Statins are the most efficacious hypolipidemic drugs available. Numerous meta-analyses of clinical trials have provided unequivocal evidence that statins are effective and safe in preventing cardiovascular morbidity and mortality in patients with and without pre-existing ischemic heart disease. With widespread usage of statins, its actions other than that of lipid-lowering have started to emerge. Although the effects of statins were initially attributed to a reduction in lipid levels, many benefits are now considered to stem from effects other than lipid modulation. In this review, we describe the mechanisms of these pleiotropic effects and the pathways involved in these effects.
Azacitidine is a pyrimidine nucleoside analog licensed for treatment of adult patients with myelodysplastic syndrome. Azacitidine acts as an inducer of cell differentiation by causing demethylation and re-expression of genes silenced by hypermethylation. We report a 56-year-old man with myelodysplastic syndrome who developed interstitial lung disease after azacitidine therapy. Open lung biopsy revealed a nonresolving organizing pneumonia pattern and bronchocentric granulomatous pattern suggestive of drug-induced lung injury. Treatment with steroids and discontinuation of azacitidine led to resolution of interstitial lung disease. The Naranjo adverse drug reaction probability scale score indicated that the association between azacitidine and interstitial lung disease was probable. Interstitial lung disease is a serious but uncommon side effect of this relatively safe drug. The mechanism underlying this is still unclear. The patient was subsequently treated with decitabine with no recurrence of interstitial lung disease.
Treatment of heart failure involves management of risk factors and control of symptoms. Traditional management of heart failure involves the use of angiotensin converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, diuretics, aldosterone antagonists, and digitalis. Metabolic modulators are a newer class of drugs that benefit these patients by modulating cardiac metabolism without altering hemodynamics. They have the potential to relieve symptoms in patients with refractory heart failure who are already on optimal medical therapy. These drugs increase glucose metabolism at the expense of free fatty acid metabolism, thereby enhancing efficient use of oxygen. This review discusses the role of 4 metabolic modulators drugs that could potentially be used for heart failure therapy: trimetazidine, ranolazine, perhexiline, and etomoxir.
Clopidogrel resistance is an emerging clinical scenario, as antiplatelet therapy has become the cornerstone of modern cardiovascular treatment. This leads to an increase in stent thromboses and recurrent ischemic events which add to the health care costs, and increased periprocedural morbidity and mortality. Management of clopidogrel resistance is challenging as there are no standardized guidelines. The arrival of newer antiplatelet drugs and the detection of genetic polymorphisms in susceptible populations may have an impact on the management. Further trials are needed regarding the target population who should be screened for clopidogrel resistance, a standardized diagnostic test to detect clopidogrel resistance, the role of pharmacogenetics, and the need for tailored therapeutic options for a patient with clopidogrel resistance.
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