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(Circulation. 2008;117:2041.)
© 2008 American Heart Association, Inc.

Clinical Summaries

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Role of Left Ventricular Stiffness in Heart Failure With Normal Ejection Fraction

 
Heart failure with normal ejection fraction (HFNEF) is an increasing problem; today, 50% of all heart failure patients have a normal ejection fraction. The mortality rate seems to be similar to that of patients with reduced ejection fraction, but our knowledge about the underlying hemodynamic pathology is limited. We performed a study investigating the diastolic function of patients with HFNEF invasively using pressure-volume loops to obtain the diastolic stiffness of the left ventricle. The highly increased diastolic stiffness in the HFNEF group, the key finding of the present study, shows that diastolic dysfunction can be demonstrated in HFNEF patients. It may further explain their main clinical symptomatology: exercise intolerance. Artificial pacing to mimic tachycardia during exercise reduced the stroke volume resulting from a leftward shift of the pressure-volume loops and therefore blunted the increase in the cardiac output, which is needed to comply with increased oxygen demand during exercise in patients with HFNEF. This was associated with a limitation of workload during exercise. Although it was shown recently that nondiastolic abnormalities also occur in patients with HFNEF, we suggest that diastolic stiffness is another important feature of HFNEF that might trigger heart rate–dependent changes in the global cardiac function and therefore contribute to heart failure symptomatology. These data further suggest that destiffening therapies might be a future goal for treating HFNEF. See p 2051.

	Noninvasive Detection and Localization of Vulnerable Plaque and Arterial Thrombosis With Computed Tomography Angiography/Positron Emission Tomography

 
The identification of vulnerable plaque can add a new dimension to the evaluation of cardiovascular atherosclerosis. Using an atherosclerotic rabbit model of plaque disruption and . . . [Full Text of this Article]

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