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Non Invasive Evaluation of Cardiac Dysfunction in β‐thalassemic Mice
Author(s) -
Stoyanova Ekatherina,
Cloutier Guy,
Felfly Hady,
Trudel Marie
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.970.27
Subject(s) - medicine , thalassemia , cardiology , circulatory system , cardiac function curve , hemolytic anemia , anemia , endocrinology , muscle hypertrophy , left ventricular hypertrophy , heart failure , blood pressure
Beta‐thalassemia is a genetic hematological disorder characterized by mutations of the hemoglobin gene causing total or partial decrease of the β‐globin chain production. This disease leads to a chronic hemolytic anemia, cardiac complications and blood circulatory problems such as transitory ischemic attacks, thromboembolic events and microcirculatory obstructions. Our objective is to study and dissect the molecular physiologic mechanism of cardiovascular dysfunction in β‐thalassemia. We have generated a murine model of β‐thalassemia major primarily for the investigation of the cardiovascular physiology. Left ventricular morphology and function were assessed by echocardiography in 13.5‐month‐old β‐thalassemic mice and age matched controls. The left ventricular mass index and total peripheral vascular resistance were significantly increased ( p < 0.05 and p < 0.01, respectively) in β‐thalassemic mice compared to wildtype controls. Furthermore, fractional shortening and cardiac output index were significantly decreased ( p < 0.01) in β‐thalassemic mice compared to age matched controls. Thus, these data in β‐thalassemic mice showed left ventricular remodeling by dilatation and hypertrophy that likely play a key role in cardiac dysfunction. This work was supported by the NIH (#RO1HL078655), CIHR (#CMI 72323), HSFC (#PG‐05‐0313).