Statins, Beta-Blockers, ACE Inhibitors: How Common Heart Drugs Work

Statins work primarily in the liver. Your liver naturally produces an enzyme called HMG-CoA reductase, which is a key step in manufacturing cholesterol. Statins block this enzyme, reducing the amount of LDL (low-density lipoprotein) cholesterol the liver releases into the bloodstream.

Lower circulating LDL means less cholesterol available to accumulate in artery walls. Over time, this can slow the progression of atherosclerosis — the gradual buildup of fatty plaques that narrows arteries and raises the risk of heart attack and stroke. Some research also suggests statins have modest anti-inflammatory effects on artery walls, though cholesterol reduction is their primary established benefit.

Common side effects include muscle aches, and in rare cases more serious muscle breakdown. Periodic liver function monitoring may be recommended depending on individual risk factors.

Your heart responds to stress hormones — primarily adrenaline (epinephrine) — by beating faster and harder. Beta-blockers work by occupying the beta-adrenergic receptors that adrenaline normally binds to, effectively muffling that signal.

The result is a slower, less forceful heartbeat. This reduces how hard the heart has to work with each contraction — a meaningful benefit in conditions like heart failure, where an overworked heart muscle gradually weakens. Beta-blockers also lower blood pressure and can stabilize irregular heart rhythms, which is why they're prescribed across a range of cardiac conditions including arrhythmias, post-heart attack recovery, and certain types of angina.

Because they slow heart rate, some people experience fatigue, cold hands and feet, or dizziness when starting beta-blockers. They are generally not stopped abruptly, as this can trigger a rebound increase in heart rate — always follow your provider's instructions on tapering.

ACE inhibitors target a hormonal pathway called the renin-angiotensin-aldosterone system (RAAS). Under normal conditions, your kidneys release an enzyme called renin, which triggers a cascade that eventually produces a hormone called angiotensin II. Angiotensin II is a potent vasoconstrictor — it signals blood vessels to tighten, raising blood pressure.

ACE inhibitors block the angiotensin-converting enzyme (ACE) that converts an inactive precursor into angiotensin II. With less angiotensin II circulating, blood vessels relax and widen. This reduces the resistance the heart pumps against, lowering blood pressure and easing the heart's workload.

ACE inhibitors are widely used for hypertension, heart failure, and kidney protection in people with diabetes. A persistent dry cough is one of their most recognized side effects, affecting a meaningful proportion of users. A related drug class — angiotensin receptor blockers, or ARBs — works on the same system but at a later step, and is sometimes used when cough becomes intolerable.