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European Journal of Heart Failure 2002 4(1):33-40; doi:10.1016/S1388-9842(01)00209-4
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© 2002 European Society of Cardiology

Normokinesia adjacent to left ventricular aneurysm: a differential risk for sudden cardiac death

Constantine A. Hassapoyannesa,b,*, Brent T. McLaurinb, Carlton A. Hornungb, Kiran Chavdaa,b and Dan-Victor Giurgiutiua

a Division of Cardiology (111C), Department of Medicine, William Jennings Bryan Dorn Veterans Affairs Medical Center WJB Dorn VAMC, 6439 Garners Ferry Road, Columbia, SC 29209-1639, USA
b University of South Carolina School of Medicine Columbia, South Carolina, USA

cahass{at}aol.com

* Corresponding author. Tel.: +1-803-776-4000 ext. 7142; fax: +1-803-695-7913


   Abstract
Top
 Abstract
1. Introduction
 2. Patients and methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 
Background: Following myocardial infarction, the ejection fraction (EF) is an indiscriminate predictor of both non-sudden cardiac death (NSCD) and sudden cardiac death (SCD). However, development of a left ventricular aneurysm (LVA) confers independent risk only for SCD. Thus, we tested the hypothesis that mechanical factors, other than the global left ventricular performance, are causally related to SCD in the presence of LVA.

Methods: A secondary analysis was conducted from a longitudinal, prospective, long-term follow-up cohort study of 66 patients with LVA (diastolic eccentricity and systolic dyskinesia) diagnosed by ventriculography. The left ventricular contour was divided into five segments and contractility scores for the residual myocardium and the segments adjacent to the aneurysm were allocated along with assessment of the EF. A normal adjacent segment was considered present when at least one segment adjacent to the aneurysm exhibited normokinesia. Presence of ventricular tachycardia was documented by Holter recording.

Results: At a 5.2-year median follow-up, there were 12 NSCD and 8 SCD. The EF was lower among patients who died vs. survivors (31.5% vs. 39.7%, P=0.01). Patients with NSCD and SCD, exhibited similar EF but disparate residual contractility scores (3.0 vs. 4.1, P<0.004). Among cardiac deaths, a decreasing residual contractility score differentially predicted NSCD (odds ratio=17.06, P<0.03), while a normokinetic adjacent segment differentially predicted SCD (odds ratio=21, P<0.02). Albeit a predictor of both NSCD and SCD, ventricular tachycardia increased markedly the model significance (P<0.004) only when tested with a normokinetic adjacent segment vis-à-vis SCD.

Conclusions: In the presence of LVA, the contractility of the non-aneurysmal myocardium is a differential predictor of death from pump failure. In contrast, a normal segment adjacent to LVA constitutes an independent and discriminate predictor of SCD, possibly through an arrhythmic substrate linked to the motion discordance between the expanding aneurysm and a normokinetic adjacent myocardium.

Key Words: Heart aneurysm • Death, Sudden, Cardiac • Arrhythmia • Stroke volume

Received March 21, 2001; Revised July 13, 2001; Accepted September 10, 2001


   1. Introduction
Top
 Abstract
 1. Introduction
2. Patients and methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 
Following myocardial infarction, the ejection fraction is a powerful, albeit indiscriminate, predictor of outcome [1–4]. However, when it develops, left ventricular aneurysm independently confers risk for sudden cardiac death, and arrhythmias may become prognostically more important than the ejection fraction [5]. Furthermore, risk of sudden cardiac death is imparted only when systolic dyskinesia is manifest [5,6] in contrast to the relative longevity of patients with rigid aneurysmal sacs [7,8]. Thus, in the context of aneurysm, either the ejection fraction is inadequate for risk stratification or there exists a distinct from myocardial failure mechanism for sudden cardiac death. We assessed the independent prognostic significance of the residual contractility and tested the hypothesis that the segmental motion adjacent to the aneurysm is pathogenetically linked to sudden cardiac death.


