Increase In Regurgitant Volume Research Articles

A Novel Aortic Regurgitation Model from Cusp Prolapse with Hemodynamic Validation Using an Ex Vivo Left Heart Simulator.

Although ex vivo simulation is a valuable tool for surgical optimization, a disease model that mimics human aortic regurgitation (AR) from cusp prolapse is needed to accurately examine valve biomechanics. To simulate AR, four porcine aortic valves were explanted, and the commissure between the two largest leaflets was detached and re-implanted 5mm lower to induce cusp prolapse. Four additional valves were tested in their native state as controls. All valves were tested in a heart simulator while hemodynamics, high-speed videography, and echocardiography data were collected. Our AR model successfully reproduced cusp prolapse with significant increase in regurgitant volume compared with that of the controls (23.2 ± 8.9 versus 2.8 ± 1.6ml, p = 0.017). Hemodynamics data confirmed the simulation of physiologic disease conditions. Echocardiography and color flow mapping demonstrated the presence of mild to moderate eccentric regurgitation in our AR model. This novel AR model has enormous potential in the evaluation of valve biomechanics and surgical repair techniques. Graphical Abstract.

Natural History of Functional Tricuspid Regurgitation: Implications of Quantitative Doppler Assessment

ObjectivesThis study sought to define the relationship between functional tricuspid regurgitation (TR) and mortality in patients with heart failure with reduced ejection fraction (HFrEF); and to establish the prognostic value of quantitative measures of TR severity (i.e., effective regurgitant orifice area [EROA] and regurgitant volume). BackgroundThe significance of TR in chronic heart failure is controversial. Earlier studies have shown an independent impact of TR on mortality, whereas more recent evidence suggests myocardial impairment to be the driving force of mortality rather than TR itself. Earlier studies have used qualitative measures of TR severity, hence the prognostic value of more quantitative measures of TR severity (i.e., EROA and regurgitant volumes) remains unclear. MethodsWe enrolled 382 patients with HFrEF on guideline-directed medical therapy and assessed TR EROA and regurgitant volume by Doppler/2-dimensional echocardiography. All-cause mortality was defined as the primary study endpoint. ResultsTR severity was associated with the HFrEF phenotype with more symptoms (p = 0.004), higher neurohumoral activation (p < 0.001), progressive right-ventricular dilatation (p < 0.001), and impaired function (p < 0.001). Cox regression showed a strong association between quantitative measures of TR with mortality (all p < 0.001). Quantitative metrics of TR severity were consistently associated with mortality with a hazard ratio of 1.009 (95% confidence interval: 1.004 to 1.013; p < 0.001) per 0.01 cm2 increase of the EROA and of 1.013 (95% confidence interval: 1.007 to 1.020; p < 0.001) per 1-ml increase in regurgitant volume. Results remained unchanged after bootstrap- or clinical confounder-based adjustment. A spline curve pattern illustrates the association with mortality with thresholds for the EROA ≥0.2 cm2, and the regurgitant volume ≥20 ml with sustained excess mortality thereafter. ConclusionsThis large-scale outcome study demonstrates the prognostic value of quantitative Doppler-echocardiographic measures of TR severity in HFrEF. The thresholds for EROA and TR regurgitant volume associated with mortality in our study fall within current ranges defining nonsevere TR. This may potentially impact therapeutic decision making, particularly timing of intervention.

Therapeutic decision-making for patients with fluctuating mitral regurgitation

Mitral regurgitation (MR) is a common, progressive, and difficult-to-manage disease. MR is dynamic in nature, with physiological fluctuations occurring in response to various stimuli such as exercise and ischaemia, which can precipitate the development of symptoms and subsequent cardiac events. In both chronic primary and secondary MR, the dynamic behaviour of MR can be reliably examined during stress echocardiography. Dynamic fluctuation of MR can also have prognostic value; patients with a marked increase in regurgitant volume or who exhibit increased systolic pulmonary artery pressure during exercise have lower symptom-free survival than those who do not experience significant changes in MR and systolic pulmonary artery pressure during exercise. Identifying patients who have dynamic MR, and understanding the mechanisms underlying the condition, can potentially influence revascularization strategies (such as the surgical restoration of coronary blood flow) and interventional treatment (including cardiac resynchronization therapy and new approaches targeted to the mitral valve).

The haemodynamic cascade

The haemodynamic cascade

Aortic valve closure for rapidly deteriorated aortic insufficiency after continuous flow left ventricular assist device implantation

A patient underwent aortic valve closure for de novo aortic insufficiency that had deteriorated to severe insufficiency during six months of support with a continuous flow left ventricular assist device (cf-LVAD). Aortic insufficiency was initially noted one month after LVAD implantation, and then deterioration quickly developed. Right heart catheterization revealed that when the rotational speed of the cf-LVAD was increased, the cardiac index was decreased by an increase in regurgitant volume, as shown by echocardiography. During surgery, fusion and shortening of the aortic leaflets as well as left coronary ostial occlusion were observed. Direct aortic closure improved hemodynamics. Thrombus formation on the aortic valve shown by echocardiography in the early postoperative period may be a trigger of aortic insufficiency. Control of the cf-LVAD rotational speed is likely required to prevent aortic insufficiency.

