Author + information
- Received December 2, 2008
- Revision received March 20, 2009
- Accepted April 21, 2009
- Published online September 8, 2009.
- ↵⁎Reprint requests and correspondence:
Dr. Jean G. Dumesnil or Dr. Philippe Pibarot, Québec Heart and Lung Institute, 2725 Chemin Sainte-Foy, Québec City, Québec G1V 4G5, Canada
Objectives This study was designed to examine the prognostic value of valvuloarterial impedance (Zva) in patients with aortic stenosis (AS).
Background We previously showed that the Zvais superior to standard indexes of AS severity in estimating the global hemodynamic load faced by the left ventricle (LV) and predicting the occurrence of LV dysfunction. This index is calculated by dividing the estimated LV systolic pressure (systolic arterial pressure + mean transvalvular gradient) by the stroke volume indexed for the body surface area.
Methods We retrospectively analyzed the clinical and echocardiographic data of 544 consecutive patients having at least moderate AS (aortic jet velocity ≥2.5 m·s−1) and no symptoms at baseline. The primary end point for this study was the overall mortality regardless of the realization of aortic valve replacement (AVR).
Results Four-year survival was significantly (p < 0.001) lower in the patients with a baseline Zva≥4.5 mm Hg·ml−1·m2(65 ± 5%) compared with those with Zvabetween 3.5 and 4.5 mm Hg·ml−1·m2(78 ± 4%) and those with Zva≤3.5 mm Hg·ml−1·m2(88 ± 3%). The risk of mortality was increased by 2.76-fold in patients with Zva≥4.5 mm Hg·ml−1·m2and by 2.30-fold in those with a Zvabetween 3.5 and 4.5 mm Hg·ml−1·m2after adjusting for other risk factors and type of treatment (surgical vs. medical).
Conclusions Increased Zvais a marker of excessive LV hemodynamic load, and a value >3.5 successfully identifies patients with a poor outcome. These findings suggest that beyond standard indexes of stenosis severity, the consideration of Zvamay be useful to improve risk stratification and clinical decision making in patients with AS.
Reduced arterial compliance is a frequent occurrence in patients with degenerative aortic stenosis (AS), where it independently contributes to increase afterload and decrease left ventricular (LV) function (1,2). Congenital bicuspid AS is also associated with impaired aortic elasticity, independent of stenosis severity or aortic size (3,4). Hence, the LV of AS patients often faces a double load: valvular plus arterial, and in these patients, the presence of symptoms and occurrence of adverse events should logically better correlate with the global burden faced by the ventricle than with the transvalvular gradient and/or aortic valve area (AVA). To this effect, we recently proposed a new index of global LV hemodynamic load, that is, the valvuloarterial impedance (Zva), which is calculated by dividing the estimated LV systolic pressure (systolic arterial pressure + mean transvalvular gradient) by the stroke volume index (SVI) (1). This index, in fact, represents the cost in mm Hg for each systemic milliliter of blood indexed for the body size, pumped by the LV during systole. And, indeed, we have shown that Zvais superior to the standard indexes of AS severity in predicting LV dysfunction (1). The objective of this study was to examine the relevance of Zvawith regard to prognosis, and in particular, to define reference values that could be used in routine clinical practice.
We retrospectively reviewed the clinical and echocardiographic data that were prospectively collected in 544 asymptomatic patients (320 men and 224 women; mean age 70 ± 14 years; range 21 to 98 years) with at least a moderate AS, defined as peak aortic jet velocity ≥2.5 m·s−1. The exclusion criteria were concomitant moderate or severe aortic insufficiency or mitral valve disease, left ventricular ejection fraction (LVEF) <50%, and the presence of symptoms at baseline.
Clinical data included age, sex, history of smoking, documented diagnosis of hypertension, hypercholesterolemia, diabetes, obesity (body mass index ≥30 kg/m2), and coronary heart disease (5).
Systemic arterial hemodynamics
Systemic arterial pressure was measured with the use of an arm cuff sphygmomanometer at the same time as the Doppler measurement of stroke volume (SV) was measured in the left ventricular outflow tract. The ratio of SVI to brachial pulse pressure (PP) was used as an indirect measure of total systemic arterial compliance: SAC = SVI/PP (1). The systemic vascular resistance was estimated by the formula: SVR = (80 × MAP)/CO, where MAP is the mean arterial pressure defined as diastolic pressure plus one-third of PP and CO is the cardiac output.
