Heart attacks in women are caused by many of the same risk factors that affect men, including high blood pressure, high cholesterol, and smoking, but the underlying biology often looks different. Women are more likely to have heart attacks triggered by mechanisms that don’t involve the classic large blockage in a coronary artery. This means some causes are routinely missed or underestimated, especially in younger women.
How Plaque Behaves Differently in Women
The textbook heart attack involves a fatty plaque in a coronary artery that ruptures, triggering a blood clot that blocks blood flow. This does happen in women, but a second mechanism called plaque erosion is far more common in women than in men. Instead of a dramatic rupture, the thin inner lining of the artery wears away, exposing the tissue beneath it to the bloodstream and triggering clot formation on a plaque that may not have been large enough to show up as a significant blockage.
Post-mortem studies have found that plaque erosion accounts for roughly 75% of sudden coronary deaths in women younger than 50. In men of the same age, the number ranges from 35% to 65%. Overall, about 40% of all acute coronary events involve erosion rather than rupture. The eroded plaques tend to have less inflammation than ruptured ones, which may be one reason standard markers of heart attack risk sometimes underestimate danger in women.
Small Vessel Disease and “Clear” Arteries
Up to half of all patients who undergo a heart catheterization for chest pain or signs of reduced blood flow turn out to have no major blockage in their large coronary arteries. In many of these cases, particularly in women, the problem is in the tiny blood vessels that branch deep into the heart muscle.
This condition, called coronary microvascular dysfunction, involves structural and functional changes in those small vessels. The vessel walls thicken, the smallest capillaries thin out, and the lining loses its ability to relax and widen when the heart needs more oxygen. The result mimics what a large blockage would do: the heart muscle doesn’t get enough blood, especially during physical or emotional stress. Risk factors like diabetes, obesity, and smoking accelerate the damage to these small vessels by impairing the lining’s ability to produce nitric oxide, the molecule that signals blood vessels to relax. Excessive constriction of these tiny arteries can also play a role, creating spasms that temporarily choke off blood flow.
Because standard imaging looks for blockages in the large arteries, microvascular disease has historically been dismissed as a non-cardiac problem. Women sent home with a clean angiogram were often told nothing was wrong, even as their small vessels were failing.
Spontaneous Coronary Artery Dissection
Spontaneous coronary artery dissection, or SCAD, is a tear in the wall of a coronary artery. Blood seeps between the layers of the artery wall, forming a pocket that compresses the channel from the outside and blocks flow. It has nothing to do with cholesterol buildup. It accounts for up to 35% of heart attacks in women under 50.
SCAD tends to strike women who don’t fit the typical cardiac risk profile. Many are physically active, have normal cholesterol, and have no family history of heart disease. The exact trigger isn’t always clear, though extreme physical exertion, emotional stress, and hormonal changes (including the postpartum period) have been associated with episodes. Connective tissue disorders and fibromuscular dysplasia, a condition where artery walls develop abnormally, also raise the risk. Fibromuscular dysplasia occurs in women about 90% of the time.
Stress Cardiomyopathy
Sometimes called “broken heart syndrome,” Takotsubo cardiomyopathy is a sudden weakening of the heart muscle triggered by intense emotional or physical stress. The heart’s pumping chamber balloons out and stops contracting normally, producing symptoms identical to a heart attack. Women, particularly postmenopausal women between 65 and 70, account for 80 to 90% of all cases.
The mechanism involves a flood of stress hormones that are directly toxic to heart muscle cells and cause the small coronary vessels to constrict. After menopause, the loss of estrogen removes a protective buffer against this kind of damage. Estrogen normally supports the blood vessel lining’s ability to produce nitric oxide, which keeps vessels relaxed and reduces inflammation. Without it, the heart becomes more vulnerable to the effects of a sudden adrenaline surge.
How Menopause Shifts the Risk
Before menopause, women develop heart disease at significantly lower rates than men of the same age. That gap narrows quickly after menopause, and the reason goes beyond simple aging. The hormonal shift itself drives measurable changes in cardiovascular risk factors over a relatively short window.
Total cholesterol rises 10 to 14% during the menopause transition. LDL cholesterol, the type most strongly linked to plaque buildup, increases by 10 to 20 mg/dL. Calcium deposits in the coronary arteries, a direct marker of atherosclerosis, are 2.37 times more likely to appear after menopause. The walls of the carotid arteries thicken at an accelerated rate during late perimenopause, a sign of early arterial disease. These are not gradual aging effects. They cluster around the hormonal transition and represent a distinct period of vascular vulnerability.
Pregnancy Complications as Warning Signs
Certain pregnancy complications are now recognized as independent risk factors for heart disease later in life. Preeclampsia, the condition marked by dangerously high blood pressure during pregnancy, roughly doubles the risk of coronary artery disease, doubles the risk of dying from cardiovascular causes, and quadruples the risk of heart failure in the decades that follow. The risk is highest for women who had preeclampsia in more than one pregnancy.
Gestational diabetes carries a similar, though somewhat smaller, signal. Women with a history of gestational diabetes face about twice the odds of developing cardiovascular disease compared to women whose pregnancies were uncomplicated. The link is partly explained by the dramatically higher risk of developing type 2 diabetes afterward (up to 10 times higher), which is itself a major driver of heart disease. But even accounting for that, the pregnancy complication appears to mark women whose cardiovascular systems are more vulnerable.
These complications don’t cause heart attacks directly. They reveal an underlying susceptibility in the blood vessels and metabolic system that, without monitoring, can go unaddressed for decades until a cardiac event occurs.
Autoimmune and Inflammatory Conditions
Chronic inflammatory diseases hit women disproportionately and carry serious cardiovascular consequences. Lupus, which affects women about nine times more often than men, increases the risk of heart attack, heart failure, and stroke by two to three times compared to the general population. In premenopausal women with lupus, the risk of heart attack is 50 times higher than in healthy women of the same age. The persistent inflammation damages blood vessel walls, accelerates plaque formation, and promotes clotting.
Rheumatoid arthritis is significant enough that it’s included as a standalone risk factor in cardiovascular risk calculators used in clinical practice. Endometriosis, which affects roughly one in ten women of reproductive age, has also been linked to a 23% higher risk of cardiovascular disease. The chronic inflammation and hormonal disruption associated with endometriosis appear to take a cumulative toll on vascular health over time.
Traditional Risk Factors Still Matter
The sex-specific causes above are important, but they layer on top of the same risk factors that drive heart disease in everyone. High blood pressure (with a treatment target below 130/80 for all adults), elevated LDL cholesterol, smoking, diabetes, obesity, and physical inactivity remain the primary drivers of atherosclerosis in women just as they are in men. Diabetes and smoking, in particular, appear to carry a proportionally greater heart attack risk in women than in men.
What makes heart attacks in women harder to predict and prevent is that these standard risk factors coexist with mechanisms like microvascular disease, plaque erosion, and SCAD that don’t follow the usual pattern. A woman can have a heart attack with arteries that look normal on a standard test, or she can develop dangerous plaque buildup silently accelerated by menopause, lupus, or a history of preeclampsia. The causes are broader and more varied than the traditional model accounts for, which is why awareness of these less obvious pathways is critical.