2007
DOI: 10.1007/s00424-007-0323-2
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A new methodological approach to assess cardiac work by pressure–volume and stress–length relations in patients with aortic valve stenosis and dilated cardiomyopathy

Abstract: In experimental animals, cardiac work is derived from pressure-volume area and analyzed further using stress-length relations. Lack of methods for determining accurately myocardial mass has until now prevented the use of stress-length relations in patients. We hypothesized, therefore, that not only pressure-volume loops but also stress-length diagrams can be derived from cardiac volume and cardiac mass as assessed by cardiac magnetic resonance imaging (CMR) and invasively measured pressure. Left ventricular (L… Show more

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Cited by 53 publications
(45 citation statements)
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“…Peak systolic wall stress was evaluated using the thick‐wall sphere model assuming that peak systolic wall stress would occur one‐third of the way into the ejection phase 15, 16…”
Section: Methodsmentioning
confidence: 99%
“…Peak systolic wall stress was evaluated using the thick‐wall sphere model assuming that peak systolic wall stress would occur one‐third of the way into the ejection phase 15, 16…”
Section: Methodsmentioning
confidence: 99%
“…21 Peak systolic wall stress was evaluated using the thick-wall sphere model assuming that peak systolic wall stress occurs one third into the ejection phase. 22,23 Systemic vascular resistance was calculated according to (systemic vascular resistance=80×mean arterial pressure/CO) and LV global afterload was estimated by valvuloarterial impedance (Zva) using the formula [Zva=(systolic blood pressure+net mean gradient)/SV index]. 24,25 Consequently, Zva was calculated using a hybrid approach with net mean gradients derived from echocardiography and SV index from CMR.…”
Section: Cardiovascular Magnetic Resonancementioning
confidence: 99%
“…Although treatment with angiotensin-converting enzyme inhibitors interferes with ventricular remodeling involving fibrosis and dilatation, an adverse increase in wall stress, 5 which is related to decreased heart rate variability, often cannot be prevented. Increased wall stress can lead to the opening of stretch-activated cation channels, increasing the risk of sudden cardiac death.…”
Section: To the Editormentioning
confidence: 99%