Pathophysiology of Tricuspid Regurgitation

Background— Respiratory dependence of tricuspid regurgitation (TR), a long-held concept suggested by murmur variation, remains unproven and of unclear mechanisms. Methods and Results— In 41 patients with mild or greater TR (median age, 67 years), we performed triple Doppler echocardiographic quantification (TR severity, right ventricular, and right atrial quantification) with simultaneous respirometer recording of respiratory phases. Expiration to inspiration changes (median) affected TR peak velocity (−40 cm/s; 25th to 75th percentile, −60 to −30 cm/s), duration (−12 milliseconds; 25th to 75th percentile, −45 to 2 milliseconds), and time-velocity integral (−17 cm; 25th to 75th percentile, −23.4 to −10 cm; all P &lt;0.001), consistent with decreased TR driving force. Nevertheless, inspiratory TR augmentation was demonstrated by increased effective regurgitant orifice (0.21 cm 2 ; 25th to 75th percentile, 0.09 to 0.34 cm 2 ) and volume (18 mL per beat; 25th to 75th percentile, 10 to 25 mL per beat; all P &lt;0.001) infrequently detected clinically (2 of 41, 5). As a result of reduced TR driving force, regurgitant volume increased less than effective regurgitant orifice (120 [25th to 75th percentile, 78.6 to 169] versus 169 [ 25th to 75th percentile, 12.9 to 226.1]; P &lt;0.001). During inspiration, right ventricular area increased (diastolic, 27.8 [25th to 75th percentile, 22.6 to 36.3] versus 26.5 [21.1 to 31.9]; P &lt;0.0001) with widening of right ventricular shape (length-to-width ratio, 1.6 [ 25th to 75th percentile, 1.37 to 1.95] versus 1.7 [1.46 to 2.1]; P &lt;0.0001), increased systolic annular diameter ( P =0.003), valve tenting height ( P &lt;0.0001) and area ( P &lt;0.0001), and reduced valvular-to-annular ratio ( P =0.006). Effective regurgitant orifice during inspiration was independently determined by inspiratory valvular-to-annular ratio ( P =0.026) and inspiratory change in right ventricular length-to-width ratio ( P =0.008) and valve tenting area ( P =0.015). Conclusions— TR is dynamic with almost universal respiratory changes of large magnitude and complex pathophysiology. During inspiration, a large increase in effective regurgitant orifice causes, despite a decline in regurgitant gradient, a notable increase in regurgitant volume. Effective regurgitant orifice changes are independently linked to inspiratory annular enlargement (decreased valvular coverage) and to inspiratory right ventricular shape widening with increased valvular tenting. These novel physiological insights into TR respiratory dependence underscore right-side heart plasticity and are important for clinical TR severity evaluation.

Exercise-Induced Changes in Degenerative Mitral Regurgitation

We sought to quantify exercise-induced changes in patients with degenerative mitral regurgitation (MR), to examine the relationship between exercise-induced changes in MR and in systolic pulmonary artery pressure (PAP), and to identify their potential impact on symptom-free survival. MR severity can change during exercise in patients with functional MR. Quantified changes in MR severity during exercise remain undetermined in patients with degenerative MR. Resting and bicycle exercise Doppler-echocardiography were performed in 61 asymptomatic patients (age 62+/-14 years) with moderate to severe degenerative MR (i.e., mitral valve prolapse or flail). Mitral regurgitation was quantified at rest and exercise with effective regurgitant orifice (ERO) area and regurgitant volume calculated with the proximal isovelocity surface area (EROP) and the quantitative Doppler (EROD) methods. At rest, EROP and EROD were well-correlated (r=0.87, p<0.0001), but EROD was larger than EROP (54+/-21 mm2 vs. 42+/-24 mm2, p<0.0001). During exercise, mean ERO and regurgitant volume markedly increased in 32% of patients by >or=10 mm2 and >or=15 ml, respectively. There was good correlation between exercise EROP and EROD (r=0.84, p<0.0001). Changes in systolic PAP were correlated with changes in ERO and regurgitant volume (r=0.59, p=0.02 and r=0.60, p=0.02). Patients with a marked increase in regurgitant volume during exercise had lower symptom-free survival than those in whom MR decreased or remained unchanged (p=0.0015). Degenerative MR might be dynamic and increases during exercise in one-third of patients. Marked changes in MR severity are associated with exercise-induced changes in systolic PAP and reduced symptom-free survival.

