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European Journal of Heart Failure 2005 7(5):852-858; doi:10.1016/j.ejheart.2005.01.019
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© 2005 European Society of Cardiology

Different prognostic impact of systolic function in patients with heart failure and/or acute myocardial infarction

Jens Jakob Thunea,*, Christian Carlsena, Pernille Buchb, Marie Seibæka, Hans Burchardtb, Christian Torp-Pedersenb, Lars Købera and on behalf of the DIAMOND investigators

a Department of Cardiology, B2141, The Heart Centre University Hospital of Copenhagen, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen O, Denmark
b Department of Cardiovascular Medicine, University Hospital of Copenhagen Bispebjerg Hospital, Bispebjerg Bakke 21, DK-2400 Copenhagen NV, Denmark

* Corresponding author. Tel.: +45 35 45 28 74; fax: +45 35 45 34 53. E-mial address: jjt{at}heart.dk


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
Aims: To study the prognostic importance of left ventricular systolic function in patients with heart failure (HF) and acute myocardial infarction (AMI) with respect to the presence of prior heart failure and known ischemic heart disease.

Methods: In 13,084 consecutive patients diagnosed with either AMI or HF, a medical history and an echocardiographic assessment of left ventricular systolic function by wall motion index (WMI) were obtained. Patients were divided into four groups: AMI with or without a history of HF, and primary HF (no recent AMI) with or without a history of ischemic heart disease (IHD). Mortality was assessed after nine years of follow-up.

Results: WMI stratified patients according to all-cause mortality in all four groups of patients (p< 0.0001). For a decrease in WMI of 0.3 (corresponding to a decrease in left ventricular ejection fraction of 0.1), the hazard ratio was 1.61 (95% CI:1.48–1.76) for AMI patients without prior HF, 1.43 (1.38–1.48) for AMI patients with prior HF, 1.26 (1.22–1.30) for primary HF patients with IHD and 1.23 (1.18–1.27) for HF patients without IHD.

Conclusion: WMI stratifies patients with IHD and/or HF according to risk of all-cause death. The presence of HF attenuates the prognostic power of WMI.

Key Words: Ejection fraction • Chronic heart failure • Acute myocardial infarction • Wall motion index • Epidemiology

Received August 24, 2004; Revised December 20, 2004; Accepted January 27, 2005


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 References
 
Reduced left ventricular systolic function is an established marker of risk of adverse cardiac events in patients with an acute myocardial infarction (AMI). In patients with chronic heart failure (HF), however, the prognostic importance of left ventricular systolic function is disputed. While a number of studies [1–4] have reported a prognostic impact of reduced systolic function in patients with chronic heart failure other studies have not [5,6] and one study found an increased risk among patients with a normal left ventricular systolic function compared to those with reduced function [7]. Recent work has demonstrated that other components of ventricular function concerning relaxation and filling during diastole are important for the prognosis in patients with HF and AMI [8–10]. Such components might be of particular prognostic importance in patients with preserved systolic left ventricular function.

The present study was thus conducted to assess the correlation between WMI and mortality in a large group of patients with myocardial infarction and/or HF who were included systematically and simultaneously into a register.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 References
 
2.1. Patients
The study population has previously been presented in detail [11]. Briefly, 5491 consecutive patients admitted due to HF and 8225 consecutive patients admitted with an AMI were screened for eligibility to the DIAMOND (Danish Investigations of Arrhythmia and Mortality on Dofetilide) studies between November 1993 and July 1996. The two studies were designed to test the prophylactic use of the selective potassium-channel blocker, dofetilide, in patients at high risk of cardiac events. Patients could be screened more than once, but for the current study only the first screening was used causing the population size to decrease by 216 patients to 13,500 (HF: 5358; AMI: 8142). In addition, 416 patients had missing information about previous HF or ischemic heart disease (IHD). Hence, the population of the current study is composed of the screening populations of both DIAMOND studies and consists of 13,084 patients (HF: 5112; AMI: 7972) for whom echocardiographic, follow-up, and essential clinical variables are available.

