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Cardiovascular Research 1997 36(1):10-20; doi:10.1016/S0008-6363(97)00174-0
© 1997 by European Society of Cardiology
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Copyright © 1997, European Society of Cardiology

Calcium sensitisers: mechanisms of action and potential usefulness as inotropes

J.A Leea,* and D.G Allenb

aUniversity Department of Pathology, The Medical School, Beech Hill Road, Sheffield, S10 2RX, UK
bDepartment of Physiology, University of Sydney, Sydney NSW 2006, Australia

* Corresponding author.

Received 22 April 1997; accepted 26 June 1997

KEYWORDS Cardiotonic agents; Calcium sensitisers; Heart failure; Inotropic agents; Cardiac muscle; Intracellular calcium

The first 150 words of the full text of this article appear below.


    1 Introduction
 
Heart failure remains a common and lethal condition, with treatment options which are less than satisfactory. Epidemiological studies [1–5]indicate an overall prevalence in the population of 1–3%, while mortality for all grades of heart failure is approximately 25% at 2 years and 50% at 4 years. Severe heart failure has a 2 year mortality as high as 75%. Although some cases are caused by correctable problems such as hypertension or valve lesions, the majority result either from loss of functioning myocardium due to ischaemic damage or from ineffective contraction of partially ischaemic or otherwise functionally disabled myocardium.

Therapy for heart failure thus has two main objectives [6–12]. Firstly, treatment of the failing pump and its main physiological consequences, fluid retention and vasoconstriction. Secondly treatment of the common associated problems which may be either primarily involved in causing heart failure (e.g. ischaemia) or which may be secondary complications (e.g. . . . [Full Text of this Article]


    2 Heart muscle activation
 

    3 Mechanisms of inotropy
 

    4 Calcium sensitisers
 

    5 Mechanisms of action of calcium sensitisers
 

    6 Effects on energetic efficiency
 

    7 Slowing of relaxation
 

    8 Potential usefulness of calcium sensitisers as inotropes
 
8.1 Effects on diseased muscle
8.2 Arrhythmias
8.3 In vivo studies

    9 Conclusions
 

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