Tissue ACE inhibition and sodium status in left ventricular dysfunction

Left ventricular (LV) dysfunction is characterized by a progressive loss of cardiac pump function, which eventually leads to the clinical syndrome of chronic heart failure (CHF). Heart failure is associated with high morbidity and mortality. The incidence of heart failure has increased during the last decades, mainly because improved survival after acute myocardial infarction. Renin angiotensin aldosterone system (RAAS) activation plays a major role in the progression of left ventricular dysfunction towards chronic heart failure. Angiotensinconverting enzyme (ACE) inhibition therapy improves cardiac function and reduces morbidity and mortality. Although ACE-inhibition slows the gradual progression of myocardial dysfunction towards overt CHF, it does not prevent it. In order to reach maximal therapy response to ACE inhibition a low sodium intake may be required. The expected underlyingmechanism was that an activated RAAS – i.e. elevated renin production – induced by sodium restriction is required for an optimal therapeutic response to ACE inhibition. Hence, the first main subject of this thesis was to study intervention with the sodium balance in order to optimize ACE-I therapy