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European Heart Journal Advance Access originally published online on June 6, 2007
European Heart Journal 2007 28(12):1454-1461; doi:10.1093/eurheartj/ehm180
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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Association of atheroma as assessed by intraoperative transoesophageal echocardiography with long-term mortality in patients undergoing cardiac surgery

Senthil K. Thambidorai, Sukaina J. Jaffer, Tushar K. Shah, William J. Stewart, Allan L. Klein* and Michael S. Lauer

Department of Cardiovascular Medicine, Cleveland Clinic, 9500 Euclid Avenue—Desk F15, Cleveland, OH 44195, USA

Received 29 September 2006; revised 22 March 2007; accepted 13 April 2007; online publish-ahead-of-print 6 June 2007.

* Corresponding author. Tel: +1216 444 3932; fax: +1 216 445 2309. E-mail address: kleina{at}ccf.org


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Conclusions
 Appendix
 Acknowledgements
 References
 
Aims: To determine whether the presence and severity of aortic atheroma predict long-term all-cause mortality among patients undergoing cardiac surgery.

Methods and results: We followed 8581 patients who underwent cardiac surgery and had routine intraoperative transoesophageal echocardiography for 2.8 years (range 0.06–6.0 years). Data regarding multiple potential confounders were prospectively collected and electronically recorded. There were 2878 (34%) patients with no atheroma; 4129 (48%) patients with mild atheroma; 1215 (14%) with moderate atheroma; and 359 (4%) with severe atheroma. There were 1000 deaths. Death rates were increased in patients with moderate [relative risk (RR) 3.29, 95% CI 2.50–4.32, P < 0.0001) and severe atheroma (RR 5.21, 95% CI 3.65–7.41, P < 0.0001). After adjusting for multiple other confounders, severe atheroma remained modestly predictive of risk (adjusted RR 1.46, 95% CI 1.07–2.00, P = 0.02); but moderate atheroma and mild atheroma were not predictive of increased risk. In a propensity analysis that matched patients with comparable range of variables, severe atheroma was no longer predictive of risk (adjusted RR 1.39, 95% CI 0.87–2.23, P = 0.17).

Conclusion: Our study shows that severe atheroma is associated with increased long-term mortality in patients undergoing cardiac surgery; however, the relationship is weak using propensity analysis, suggesting no causal association.

Key Words: Atheroma • Intraoperative echocardiography • Survival


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Conclusions
 Appendix
 Acknowledgements
 References
 
Aortic atheroma has been shown to be a marker of generalized atherosclerosis and is associated with coronary artery disease (CAD),1 carotid artery disease,2 and peripheral vascular disease (PVD).3,4 Numerous studies have shown aortic atheroma to be predictive of adverse cerebral outcomes—mostly intraoperative and delayed stroke.5–10 Initial studies using intraoperative epiaortic ultrasound and intraoperative transoesophageal echocardiography (TEE) have shown severity of aortic atheroma to correlate with long-term mortality in high-risk patients, but not in the general population.6,11–14 Clinical variables involved in predicting long-term mortality in patients undergoing cardiac surgery have been studied in great detail over the past several years15–19 and were not included in these previous studies. These studies were also limited in that they used only one portion of the thoracic aorta to identify the atheroma. In contrast, a population-based TEE study recently showed that thoracic aortic atherosclerosis was not independently predictive of long-term mortality in addition to clinical risk factors based on ACC/AHA guidelines. Thus, this brings into question the significance of aortic atheroma.

TEE is very sensitive in diagnosing aortic atheroma and intraoperative TEE is now routinely performed during most cardiac surgeries. In view of conflicting results, we sought to determine the impact of varying severity of aortic atheroma on long-term, all-cause mortality in patients undergoing cardiac surgery.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Conclusions
 Appendix
 Acknowledgements
 References
 
Patients
The study sample was derived from 12,056 consecutive adult patients undergoing first-time cardiac surgery at the Cleveland Clinic Foundation between 1996 and 2001. Patients who had prior coronary artery bypass graft surgery (CABG) or valve surgery were excluded. Only patients with Social Security numbers were included in the study. Patients who did not have a complete echocardiographic evaluation were excluded as well. A total of 3475 patients were excluded on the basis of these criteria. Thus, 8581 patients comprised our study population. There were no major differences in the baseline clinical and surgical characteristics between the excluded cohort of patients and the patients included in the final study group (Table A2). Approval was obtained from the Cleveland Clinic Foundation Institutional Review Board.

