Literature DB >> 1827970

Significance of diastolic dysfunction of the heart.

B H Lorell1.   

Abstract

Diastolic dysfunction is an important cause of the clinical syndrome of congestive heart failure. Traditionally, the syndrome of pulmonary congestion due to the elevation of left heart filling pressure has been attributed to the depressed ability of the heart to eject blood during systole, with a secondary increase in left ventricular volume. However, heart failure can also occur when the left ventricle fails to receive blood during diastole at low filling pressures. With a mild degree of resistance of the left ventricle to diastolic filling, the initial hemodynamic manifestation may just be the elevation of left ventricular diastolic pressure and pulmonary venous pressure. More severe resistance to left ventricular filling may cause an inadequate extent of diastolic filling and insufficient myofiber stretch, which results in the depression of stroke volume. In this review, the factors contributing to diastolic dysfunction are discussed, with a particular focus on the role of diastolic heart failure in patients with ischemic heart disease or hypertrophy.

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Year:  1991        PMID: 1827970     DOI: 10.1146/annurev.me.42.020191.002211

Source DB:  PubMed          Journal:  Annu Rev Med        ISSN: 0066-4219            Impact factor:   13.739


  13 in total

1.  Diastolic Heart Failure.

Authors: 
Journal:  Curr Treat Options Cardiovasc Med       Date:  2000-10

2.  Thyroid hormone improves function and Ca2+ handling in pressure overload hypertrophy. Association with increased sarcoplasmic reticulum Ca2+-ATPase and alpha-myosin heavy chain in rat hearts.

Authors:  K C Chang; V M Figueredo; J H Schreur; K Kariya; M W Weiner; P C Simpson; S A Camacho
Journal:  J Clin Invest       Date:  1997-10-01       Impact factor: 14.808

Review 3.  Diuretic therapy in elderly heart failure patients with and without left ventricular systolic dysfunction.

Authors:  D J van Kraaij; R W Jansen; F W Gribnau; W H Hoefnagels
Journal:  Drugs Aging       Date:  2000-04       Impact factor: 3.923

4.  In vivo acceleration of heart relaxation performance by parvalbumin gene delivery.

Authors:  M L Szatkowski; M V Westfall; C A Gomez; P A Wahr; D E Michele; C DelloRusso; I I Turner; K E Hong; F P Albayya; J M Metzger
Journal:  J Clin Invest       Date:  2001-01       Impact factor: 14.808

5.  Ca2+ transient decline and myocardial relaxation are slowed during low flow ischemia in rat hearts.

Authors:  S A Camacho; R Brandes; V M Figueredo; M W Weiner
Journal:  J Clin Invest       Date:  1994-03       Impact factor: 14.808

6.  Correcting diastolic dysfunction by Ca2+ desensitizing troponin in a transgenic mouse model of restrictive cardiomyopathy.

Authors:  Yuejin Li; Pierre-Yves Jean Charles; Changlong Nan; Jose Renato Pinto; Yingcai Wang; Jingsheng Liang; Gang Wu; Jie Tian; Han-Zhong Feng; James D Potter; J-P Jin; Xupei Huang
Journal:  J Mol Cell Cardiol       Date:  2010-05-15       Impact factor: 5.000

Review 7.  Load dependent diastolic dysfunction in heart failure.

Authors:  T C Gillebert; A F Leite-Moreira; S G De Hert
Journal:  Heart Fail Rev       Date:  2000-12       Impact factor: 4.214

8.  Optimal range for parvalbumin as relaxing agent in adult cardiac myocytes: gene transfer and mathematical modeling.

Authors:  Pierre Coutu; Joseph M Metzger
Journal:  Biophys J       Date:  2002-05       Impact factor: 4.033

9.  Influence of preload on left ventricular relaxation in isolated ejecting hearts during myocardial depression.

Authors:  Stefan Fj Langer; Hanno D Schmidt
Journal:  Exp Clin Cardiol       Date:  2003

10.  Noncanonical EF-hand motif strategically delays Ca2+ buffering to enhance cardiac performance.

Authors:  Wang Wang; Matthew S Barnabei; Michelle L Asp; Frazer I Heinis; Erik Arden; Jennifer Davis; Elizabeth Braunlin; Qi Li; Jonathan P Davis; James D Potter; Joseph M Metzger
Journal:  Nat Med       Date:  2013-02-10       Impact factor: 53.440

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