   2. Patients and methods
Top
 Abstract
 1. Introduction
 2. Patients and methods
3. Results
 4. Discussion
 5. Conclusions
 References
 
This study represents a secondary analysis of data collected to examine the risk of sudden and non-sudden cardiac death associated with ventricular aneurysm following myocardial infarction as we have described in detail elsewhere [5]. All patients with left ventricular aneurysm diagnosed in the course of hospitalization for evaluation of coronary artery disease between 1977 and 1985 were identified. Follow-up continued until January 1989 when the last patient identified would have been followed for at least 4 years. The definition of left ventricular aneurysm used herein, diastolic eccentricity and systolic dyskinesia, was met by 66 patients: 61 (92%) by contrast ventriculography and five (8%) by nuclear scintigraphy. All patients had a history of healed myocardial infarction with the minimum interval between ventriculography and the culprit myocardial infarction being 1 month.

Predictor variables considered included baseline demographics, social habits, co-morbidities, pertinent clinical and angiographic data as well as therapeutic modalities. A 24-h pre-discharge Holter recording was obtained in all patients. No studies were obtained within 72 h of an acute myocardial infarction. Ventricular tachycardia was defined as ≥3 sequential ectopic complexes at a rate of ≥110 beats/min. Measurement of the left ventricular ejection fraction was available, by contrast and nuclear ventriculography in 28 patients, by contrast ventriculography alone in 33 patients, and by nuclear ventriculography alone in five patients. When the estimate of the ejection fraction was available by both techniques, we chose the value obtained by nuclear scintigraphy.

By means of cine-ventriculography in the 30° right anterior oblique position (61 patients) or gated blood pool scintigraphy in the anterior position (5 patients), the left ventricular silhouette was divided into five segments (anterobasal, anterolateral, apical, inferoapical and inferobasal) for which scores were allocated based on wall motion (normal or hyperkinesia 5, mild hypokinesia 4, moderate hypokinesia 3, severe hypokinesia 2, akinesia 1, dyskinesia –1). When at least one myocardial segment adjacent to the aneurysm exhibited normal wall motion, a normal adjacent segment was considered present. The number of aneurysmal myocardial segments was recorded. In addition, we derived three contractility indices modified from the Coronary Artery Surgery Study protocol [9]: (1) a total contractility score obtained by averaging scores from all segments; (2) a corrected contractility score as above except that dyskinesia, like akinesia, was scored as a 1; and (3) a residual contractility score by averaging scores from the non-aneurysmal myocardium only. These indices can be conceptualized as: Total contractility score=d/(a+b); Corrected contractility score=(c+d)/(a+b); Residual contractility score=(c+d)/a, where a, is the end-diastolic volume of the non-aneurysmal myocardium; b, the end-diastolic volume of the aneurysmal sac; c, the volume displaced into the aneurysmal sac during systole; and d, the blood volume ejected into the aorta per stroke (effective stroke volume). Hence, the effective stoke volume plus the volume displaced into the aneurysmal sac during systole represents the stroke volume of the residual myocardium, i.e. the actual stroke volume (c+d). Thus, the total contractility score is analogous to the volume exiting the left ventricle expressed as a fraction of the left ventricular end-diastolic volume, i.e. the ejection fraction; the corrected contractility score, to the actual stroke volume expressed as a fraction of the total left ventricular end-diastolic volume; and the residual contractility score to the actual stoke volume expressed as a fraction of the end-diastolic volume of the non-aneurysmal myocardium only.

Two observers independently assessed segmental wall motion based on cine display using superimposition of the realigned end-diastolic and end-systolic frames. The presence of both diastolic eccentricity and systolic dyskinesia had to be documented by each observer prior to patient entry. Inter-observer variability of contractility scores was 0.6 grade in a 6-grade system (10%). There was no disagreement regarding the presence of at least one normal or hyperdynamic adjacent segment.

Follow-up was defined as the interval from the culprit myocardial infarction until January 1989. Those patients who died or were censored due to loss of contact prior to January 1989 were included in the cohort. Cardiac death was classified as sudden when the event occurred within 1 h of symptom-onset, and acute ischemia, myocardial infarction or left ventricular failure was not the cause. The mean interval between the culprit myocardial infarction and the cardiac catheterization was 9.1±2.2 months for the entire cohort. The mean intervals from the culprit myocardial infarction to cardiac catheterization among survivors, cardiac death, non-sudden cardiac death, and sudden cardiac death population subsets were 7.5±2.3, 12.7±5.0, 9.9±5.0 and 16.9±10.6 months, respectively. The difference between these intervals was not significant (survivors vs. total cardiac death population: P=0.91; survivors vs. non-sudden cardiac death population: P=0.81; survivors vs. sudden cardiac death population: P=0.90; and non-sudden vs. sudden cardiac death population: P=0.79).

