1999
DOI: 10.1016/s0008-6363(99)00099-1
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Afterload induced changes in myocardial relaxation A mechanism for diastolic dysfunction

Abstract: Diastolic LV dysfunction was induced by elevated afterload in healthy hearts of rabbits and dogs. If this mechanism could be shown to be operative in the failing heart, reversal of diastolic dysfunction should contribute to the beneficial effects of vasodilating and inotropic therapy on pulmonary congestion.

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Cited by 235 publications
(194 citation statements)
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References 40 publications
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“…30 An impaired cardiac relaxation may cause elevation of LV DBP, which increase extravascular compression forces on the coronary arterioles resulting in increased coronary microcirculatory resistance and consequently to the reduction of coronary flow in the subendocardial layers. 31 Thus, enhanced wave reflections exert a negative impact on LV myocardial relaxation 32,33 and may cause subendocardial ischaemia. 11,32,34,35 Chronic subendocardial ischaemia has been associated with myocardial fibrosis and LV diastolic dysfunction.…”
Section: Association Of Cai and Aos With LV Diastolic Dysfunctionmentioning
confidence: 99%
“…30 An impaired cardiac relaxation may cause elevation of LV DBP, which increase extravascular compression forces on the coronary arterioles resulting in increased coronary microcirculatory resistance and consequently to the reduction of coronary flow in the subendocardial layers. 31 Thus, enhanced wave reflections exert a negative impact on LV myocardial relaxation 32,33 and may cause subendocardial ischaemia. 11,32,34,35 Chronic subendocardial ischaemia has been associated with myocardial fibrosis and LV diastolic dysfunction.…”
Section: Association Of Cai and Aos With LV Diastolic Dysfunctionmentioning
confidence: 99%
“…[30][31][32] It is possible that the contribution of afterload is underestimated in our study. Many studies, including our own, utilize compliance of the aorta or large proximal arteries as measures of afterload.…”
Section: Discussionmentioning
confidence: 99%
“…15,16 These changes are also reflected by elevation in the end-systolic pressurevolume ratio accompanied by a rise in Ees and a reduction in stroke volume and further progression of the diastolic dysfunction via impaired and raised diastolic pressure. 17 Additionally, high Ees accompanied by diastolic dysfunction can increase myocardial oxygen consumption, thus limiting myocardial perfusion reserve. 15 Of interest, the results of this study showing no significant change in Ees in MHT vs. essential hypertension, which accords with the previous observation of preserved myocardial perfusion reserve in MHT despite impairment of endothelial dysfunction.…”
Section: Vascular Ventricular Coupling In Malignant Hypertensionmentioning
confidence: 99%