Cardiovascular disease - heart attacks, strokes, heart failure, and related conditions - is the leading cause of death in the United States and most of the developed world. It accounts for roughly one in three deaths globally.

But cardiovascular disease is not simply a disease. It is, in many ways, a manifestation of accelerated aging in the vascular system. The same processes that drive biological aging - inflammation, oxidative stress, cellular senescence, mitochondrial dysfunction - are the processes that damage arteries, stiffen the heart, and ultimately cause cardiovascular events.

This means that understanding cardiovascular aging is not separate from understanding longevity. It is central to it.

The cardiovascular system undergoes predictable changes with age, even in the absence of disease:

Arterial stiffening. The aorta and large arteries become progressively stiffer with age due to changes in the extracellular matrix - particularly the cross-linking of collagen and the degradation of elastin. Arterial stiffness increases the workload on the heart and is an independent predictor of cardiovascular events and mortality.

Endothelial dysfunction. The endothelium - the single-cell layer lining blood vessels - loses its ability to produce nitric oxide, the molecule that causes blood vessels to dilate. Endothelial dysfunction is one of the earliest detectable signs of cardiovascular aging and precedes atherosclerosis by decades.

Left ventricular hypertrophy. The heart muscle thickens with age in response to increased afterload from arterial stiffness. This reduces the heart's ability to relax and fill properly - a condition called diastolic dysfunction.

Reduced cardiac reserve. Maximum heart rate and cardiac output during exercise decline with age, reducing the heart's ability to respond to physical demands.

Atherosclerosis. The accumulation of lipid-laden plaques in arterial walls is a chronic inflammatory process that begins in childhood and accelerates with age, particularly in the presence of risk factors.

Several modifiable risk factors dramatically accelerate the normal aging of the cardiovascular system:

Hypertension. Chronically elevated blood pressure is the single most important modifiable cardiovascular risk factor. It accelerates arterial stiffening, promotes left ventricular hypertrophy, damages the endothelium, and drives atherosclerosis. The relationship between blood pressure and cardiovascular risk is continuous - there is no threshold below which lower is not better, down to approximately 110/70 mmHg.

Dyslipidemia. Elevated LDL cholesterol, particularly small dense LDL particles, drives atherosclerosis. The relationship between LDL and cardiovascular risk is causal, not merely associative - Mendelian randomization studies and statin trials have established this beyond reasonable doubt.

Insulin resistance and type 2 diabetes. Metabolic dysfunction accelerates virtually every aspect of cardiovascular aging. Elevated glucose and insulin damage the endothelium, promote inflammation, and accelerate atherosclerosis.

Smoking. Tobacco smoke causes direct endothelial damage, promotes oxidative stress, and dramatically accelerates atherosclerosis. Smoking cessation is the single most impactful cardiovascular intervention available.

Chronic inflammation. Elevated CRP and other inflammatory markers predict cardiovascular events independently of traditional risk factors. The JUPITER trial demonstrated that statin therapy reduces cardiovascular events even in people with normal LDL but elevated CRP - evidence that inflammation is a causal driver, not just a marker.

Sedentary behavior. Physical inactivity is an independent cardiovascular risk factor. The cardiovascular system is designed for regular physical stress, and its absence accelerates aging in every measurable parameter.

Several cardiovascular biomarkers are particularly informative for longevity assessment:

VO2 max. Cardiorespiratory fitness, measured as VO2 max, is the strongest known predictor of cardiovascular mortality and all-cause mortality. A low VO2 max carries a higher mortality risk than smoking, hypertension, or diabetes in some analyses. Improving VO2 max through aerobic exercise is one of the highest-return longevity investments available.

Coronary artery calcium (CAC) score. A CT scan that measures calcified plaque in the coronary arteries. A CAC score of zero in a middle-aged adult is associated with very low cardiovascular risk even in the presence of traditional risk factors. A high CAC score identifies people who benefit most aggressively from risk factor management.

ApoB. Apolipoprotein B is a protein found on every atherogenic lipoprotein particle. ApoB is a more accurate predictor of cardiovascular risk than LDL cholesterol because it counts particles rather than cholesterol mass. Many longevity physicians now consider ApoB the primary lipid metric to optimize.

Blood pressure variability. Not just average blood pressure, but its variability over time, predicts cardiovascular outcomes. Home blood pressure monitoring provides more prognostic information than office measurements.

Resting heart rate. A lower resting heart rate reflects better cardiovascular fitness and autonomic function. Each 10 bpm increase in resting heart rate is associated with approximately 10% higher cardiovascular mortality.

Exercise - particularly aerobic exercise. The cardiovascular benefits of regular aerobic exercise are among the most consistently demonstrated findings in all of medicine. Exercise improves endothelial function, reduces arterial stiffness, lowers blood pressure, improves lipid profiles, reduces insulin resistance, and directly increases VO2 max. The dose-response relationship is steep at low fitness levels - going from sedentary to moderately active produces larger risk reductions than going from moderately active to very active.

Blood pressure control. Treating hypertension reduces cardiovascular events more reliably than almost any other intervention. The SPRINT trial demonstrated that targeting systolic blood pressure below 120 mmHg (rather than the traditional 140 mmHg) significantly reduced cardiovascular events and mortality.

LDL and ApoB reduction. The evidence for reducing atherogenic lipoproteins is overwhelming. Statins, ezetimibe, and PCSK9 inhibitors all reduce cardiovascular events in proportion to the degree of LDL/ApoB reduction. The lower the LDL, the lower the risk - with no established floor.

Dietary quality. The Mediterranean diet has the strongest evidence base of any dietary pattern for cardiovascular protection. The PREDIMED trial demonstrated a 30% reduction in major cardiovascular events with a Mediterranean diet supplemented with olive oil or nuts, compared to a low-fat control diet.

Sleep. Both short sleep (less than 6 hours) and long sleep (more than 9 hours) are associated with increased cardiovascular risk. Seven to eight hours of quality sleep is associated with the lowest cardiovascular mortality.

Stress management. Chronic psychological stress activates the sympathetic nervous system and the HPA axis, raising blood pressure, promoting inflammation, and increasing cardiovascular risk. The relationship between psychological stress and cardiovascular events is well established.

One of the most important developments in cardiovascular medicine over the past decade has been the recognition that inflammation is not just a marker of cardiovascular disease - it is a driver.

The CANTOS trial demonstrated that canakinumab, an anti-inflammatory drug that targets IL-1beta, reduced cardiovascular events in people with prior heart attacks and elevated CRP - without affecting lipids at all. This was proof-of-concept that targeting inflammation directly reduces cardiovascular risk.

This finding has shifted attention toward anti-inflammatory lifestyle interventions as cardiovascular protective strategies: exercise, dietary quality, sleep, stress management, and weight management all reduce chronic inflammation and, through that mechanism, reduce cardiovascular risk.

Cardiovascular health is not a separate domain from longevity - it is central to it. The interventions that protect the heart and vasculature are largely the same ones that protect every other system: regular exercise, dietary quality, sleep, stress management, and avoidance of smoking.

What is distinctive about cardiovascular health is the availability of powerful pharmacological interventions - statins, antihypertensives, antiplatelet agents - that can dramatically reduce risk when lifestyle alone is insufficient. These are not alternatives to lifestyle; they are complements to it.

The most important thing most people can do for their cardiovascular longevity is not a drug or a supplement. It is improving their cardiorespiratory fitness. The mortality risk reduction from moving from low to moderate fitness is larger than the risk reduction from most cardiovascular drugs. And unlike drugs, it improves every other system simultaneously.