Screening of patients was conducted following provision of informed consent and consisted of a medical history and an echocardiographic examination stored on videotape. To be considered for screening patients had to be diagnosed with either HF or AMI within 7 days. HF patients were defined as patients treated with diuretics for suspected HF and who had been in NYHA class 3 or 4 within the last month of screening. HF was not necessarily the primary diagnosis at admission. AMI was defined as chest pain lasting >20 min and/or electrocardiographic changes indicative of AMI accompanied by a significant elevation of cardiac enzymes. For the current study patients were further divided into HF patients with or without IHD and AMI patients with or without HF. The presence of IHD was assessed during screening and required a history of AMI or angina pectoris and did not require objective confirmation but the majority of patients had been hospitalised previously due to AMI.

In the AMI population the presence of HF was assessed on screening and based on history and required diuretic treatment because of HF. To ensure that AMI patients diagnosed with chronic HF indeed had a chronic history, we retrospectively defined that in order to be chronic duration of HF had to be ≥30 days. Many patients had been investigated for other diseases such as chronic pulmonary disease but this was not a prerequisite for the classification of HF in the register as it was not feasible with such a large screening population.

Thus, the assessment of the presence of IHD, AMI, and HF was done at the inclusion of patients into the DIAMOND studies while the construction of the four patient groups for this report was done retrospectively and not part of the original protocol.

Creatinine clearance was calculated from serum creatinine values using the Cockcroft–Gault formula. Data on the use of beta-blockers were not available.

The DIAMOND studies were approved by all local ethical committees.

2.2. Echocardiographic examination
All patients were examined with standard 2-dimensional echocardiography according to recommendations [12]. Staff at the 34 participating centres was trained in echocardiography with special attention to imaging technique. Examinations were stored on videotape and evaluated centrally. Data on intra- and inter-observer variability for the centres and the core-laboratory have been reported previously [13].

For grading of wall motion a 16-segment scoring system was used where –1 represents dyskinesia, 0 akinesia, 1 hypokinesia, 2 normokinesia, and 3 hyperkinesia. With this reverse scoring system, wall motion index multiplied by 30% provides an acceptable approximation of LVEF [14]. For this reason no other methods for assessing LVEF were used. For the analyses wall motion index was categorized into these four groups (with approximate left ventricular ejection fraction shown in parentheses): <0.9 (<0.25), 0.9–1.2 (0.25–0.37), 1.3–1.6 (0.37–0.50), and >1.6 (>0.50).

2.3. Mortality status
Survival status was obtained from the Danish Civil Register which registers all deaths of Danish citizens within two weeks. The register was interrogated for survival status in April 2003 providing a follow-up time between 7 and 10 years.

2.4. Statistical analyses
All analyses were performed using SAS version 8.02. A p-value below 0.05 was considered significant in all analyses. Baseline variables were compared using a continuity-adjusted {chi}2-test for discrete variables and the Wilcoxon Rank Sum test for continuous variables. Life-table plots were constructed using the Kaplan–Meier method and death rates were compared using a log-rank test. Hazard ratios were calculated with a multivariate Cox proportional hazards model where model assumptions (proportional hazard, lack of interaction and log-linearity of continuous variables) were valid unless otherwise indicated. For patients with prior chronic HF the wall motion index did not meet the requirements of log-linearity necessary for the Cox proportional hazards model because of a high mortality in the group of patients with HF and preserved systolic function. To accommodate this, wall motion index was set to 1.7 for all patients with a wall motion index above 1.6, after which all variables in the Cox model demonstrated log-linearity. The problem with non-linearity was a result of the fact that there was no difference in survival with higher WMI in this group and therefore no biological information has been compromised by fusing the patients into one group as WMI=1.7 and above. Since this group represents an approximate ejection fraction range from 0.51 to 0.60 this is in accordance with the rest of the literature where an LVEF> 0.50 is considered preserved.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 References
 
Baseline demographics for the study population are presented in Table 1. All baseline variables except prevalence of hypertension differed significantly between groups. The overall mortality rates for the four patient groups are shown in Fig. 1. The three HF groups show a very high and almost identical mortality rate while the AMI patients without prior chronic HF have a much lower mortality rate. There were significant differences between all groups (p < 0.001) except between the group with AMI and prior HF and the group with HF and IHD (p=0.10).


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  		Table 1 Baseline demographics*,a

 


Figure 1
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  		Fig. 1 Kaplan–Meier life-table plots of mortality in the four patient groups (p<0.001 for overall difference). For between-group comparisons please see text.