2.1. Statistics
Kaplan–Meier curves were used to depict the survival of patients with high vs. those with low residual contractility score with respect to non-sudden cardiac death, and the survival of patients with presence vs. those with absence of a normokinetic adjacent segment with respect to sudden cardiac death. Since we previously demonstrated that in the presence of left ventricular aneurysm, the ejection fraction and ventricular arrhythmias were independent, albeit non-differential, predictors of outcome [5], univariate and multivariate Cox proportional hazards regression models (Statistical Package for the Social Sciences-7.5.1) were used to compare the contractility scores and normal adjacent segment to the ejection fraction and ventricular tachycardia in order to assess their effect on the risk of sudden and non-sudden cardiac death. Logistic regression was used to determine the ability of previously identified independent predictors to also discriminate between sudden and non-sudden cardiac death, from the population of cardiac deaths. Two non-cardiac deaths were also excluded. The null hypothesis was rejected for P<0.05 (two-tail).


   3. Results
Top
 Abstract
 1. Introduction
 2. Patients and methods
 3. Results
4. Discussion
 5. Conclusions
 References
 
Apical was the predominant aneurysm location (apical 91%, anterolateral 39%, inferior 24%). At a median follow-up of 5.2 years, there were 22 deaths. Of these deaths, 20 were cardiac, 8 sudden. Kaplan–Meier curves showed that with respect to sudden cardiac death, the survival of patients with presence vs. those with absence of a normokinetic adjacent segment diverged from the outset (Fig. 1); with respect to non-sudden cardiac death, the survival of patients with residual contractility score =3.5 and >3.5 diverged after 6 years (Fig. 2).


Figure 1
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  		Fig. 1 Cumulative percent survival comparing the groups with and without normal adjacent segment (NAS) for sudden cardiac death.

 


Figure 2
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  		Fig. 2 Cumulative percent survival comparing the groups with residual contractility score (RCS) =3.5 and >3.5 for non-sudden cardiac death.

 
3.1. Ejection fraction vs. contractility scores
The ejection fraction correlated with the total contractility score (Fig. 3) but not with the residual contractility score (R=0.19, P=0.14). Like the ejection fraction, the total and corrected contractility scores, which also reflect global rather than segmental ventricular performance, were lower among the total cardiac death population vs. survivors but did not discriminate between non-sudden and sudden cardiac death (Table 1). In contrast, the residual contractility score diverged between patients with non-sudden and sudden cardiac death (P=0.004, Fisher's Exact Test), even though these patients had a similar and proportionately distributed ejection fraction (Fig. 4).


Figure 3
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  		Fig. 3 Relation between the total contractility score and the ejection fraction.

 


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  		Table 1 Contractility characteristics

 


Figure 4
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  		Fig. 4 Distribution of sudden and non-sudden cardiac death by residual contractility score and ejection fraction. Horizontal and vertical interrupted lines correspond to the cohort's median residual contractility score and ejection fraction, respectively.

 
3.2. Risk stratification by outcome
According to the criteria used herein (Table 2), the prevalence of one, two, and three-vessel coronary artery disease among patients with sudden cardiac death and non-sudden cardiac death was: 42.9 vs. 22.2%, P=0.26; 14.3 vs. 63.6%, P=0.04; and, 14.3 vs. 9.1%, P=0.07, respectively. There was also a difference between the non-sudden and sudden cardiac death populations in gender distribution and prevalence of right coronary artery disease (Table 2). We [5] and others [10] have shown right coronary artery stenosis >70% to be a predictor of non-sudden cardiac death, since it reflects more myocardium in jeopardy when the majority of patients also manifest left coronary system disease. In turn, the gender difference is consistent with the higher prevalence of right coronary artery disease among women. Of all contractility (Table 1) and clinical (Table 2) characteristics, only the residual contractility score and normal adjacent segment discriminated between non-sudden and sudden cardiac death, and between these respective outcomes and survivorship.


