Heart failure (HF) is a prevalent syndrome resulting in a high mortality rate. HF may be associated with zinc deficiency through a reduction in dietary intake, decreased absorption due to gastrointestinal edema, impaired motility or intestinal zinc losses. Diseases concomitant with HF such as diabetes mellitus (DM) and hypertension may enhance zinc deficiency. Medications given for HF may affect zinc metabolism in different ways. It was shown that thiazides may cause zincuria and a decrease in tissue zinc concentration. There is conflicting evidence about furosemide, even though patients with chronic furosemide treatment showed low tissue zinc levels in autopsies. Treatment with angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) resulted in zincuria and zinc deficiency, but this outcome was not consistent in all studies. Beta-blockers did not alter plasma zinc concentration. Matrix metalloproteinases (MMPs) and ACE are zinc-containing enzymes, which play a role in the process of remodeling in HF. It was shown that ACE inhibitors may inhibit the activity of different MMPs. The exact interrelationship between HF, zinc-containing enzymes, zinc deficiency and the clinical manifestation of HF has to be investigated.
|Number of pages||6|
|Journal||Heart Failure Reviews|
|State||Published - Mar 2006|
- Angiotensin receptor blockers
- Angiotensin-converting enzyme inhibitors
- Heart failure