Clinical data
At the time of cardiac surgery, the data on baseline demographics, medical history, stroke risk factors, and medication use were prospectively recorded using the Cardiovascular Information Registry (CVIR) at the Cleveland Clinic Foundation. All data were entered prior to the surgery. Medication use was recorded preoperatively (30 days prior to surgery); intraoperatively; and postoperatively (while leaving the operating room (OR)). Blood pressure was measured to the nearest 1 mmHg using indirect mercury column sphygmomanometry. Height and weight were directly measured and body mass index was calculated as weight in kilograms divided by the square of height in metres. Diabetes was considered present if insulin or oral hypoglycaemic medications were being used or if the patient had been prescribed a diabetic diet. Hypertension was defined as a resting blood pressure ≥ 140 mmHg, a resting diastolic blood pressure ≥ 90 mmHg, or use of medications to reduce blood pressure. Mild CAD was defined as the presence of at least one coronary artery stenosis (50% or greater diameter) on coronary angiography, and severe CAD was defined as the presence of two or more coronary arteries with stenosis. Date of first and most recent myocardial infarction (MI) was noted. PVD was noted from the patient's record. Patient's rhythm was verified by electrocardiography on admission and on discharge. Carotid artery disease was coded as present if > 20% stenosis was seen on carotid artery ultrasound. History of recent (<2 weeks) or remote (>2 weeks) stroke was noted. Previous history of systemic embolus was noted.

Intraoperative echocardiography and detection of atheroma
A standard TEE study was performed during cardiac surgery in each patient by use of a multiplane 5–7.5 MHz transducer attached to an echocardiographic machine. All studies were recorded on standard VHS tape and interpreted subsequently. The echocardiographic images were evaluated for the presence of aortic atheroma, thickness of the atheroma, and the characteristic of the atheroma (mobile/protruding/sessile) in the ascending, arch, and descending thoracic aorta. Aortic atheroma was graded as absent; mild (<4 mm without complex features); moderate (≥4 mm without complex features); and severe (any size with protruding or mobile components).9 Since the prognosis for plaques < 4 mm does not vary, we included any plaque < 4 mm as mild atheroma.9 All TEE images were reviewed by two different cardiologists. It should be noted that only patients with a complete echocardiographic evaluation of all segments of the aorta were included in the study. All patients had an ejection fraction (EF) noted during the intraoperative TEE or with a transthoracic echocardiography within 1 week prior to the surgery.

Outcomes
The primary outcome was all-cause mortality. We used the Social Security Death Index (SSDI), which has been shown to be highly specific (>99.5%) and unbiased.20,21 We have previously compared our CVIR registry survival data based on active follow-up with SSDI and found a sensitivity of 97%.22 The mean follow-up was 2.8 years (range 0.06–6 years), and the median follow-up was 2.6 years (interquartile range 1.5–4.2 years).

Statistical analysis
Baseline characteristics are recorded as mean ± standard deviation for continuous variables and number (%) for categorical variables. Differences in baseline characteristics according to atheroma severity were tested using the Kruskal–Wallis and Mantel–Haenszel {chi}2 extension tests as appropriate. The unadjusted association of atheroma severity with survival was examined by the construction of Kaplan–Meier curves, with differences tested by means of the log-rank {chi}2 statistic. Multivariable modelling was performed using a wholly parametric method, taking into account an early phase immediately following surgery and a late phase that continued years into follow-up.23 This approach accounts for the possibility of non-proportional hazards, a common occurrence when considering outcomes following cardiac surgery. We carefully tested for non-linear associations for all continuous variables by means of appropriate transformations. We created dummy variables for mild, moderate, and severe atheroma with no atheroma serving as the primary comparison. In a sensitivity analysis, we treated atheroma as a purely ordinal variable (with values 0, 1, 2, and 3 for none, mild, moderate, and severe, respectively) and obtained essentially similar results.

