The incidence of sudden death appears to be reduced by ACE inhibitor therapy. Apart from a prevention of the deterioration in abnormal left ventricular function, patients treated with ACE inhibitors appear to have a reduction in arrhythmias. This may be explained by the decrease in the release of catecholamines that is increased by angiotensin II. Excess catecholamines have been documented to cause serious arrhythmias, and their blockade by the beta-blocking drugs results in the proven beneficial effects of these agents. Patients carrying the ACE DD genotype with angiotensin II type 1C allele appear to be at higher risk for serious ventricular arrhythmias.
ACE 2 has recently been defined. The renin-angiotensin system is obviously much more complicated than extensive research over the past 20 years has suggested. The recently discovered enzyme ACE 2 has beneficial effects on the
function of the heart. ACE 2 converts angiotensin I to angiotensin 1–9 containing 9 amino acids that can be converted by ACE to a shorter peptide angiotensin 1–7, a dilator of blood vessels whereas angiotensin II containing 8 amino acids is a potent vasoconstrictor (see Fig. 1). Thus, ACE 2 appears to prevent the formation of excess angiotensin II, and this action is beneficial. It appears that ACE 2 increases cardiac contractility, has cardioprotective properties, and may be an important regulator of cardiac function. Intensive research is required to obtain compounds that could increase the production of beneficial ACE 2 and decrease the deleterious actions of angiotensin II.

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