Aortic dissection is a fatal disease due to abrupt tearing of the aortic wall, which is accompanied by severe pain and has largely unknown pathogenesis. However, aortic dissection may often occur suddenly without preceding clinical signs or symptoms. Aortic dissection represents a serious medical emergency. Recent advances in diagnostic modalities and surgical techniques have improved the diagnosis, although emergency surgery is still associated with high mortality (10%–35%) even at experienced centers. The mortality is also high in patients unable to reach the hospital and includes about a 20 % of patients.
Apart from keeping the lowest tolerable blood pressure and heart rate values, there are no drugs available to stabilize the damaged aortic wall after the development of aortic dissection.
The prevention of aortic dissection is still a main issue, since no specific intervention / drugs have been proposed, in addition to standard measures of cardiovascular prevention, including the optimal control of blood pressure and heart rate.
High salt intake has been proposed for a long time as a risk factor hypertension and cardiovascular diseases; in particular, the association between high salt intake and aortic enlargement, aortic aneurysms development and aortic rupture has been described. However, the relationship between aortic dissection and high salt intake has not completely understood and the present study has the merit of examining the effect of high-salt diet on a mouse model of aortic dissection.
In this study by Nishida et al aortic dissection was induced in male mice by continuous infusion of β-aminopropionitrile, a collagen/elastin cross-link inhibitor, and Angiotensin II for 14 days. Authors have examined 2 groups of male ( male sex is associated with a greater development of aortic dissection) mice: a wild type and a Interleukin 17 knockout (interleukin 17KO ) mice. The cytokine Interleukin-17 is secreted from T helper lymphocytes, is increased in aortic dissection tissues; high salt intake increases T helper lymphocytes and inflammation.
Therefore authors have investigated the possible relationship between high salt intake, Interleukin-17, and aortic dissection development.
High-salt administration was performed through drinking water, substituting 1% NaCl for drinking water for the indicated time period, mimicking what happens in humans that usually add salt to the diet.
The high salt administration was performed 1 week before and during the β-aminopropionitrile and Angiotensin II infusion and the effects were compared with the normal-salt-intake group. The high-salt challenge did not affect the systolic blood pressure or pulse rate of the mice
In the normal-salt condition, wildtype and interleukin 17KO mice groups exhibited the same length of aortic wall destruction, indicating the severity of aortic damage.
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