As an additional test of independent prediction, we performed propensity score matching.24–26 Propensity analysis allows one to assure that enough overlap of baseline characteristics is present to allow for valid adjustments for confounding and selection bias.27,28 We generated a propensity score for atheroma severity as a function of all the baseline characteristics listed in Tables 1 and 2 with a non-parsimonious logistic regression model. Variables used to generate the propensity score are listed in the appendix (Table A1). The c-statistic (analogous to an ROC curve) for the logistic model was 0.92, indicating excellent discrimination. The score was then used to match subjects with mild, moderate, or severe atheroma with subjects with no atheroma by means of a greedy-matching algorithm. We confirmed excellent matching by carefully examining the distribution of propensity scores (and their variances) along with all baseline characteristics in the matched cohorts. For example, in the cohort that matched severe atheroma to no atheroma, the propensity score in the severe group was 0.369 + 0.213, and in the no atheroma group, it was 0.368 + 0.215. Subsequently, parametric survival modelling was repeated on the matched cohorts with the incorporation of the propensity score as a continuous covariate. All analyses were performed using SAS software versions 8.2 and 9.1 (SAS Inc., Cary, NC, USA). All P-values were two-sided, with those < 0.05 considered statistically significant.


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  		Table 1 Variables of patient data according to severity of atheroma

 

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  		Table 2 Surgical characteristics according to the severity of atheroma

 

   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Conclusions
 Appendix
 Acknowledgements
 References
 
Baseline characteristics
There were 2878 (34%) patients with no atheroma; 4129 (48%) patients with mild atheroma; 1215 (14%) with moderate atheroma; and 359 (4%) with severe atheroma (Table 1). Compared with those with no atheroma, patients with severe atheroma were much older, much more likely to have PVD, and much more likely to have had prior MI and a lower EF. Cigarette smoking was not significantly different among the groups. Patients with severe atheroma were more likely to have severe CAD and more likely had a remote cerebrovascular accident. Patients with severe atheroma had a higher baseline creatinine. Patients with any atheroma grade had slightly higher rates of atrial fibrillation than those without any atheroma. Patients with severe atheroma were more likely to be undergoing CABG (Table 2).

Severity of atheroma and mortality
There were a total of 1000 deaths. Death rates were increased in patients with moderate [relative risk (RR) 3.29, 95% CI 2.50–4.32, P < 0.0001] and severe atheroma (RR 5.21, 95% CI 3.65–7.41, P < 0.0001) (Figure 1). Survival rates for none, mild, moderate, and severe aortic atheroma were 95, 92, 83, and 72% at 3 years and 90, 86, 76, and 66% at 5 years, respectively. After adjusting for age, gender, diabetes, hypertension, smoking, renal function, EF, coronary disease severity, PVD, prior stroke, type of surgery, MI history, and multiple other confounders, severe atheroma remained modestly predictive of risk (adjusted RR 1.50, 95% CI 1.10–2.04, P = 0.01); but moderate atheroma and mild atheroma were not predictive of increased risk. A detailed description of the two-phase parametric model is shown in Table 3. When atheroma was treated as an ordinal variable (0, no atheroma; 1, mild atheroma; 2, moderate atheroma; 3, severe atheroma) and an overall test was performed, it was a significant predictor of late-phase mortality (parameter estimate = 0.13, standard error = 0.058, P = 0.028).


Figure 1
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  		Figure 1 Kaplan–Meier survival curves relating atheroma grades (none, mild, moderate, or severe) to mortality. Note there is worse survival with increasing grade of atheroma.

 

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  		Table 3 Multivariable model with the phase-related variables and coefficients

 
Severity of atheroma and mortality: propensity analysis
The variables used to generate the propensity score are listed in the appendix (Table A1). The propensity score was strongly predictive of mortality (P = 0.02 for the early phase and P < 0.0001 for the late phase). In this propensity analysis that matched patients with severe atheroma and no atheroma using comparable range of variables, severe atheroma was no longer predictive of risk (adjusted RR 1.39, 95% CI 0.87–2.23, P = 0.17) (Figure 2).


Figure 2
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  		Figure 2 Kaplan–Meier survival curves after propensity matching relating no atheroma and severe atheroma. Note there is no early separation of survival curves after propensity analysis.

