Cardiac arrest, chronic total occlusion, and occluded stent in a 16-year-old boy with Kawasaki disease: a case report.

BACKGROUND: Kawasaki disease is the leading cause of premature coronary artery disease in developed countries. As such, patients may require revascularisation as children. However, there are no randomized data guiding treatment so this must be individualized. This case report describes the decision-making in a young patient requiring revascularization who had already suffered stent occlusion. CASE SUMMARY: Our patient, a 16-year-old boy with Kawasaki disease, presented with cardiac arrest during exercise. Coronary angiography showed that a proximal left anterior descending artery stent implanted at the age of 8 years had occluded some time ago and his right coronary artery was also chronically occluded. He has discussed in several Heart Team meetings and with international colleagues and a consensus reached to revascularize him surgically. DISCUSSION: It is vital that young patients with complex coronary disease are discussed in an extensive multidisciplinary setting to determine the most suitable means of treatment. The previously occluded stent was crucial in the individualized decision-making in this patient.

Limitations of the MRL mouse as a model for cardiac regeneration.

OBJECTIVE: Myocardial repair following injury in mammals is restricted such that damaged areas are replaced by scar tissue, impairing cardiac function. MRL mice exhibit exceptional regenerative healing in an ear punch wound model. Some myocardial repair with restoration of heart function has also been reported following cryoinjury. Increased cardiomyocyte proliferation and a foetal liver stem cell population were implicated. We investigated molecular mechanisms facilitating myocardial repair in MRL mice to identify potential therapeutic targets in non-regenerative species. METHODS: Expressions of specific cell-cycle regulators that might account for regeneration (CDKs 1, 2, 4 and 6; cyclins A, E, D1 and B1; p21, p27 and E2F5) were compared by immunoblotting in MRL and control C57BL/6 ventricles during development. Flow cytometry was used to investigate stem cell populations in livers from foetal mice, and infarct sizes were compared in coronary artery-ligated and sham-treated MRL and C57BL/6 adult mice. KEY FINDINGS: No differences in the expressions of cell cycle regulators were observed between the two strains. Expressions of CD34+Sca1+ckit-, CD34+Sca1+ckit+ and CD34+Sca1-ckit+ increased in livers from C57BL/6 vs MRL mice. No differences were observed in infarct sizes, levels of fibrosis, Ki67 staining or cardiac function between MRL and C57BL/6 mice. CONCLUSIONS: No intrinsic differences were observed in cell cycle control molecules or stem cell populations between MRL and control C57BL mouse hearts. Pathophysiologically relevant ischaemic injury is not repaired more efficiently in MRL myocardium, questioning the use of the MRL mouse as a reliable model for cardiac regeneration in response to pathophysiologically relevant forms of injury.

Post-infarction remodeling is independent of mitogen-activated protein kinase kinase 3 (MKK3).

OBJECTIVES: Our aim was to examine the role of mitogen-activated protein kinase kinase 3 (MKK3) in the development of left ventricular (LV) remodeling following myocardial infarction (MI). METHODS: MKK3-null mice were subjected to permanent coronary artery ligation. Twenty-eight days after MI, haemodynamics in male mkk3+/+(WT) and mkk3-/-(KO) littermates were assessed using a pressure-conductance catheter. MI groups were compared to un-operated time-matched WT and KO controls. RESULTS: MI caused significant LV contractile dysfunction and dilatation which did not differ by genotype. Detailed morphometric analysis of excised hearts confirmed these similar global indices of remodeling and also demonstrated that pathological changes within remote myocardium and scar did not differ between KO and WT hearts. CONCLUSIONS: Despite numerous lines of evidence suggesting MKK3 is the relevant kinase upstream of p38 mitogen-activated protein kinase in LV remodeling these processes can continue in its absence.