Doppler echocardiographic data
Aortic Valve Stenosis Severity
The Doppler echocardiographic indexes of AS severity included: the mean transvalvular pressure gradient obtained with the use of the modified Bernoulli equation, the AVA obtained with the use of the standard continuity equation, and the energy loss index (ELI) as previously described in Garcia et al. (6). Severe AS was defined as an AVA ≤1.0 cm2.
Two-dimensionally directed LV M-mode dimensions were measured in the left parasternal long-axis view following the recommendations of the American Society of Echocardiography. Left ventricular minor axis internal dimension (LVID), posterior wall thickness (PWT), and interventricular septal thickness (IVST) were measured at end-diastole (d). The LV mass was calculated using the corrected formula of the American Society of Echocardiography and was indexed for body surface area. Significant LV hypertrophy was defined as LV mass index >134 g/m2in men and >110 g/m2in women. The relative wall thickness (RWT) was calculated with the formula: RWT = (PWTd + IVSTd)/LVIDd.
LV Systolic Function
Diastolic function was assessed as previously described (7). The LVEF was determined in all patients using the Quinones method, the Dumesnil method (8), and visual estimate. In the case of a disagreement among these methods, the reviewing cardiologist selected the value that seemed the most representative.
Global LV Hemodynamic Load
As a measure of global LV load, we calculated the valvuloarterial impedance: Zva= (SAP + MG)/SVI, where SAP is the systolic arterial pressure and MG is the mean transvalvular pressure gradient (1). Hence, Zvarepresents the valvular and arterial factors that oppose ventricular ejection by absorbing the mechanical energy developed by the LV.
The primary end point for this study was overall death regardless of whether or not there was aortic valve replacement (AVR). Hence, this includes the deaths occurring in patients who did not undergo AVR as well as those occurring after operation in patients who underwent AVR. The outcome data were retrospectively obtained from patients' charts or death certificates.
We subdivided the patients into 3 groups according to the level of Zva: 1) Zva≤3.5 mm Hg·ml−1·m2(low Zvagroup, n = 172; 32%); 2) 3.5 < Zva<4.5 mm Hg·ml−1·m2(medium Zvagroup, n = 192; 35%); and 3) Zva≥4.5 mm Hg·ml−1·m2(high Zvagroup, n = 180, 33%). These 3 groups correspond approximately to the tertiles of Zva.
Continuous data were expressed as mean ± SD and compared among the 3 Zvagroups using a 1-way analysis of variance followed by a Tukey test. Categorical data were given as a percentage and compared with a chi-square test. Cumulative probability of survival was estimated with the Kaplan-Meier method and compared between groups using a log-rank test. The survival observed in these groups was also compared with that of the general population in the Québec province matched for age and sex. The survival data of this control population were derived from the 2002 life tables of Canada Statistics. The effect of the clinical and Doppler echocardiographic variables on survival was assessed with the use of a Cox proportional hazards model. All of the variables presented in Tables 1, 2, and 3⇓⇓as well as the type of treatment (medical vs. surgical, i.e., AVR) were tested in univariate analysis, and those with a p value <0.20 on univariate analysis were incorporated into the multivariate models. Age was forced into the model. To avoid colinearity among a subset of several variables measuring the same phenomenon (e.g., AVA, peak gradient, mean gradient, ELI), we entered in the multivariate models the variable that had the strongest association with mortality on univariate analysis. We constructed a first series of multivariate models with independent variables entered in continuous format and then a second series with these variables entered in dichotomous formats.
Table 1shows the baseline characteristics of the patients in the 3 Zvagroups. Patients with high and medium Zvawere significantly older and had a higher prevalence of systemic arterial hypertension compared with those with low Zva. There was no significant difference among the 3 groups with regard to sex distribution, body surface area, body mass index, and prevalence of hypercholesterolemia, diabetes, and coronary artery disease.
Table 2shows the data of the Doppler echocardiographic and systemic arterial indexes reflecting the valvular load (i.e., AS severity) and the arterial load. As expected, patients with high Zvahad a higher valvular load, that is, more severe valvular stenosis, as reflected by smaller AVA and ELI and higher transvalvular gradients compared with patients with medium or low Zva(Fig. 1).Patients with medium Zvaalso had significantly smaller AVA but similar gradients compared with patients with low Zva. Patients with higher levels of Zvaalso had a higher vascular load as reflected by reduced systemic arterial compliance, increased systemic vascular resistance, and higher systolic and diastolic arterial pressures.
