Existence of the Frank-Starling Mechanism in the Failing Human Heart

Holubarsch, Christian; Ruf, Thorsten; Goldstein, Daniel J.; Ashton, Robert C.; Nickl, Werner; Pieske, Burkert; Pioch, Katja; Lüdemann, Jens; Wiesner, S; Hasenfuß, Gerd; Posival, Herbert; Just, Hanjörg; Burkhoff, Daniel

doi:10.1161/01.cir.94.4.683

Cited by 216 publications

(66 citation statements)

References 42 publications

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“…In end-stage heart failure, the Frank-Starling relationship has been reported to be depressed (13,29). LDA is believed to be the cellular basis of the Frank-Starling mechanism (26,34).…”

Section: Discussionmentioning

confidence: 99%

Length-dependent activation is modulated by cardiac troponin I bisphosphorylation at Ser23 and Ser24 but not by Thr143 phosphorylation

Wijnker

Sequeira

Foster

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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“…In end-stage heart failure, the Frank-Starling relationship has been reported to be depressed (13,29). LDA is believed to be the cellular basis of the Frank-Starling mechanism (26,34).…”

Section: Discussionmentioning

confidence: 99%

Length-dependent activation is modulated by cardiac troponin I bisphosphorylation at Ser23 and Ser24 but not by Thr143 phosphorylation

Wijnker

Sequeira

Foster

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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“…Snap-frozen biopsies were obtained in 20 patients (Table 1, patients [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] for determination of NOS2 (n ϭ 20), NOS3 (n ϭ 20), heme oxygenase (HO)-1 (n ϭ 14), and TNF-␣ mRNA (n ϭ 10). RNA extraction, internal standard preparation, and oligonucleotides used for RT-PCR and quantitative RT-PCR protocol, using a defined amount of specific RNA mutant as an internal standard, have been extensively described previously (13).…”

Section: Methodsmentioning

confidence: 99%

“…The enhancement of PR-LVSW in DCM results from a rightward displacement of the diastolic LV pressurevolume relation (15). Limitation of this rightward displacement is accompanied by a restrictive LV filling pattern on the Doppler mitral inflow signal, by exacerbation of symptoms, and by poor prognosis (25).…”

Section: No Fibrosis and LV Preload Reservementioning

confidence: 99%

Myocardial fibrosis blunts nitric oxide synthase-related preload reserve in human dilated cardiomyopathy

Bronzwaer

Heymes

Visser

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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. Myocardial fibrosis blunts nitric oxide synthase-related preload reserve in human dilated cardiomyopathy. Am J Physiol Heart Circ Physiol 284: H10-H16, 2003; 10.1152/ajpheart.00401.2002.-The purpose of the study was to investigate interactions between myocardial nitric oxide synthase (NOS) and myocardial fibrosis, both of which determine left ventricular (LV) preload reserve in patients with nonischemic dilated cardiomyopathy (DCM). In previous animal experiments, chronic inhibition of NOS induced myocardial fibrosis and limited LV preload reserve. Twenty-eight DCM patients underwent LV catheterization, balloon caval occlusions (BCO; n ϭ 8), intracoronary substance P infusion (n ϭ 8), and procurement of LV endomyocardial biopsies for determinations of collagen volume fraction (CVF), of gene expression of NOS2, NOS3, heme oxygenase (HO)-1, and TNF-␣, and of NOS2 protein. CVF was unrelated to the intensity of NOS2, NOS3, HO-1, or TNF-␣ gene expression or of NOS2 protein expression. Preload recruitable LV stroke work (PR-LVSW) correlated directly with NOS2 gene expression (P ϭ 0.001) and inversely with CVF (P ϭ 0.04). High CVF (Ͼ10%) reduced baseline LVSW and PR-LVSW at each level of NOS2 gene expression. In DCM, myocardial fibrosis is unrelated to the intensity of myocardial gene expression of NOS, antioxidative enzymes (HO-1), or cytokines (TNF-␣) and blunts NOS2-related recruitment of LV preload reserve. collagen; diastole; myocardial contraction HIGHER LEFT VENTRICULAR (LV) endomyocardial nitric oxide (NO) synthase (NOS) gene expression enables patients with dilated cardiomyopathy (DCM) to recruit LV preload reserve as evident from their higher LV stroke work (LVSW) at elevated LV filling pressures (13). This ability to recruit LV preload reserve could result from an acute direct myocardial action of NO, because intracoronary infusion of substance P, which releases NO from the coronary endothelium, induces an instantaneous increase in LVSW in DCM patients with elevated LV filling pressures (13). This increase in LVSW is accompanied by a rightward shift of the diastolic LV pressure-volume relation. A similar NOrelated rightward shift of the diastolic LV pressurevolume relation was previously observed in control and aortic stenosis patients after intracoronary infusion of a NO donor (20,24) and in DCM patients after intracoronary infusion of enalaprilat (37). Acute effects of NO on myocardial diastolic distensibility have also been reported in experimental preparations. In isolated rat cardiomyocytes, exposure to cGMP, the second messenger of NO, increases diastolic cell length (32), and, in isolated guinea pig hearts, a coronary perfusate containing a specific NOS inhibitor results in an acute reduction of LV stroke volume because of a leftward shift of the diastolic LV pressure-volume relation (27).The ability of NO to preserve LV diastolic distensibility could result not only from its acute direct myocardial actions but also from chronic effects on LV hypertrophy and on collagen turnover within the cardiac i...

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“…The FFR and the Frank-Starling law are the essential mechanisms by which cardiac tissue adjusts mechanical performance in response to hemodynamic needs (20,21). Loss of positive FFR has been reported in human and animal models of heart failure (1,22).…”

Section: Effects Of Celacade On the Ffrmentioning

confidence: 99%

Effects of therapy using the Celacade system on structural and functional cardiac remodelling in rats following myocardial infarction

Zhang¹,

Mei²,

Archer³

et al. 2009

Canadian Journal of Cardiology

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Existence of the Frank-Starling Mechanism in the Failing Human Heart

Abstract: The Frank-Starling mechanism is maintained in end-stage failing human hearts, whereas significant alterations of diastolic myocardial distensibility are evident in chronic heart failure.

Cited by 216 publications

References 42 publications

Length-dependent activation is modulated by cardiac troponin I bisphosphorylation at Ser23 and Ser24 but not by Thr143 phosphorylation

Length-dependent activation is modulated by cardiac troponin I bisphosphorylation at Ser23 and Ser24 but not by Thr143 phosphorylation

Myocardial fibrosis blunts nitric oxide synthase-related preload reserve in human dilated cardiomyopathy

Effects of therapy using the Celacade system on structural and functional cardiac remodelling in rats following myocardial infarction

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