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Conclusions
 Appendix
 Acknowledgements
 References
 
The significance of aortic atheroma in relation to all-cause mortality has been studied only in high-risk patients (undergoing CABG and patients referred for embolic episodes).6,11–14 The present study involving 8581 patients is the largest study on the association of aortic atheroma with long-term survival in patients undergoing any cardiac surgery. Our findings suggest that severe atheroma detected by intraoperative TEE is associated with increased long-term mortality in patients undergoing any cardiac surgery (RR 1.50, 95% CI 1.10–2.04, P = 0.01). The relationship is weak when using a propensity analysis, suggesting that severe aortic atheroma may be a marker for mortality associated with known complications of atherosclerosis rather than mortality due to aortic atheroma itself. Mild atheroma and moderate atheroma detected by TEE do not increase the risk of long-term mortality in these patients.

Prevalence of severe aortic atheroma
The prevalence of severe atheroma (4%) in our study was comparable with a postsurgical study (5%)12 and the recently published SPARC data (7%), which was a population-based non-surgical study.13 The slightly increased rates in the SPARC study were due to the classification into only two groups, not three groups as in our study. In addition, patients with severe aortic atheroma may not be referred to cardiac surgeries and hence there were lower rates in cardiac surgical studies compared with the SPARC study, which was undertaken among the general population. Other case–control studies have shown similar prevalence of severe atheroma in the control subjects (929 and 4%30).

Aortic atheroma and postsurgical mortality rates
There have been only few studies that evaluated long-term postsurgical survival in patients with severe atheromatous disease.12,31 Although our study included both CABG and/or valve surgeries, 3 year survival rates for severe atheroma (~72%) in our study was comparable with a recent study that included only CABG patients with severe atheromatous disease.31 In another study that included both CABG and valve surgeries in different proportions, the survival rates were similar to our study.12 In the AWESOME trial, patients with high-risk features (based on clinical/laboratory criteria) undergoing CABG had 3 year survival rates of 79%.32 Also, the postsurgical survival rates for absent and mild aortic atheromatous disease in our study is comparable with previously published reports in low-risk patients (based on clinical/laboratory criteria).33 It is reasonable to conclude that patients with severe atheroma have postsurgical survival rates similar to high-risk (clinical/laboratory) patients; and patients with absent or mild atheroma have rates similar to low-risk (clinical/laboratory) patients. The survival curves (Figure 1) separate early and increase after mean follow-up, suggesting early and sustained risk with increasing severity of aortic atheroma. However, this is not seen in the propensity-matched analysis in Figure 2, suggesting that the increased early risk seen with severe aortic atheroma may be due to its association with high-risk clinical features.

Aortic atheroma and long-term survival predictors
There have been numerous studies that have looked at long-term predictors of mortality in patients undergoing cardiac surgery, with most of them being CABG.15–19 Among various studies reviewed by the ACC/AHA committee, consistent predictors of long-term mortality subsequent to CABG included advanced age, low EF, diabetes, severity of CAD, type of graft, hypertension, history of MI, renal dysfunction, and congestive heart failure.34 The fact that independent associations exist between aortic atheroma and most of the aforementioned predictors has given rise to the interest in aortic atheroma as a predictor of long-term mortality. Previous studies have shown aortic atheroma to be independently predictive of long-term mortality.6,11,12 In a study of 1957 cardiac surgical patients, aortic atheroma was independently predictive of long-term survival.12 This study was limited by the fact that the authors used only six predefined predictors of mortality in the multivariate model and aortic atheroma was visualized only in the ascending aorta. Another study of 189 patients revealed that an advancing aortic atheroma grade was a strong predictor of death after CABG.6 This study was limited by a small sample size and a follow-up period of only 6 months. A recent prospective study of 125 patients showed that complex aortic atheroma was associated with a high risk of cardiac events but this study included only patients referred for sources of embolism and had a selection bias.11 The rates of complex atheroma in this study were ~40% and did not represent the general population. These studies involving non-surgical patients were generally limited by sample sizes and were restricted to stroke/TIA patients. A previous study by Montgomery et al.35 assessing the natural progression of aortic atheroma in a random population did point out that although aortic atheroma was associated with CAD, carotid artery disease, and PVD, it did not have an independent effect on mortality. This study was limited by sample size as well.35 Recently published SPARC data in 579 patients13 also revealed that aortic atherosclerosis is not an independently significant risk factor in cardiac or cerebrovascular events in a general population.

