The heart is a muscular pump about the size of a clenched fist, roughly 250-350 g in adults, sitting slightly left of center in the mediastinum. It contracts about 100,000 times a day, pumps about 5 L per minute at rest and up to 25 L per minute under maximal exercise, and has its own blood supply — the coronary arteries — which is both a marvel of engineering and the site where most cardiovascular disease plays out.
At a glance
What it does
Circulates blood. The right side pumps deoxygenated blood to the lungs through the pulmonary circulation; the left side pumps oxygenated blood to the rest of the body through the systemic circulation. The two sides are in series — every drop passes through both — which means any pump failure on either side eventually backs up into the other.
Four chambers. Right atrium and ventricle on one side, left atrium and ventricle on the other, separated by valves (tricuspid and mitral between atria and ventricles, pulmonary and aortic at the outflow tracts). Each valve's job is to keep blood moving one direction only. Each chamber's wall thickness matches its workload — the left ventricle, pushing against systemic pressure, is 8-15 mm thick; the right, pushing against pulmonary pressure, is 3-5 mm.
How it works
The sinoatrial node sits in the right atrium and fires spontaneously about 60-100 times per minute. Each impulse spreads across the atria, reaches the atrioventricular node (which delays it briefly to let the atria fill the ventricles), then races down the bundle of His and Purkinje fibers to depolarize the ventricles from apex to base. This electrical pattern is what an ECG records.
Mechanically, the cardiac cycle has two main phases. During systole, the ventricles contract and push blood out against closed atrioventricular valves and open semilunar valves. During diastole, the ventricles relax and fill through open atrioventricular valves while the semilunars snap shut. Most coronary artery perfusion happens during diastole — which is part of why tachycardia (shorter diastole) can precipitate ischemia in someone with coronary disease.
The heart is preload-dependent (Starling's law — stretch it more, it contracts harder up to a limit), afterload-sensitive (harder to pump against high resistance), and chronotropically regulated by the autonomic nervous system (sympathetic speeds it, parasympathetic slows it through the vagus).
When it goes wrong
Coronary artery disease is the dominant failure mode and the leading cause of death worldwide. Decades of apoB-containing lipoproteins (LDL, VLDL, Lp(a)) penetrating the arterial wall drive plaque formation. When a plaque's fibrous cap ruptures, platelets swarm the exposed core, a clot forms, and the downstream myocardium dies — myocardial infarction. Survivors often develop heart failure from the dead muscle that no longer contracts.
Stress does not cause most heart attacks. Atherosclerosis does. The framing of "my uncle died of stress" is usually a story about a man who had 30 years of accumulating plaque, a sedentary lifestyle, high apoB, likely hypertension, and a triggering event. Taking the stress blame off the root causes is one of the reasons cardiovascular disease remains so common. The actual modifiable drivers are lipids (apoB is a better target than LDL-C), blood pressure, smoking, insulin resistance, and fitness.
Heart failure comes in two main flavors: reduced ejection fraction (the pump is weak — often from prior MI or dilated cardiomyopathy) and preserved ejection fraction (the ventricle cannot relax and fill normally — often from longstanding hypertension, obesity, and aging). Treatment and prognosis differ substantially.
Arrhythmias range from nuisance (premature beats) to fatal (ventricular fibrillation). Atrial fibrillation is the common clinical one, and the main danger is stroke from clot formation in the left atrium, which is why anticoagulation is the standard of care above a certain risk threshold.
Interactions
Cortisol sensitizes the vasculature to catecholamines, which is why chronic HPA activation correlates with hypertension. Thyroid hormone is directly chronotropic and inotropic — hyperthyroidism causes tachycardia and can precipitate atrial fibrillation in older adults. Testosterone and estrogen both have cardiovascular effects: estrogen is generally vascular-protective until menopause, testosterone's effects are more complex and TRT's net cardiovascular risk remains an active area of research with the TRAVERSE trial suggesting no major increase in MACE in symptomatic hypogonadal men.
The two exercise inputs with the best data are zone 2 aerobic work (for cardiac output, mitochondrial biogenesis, insulin sensitivity) and resistance training (for metabolic health, muscle mass, fall prevention). Both are non-negotiable for cardiovascular health past age 40. Adding high-intensity interval work improves VO2max faster; VO2max is one of the strongest predictors of all-cause mortality available.
Honest take
If you want one number to move, it is apoB — the count of atherogenic particles. LDL-C is a proxy that is usually correlated but not always; apoB is the actual thing doing the damage. Modern lipid-lowering (statins, ezetimibe, PCSK9 inhibitors, bempedoic acid) is one of the best-evidenced interventions in medicine, and cumulative apoB exposure over a lifetime predicts event rates far better than a single "at least you're normal" reading at 50. Meanwhile, the obsession with "heart-healthy" stress management supplements is mostly theater — sleep 7+ hours, move most days, do not smoke, keep blood pressure below 130/80, and keep apoB aggressively low if your risk warrants. That set of interventions has better data than any supplement aisle.
Sources
- Grundy et al., Circulation — ACC/AHA cholesterol guideline.
- Visseren et al., European Heart Journal — ESC guidelines on cardiovascular disease prevention.
- Lincoff et al., NEJM (2023) — TRAVERSE trial on testosterone therapy and cardiovascular events.
- Sniderman et al., JAMA Cardiology — apoB as primary lipid target.