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  		Table 2 Clinical characteristics in percent

 
3.3. Predictors of outcome (multivariate analysis)
In a univariate Cox regression model, decreasing ejection fraction as well as decreasing total, corrected and residual contractility scores predicted only non-sudden cardiac death [rate ratio (RR)=1.05, P<0.05; RR=2.7, P<0.02; RR=5, P<0.01; RR=2.5, P<0.02, respectively], whereas the presence of a normal adjacent segment predicted sudden cardiac death (RR=8.23, P<0.05). Importantly though, only two of these measures of contractility emerged as differential (discriminate) predictors of outcome: by univariate Cox regression analysis, a decreasing residual contractility score predicted non-sudden but not sudden cardiac death (RR=2.50, P<0.02), while the presence of a normal adjacent segment predicted sudden but not non-sudden cardiac death (RR=8.23, P<0.05). Moreover, when the population of cardiac deaths was considered separately, a decreasing residual contractility score differentially predicted non-sudden cardiac death (logistic regression model: non-sudden=1, sudden=0; OR=17.06, P<0.03), while presence of a normal adjacent segment differentially predicted sudden cardiac death (logistic regression model: sudden=1, non-sudden=0; OR=21.0, P<0.02). Consequently, these two factors along with ventricular tachycardia, the ‘expected’ predictor of sudden cardiac death, were tested further in multivariate models (Table 3).


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  		Table 3 Cox regression models: predictors of outcome

 
3.4. Non-sudden cardiac death
A decreasing residual contractility score consistently predicted non-sudden cardiac death whether tested in a single-factor model, in two-factor models with normal adjacent segment (two-factor model A) and ventricular tachycardia (two-factor model B), or in a three-factor model (Table 3). Ventricular tachycardia also consistently emerged as an independent predictor. However, the relative stability of the rate ratios for residual contractility score and ventricular tachycardia, with and without control for each other, indicates a minimal interaction effect between these factors with respect to non-sudden outcome. The effect of normal adjacent segment was insignificant in all models.

3.5. Sudden cardiac death
In single-factor models, normal adjacent segment and ventricular tachycardia emerged as significant and nearly significant predictors, respectively. When tested simultaneously (two-factor model C), the significance for each factor almost doubled, and the significance of the model also increased (P<0.004) indicating that each factor was an independent predictor and that together they enhanced risk. Moreover, with simultaneous control for the residual contractility score (three-factor model vs. two-factor model C), the rate ratio associated with normal adjacent segment doubled, which corroborates that only the motion of the segment(s) adjacent to the aneurysmal sac is linked to sudden cardiac death.


   4. Discussion
Top
 Abstract
 1. Introduction
 2. Patients and methods
 3. Results
 4. Discussion
5. Conclusions
 References
 
This is the first study to show that, in the presence of left ventricular aneurysm, normokinesia adjacent to the dyskinetic sac is a discriminate predictor of sudden cardiac death, while decreasing contractility of the residual myocardium differentially predicts non-sudden cardiac death. Moreover, we confirmed that ventricular arrhythmias are an indiscriminate predictor of mechanism of death but are linked to the kinesia of the adjacent to the aneurysm myocardial segment only with respect to sudden cardiac death, which has not been previously reported.

There is paucity of information on the association between the contractility in the vicinity of left ventricular aneurysm and ventricular arrhythmias [11] or sudden cardiac death [6]. Woelfel et al. demonstrated that proximity of a normokinetic myocardium to the aneurysmal sac greatly promoted the inducibility of ventricular tachycardia [11]. In a population with functional aneurysm and with preserved adjacent wall motion, Meizlish et al. found a high 1-year mortality with the majority of deaths being sudden [6]. Accordingly, we showed that seven out of eight patients with sudden cardiac death manifested at least one normokinetic adjacent segment, while among patients with preserved contractility of the residual myocardium but hypokinetic adjacent segment, none died suddenly. Furthermore, the risk of sudden cardiac death was potentiated in the presence of both normal adjacent wall motion and ventricular tachycardia. A plausible explanation for these findings is motion discordance between a normokinetic adjacent segment and the aneurysmal sac. During cardiac systole, the increased elastance (stiffness) of a normal compared to a hypokinetic or akinetic adjacent segment would enhance the passive stretch at the border [12–14]. In diastole, the adjacent segment also undergoes non-uniform extension and stretch since its compliance exceeds that of the aneurysmal myocardium and is greater in a normal vs. hypokinetic adjacent segment [12]. Stretch can depolarize Purkinje fibers thus creating a potential for electrical instability [1].