Aortic atheroma has been associated with advancing age,8,36 CAD severity,1 hypertension,37 renal dysfunction,38 and diabetes.39 In our study, severity of aortic atheroma was univariately associated with advanced age, low EF, increased creatinine, severity of CAD, and history of MI. Low EF could be secondary since severe aortic atheroma is more often associated with severe CAD and previous MI. Also in our study, patients with severe aortic atheroma were more likely to undergo CABG than those without severe aortic atheroma—again probably due to the higher prevalence of severe CAD (60%) among patients with severe aortic atheroma, compared with those with no atheroma (16%). Our data suggest that a strong association exists between severe aortic atheroma and increased mortality by univariate analysis (RR 5.21; P < 0.001). After adjusting for multiple confounders (known clinical/imaging risk factors), severe aortic atheroma was associated with increased long-term mortality (RR1.50, P = 0.01). The association was weak and lost statistical significance (RR 1.39; P = 0.17) after propensity analysis, implying an absence of causal association between severe aortic atheroma and increased long-term mortality.

Mechanisms of atheroma and mortality
Various mechanisms have been described for the association of aortic atheroma with known markers of mortality.1,8,12,36 Inflammation plays a key role in atherosclerosis40 and could be a unifying factor. Elevated levels of C-reactive protein have been shown to be associated with severe aortic atheroma.39,41 A recent in vivo study showed that C-reactive protein is an active participant in the atherogenic process.42 Inflammation, as represented by C-reactive protein, has been shown to be independently predictive of cardiovascular events and mortality.43 Hence, the association of severe aortic atheroma and mortality by multivariable analysis could be explained by its association with inflammatory markers. Severe aortic atheroma is a marker of generalized atherosclerosis and thus could be a marker of various complications of atherosclerosis that increases the risk of mortality.

Limitations
The main limitation of the study is that the prevalence of severe aortic atheroma was low and hence may have lacked statistical power. Aortic atheroma is primarily a disease of the elderly and our patient population had many younger patients (<60 years) and non-CABG patients who could have decreased the strength of the association. There may be an inherent selection bias since patients with severe aortic atheroma may not have been referred to cardiac surgery. However, our study has prevalence rates comparable with other studies in cardiac surgical patients and in the general population. Since this study involved only cardiac surgical patients, extrapolating the results to the general population may be difficult. The study did not look at the impact of the location of atheroma primarily since stroke was not an endpoint in this study. There were 3169 patients with missing echocardiography data and 306 patients with no clinical data recorded. Comparison of the baseline clinical and surgical characteristics of the excluded cohort with the final study population showed no major differences (Table A2). The final limitation is that since the patients were operated during a relatively short period (1996–2001), we were unable to examine the long-term secular trends.


   Conclusions
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
Appendix
 Acknowledgements
 References
 
Intraoperative TEE is currently performed routinely during most cardiac surgeries and is the diagnostic modality of choice for assessing atheromatous burden in the aortic arch, descending thoracic aortic atheroma, and most of ascending aortic atheroma.31,44 Current data have consistently shown that severity of aortic arch atheroma by intraoperative TEE is related to stroke and other adverse cerebral outcomes.5–10 On the basis of our current study, severe aortic atheroma is associated with increased long-term mortality (RR 1.50 95% CI 1.10–2.04) and may have prognostic information in addition to the existing AHA/ACC guidelines risk stratification schemes in predicting long-term mortality in all cardiac surgical patients. The propensity analysis shows that severe atheroma is not an independent predictor of long-term mortality and it may be due to the association of severe aortic atheroma with known complications of atherosclerosis that causes an increased mortality. Further studies are required to elucidate causal association.


