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Myocardial contractility represents the intrinsic ability of the heart/myocardium to contract. Changes in the ability to produce force during contraction result from incremental degrees of binding between myosin (thick) and actin (thin) filaments. The degree of binding that occurs depends on concentration of calcium ions in the cell. Within an in vivo intact heart, it is generally the action/response of the sympathetic nervous system driven by precisely time released catecholamine that determines the concentration of calcium ions in the cytosol of cardiac muscle cells. All factors that cause an increase in contractility work by causing an increase in intracellular [Ca++] during contraction.[citation needed]


Measurable relative increase in contractility is a property of the myocardium similar to the term inotropy. Contractility may be iatrogenically altered by the administration of inotropic agents. Drugs that positively render the effects of catecholamines such as (norepinephrine and epinephrine) that enhance contractility are considered to have a positive inotropic effect. The ancient herbal remedy digitalis appears to have both inotropic and chronotropic properties that have been recorded encyclopedically for centuries and it remains advantageous today.

Model as a contributing factor[edit]

Under one existing model[citation needed], the five factors of myocardial performance are considered to be

By this model, if myocardial performance changes while preload, afterload, heart rate, and conduction velocity are all held constant, then the change in performance must be due to a change in contractility. However, changes in contractility alone generally do not occur.[citation needed] Other examples:


  1. ^ a b Klabunde, Richard. "Cardiac Inotropy (Contractility)". Cardiovascular Physiology Concepts. Retrieved 27 January 2011.