 
Mortality rates for the four patient groups stratified according to wall motion index groups are shown in Fig. 2a–d. Overall, there is a decrease in survival with decreasing WMI in all four patient groups (p<0.001). However while the curves are significantly different for all four subgroups it can readily be appreciated that risk stratification with wall motion index is most powerful in AMI patients without a history of HF (Fig. 2A). In this group there was a significant difference in survival between all four WMI-groups (p<0.001). For the group of patients with AMI and prior chronic HF (Fig. 2B) there was a significant difference in survival only between the two groups with WMI>1.6 and WMI<0.9 (p<0.01). For patients with HF and IHD (Fig. 2C) there was a significant difference between all groups (all p<0.001) except between the groups with WMI>1.6 and WMI 1.3–1.6 (p=0.12). For HF patients without signs of IHD (Fig. 2D) there was no difference in survival between the three groups with decreased WMI (all p>0.05) while the group with preserved systolic function had a significantly better survival than the three lower groups (p<0.03). There was a significant interaction between history of atrial fibrillation and the predictive value of WMI in the group of patients with chronic HF without IHD so that a history of atrial fibrillation in this group of patients made the predictive value of WMI insignificant (p=0.08).


Figure 2
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  		Fig. 2 Kaplan–Meier life-table plots of mortality in the four patient groups stratified according to WMI (p<0.0001 for overall difference for all four figures). For comparisons between the four WMI-groups please see text.

 
Fig. 3 illustrates the hazard ratio associated with decreasing wall motion index in the four subgroups in univariate analyses.


Figure 3
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  		Fig. 3 Hazard ratios of all-cause mortality associated with decreasing WMI for the four patient groups. Univariate analysis (p<0.001 for all four patient groups).

 
The results of a Cox proportional hazards analysis are shown in Table 2. A decrease in wall motion index of 0.33 (corresponding to a decrease in LVEF of 10%) confers a 60% higher risk for AMI patients without prior chronic HF, a 43% higher risk for AMI patients with prior chronic HF and an approximately 25% higher risk for the two groups presenting with HF.


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  		Table 2 Hazard ratios attributable to a decrease in WMI of 0.33*

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
References
 
The present study shows that the prognostic value of global systolic function, as expressed by wall motion index, is present across a spectrum of heart diseases. However, the prognostic importance differs markedly between subsets of heart disease, which, to our knowledge, has not been investigated previously.

The present study is unique in that both AMI and HF patients were examined at the same institutions, by the same physicians, and during the same time period and WMI was assessed by four of the authors blinded to the diagnosis of the patients. This makes it possible to compare the value of wall motion index across disease subsets because problems with changes in practice over time or with changing investigators are eliminated. Furthermore, this is the largest population of consecutively included patients with AMI or HF with an extensive follow-up period presented to date. This provides mortality rates between 70% and 80% for patients with HF, which makes the detection of even small differences in risk possible.

However, some considerations concerning the present population must be taken into account. One is the limitation that the definition of chronic HF required an exacerbation of HF within the recent month. Thus the HF population in the present study consists of unstable HF patients who are at an increased risk of adverse events and they are therefore not representable of all HF patients in general. Furthermore, the diagnosis of HF was not as stringent at the time of the study and was left to the individual physicians. However, uniform requirements for screening were used in all centres.

A second concern is regarding the allocation of HF patients into the categories of ischemic and non-ischemic. In the present study 57% of patients with HF presenting without an AMI were considered to have IHD. Knowing that IHD can cause HF despite the lack of symptomatic ischemia this is more likely to be an underestimation than an overestimation of the prevalence of IHD in the HF population. The prevalence however is in concordance with the reported prevalence of IHD of 52% in patients with HF from an invasive study of coronary artery morphology [15]. For patients with a depressed LVEF without structural heart disease the prevalence of IHD determined invasively has been reported as high as 82% but this was in a population referred for cardiac catheterization [16]. The two HF groups in this study are very similar in mortality rate and impact of wall motion index so assuming that the majority of IHD patients are allocated correctly the misclassification of a smaller group of patients is not likely to influence results.