The precise role of the ejection fraction as a prognostic indicator of sudden cardiac death in the presence of left ventricular aneurysm is unclear [5,6,9]. Although a useful index of effective ventricular performance, the ejection fraction has been shown in the mathematical model to be insensitive to changes in contractility of the non-aneurysmal segment because the compliance of the aneurysmal sac dissipates the effect of an increase in inotropy of the residual myocardium [15]. We demonstrated that the residual contractility differentially predicts death from pump failure but is poorly reflected by the ejection fraction. This may, in part, be the reason why the ejection fraction fails to discriminate mechanism of death.

In accordance with earlier data [1], we showed that ventricular tachycardia as a risk factor following myocardial infarction cannot differentially predict outcome. However, in the presence of an aneurysm, it predicts both types of cardiac death but in two pathophysiologically distinct ways. With respect to non-sudden cardiac death, ventricular tachycardia did not interact with indices of contractility indicating that it is only a marker (correlate) of ventricular dysfunction. Nevertheless, ventricular tachycardia and a mechanical factor (i.e. normokinetic as opposed to hypokinetic segment adjacent to the aneurysm) were mutually potentiated and linked only in predicting sudden cardiac death.

Since use of digitalis was significantly higher among patients who died suddenly compared to survivors, a possible influence on outcome or introduction of bias in the results was further evaluated. Importantly, the prevalence of digitalis use did not differ between sudden and non-sudden cardiac death populations. Moreover, in the logistic regression analysis, digitalis failed to emerge as an independent predictor of either sudden or non-sudden cardiac death. Thus, although the possible contribution of digitalis to fatal arrhythmias cannot be excluded, a bias in the results due to digitalis use is unlikely.

The translational and rotational motions of the heart exert a confounding effect on segmental wall motion analysis, especially in the presence of left ventricular aneurysm. Thus, quantitative analysis, which eschews realignment [16], was avoided in this study. Instead, two observers independently assessed segmental wall motion semi-quantitatively. In order to increase the likelihood of accurate diagnosis of left ventricular aneurysm, the presence of both diagnostic criteria had to be agreed upon by each observer, a requirement that eliminated diagnostic inter-observer variability. The inter-observer variability for contractility scores was limited to 0.6 grade in a 6-grade system (10%), while there was no disagreement regarding the presence of at least one normal or hyperdynamic adjacent segment.

4.1. Limitations
Although exciting, these data should be interpreted with caution. Bias due to population selection, locality, or relatively small sample size are possible. The latter is of particular important when negative findings are considered. The cine-ventriculography and nuclear scintigraphy projections chosen here may under-represent posterior-lateral aneurysm. Finally, differences in projection angle by cine-venrticulography compared to nuclear scintigraphy could have resulted in error.


   5. Conclusions
Top
 Abstract
 1. Introduction
 2. Patients and methods
 3. Results
 4. Discussion
 5. Conclusions
References
 
We conclude that, in the left ventricular aneurysm model, normokinesia adjacent to the aneurysm constitutes a discriminate predictor of late sudden cardiac death while decreasing residual contractility differentially predicts non-sudden cardiac death. Although indiscriminate for type of death, ventricular tachycardia is linked to the mechanical substrate, i.e. a normokinetic adjacent segment, only with respect to sudden cardiac death. These data strongly suggest electrical discontinuity in result of mechanical dyssynchrony as the mechanism for sudden cardiac death as opposed to failure of the residual myocardium as the mechanism for non-sudden cardiac death.


   Acknowledgements
 
We would like to thank Mya D. Kline and Felicitas Brown for their technical support and greatly appreciate the critique of Drs Ernest P. McCutcheon, Francis L. Abel and Kirby L. Jackson.


   References
Top
 Abstract
 1. Introduction
 2. Patients and methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 

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