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FR183998 inhibits Na+/H+ exchange and IL-8 accumulation following cardiac ischemia Cardiovascular diseases have been the most common cause of death in the US each year with the exception of 1918. In 1998, this group of diseases claimed almost 1 million lives which translates to 40% of all deaths and 1 death every 30 seconds. Strikingly, more people die from cardiovascular disease that the next six leading causes of death combined, and if cardiovascular disease were to be eliminated, the average life expectancy would rise by 7 years. Coronary heart disease is by far the leading cause of deaths from cardiovascular disease. Of the 12 million or so Americans with coronary heart disease, some 1 million suffer new or recurrent coronary attack each year. 40 percent of these patients die. First line treatments include the use of thrombolytic drugs despite their high cost and association with bleeding. The aim of these drugs is to re-establish perfusion of cardiac tissue thereby limiting ischemia. An alternative approach however is to limit the death resulting from ischemia when it occurs. The initial period of ischemia causes the accumulation of myocardial Na(+) and consequently Ca(2+) and consequently cell death. During subsequent reperfusion, IL-8 causes the migration of inflammatory cells resulting in further cell death. Fujisawa are developing FR183998, an inhibitor of Na+/H+ exchange. This therapeutic candidate is able to prevent ionic imbalances during ischemia reducing or completely abolishing cardiac ventricular fibrillation and mortality following ischemia/reperfusion. The drug can also reduce infarct size following cerebral ischemia. Most recently however, FR183998 has also been shown to reduce IL-8 levels following cardiac ischemia/reperfusion suggesting that it is able to both prevent direct cell death and also inflammatory damage following ischemic crisis. Link to journal abstract:
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