   Appendix
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 Appendix
Acknowledgements
 References
 

Table A1 Variables used in the propensity analysis with the parameter estimates and coefficients

Parameter Estimate Standard error Wald {chi}2 P-value
Age 0.0901 0.00898 100.6319 <0.0001
Male sex 0.3381 0.1503 5.0592 0.0245
Body mass index –0.0132 0.0137 0.9263 0.3358
EF –0.00404 0.00597 0.4576 0.4987
PVD 1.0903 0.1559 48.8975 <0.0001
Chronic obstructive pulmonary disease 0.7490 0.1602 21.8582 <0.0001
Insulin-dependent diabetes –0.0216 0.2630 0.0068 0.9345
Non-insulin-dependent diabetes 0.3610 0.1855 3.7871 0.0516
Creatinine 0.2855 0.0703 16.5191 <0.0001
Current smoker 0.7250 0.2182 11.0447 0.0009
Previous MI 0.3288 0.1832 3.2196 0.0728
Atrial fibrillation 0.1470 0.2461 0.3570 0.5502
Pacemaker –0.4068 0.3966 1.0523 0.3050
Hypertension 0.9326 0.1943 23.0326 <0.0001
MI within the last week 0.2178 0.3392 0.4121 0.5209
Recent stroke (<2 weeks) 0.1446 1.4040 0.0106 0.9180
Remote stroke (>2 weeks) 0.0620 0.2709 0.0524 0.8189
Aortic valve replacement 0.2872 0.1724 2.7737 0.0958
Aortic valve repair –0.1562 0.5784 0.0729 0.7872
Mitral valve replacement 0.4512 0.3338 1.8276 0.1764
Mitral valve repair 0.00884 0.2788 0.0010 0.9747
Tricuspid valve repair –0.2294 0.37773 0.3688 0.5437
Unilateral internal mammary graft 0.3622 0.2070 3.0617 0.0802
Bilateral internal mammary graft 0.8360 0.4620 3.2749 0.0703
Mitral valve regurgitation –0.0163 0.0785 0.0429 0.8360
Mild CAD 0.6833 0.3149 4.7101 0.03
Severe CAD 1.2651 0.35 13.0635 0.0003
Emergent surgery –1.7055 0.5623 9.1982 0.0024
Intra-aortic balloon pump –0.8797 0.5751 2.3398 0.1261
Coronary artery bypass surgery 0.0761 0.3117 0.0596 0.8071
Electrocardiogram evidence of infarction –0.0855 0.2151 0.1580 0.6910


Table A2 Comparison of baseline characteristics between study cohort and patients excluded due to missing echocardiography dataa

Variables Total patient population
Excluded patients (N = 3169), n (%) Included patients (N = 8581), n (%)
Age (years) 61 ± 14 62 ± 14
Male sex 2159 (68) 5443 (63)
Body mass index (actual number) 28 ± 5 28 ± 5
PVD 1025 (32) 2719 (32)
Insulin-dependent diabetes 208 (9) 619(7)
Non-insulin-dependent diabetes 499 (16) 1108 (13)
Current smoker 1828 (58) 3956 (46)
Previous MI 1232 (39) 2840 (33)
Electrocardiogram evidence of infarction 557 (18) 1273 (15)
Atrial fibrillation 259 (8) 932 (11)
Hypertension 1921 (62) 5165 (62)
Creatinine (actual number) 1.17 ± 1 1.14 ± 0.9
Aortic valve replacement 732 (23) 2477 (28)
Aortic valve repair 135 (4) 322 (4)
Mitral valve replacement 271 (9) 704 (8)
Mitral valve repair 731 (23) 2574 (30)
Unilateral internal mammary graft 1343 (42) 3158 (37)
Bilateral internal mammary graft 174 (5) 271 (3)
Mild CAD 756 (24) 2077 (24)
Severe CAD 1140 (36) 2497 (29)
Emergent surgery 178 (5) 277 (3)
Coronary artery bypass surgery 1836 (58) 4399 (51)

aOf the 3475 patients excluded, 306 had no clinical data for comparison.


   Acknowledgements
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 Appendix
 Acknowledgements
References
 
M.S.L. is funded by NHLBI grants (RO1 HL-66004-2, RO1 HL-072771-02, and P50 HL-77107-1). We thank Marie Campbell for her editorial assistance.

Conflict of interest: none declared.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 Appendix
 Acknowledgements
 References
 

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The Year in Echocardiography
J. Am. Coll. Cardiol., March 25, 2008; 51(12): 1221 - 1229.
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