Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Lorenzoni, R. et al.

Coronary vasodilator reserve is impaired in patients with hypertrophic cardiomyopathy and left ventricular dysfunction.

BACKGROUND: We tested the hypothesis that a reduced delivery of blood to the myocardium is involved in the development of systolic dysfunction of patients with hypertrophic cardiomyopathy (HCM). METHODS AND RESULTS: Eighty-four patients with HCM (62 men, age 43 +/- 12 years) were studied. Left ventricular dimensions and function (fractional shortening) were evaluated by 2-dimensional echocardiography. Myocardial blood flow (MBF) was measured by N13 -ammonia or O15 -water and positron emission tomography at baseline and after dipyridamole; coronary vasodilator reserve (CVR) was calculated as dipyridamole/baseline MBF. Patients with HCM in advanced New York Heart Association (NYHA) classes had lower dipyridamole MBF (NYHA class I = 1.57 +/- 0.64 vs class II = 1.52 +/- 0.58 vs class III = 0.96 +/- 0.32 mL/min per gram; analysis of variance, P <.05) and CVR (NYHA class I = 1.93 +/- 0.64 vs class II = 1.69 +/- 0.54 vs class III = 1.40 +/- 0.43; analysis of variance, P <.05). A positive linear correlation between fractional shortening and dipyridamole MBF was demonstrated (R = 0.23, P <.05), and patients with abnormal fractional shortening had lower dipyridamole MBF (1.07 +/- 0.43 vs 1.58 +/- 0.62 mL/min per gram, P <.01). CONCLUSIONS: Systolic dysfunction in HCM may be caused by a more severe alteration of the coronary vasodilator capacity.[1]

References

Coronary vasodilator reserve is impaired in patients with hypertrophic cardiomyopathy and left ventricular dysfunction. Lorenzoni, R., Gistri, R., Cecchi, F., Olivotto, I., Chiriatti, G., Elliott, P., McKenna, W.J., Camici, P.G. Am. Heart J. (1998) [Pubmed]

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