Table 3shows the echocardiographic data of LV geometry and function. Patients in the high Zvagroup had thicker LV walls, a smaller LV cavity, and a higher relative wall thickness ratio compared with those in the medium and low Zvagroups. Patients with high Zvaalso had a lower LVEF, SV, cardiac output, and mean transvalvular flow rate compared with patients with lower Zva. The indexes of LV systolic function, except LVEF, were also significantly lower in the medium Zvagroup than in the low Zvagroup.
Moreover, as shown in Figure 1, the proportion of patients with a paradoxical low flow pattern, defined as stoke volume index ≤35 ml·m−2in the setting of LVEF ≥50%, was much higher (p < 0.001) in the high Zvagroup (n = 90, 50%) than that in the medium Zvagroup (n = 28, 15%) or in the low Zvagroup (n = 7, 4%), which is consistent with our previous study showing that patients with paradoxical low flow are characterized by a markedly increased Zva(5). Hence, among the 125 patients with paradoxical low flow, 90 (72%) had a high Zva, and of these patients 74 (82%) had a severe AS.
Type of treatment
Aortic valve replacement was performed during follow-up in 54 (31%) patients in the low Zvagroup, 58 (30%) in the medium Zvagroup, and 64 (36%) in the high Zvagroup. Coronary artery bypass grafting (CABG) was performed concomitantly in 75 of 176 (43%) patients. Among the 176 patients undergoing AVR, 166 (94%) had severe AS at the time of operation (67 of these patients underwent CABG) and 10 (6%) had moderate AS (8 underwent CABG).
The mean follow-up time in the total cohort was 2.5 ± 1.8 years (median 2.1 years). The follow-up was complete in all patients, and there was no significant difference between groups with regard to the duration of follow-up.
Overall, there were 91 deaths: 15 (9%) in the low Zvagroup, 36 (19%) in the medium Zvagroup, and 40 (22%) in high Zvagroup. Among them 51 (56%) were from a cardiovascular cause: 7 (4%) in low Zvagroup, 19 (10%) in the medium Zvagroup, and 25 (14%) in the high Zvagroup. Seventy-eight of the 91 deaths occurred in patients treated medically, whereas 13 occurred after AVR. Six of these post-operative deaths occurred in the early post-operative period (<30 days).
Four-year survival was significantly (p < 0.001) lower in the high Zvagroup (65 ± 5%) than in the medium (78 ± 4%) and low (88 ± 3%) Zvagroups. Survival was also significantly (p = 0.007) lower in the patients with medium Zvacompared with those with low Zva(Fig. 2).Patients with low Zvahad similar survival compared with that of the general population in Quebec, whereas patients in the medium and high Zvagroups had lower (p < 0.05) survival than in this control population.
Figure 3shows the survival as a function of the 3 levels of Zvaand the type of treatment. Particularly noteworthy is the fact that survival of patients in the 3 groups treated surgically was similar or better than that of the control population, albeit there was a statistical difference (p = 0.02) between the high and low Zvagroups treated surgically. Likewise, survival of patients in the low Zvagroup treated medically was no different from that of the control population. Conversely, patients with high and moderate Zvatreated medically had markedly lower survival compared with the control population (p = 0.002 and p =0.002, respectively) and with the patients with low Zva(p = 0.0003 and p = 0.02, respectively). Moreover, although significantly different in both groups, the magnitude of the protective effect of AVR was most important in patients with higher Zva(4-year survival: 87 ± 5% vs. 42 ± 9% for patients treated medically, p < 0.001) than in patients with moderate Zva(4-year survival: 89 ± 5% vs. 74 ± 4% for patients treated medically, p = 0.001). Overall, these results seem to identify Zva>3.5 mm Hg·ml−1·m2as the logical threshold to identify patients likely to be at higher risk if treated medically rather than surgically.
