Ranolazine is effective for acute or chronic ischemic dysfunction with heart failure.
e congratulate Morrow et al. (1) for their interesting study on the effects f ranolazine in patients with non–ST-segment elevation myocardial nfarction. Ranolazine reduced the composite primary end point of ardiovascular death, myocardial infarction, and recurrent ischemia in atients with B-type natriuretic peptide 80 pg/ml. Interestingly, there as a decrease in composite arrhythmia end points consisting of ventriclar tachycardia ( 100 beats/min for 3 beats), supraventricular tachyardia ( 120 beats/min for 4 beats), and bradycardia ( 40 beats/min, ause 2.5 s or 3 atrioventricular block). Ranolazine usage showed a rend toward reduction across all arrhythmia types: ventricular tachycardia p 0.13), supraventricular tachycardia (p 0.001), atrial fibrillation p 0.4), and sudden cardiac death (p 0.11). These effects were bserved over a mean duration of 343 days. We recently reported successful use of ranolazine in a patient with hronic ischemic cardiomyopathy, symptomatic premature ventricular omplexes (PVC [ 36% of all beats]), and monomorphic ventricular achycardia who had failed amiodarone and mexilitine therapy. anolazine decreased the total number of PVCs to 1% to 2% of all eats, eliminated the ventricular tachycardia, and led to complete esolution of symptoms (2). Inhibition of the late sodium current (INa) is the proposed echanism of both the anti-ischemic and anti-arrhythmic benefits of anolazine. Activity in late INa activity is increased significantly in schemia as well as congestive heart failure (3). Increased late INa ctivity produces higher intracellular sodium, which results in calcium verload through the sodium-calcium exchange. Ranolazine inhibits ate INa 10-fold more selectively than peak INa. This mechanism, long with its 1, 2, and calcium-channel antagonism, produces its nti-ischemic and antiarrhythmic benefits (3). The present study shows beneficial effects of ranolazine in the setting f acute ischemia with evidence of heart failure. Our patient had a chronic schemic cardiomyopathy with severe myocardial dysfunction (ejection raction 15%) for which ranolazine produced excellent symptomatic relief. uture studies using ranolazine are needed to evaluate patients with acute nd chronic ischemia in the presence of elevated B-type natriuretic eptide/left ventricular dysfunction to further clarify its benefits. It ay be this category of patients who have the highest risk–benefit atio from ranolazine therapy.