Quantitation of functional mitral regurgitation during bicycle exercise in patients with heart failure

OBJECTIVESWe sought to examine the feasibility and reliability of quantifying mitral regurgitation (MR) during exercise by Doppler echocardiography in patients with heart failure and to assess the relationship between dynamic MR and systolic pulmonary artery pressure changes.BACKGROUNDThe severity of MR can be quantified by using several echocardiographic methods. Quantitation of MR during dynamic exercise has not yet been performed.METHODSSymptom-limited, semi-supine two-dimensional and Doppler echocardiograms during bicycle exercise were obtained in 27 consecutive patients with heart failure and functional MR. Regurgitant volume was measured at rest and during exercise by the proximal isovelocity surface area (PISA) method and by quantitative Doppler echocardiography. Exercise-induced changes in regurgitant volume were compared with changes in the regurgitant jet area to left atrial area ratio, vena contracta width and trans-tricuspid pressure gradient.RESULTSThe regurgitant volume measured by the PISA method increased from 21 ± 12 ml (range 5 to 55) at rest to 39 ± 23 ml (range 8 to 85) during exercise (p < 0.0001). The difference between two observers was low for both rest (2.0 ± 2.7 ml) and exercise measurements (3.5 ± 6.2 ml). The regurgitant volume measured by quantitative Doppler echocardiography increased from 29 ± 13 to 49 ± 24 ml (p = 0.0001). Excellent correlation between the two methods was obtained with exercise (r = 0.92). Exercise-induced changes in regurgitant volume, as measured by the PISA method, correlated well with regurgitant volume changes measured by quantitative Doppler echocardiography (r = 0.88), changes in vena contracta width (r = 0.82) and changes in trans-tricuspid pressure gradient (r = 0.73), but not with changes in regurgitant jet area to left atrial area ratio (r = 0.29). Seventeen patients stopped exercise because of fatigue and 10 because of dyspnea. These 10 patients exhibited greater increases in regurgitant volume (34 ± 6 vs. 11 ± 8 ml), corresponding to a significant elevation of the trans-tricuspid gradient (48 ± 14 vs. 20 ± 14 mm Hg).CONCLUSIONSQuantitation of functional MR during exercise is feasible in patients with heart failure. There is a good correlation between regurgitant volume measured during exercise by the PISA method and that obtained by quantitative Doppler echocardiography, suggesting that the technique is reliable. An increase in mitral regurgitant volume during dynamic exercise correlates well with elevation of systolic pulmonary artery pressure.

Quantification of mitral regurgitant volume by the color doppler proximal isovelocity surface area method: A clinical study

In vitro studies have demonstrated that regurgitant flow rate can be estimated by the color Doppler "proximal isovelocity surface area" (PISA) method. By applying the PISA method and continuity principle, we developed a formula to calculate mitral regurgitant volume: 2 pi r2.VN.FVI/Vo, where r = distance from the first jet alias to mitral leaflets, VN = aliasing velocity, FVI = flow velocity integral or regurgitant jet, and Vo = peak velocity through the regurgitant orifice. Doppler echocardiography was performed in 20 patients with mitral regurgitation. The mitral regurgitant volume was estimated by PISA and compared to cine ventriculographic grading. The results showed an increase in regurgitant volume by PISA compared with increasing angiographic grades of mitral regurgitation: 19 +/- 0.6, 18 +/- 5, 25 +/- 12, and 44 +/- 4 ml for grades 1+ to 4+, respectively (r = 0.77). Thus a formula developed from PISA is able to identify patients with a severe grade of mitral regurgitation and to provide an alternate approach to the noninvasive quantitation of mitral regurgitation.

Load dependence of the effective regurgitant orifice area in a sheep model of aortic regurgitation

Treatment of patients with aortic regurgitation with vasodilators reduces regurgitant volume, ventricular dilation and left ventricular mass. Although these effects are presumably due to afterload reduction, it is also possible that the aortic regurgitant orifice area is not constant. To test the latter hypothesis, aortic regurgitation was created in 10 open chest sheep by partial resection of the noncoronary leaflet under direct visualization. Regurgitant flow was measured with an aortic supravalvular electromagnetic probe; aortic and left ventricular pressures were measured with catheter-tipped micromanometer pressure transducers.The effective regurgitant orifice area was calculated by a modification of the continuity equation in a manner similar to the Gorlin equation. The regurgitant orifice area was measured three times: after aortic regurgitation was created, after mean arterial pressure was increased by 15 to 25 mm Hg with intravenous dopamine and after mean arterial pressure was reduced by 15 to 25 mm Hg with intravenous sodium nitroprusside. Comparison of regurgitant volumes and areas obtained after creation of aortic regurgitation and at the conclusion of the experiment in the absence of dopamine or sodium nitroprusside demonstrated no significant change over time.Dopamine administration was associated with an 86 ± 81% increase in regurgitant volume (p < 0.01) and a 38 ± 44% increase in regurgitant orifice area (p < 0.01). Sodium nitroprusside administration resulted in a 51 ± 14% decrease in regurgitant volume (p < 0.001) and a 28 ± 21% reduction in regurgitant orifice area (p = 0.007).In this model of acute aortic regurgitation, the effective regurgitant orifice area was altered by increasing or decreasing the aortic transvalvular pressure gradient. This dynamic nature of the regurgitant orifice area may be secondary to changes in aortic root geometry at various aortic pressures. Reduction of this area may be one of the mechanisms of the beneficial effect of afterload reduction in patients with aortic regurgitation, particularly when the elasticity of the aortic valve apparatus has not been impaired by fibrosis or calcification.