Predictors of outcome
Table 4shows the univariate and multivariate predictors of mortality. Mortality risk increased by 1.41-fold (95% confidence interval [CI]: 1.17 to 1.67, p = 0.0004) per 1-U increase in Zvaon univariate analysis and by 1.36-fold (95% CI: 1.03 to 1.75, p = 0.03) on multivariate analysis (Model 1 in Table 4). When Zvawas expressed in a categorical format, a value of Zva≥4.5 mm Hg·ml−1·m2was associated with a hazard ratio for mortality of 2.95 (95% CI: 1.67 to 5.53, p = 0.0001), whereas a value of Zva>3.5 and <4.5 mm Hg·ml−1·m2was associated with a hazard ratio of 2.24 (95% CI: 1.25 to 4.22, p = 0.006). On multivariate analysis, the independent risk factors for mortality were older age, increased LV mass index, and increased Zva, whereas the surgical treatment (AVR with or without CABG) was highly protective (models 1 and 2 in Table 4). The risk of mortality was increased by 2.76-fold (95% CI: 1.32 to 5.92; p = 0.01) in patients with Zva≥4.5 mm Hg·ml−1·m2and by 2.30-fold (95% CI: 1.16 to 4.71; p = 0.03) in those with a Zvacomprised between 3.5 and 4.5 mm Hg·ml−1·m2after adjustment for other risk factors and type of treatment (surgical vs. medical) (Model 2 in Table 4). With regard to the risk of cardiovascular mortality, a value of Zva≥4.5 mm Hg·ml−1·m2was associated with a hazard ratio for mortality of 3.71-fold (95% CI: 1.47 to 10.17; p = 0.001) whereas a value of Zva>3.5 and <4.5 mm Hg·ml−1·m2was associated with a hazard ratio of 3.11 (95% CI: 1.28 to 8.20, p = 0.014).
The most important finding of the present study is that Zvapredicts adverse outcome in asymptomatic patients with at least moderate AS, even after adjustment for standard indexes of stenosis severity, LV geometry and function, and type of treatment. A value of Zva≥4.5 mm Hg·ml−1·m2was indeed associated with a 2.76- and a 3.71-fold increase in the risk of overall and cardiovascular mortality, respectively, whereas a value of Zvabetween 3.5 and 4.5 was associated with 2.30- and 3.11-fold increases of the same risks. The fact that the adverse impact of Zvaon survival was most evident in patients with moderately (>3.5 and <4.5 mm Hg·ml−1·m2) or severely (≥4.5 mm Hg·ml−1·m2) increased Zvatreated medically whereas survival of patients treated surgically or with a low Zva(≤3.5 mm Hg·ml−1·m2) was similar or better than that of the general population in Quebec is also compelling evidence that this parameter should be highly useful for risk stratification and clinical decision making and that the logical reference value for this purpose would seem to be a Zva>3.5 mm Hg·ml−1·m2.
The valvuloarterial impedance provides an estimate of the global LV hemodynamic load that results from the summation of the valvular and vascular loads, and the concept is very useful because it incorporates stenosis severity, volume flow rate, body size, and systemic vascular resistance. Moreover, Zvacan easily be calculated using Doppler echocardiography from 3 simple measurements, that is, the SVI in the LV outflow tract, the transvalvular mean gradient, and systolic arterial pressure, and as previously shown (1), it is superior to the standard indexes of AS severity in predicting LV dysfunction. These results have been independently corroborated by a substudy of the SEAS (Simvastatin and Ezetimibe in Aortic Stenosis) trial (9), in which increased Zvawas a powerful independent predictor of myocardial systolic dysfunction in asymptomatic patients with mild to severe AS. Moreover, in a recent study (5) including only patients with severe AS, a value of Zva>5.5 mm Hg·ml−1·m2was associated with a 2.5-fold increase in the risk of overall mortality, regardless of the type of treatment (AVR or medical). An important limitation of that study, however, is that many patients were already symptomatic at baseline.
Comparison with previous studies
Previous studies of patients with asymptomatic AS have identified older age, hemodynamic severity of AS, severe aortic valve calcification, physical inactivity, coronary artery disease, and renal failure as independent predictors of adverse events generally defined as AVR (or onset of symptoms) and death (10–12). In the present study, we identified some of these factors, such as age and baseline AVA, as predictors of mortality. It should also be emphasized that Zvawas not determined in previous studies. Moreover, we selected overall mortality as the end point for the present study rather than a combined end point of AVR or death as used in some previous studies.
