Inhibitors of the Slow Calcium Current and Early Ventricular Arrhythmias

  • James R. Parratt


The effects of ‘calcium antagonist’ drugs on cardiac muscle are due to interference with those ‘slow channels’ in the cell membrane through which Ca2+ ions enter the cell (for example, during the plateau phase of the action potential in normal ventricular and Purkinje fibres). Calcium ions are also at least partly responsible for so called ‘slow potentials’ which occur in normal sinus and atrioventricular nodal cells and under conditions, for example during myocardial ischaemia, in which cells are partially depolarised, thereby inactivating Na+-mediated ‘fast responses’. The most obvious effects of cardiac cellular ‘Ca2+ deprivation’ are as follows:
  1. (1)

    Impairment of excitation-contraction coupling, leading to a decline in myocardial contractile force but with no initial alteration in the cardiac muscle action potential.

  2. (2)

    Depression of pacemaker activity, leading to a decrease in spontaneous (phase 4) depolarisation at the SA and AV nodes and to slowing of AV conduction. These are precisely the effects of inorganic ions such as CO2+, Ni2+ and La3+ or of specific ‘calcium antagonist’ drugs which powerfully and selectively inhibit Ca2+ flux across the sarcolemma through specific channels. This chapter is concerned particularly with synthetic drugs that inhibit the slow channel transport of calcium.



Ventricular Arrhythmia Left Anterior Descend Calcium Antagonist Ventricular Fibrillation Conduction Delay 
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