Key result
In three patients with acute myocardial rupture following myocardial infarction, Factor XIII levels were significantly reduced to 57-68% of normal (p<0.01), and supplementation aided wound healing.
Why the study?
Does Factor XIII deficiency impair wound healing and increase the incidence of cardiac rupture after myocardial infarction?
Case Report (n=3)
No
Does Factor XIII deficiency impair wound healing and increase the incidence of cardiac rupture after myocardial infarction?
p-value: p=<0.01
Clinical observations suggest that Factor XIII deficiency may contribute to impaired wound healing and increased risk of cardiac rupture post-myocardial infarction.
Hypothesis-generating for Factor XIII in post-MI rupture; prospective trials needed before clinical adoption.
Inadequate healing of myocardial infarction may contribute to local expansion of the infarct, frequently leading to chamber dilation, heart failure, or myocardial rupture. Experimental evidence in mouse models suggests that Factor XIII might play a key role in wound healing, and low persistent values lead to increased incidence of cardiac rupture following myocardial infarction. Here we would like to share our initial clinical experiences with strikingly similar observations in patients with this grave disease, and compare these observations to experimental findings.
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Nahrendorf et al. (2006) conducted a case report in Acute myocardial rupture following myocardial infarction (n=3). Factor XIII deficiency vs. Normal Factor XIII levels was evaluated on Factor XIII levels (p=<0.01). In three patients with acute myocardial rupture following myocardial infarction, Factor XIII levels were significantly reduced to 57-68% of normal (p<0.01), and supplementation aided wound healing.