AS: a disease not only limited to the valve
There is now a strong body of evidence suggesting that degenerative AS is an active disease akin to atherosclerosis (13,14), and in this context, it is not surprising that many patients with degenerative AS also have manifestations of atherosclerosis in other target organs. Many patients with degenerative AS thus also may present with concomitant systolic hypertension, and indeed, a markedly reduced arterial compliance was previously found to be present in up to 40% of patients with at least moderate AS (1). As well, such patients also may have alterations of LV function that might not only be caused by AS as such but also by hypertension and/or associated coronary artery disease and in varying proportions depending on the severity of each entity. Thus, degenerative AS cannot be viewed as an isolated disease strictly limited to the valve, but rather as part of a continuum that may also include a reduction in systemic arterial compliance and/or alterations of LV function. From the results of the present study, it would indeed seem that the pathophysiology of adverse outcomes in AS is primarily related to an imbalance between the global increase in LV overload, independent of whether it be of valvular and/or vascular origin, and LV reserve both at rest and during exercise; as well, it becomes evident that Zvais the best-suited and most relevant parameter to clinically quantify this “global or total” increase in LV hemodynamic load.
The chronic exposure to a high level of afterload may eventually lead to a reduction in the coronary vasodilatory reserve, an intrinsic impairment of myocardial contractile function, and a decrease in cardiac output (1,5,9,15). To this effect, previous studies from our laboratory (1,5) and from the SEAS investigators (9) have reported that patients with a markedly increased Zvaoften have decreases in LVEF, mid-wall fractional shortening, and cardiac output. The consequences of a reduction in cardiac output are a reduction of transvalvular gradients and a pseudo-normalization of peripheral blood pressure, which may occur in up to 30% of patients (1,5). Clinically, this situation is highly insidious because both AS and hypertension may appear less severe on the basis of the transvalvular gradients and blood pressure, whereas, in fact, these patients are at a more advanced stage of their disease. In this regard, the calculation of Zvamay be useful for identifying the patients in whom disease severity is masked by this pseudo-normalization phenomenon.
These results strengthen the need for a more comprehensive evaluation of AS that should include indexes such as: 1) AVA and ELI (in patients with a small aorta) for the assessment of valvular load; 2) systemic arterial compliance and vascular resistance for the assessment of arterial load; and finally, 3) Zvato quantify global LV load. The consideration of these indexes easily measurable by Doppler echocardiography allows the clinician to better quantify the severity of the disease and could be particularly helpful in the 3 following clinical situations.
Asymptomatic Patients with Severe AS
Management of these patients remains a source of debate (16,17), and recent studies have suggested that those treated surgically may have better survival than those treated medically (18–20). This difference may be related to underestimation of symptoms and/or stenosis severity in some patients, especially in the elderly sedentary patients (5,19,20). Moreover, it has been argued that a “wait for symptoms” strategy may result in some patients undergoing surgery too late (i.e., at a stage of the disease when myocardial impairment has become, at least in part, irreversible) (21). On the other hand, AVR is not without risk (22), and the decision to operate on such patients therefore requires careful weighing of benefits against risks. To this effect, Zvamay be useful for identifying patients who are at higher risk and may be an indication for closer follow-up and further investigation. In this context, exercise stress testing may be particularly useful to corroborate symptomatic status in patients with a Zva>4.5 mm Hg·ml−1·m2who claim to be asymptomatic. If the exercise test is abnormal (exercise-limiting symptoms, decrease in blood pressure), AVR can be contemplated (16), whereas in the case of a normal test, the patient can be followed up more closely with a clinical brain natriuretic peptide level and/or echocardiographic evaluation every 6 to 12 months (23).
Symptomatic Patients with Moderate AS
Patients with moderate AS may become symptomatic because of concomitant hypertension. The calculation of Zvamay thus help to reconcile the apparent discrepancy between stenosis severity and symptomatic status. If the Zvais <3.5 mm Hg·ml−1·m2, the symptoms could be related to a concomitant disease such as coronary artery disease, whereas if it is >3.5 mm Hg·ml−1·m2, the symptoms could be caused by the additive effects of the moderate AS and reduced arterial compliance and/or increased vascular resistance.
In such patients, the logical first step would be to treat their hypertension and then to re-evaluate symptomatic status and Zvaunder treatment. Traditionally, vasodilator therapy has been considered relatively contraindicated in patients with AS because of its hypotensive effects, but recent studies, however, suggest that except in patients with very severe disease, it can be applied both safely and beneficially (23,24). Nonetheless, therapy should be introduced cautiously, particularly in patients with severe AS. Further studies will, however, be necessary to determine whether symptomatic status and outcome can be significantly improved in this fashion. Indeed, because AS patients often have reduced arterial compliance (1), blood pressure levels may not be completely normalized by treatment.
