3 HO"


73 Eicosapentaenoic acid

74 docosahexaenoic acid

Figure 22 Examples of o-3 polyunsaturated fatty acids.

readily that all arrhythmias are similar. This is not so. With this in mind, various approaches can be considered such as:

1. Prevention of the generation, release, or action of arrhythmogens. Obvious examples of such an approach are class 2 antiarrhythmics which prevent the arrhythmogenic effects of catecholamines. Unfortunately, none of the other identified arrhythmogens have proved to be important enough to warrant targeting them with a full-scale research program. Similarly, a combination of arrhythmogens may also not be that important.3

2. Blockade of particular channels whose activation generates arrhythmias. Examples include IKATP and stretch channels. However, evidence for any particular channel being a sine qua non for arrhythmias is not overwhelming. It is the altered behavior of normal ion channels due to diverse pathology that appears to cause many arrhythmias.

3. Correction of pathologically disturbed normal channels to either revert behavior to normal; block them; or prevent their participation in the genesis/maintenance of arrhythmias.

4. Correction of the mutated channels responsible for the generation/maintenance of arrhythmias. The classic examples are those responsible for the prolonged QT syndrome, and associated torsades. It may prove possible in the future to use gene therapy, but currently drugs are needed to selectively alter the behavior of such aberrant channels, or prevent the consequence of their activation, e.g., intracellular calcium loading.

5. Selective blockade or activation of particular ion channels (e.g., INa, ICa, IK„ IKur, If) might yet prove to be a useful antiarrhythmic strategy, for example, blockade of IKur for atrial selective drugs.

6. Combination blockers of various ion channels. Amiodarone probably owes its antiarrhythmic actions to simultaneous block of a number of different type of channels. The important question of which channels to block, and what degree of blockade, is currently difficult to answer.

7. Selective ion blocking actions confined to cardiac tissue that is subject to the pathological conditions causing an arrhythmia. The most obvious example is pathology due to myocardial ischemia and infarction. Similarly, damage due to infarction, or to stretch of cardiac tissue, provides another particular target. In the case of ischemia, its special conditions might be used to activate drugs so that they are only active in ischemic tissue.

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