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Cardiothoracic Surgery, Leiden University Medical Center, Postbus 9600, Leiden 2300 RC, The Netherlands
(Email: j.braun{at}lumc.nl).
Finite element modeling is more and more used to study questions that are not easily assessed in a clinical setting—or even cannot be assessed at all. The study presented by Wenk and coworkers [1] tries to shed some more light on what happens in the myocardial borderzone (the normally perfused but hypocontractile area adjacent to an infarcted area) in a patient with a previous myocardial infarction (MI). Earlier work in an ovine model from this group showed that infarction-induced left ventricular geometry changes are not simply related to passive changes resulting from increased wall stress but that intrinsic myocardial changes leading to hypocontractility also play an important role [2, 3].
So where should we place the current contribution from this group? First, we should appreciate that this is an attempt to demonstrate impaired contractility in the borderzone of a human being. The finite element model was created using input from cardiac catheterization (left ventricular pressures) and 3-dimensional magnetic resonance imaging (myofiber strain and left ventricular geometry), enabling myofiber stress to be calculated. The reader should not be distracted by the inevitable mathematic formulas presented here, but focus on the core message, which is that—as in the ovine model— borderzone myofibers also show reduced contractility in a human heart.
Now, there are some important remarks to be made with regard to this particular study, especially concerning the relationship with animal models and the extent to which results from previous experimental settings may be extrapolated: First, this is a single-patient study. Second, the studied heart experienced a MI 25 years before the current data collection, and therefore, it is hard to relate the current data to the results derived from acute animal models. As the authors correctly state in their introduction, this is a "remodeled heart," so the borderzone here inevitably will contain some degree of fibrosis and contractility will have changed.
In addition, the ovine experiments were performed in animals with healthy coronary arteries, allowing the researchers to study true infarctions with true borderzones. In human coronary artery disease, collateral circulation might not provide a clearly delineated borderzone after a MI. In this patient, it is assumed that the area targeted as borderzone was indeed normally perfused because before coronary artery bypass grafting, there were "reversible defects amenable to surgical revascularization" on a Persantine thallium stress assessment. However, this remains an assumption that should preferably be tested again in more patients with MIs of more recent onset, who should then be monitored longitudinally.
In summary, this study shows the feasibility of creating a finite element model to assess reduced myofiber contractility and increased stress in the area that represents at least the remains of a borderzone in a remodeled human heart. By using this model, more patients with more recent MIs can be examined. This will help us further understand the post-MI remodeling process in a clinical setting and, hopefully, provide new tools to attenuate this deleterious process.
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