chordal preservation. Echocardiography and sphygmomanometer blood pressures were obtained in 15 patients with pure chronic mitral regurgitation before and 7-10 days after mitral valve surgery. These measurements were used to calculate ventricular volume, wall stress, and ejection fraction. Seven patients underwent MVR with chordal transection (MVR-CT), and eight patients underwent MVR-CP. MVR-CT resulted in no postoperative change in LV end-diastolic volume, a significant increase in LV end-systolic volume, a significant increase in end-systolic stress, from 89 +/- 9 to 111 +/- 12 g/cm2 (p < 0.05), and a significant decrease in ejection fraction, from 0.60 +/- 0.02 to 36 +/- 0.02 (p < 0.05). In contrast, patients who underwent MVR-CP had a significant decrease in LV end-diastolic and end-systolic volumes. End-systolic wall stress actually fell from 95 +/- 6 to 66 +/- 6 g/cm2 (p < 0.05), and ejection fraction was unchanged (0.63 +/- 0.01 before and 0.61 +/- 0.02 after mitral valve surgery) instead of reduced. MVR-CT resulted in a decrease in ejection performance caused in part by an increase in end-systolic stress, which in turn increased end-systolic volume. Conversely, MVR-CP resulted in a smaller LV size, allowing a reduced end-systolic stress and preservation of ejection performance despite closure of the low-impedance left atrial ejection pathway.

Hemodynamic and volume correlates of left ventricular diastolic relaxation and filling in patients with aortic stenosis

Objective. The aim of the present study was to evaluate the hemodynamic and volume correlates of early diastolic filling and isovolumetric relaxation in patients with aortic stenosis.Background. Left ventricular diastolic relaxation and filling have been found to be heterogeneous in patients with aortic stenosis. Potential mechanisms underlying this heterogeneity include individual differences in the severity of muscle hypertrophy or systolic dysfunction, or both, in the presence and severity of mitral regurgitation and in the level of left atrial pressure.Methods. Right (fluid-filled) and left (high fidelity micromanometer) ventricular pressures, left ventricular volumes (contrast angiography) and transmitral inflow dynamics (Doppler echocardiography) were measured in 17 patients with isolated severe aortic stenosis (valve area < 0.75 cm2). Measurements included left ventricular end-diastolic and end-systolic volumes, left ventricular ejection fraction, peak positive and negative first derivative of left ventricular pressure (dP/dt), the time constant of isovolumetric relaxation (tau), left ventricular end-diastolic pressure, left ventricular mass, left ventricular end-systolic stress, mean capillary wedge pressure and peak early (E) and late (A) transmitral filling velocities. Patients were subclassified according to left ventricular ejection performance at rest and mean capillary wedge pressure.Results. Patients with normal ejection performance and normal mean capillary wedge pressure had a normal rate of isovolumetric left ventricular pressure decay and an abnormal diastolic filling pattern, with diastolic filling occurring primarily during atrial systole. In contrast, in patients with systolic dysfunction and elevated mean capillary wedge pressure, isovolumetric pressure decay was prolonged and diastolic filling occurred essentially during the rapid filling period, with reduced atrial contribution to left ventricular filling and a short isovolumetric relaxation period. Stepwise multiple linear regression analysis identified two variables as independent predictors of transmitral velocity profile and three variables independently predictive of the rate of left ventricular pressure decay. The single most important predictor of transmitral filling pattern was the pulmonary capillary wedge pressure (p < 0.0001), followed by the left ventricular peak negative dP/dt (p = 0.002). The single most powerful predictor of the rate of reduction in left ventricular pressure was left ventricular mass index (p < 0.0001), followed by end-systolic volume index (p = 0.0002) and left ventricular peak negative dP/dt (p= 0.0029).Conclusions. In patients with aortic stenosis, left ventricular filling is essentially determined by left atrial pressure, whereas isovolumetric relaxation more closely depends on the severity of muscle hypertrophy and chamber dilation.

Left ventricular ejection performance in mitral stenosis, and effects of successful percutaneous transvenous mitral commissurotomy

Impaired left ventricular ejection performance was reported in pure mitral stenosis. The speculative mechanisms included insufficient preload, increased wall stress, high right ventricular pressure and unknown myocardial factors, but no definitive mechanism has been established. Fifteen patients with tight mitral stenosis who underwent successful percutaneous transvenous mitral commissurotomy were studied to ascertain whether ejection performance would improve with sufficient blood filling. The indexes of preload (end-diastolic volume) and ejection performance (stroke volume, ejection fraction, and mean systolic and mean normalized ejection rates) were calculated angiographically before and immediately after mitral commissurotomy. Improved blood filling (the result of successful mitral commissurotomy) produced an increase in end-diastolic volume (mean ± SD 99.0 ± 30.2 to 112.1 ± 30.1 ml/m 2; p < 0.05). All 4 indexes of ejection performance also improved. There was good correlation between end-diastolic and stroke volumes before intervention (stroke volume = 0.476 × end-diastolic volume + 16.77; r = 0.76), and the relation between them showed no change even after mitral commissurotomy. It is concluded that both left ventricular preload and ejection performance improved after successful percutaneous transvenous mitral commissurotomy. Insufficient preload could affect ejection performance in patients with tight mitral stenosis.

Left ventricular ejection performance, wall stress, and contractile state in aortic regurgitation before and after aortic valve replacement.

Left ventricular ejection performance, wall stress, and contractile state were evaluated in 35 patients with chronic aortic regurgitation. Cineangiography and pressure measurements were obtained before and a mean of 26 months after aortic valve replacement, and data were compared with those from 30 normal control subjects. The relation between quantitative changes in wall stress and changes in ejection fraction after surgery was determined. Preoperatively, end-systolic stress was elevated in patients with aortic regurgitation (218 +/- 45 vs. 160 +/- 23 kdynes/cm2 [mean +/- SD] for control subjects, p less than 0.01), and ejection fraction was depressed (0.46 +/- 0.11 vs. 0.65 +/- 0.05, p less than 0.01). End-systolic stress decreased postoperatively (151 +/- 41 kdynes/cm2, p less than 0.01) and ejection fraction increased (0.58 +/- 0.11, p less than 0.01). The magnitude of increase in ejection fraction correlated significantly and negatively (r = -0.65) with the quantitative change in end-systolic stress after surgery. Contractile function, as assessed by the ejection phase index-end-systolic stress relation, did not significantly change: 23 of 35 patients preoperatively and 18 of 35 patients postoperatively had values that clearly fell below the 95% confidence limit of the ejection fraction-end-systolic stress relation for controls. After surgery, individual ejection fraction-end-systolic stress relationships demonstrated a shift parallel to the regression curve for the control subjects. Moreover, persistent postoperative left ventricular hypertrophy was significantly associated with persistent contractile dysfunction. Thus, late improvement in left ventricular ejection performance after aortic valve replacement can be attributed to the reduction in end-systolic stress. Contractile function itself was not improved by surgery. Persistent postoperative hypertrophy may be a marker for myocardial contractile dysfunction.