What I learned from my mentor when I was a research fellow is that it supposedly worked by inhibiting the late sodium current which would decrease Na-i and in turn improve Ca-i efflux. I don't think the clinical trials produced the desired anti-arrythmogenic results, however.
Randomized controlled trials (RCTs) on the use of ranolazine (RN) for prevention and cardioversion of atrial fibrillation (AF) have yielded сontradictory results.
PubMed and EMBASE were searched until June 2016. Of 484 initially identified studies, 8 RCTs were finally analyzed. Meta-analysis suggests that RN may be effective in AF prevention, whereas it potentiates and accelerates the conversion effect of amiodarone of recent-onset AF. Larger RCTs with long-term follow-up in diverse clinical settings are needed to further clarify the impact of RN on AF therapy. (PMID: 27746384 DOI: 10.1016/j.hrthm.2016.10.008)
https://www.ncbi.nlm.nih.gov/pubmed/27746384#
Ranolazine is an antianginal compound that inhibits potassium and sodium currents and increases glucose metabolism at the expense of free fatty acid metabolism, thereby enhancing the efficient use of oxygen. At present, there is insufficient evidence to recommend ranolazine as an antiarrhythmic drug, alone or in combination with other antiarrhythmic drugs.
http://www.cardio.se/sites/default/files/ESC%20Guidelines%20for%20the%20management%20of%20atrial%20fibrillation%202016.pdf
Everything has been said! Agree with college of mine who wrote upper answers!
From the meta-analysis it seems that ranolazine probably has some effect in AF prevention. Some case reports have shown that it can covert refractory cases of AF along with other Antiarrhymic drugs. Some well designed larger study is needed.
https://www.ncbi.nlm.nih.gov/pubmed/25602175
http://journals.sagepub.com/doi/abs/10.1177/1060028016673073
https://clinicaltrials.gov/ct2/show/NCT01534962
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