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See Latest ArticlesIs remodeling the dominant compensatory mechanism in both chronic heart failure with preserved and reduced left ventricular ejection fraction
Basic Research in Cardiology , 09/28/09
MacIver DH – Normalization of stroke volume by remodeling resulted in a marked increase in end–diastolic volume in the absence of hypertrophy and an end–diastolic volume similar to normal in the presence of concentric hypertrophy. The model predicts that the dominant compensatory mechanism in chronic heart failure is remodeling with normalization of stroke volume. Observational data cited supports this conclusion.
David H. MacIver, 09/29/09
| The pathophysiological processes in heart failure are thought to be complex and involve multiple processes. Stroke volume is reduced in acute heart failure and decompensated chronic heart failure and yet is relatively normal in chronic stable heart failure. What is the primary mechanism of normalisation of the stroke volume? Evidence suggests it is unlikely to be due to neuro-humoral activation or the Frank-Starling mechanism. One candidate is the change in end-diastolic volume as may be seen in normal growth, pregnancy and following training. Modelling suggest that the end-diastolic volume should be relatively normal in heart failure and a preserved ejection fraction and elevated in low ejection fraction heart failure if the stroke volume is normal. The physiological change of end-diastolic volume is probably the main compensatory mechanism in chronic heart failure regardless of the ejection fraction. This provides a considerable simplification of our understanding of heart failure. |
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