When considering taking these medicines, it is important to note the variations in their ability to offset the nongenomic effects of aldosterone.Currently, there is not enough evidence available from the randomized controlled trials on side effects of eplerenone to do a benefit versus risk assessment in people with primary hypertension. Interactions
Eplerenone is primarily metabolized by the cytochrome P450 enzyme CYP3A4. Thus the potential exists for adverse drug interactions with other drugs that induce or inhibit CYP3A4. Specifically, the concomitant use of the CYP3A4 potent inhibitors ketoconazole and itraconazole is contraindicated. Other CYP3A4 inhibitors including erythromycin, saquinavir, and verapamil should be used with caution. Other drugs that increase potassium concentrations may increase the risk of hyperkalemia associated with eplerenone therapy, including salt substitutes, potassium supplements and other potassium-sparing diuretics. Pharmacology
Eplerenone is an antimineralocorticoid, or an antagonist of the mineralocorticoid receptor (MR). Eplerenone is also known chemically as 9,11α-epoxy-7α-methoxycarbonyl-3-oxo-17α-pregn-4-ene-21,17-carbolactone and "was derived from spironolactone by the introduction of a 9α,11α-epoxy bridge and by substitution of the 17α-thoacetyl group of spironolactone with a carbomethoxy group." The drug controls high blood pressure by blocking the binding of aldosterone to the mineralocorticoid receptor (MR) in epithelial tissues, such as the kidney. Blocking the action of aldosterone decreases blood volume and lowers blood pressure. It has 10- to 20-fold lower affinity for the MR relative to spironolactone, and is less potent in vivo as an antimineralocorticoid. However, in contrast to spironolactone, eplerenone has little affinity for the androgen, progesterone, and glucocorticoid receptors.
This is most commonly the result of longstanding high blood pressure, or hypertension, which has caused a maladaptive change to the wall of the main pumping chamber of the heart, the left ventricle. Increased blood pressure means that the heart must pump even harder to adequately circulate blood throughout the body. If the heart does this for a prolonged period of time due to uncontrolled hypertension, the left ventricle can hypertrophy (grow larger) in a way that decreases the effectiveness of the heart. Left ventricular hypertrophy can be demonstrated on echocardiogram and electrocardiogram (EKG).A 1999 review of sudden cardiac deaths in the United States found that structural heart diseases accounted for over 30% of sudden cardiac arrests for those under 30 years. A study of military recruits age 18-35 found that this accounted for over 40% of sudden cardiac deaths.Congestive heart failure increases the risk of sudden cardiac death fivefold.Structural abnormalities of the cardiac conduction system (notably the Atrioventricular Node and His-Purkinje system) may predispose an individual to arrhythmias with risk of progressing to sudden cardiac arrest, albeit this risk remains low. Many of these conduction blocks can be treated with internal cardiac defibrillators for those determined to be at high risk due to severity of fibrosis or severe electrophysiologic disturbances. : 833

Inherited arrhythmia syndromes
Arrhythmias that are not due to structural heart disease account for 5 to 10% of sudden cardiac arrests. These are frequently caused by genetic disorders that lead to abnormal heart rhythms.