Paradoxical Low-flow, Low-gradient, Severe AS
We recently reported that an important proportion of the patients with severe AS on the basis of AVA paradoxically have a low transvalvular flow rate (SVI <35 ml/m2) and thus a low gradient (<40 mm Hg) despite the presence of a preserved LVEF (≥50%) (5). When compared with patients with severe AS, normal LV output and thus high gradient, these patients with paradoxical low flow were characterized by a higher degree of LV concentric remodeling, a lower LVEF (although still within the normal range), a reduced mid-wall shortening, a markedly higher level of LV global load reflected by a higher Zva, and a worse prognosis if treated medically. Hence, it can be conceived that a greater and more longstanding increase in afterload may result in more pronounced LV concentric remodeling, a smaller LV cavity size, and a decrease in intrinsic myocardial function. This paradoxical low-flow, low-gradient AS pattern may bring some uncertainty about the actual severity of AS and may lead clinicians to erroneously conclude that the stenosis is not severe and that surgery is not indicated. Hence, the consideration of Zvamay be helpful in these patients to determine the actual level of global LV hemodynamic load that is often underestimated because of a reduction of transvalvular gradients and a pseudo-normalization of arterial pressures inherent to the low-flow state. If the Zvais high, it is likely that the excessive hemodynamic load imposed by AS and/or hypertension contributed to the alteration of LV geometry and function that, in turn, led to the paradoxical low-flow state. In the present series, the vast majority (72%) of patients with paradoxical low flow had high Zva, and among these patients >80% had a severe AS. In the subset of patients with moderate AS, the severe augmentation of Zvais most likely caused by the coexistence of hypertension. On the other hand, if Zvais low, the alteration of the LV geometry and function leading to a paradoxical low-flow state may be caused by concomitant risk factors or diseases such as diabetes, metabolic syndrome, or hypertrophic cardiomyopathy.
One limitation of this study is its retrospective design. The baseline data were prospectively collected in consecutive patients with asymptomatic AS referred to the echocardiographic laboratory. However, the outcome data were retrospectively obtained from patients' charts or death certificates. Consequently, we did not have the information on: 1) the exact timing of symptom onset during follow-up; 2) the proportion of patients in whom severe symptomatic AS developed and who were not referred to AVR because of advanced age, comorbidities, or inappropriate management; and 3) the primary reason that motivated AVR. These limitations were, at least in part, compensated by the fact that we used overall survival (and not AVR) as the primary end point for this study and that we adjusted for the type of treatment in the multivariate analyses.
Patients with more than mild aortic insufficiency were excluded from the study. In the presence of significant aortic insufficiency, both the numerator (transvalvular gradient) and the denominator (SVI measured in the LV outflow tract) of Zvamay increase, which may reduce the ability of this index to correctly quantify the severity of the hemodynamic load in patients with mixed valvular dysfunction, and further studies are thus needed to examine the applicability and utility of Zvain patients with mixed dysfunction.
Increased Zvais a marker of excessive LV hemodynamic load and identifies patients with a poor outcome. These findings suggest that beyond standard indexes of stenosis severity, LV geometry, and function, the consideration of Zvamay be useful to improve risk stratification and clinical decision making in patients with AS.
The authors thank Dominique Labrèche, PhD, Isabelle Laforest, MS, Isabelle Fortin, and Marie-Annick Clavel, DVM, for data collection and validation, and Claudia Blais, PhD, Valérie Jomphe, MS, and Nicolas Girerd, MS, for their assistance in the statistical analyses.
This work was supported by a grant from the Canadian Institutes of Health Research (MOP-82873), Ottawa, Canada.
Dr. Pibarot holds the Canada Research Chair in Valvular Heart Diseases, Canadian Institutes of Health Research, Ottawa, Ontario, Canada.
- Abbreviations and Acronyms
- aortic stenosis
- aortic valve area
- aortic valve replacement
- coronary artery bypass graft
- confidence interval
- energy loss index
- left ventricle/ventricular
- left ventricular ejection fraction
- pulse pressure
- stroke volume
- stroke volume index
- valvuloarterial impedance
- Received December 2, 2008.
- Revision received March 20, 2009.
- Accepted April 21, 2009.
- American College of Cardiology Foundation
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