Our findings are consistent with the earlier report from the DIAMOND-HF database that wall motion index is prognostic in HF [17]. Our results, that WMI is a powerful tool for risk stratification in patients presenting with an acute or recent myocardial infarction, are in line with reports from several other groups [18–20] and we have extended this finding by showing that WMI performs better as a marker of risk in an AMI population without prior HF than in a population with AMI and prior HF. Furthermore, though significantly prognostic in patients included in the study due to HF, WMI has a much smaller influence on overall mortality in this group. This is consistent with reports that HF with preserved LVEF carries almost as dismal a prognosis as HF with an impaired LVEF [1–3].

In the present study approximately half of the patients with HF did not have a substantial decrease in LVEF and as in other studies this group still had a high mortality [5,7,8]. The syndrome of HF with preserved LVEF is still widely unexplained. To suggest that all patients with this syndrome simply have so-called diastolic HF would probably be an oversimplification particularly in view of the fact that most patients with HF and preserved LVEF do not have echocardiographic signs of an elevated left ventricular filling pressure [21,22]. The only invasive study to address this problem found that all patients with HF and preserved LVEF had diastolic dysfunction [23,24] but in that study all subjects had concentric remodeling on echocardiography [25] wherefore the result is not surprising and does not fully answer the question. An invasive study on patients with HF and preserved LVEF without obvious signs of elevated left ventricular pressures is necessary to resolve this debate. However, whether all patients with HF and preserved LVEF have so-called diastolic HF or not, in our view the presence of HF with preserved LVEF does constitute a unique syndrome which should be considered distinct from HF with impaired LVEF.

What then is the cause of the variable impact of WMI across these different disease subgroups? In all likelihood the prognostic value of WMI is high in patients without HF because global left ventricular systolic function correlates quite accurately to the degree of affected cardiac function in these patients. The presence of HF however signifies a syndrome involving neurohumoral and haemodynamic changes which influence prognosis [26] and this might attenuate the predictive power of WMI. WMI is most suited for detecting reductions in regional function and the haemodynamic and neurohumoral factors involved in HF are presumably predominantly affecting left ventricular function globally. Thus, the WMI might not correlate as well to the extent of impaired myocardial performance when these global influences are present. Furthermore not only the heart but the entire body is affected in patients with HF by way of cytokines and neurohormones which cause failure of other organs and wasting of skeletal muscle and therefore WMI as a parameter of cardiac function would be likely to lose some of its prognostic value.

From our results it would seem that WMI primarily is a marker of risk for patients with AMI and that the presence of HF attenuates the prognostic importance of WMI. Thus, diverging results reported on the prognostic importance of left ventricular systolic function can be explained, at least in part, by different populations, and especially in different proportions of patients with HF.

Another important aspect to bear in mind when considering our results is that, in order to be included in this study, HF patients had to have survived for at least a period of time. These patients had thus already demonstrated an ability to survive despite a reduced left ventricular systolic function. In this patient group the duration of HF and how long patients had survived despite symptomatic HF might provide important information in addition to merely the actual level of left ventricular impairment. This observation could have important clinical implications for patient treatment as well as for clinical trials. Often HF patients are selected for trials based on left ventricular systolic function alone, and this might explain why many trials report a surprisingly low risk among patients with severe left ventricular dysfunction, since all off these patients have demonstrated an ability to survive and are capable of entering a study.

Summed up, the main limitations of the study are that patients had to have been hospitalised due to AMI or HF thus putting our study population at a higher risk than HF patients or IHD patients in general, and that the diagnosis of IHD in the HF population was based on history and not requiring objective assessment. Furthermore, the diagnosis of HF differed from current guidelines as it was based upon the use of diuretics on suspicion of HF.

In conclusion, the underlying cause of impaired left ventricular function needs to be taken into consideration when left ventricular systolic function is used to assess prognosis. WMI stratifies patients with IHD and/or HF according to risk of all-cause death, but WMI is best at risk stratification in patients with AMI without a history of HF and least in patients hospitalised with chronic HF.


   Acknowledgement
 
Funding source: The DIAMOND studies were sponsored by a grant from Pfizer Central Research, Sandwich, UK. This study was supported by a grant from the Danish Heart Association. No additional funding or conflicts of interest.


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 

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