Myocardial infarction, the death of heart muscle when its coronary blood supply is interrupted, is the most visible event in ischaemic heart disease, the disease of reduced blood supply to the heart muscle. The population it happens to has changed over the last two decades. Most acute infarctions now present without ST elevation, and the risk factors that produce them are common, measurable and — with a few exceptions — modifiable.
How common it is
Ischaemic heart disease carries the largest age-standardised burden of any condition measured by the Global Burden of Disease study, at roughly 2,276 disability-adjusted life-years per 100,000 people. Age-standardised figures adjust for differences in the age structure of populations, and a disability-adjusted life-year counts one year of healthy life lost, whether to illness, disability or early death. Age-standardised incidence, disability and mortality all fell between 1990 and 2021, so the burden is shrinking even while it remains the largest.
Why most infarctions now present without ST elevation
ST elevation is the ECG sign that generally reflects an acutely occluded coronary artery, and ST-elevation myocardial infarction (STEMI) is the presentation that triggers immediate reperfusion by default. Infarction without it is non-ST-elevation myocardial infarction (NSTEMI).
In a United States registry, NSTEMI rose from 52.8% of acute infarctions in 2002 to 68.6% in 2011, and STEMI became correspondingly less common. The registry describes an American population, and the same pattern is reported elsewhere, so the non-ST-elevation presentation is now the majority of what a clinician meets rather than the minority. That shift changes where the diagnostic work happens: most patients need risk stratification — an estimate of their risk that sets how urgently angiography is done — and timing decisions rather than an immediate catheterisation trigger.
What raises risk
Risk factors divide into those that cannot be changed — age, male sex, and a family history of premature coronary disease among them — and those that can. The modifiable group is where prevention acts, and knowing which exposures carry the most weight is what separates a useful risk-factor history from a checklist.
The INTERHEART study measured that weight directly. It was a case-control study, comparing past exposures in people who already had the disease with those in people who did not: 15,152 people with a first myocardial infarction and 14,820 controls across 52 countries, recruited between 1999 and 2003. It reported the following associations, expressed as odds ratios — how much higher the odds of an exposure were among cases than among controls. The strongest, the ApoB/ApoA1 ratio, compares apolipoprotein B, the protein of atherogenic lipoproteins such as low-density lipoprotein (LDL), with apolipoprotein A1, the main protein of high-density lipoprotein (HDL).
| Exposure | Odds ratio for a first myocardial infarction |
|---|---|
| Raised ApoB/ApoA1 ratio | 3.25 |
| Current smoking | 2.87 |
| Psychosocial factors | 2.67 |
| Diabetes | 2.37 |
| Hypertension | 1.91 |
| Abdominal obesity | 1.62 |
Two cautions belong with the table. These are odds ratios from a case-control design, not relative risks, and they describe the populations studied rather than a fixed biological constant.
What matters beyond the individual figures is the total. The population-attributable risk is the share of cases in a population that would be avoided if an exposure were removed, and the nine modifiable factors in the study, six of which appear in the table, together accounted for about 90% of the population-attributable risk in men and 94% in women. Myocardial infarction, in aggregate, is a largely preventable disease, and the two strongest associations in the table — dyslipidaemia (an abnormal blood lipid profile) and smoking — are also the two that treatment attacks first after an event (see Post-MI Long-Term Management).
What a table of associations cannot show is how a risk factor becomes an artery that closes within minutes.