Ischaemic heart disease (IHD) is the most common cause of death globally but in Europe mortality has been falling over the past 30 years.[1] IHD now accounts for almost 1.8 million deaths per year across Europe, around 20% of all deaths, but rates vary significantly between countries.[1] 

In Sweden, which keeps the most comprehensive European STEMI registry, the annual incidence of STEMI in 2015 was 58 per 100,000.[1] Across Europe, incidence estimates range from 43 to 144 per 100,000 per year.[1]

The incidence of STEMI has been declining over the past 20 years. In the UK, it now averages around 500 hospitalised episodes per million people per year.[5] The UK prevalence of people who have had a STEMI at some point in their lives is likely to be between 750 to 1250 per million people.[5] The reported adjusted incidence rate of STEMI in the US fell from 133 per 100,000 in 1999 to 50 per 100,000 in 2008.[1]

There is a consistent pattern for STEMI to be more common in younger than older people and more common in men than in women.[1]

MI tends to occur at a younger age in men. The incidence in women increases after the menopause. The average age of a person having a first MI is 65.1 years for men and 72 years for women.[4] In women with STEMI, younger age is associated with higher 30-day mortality rates even after adjustment for medications, primary percutaneous coronary intervention, and other co-existing comorbidities.[6]

Risk factors

Single most important modifiable risk factor.

People who smoke 20 or more cigarettes a day have a 2- to 3-fold increased risk of dying from coronary heart disease compared with non-smokers or those who have quit for >10 years. Even mild and passive smoking is associated with increased risk.[4]

Only 2 out of 3 patients with hypertension are diagnosed and only 1 in 3 are adequately controlled on treatment.

Systolic blood pressure (SBP) and diastolic blood pressure (DBP) both contribute to development of coronary artery disease.

Even pre-hypertension (untreated SBP 120-139 mmHg and untreated DBP 80-89 mmHg, or both) increases risk 2-fold compared with normal levels.[4]

Patients with diabetes have impaired endothelial and smooth muscle function with increased leukocyte adhesion, promoting atherosclerosis.

They have a 4-fold increased risk of cardiovascular disease compared with people who do not have diabetes.[8]

An HbA1c of <53 mmol/mol (<7%) is the goal of treatment for patients with diabetes.[4][9] However, for patients with coronary heart disease, this goal may be less stringent (i.e., <64 mmol/mol [<8%]).[9]

Increased risk in patients with a body mass index >25.[4]

May be present in men with a waist circumference >100 cm (>39 inches) and women with a waist circumference >90 cm (>35 inches).[10]

Characterised by glucose intolerance, hyperinsulinaemia, elevated triglycerides, low HDL-cholesterol, and central obesity and is a marker for increased risk of coronary artery disease, even in patients without diabetes.[4][11]

Physical inactivity is responsible for 12.2% of the global burden of MI after accounting for other cardiovascular disease risk factors such as cigarette smoking, diabetes mellitus, hypertension, abdominal obesity, lipid profile, alcohol intake, and psychosocial factors.[4]

Elevated LDL-cholesterol, elevated triglycerides, decreased HDL, and elevated ratio of LDL to HDL are all independently associated with increased risk of atherosclerosis.

Early studies on cholesterol showed that a reduction in serum cholesterol by diet and medications reduces non-fatal MI by 25% and fatal MI by 14%.[10]

Current guidelines recommend high-dose statin therapy in patients with known coronary artery disease (CAD) or CAD equivalent, irrespective of LDL levels.[12] Other lipid-lowering treatments can be considered in patients who are contraindicated or intolerant of statins.

Renal dysfunction is a marker of vascular damage.[13]

Excess cardiovascular disease in patients with chronic kidney disease is caused, at least in part, by higher prevalence of traditional risk factors in this group.[4]

18% of coronary events are in patients with preceding long-standing angina pectoris.[4]

Onset affecting first-degree male family member aged <55 years or female family member <65 years.[4]

Regular use of cocaine predisposes young people (aged 18-45 years) to MI.

The risk is increased by 24 times over baseline 1 hour following cocaine use, and chronic exposure appears to accelerate atherosclerosis.[14]

Men have an increased risk of acute MI compared with premenopausal women of the same age. The incidence is similar in post-menopausal women and men of the same age.

Older patients are at an increased risk of acute MI. The number of men being diagnosed with an MI or fatal coronary heart disease rises from 25 per 1000 for men aged 35-44 years to 135 per 1000 for men aged 65-74 years.[4] For women, the incidence also increases with age.

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