Epidemiology
Cardiovascular disease (CVD) is the number one cause of death worldwide, accounting for 17.9 million deaths per year.[6] Ischaemic heart disease (IHD) is the most common cause of cardiovascular death; data from the European Society of Cardiology in 2019 showed that IHD accounted for 38% of CVD deaths in females and 44% in males.[1][7] Coronary heart disease mortality has fallen over the last 30 years in Europe and is decreasing in many developed countries, but is increasing in developing and transitional countries, with more than 75% of CVD deaths occurring in developing countries.[6] These trends reflect changes in population longevity, urbanisation, and lifestyle changes.[6]
Despite the overall reduction in incidence and mortality of CVD, in the UK the prevalence remains at about 3%, with CVD accounting for about 1.2 million hospitalisations per year.[8] In the UK in 2022-2023 there were 81,735 confirmed myocardial infarctions, of which 52,470 were non-ST-elevation myocardial infarction (NSTEMI), a reduction of about 4% on the number recorded in 2017-2018.[9] IHD is more common in men than in women.[7][10]
Epidemiology data have shown that acute coronary syndrome (ACS) cases with ST-elevation myocardial infarction (STEMI) appear to be declining and that NSTEMI occurs more frequently than STEMI.[10] In the US, it is estimated that >780,000 people will experience an ACS each year, and approximately 70% of these will have NSTEMI.[1] International data suggest that the incidence of NSTEMI continues to rise.[9][11] This is likely to be due to the advent of more sensitive assays for myocardial injury, earlier pharmacotherapy, and reperfusion (and prevention) of STEMI.[12]
Risk factors
Smoking causes nearly 1 in 5 deaths in the US and is the single most important modifiable risk factor for cardiovascular disease (CVD).[16] Cigarette smokers are substantially more likely than non-smokers to develop coronary artery disease (CAD), to have a stroke, and to develop peripheral vascular disease, and are at increased risk of fatal and non-fatal recurrences of these diseases.[16][17][18]
Smoking increases risk for CAD by direct promotion of atherosclerosis, reduced oxygen delivery in the blood, increased thrombogenesis, and direct coronary artery spasm.[19] Even mild and passive smoking, and exposure to environmental tobacco, is associated with increased risk; risk increases further as the number of cigarettes smoked per day increases.[4][10][17][20][21] Current use of smokeless tobacco also increases the risk of CAD compared with people who have never used.[10][21] Patients who stop smoking reduce their risk of recurrent cardiovascular disease by about one third compared with patients who do not stop smoking.[22]
Surprisingly, current smoking is associated with a lower risk of acute death in the setting of acute coronary syndrome (ACS).[2] This is referred to as the 'smoker's paradox' and reflects the tendency for smokers to develop thrombi on less severe plaques and at an earlier age than non-smokers.
A major risk factor for ACS, and for poor outcomes in patients with ACS. About 69% of people who have a first myocardial infarction (MI) have BP >140/90 mmHg.[1] Hypertension is one of the most prevalent risk factors for CAD in the US; approximately 30% of Americans have BP >140/90 mmHg, placing them at greater risk of MI, and of poor outcomes in the event of ACS.[1][2][23][24] Even pre-hypertension (untreated systolic BP 120-139 mmHg and untreated diastolic BP 80-89 mmHg, or both) increases risk twofold compared with normal levels.[10] High blood pressure induces ventricular hypertrophy and endothelial dysfunction/damage, and promotes atherosclerosis, all of which predispose patients to cardiac events. By increasing cardiac after-load and myocardial oxygen consumption, uncontrolled hypertension can contribute to and worsen anginal symptoms.
Effective treatment of hypertension dramatically reduces the risk of cerebrovascular events, heart failure, and future MI.[1]
Patients with diabetes mellitus are at increased risk of CAD.[2] They have a two- to fourfold increased risk of cardiovascular disease compared with people who do not have diabetes.[25] The mechanisms are not fully known but they may reflect vascular abnormalities of inflammation, endothelial and smooth muscle function, obesity, hypertension, dyslipidaemia, and hypercoagulability.
CAD accounts for 75% of all deaths in the diabetic population.[2] Diabetes is associated with more extensive CAD, unstable lesions, and less favourable long-term outcomes (death, MI, ACS re-admission), with approximately double the risk of long-term mortality from CAD than that of people without diabetes following MI.[2][23]
An HbA1c of <53 mmol/mol (<7%) is the goal of treatment for patients with diabetes.[10][26] However, for patients with coronary heart disease, this goal may be less stringent (i.e., <64 mmol/mol [<8%]).[26]
Estimates suggest that more than half of adults in Western society are overweight or obese.[10][27][28] Adipokines and other hormones secreted by adipose tissue are highly linked to inflammation and atherosclerosis.[29] Obesity is associated with diastolic dysfunction and is a strong stimulus for left ventricular hypertrophy.[30][31] Obesity and the metabolic phenotype (abdominal obesity with known history of hyperlipidaemia, hypertension, and insulin resistance) predispose to CAD, and increase cardiovascular and all-cause mortality.[2][10][28][30][32] Bariatric surgery for weight loss reduces risk of major cardiovascular events (fatal ACS and stroke), incident heart failure and cardiovascular mortality.[33]
Sedentary behaviour is associated with an increased risk of CVD.[10] Epidemiological studies suggest a cause-and-effect relationship between physical activity and cardiorespiratory fitness and reduced cardiovascular mortality.[34] The relative risk of CAD associated with physical inactivity ranges from 1.5 to 2.4, an increase comparable to that for high cholesterol, high blood pressure, and cigarette smoking.[35]
Physical activity has anti-atherosclerotic, psychological, antithrombotic, anti-ischaemic, and anti-arrhythmic effects that are important in primary and secondary prevention of CAD.[34] Regular exercise increases cardiorespiratory fitness and lowers myocardial oxygen demand.[36] Sustained, regular physical activity lowers blood pressure, reduces lipid levels, reduces adiposity, increases insulin sensitivity, and decreases inflammation, stress, and adrenergic activity.[37] In patients with CAD, there is a direct correlation between the volume of moderate to vigorous physical activity and reduction in cardiovascular risk and mortality.[38][39]
Elevated low-density lipoprotein (LDL)-cholesterol, elevated triglycerides, decreased high-density lipoprotein (HDL), and elevated ratio of LDL to HDL are all independently associated with increased risk of atherosclerosis.[40] There is a linear relationship between reduction in LDL-cholesterol and risk of MI or other major vascular events; absolute risk reduction of major vascular events depends on the baseline risk of cardiovascular events and degree of LDL-cholesterol lowering.[41] In postmenopausal women, dysfunctional HDL may mean that high HDL levels (usually considered protective) are also associated with an increased risk of atherosclerosis.[42]
Lipid-lowering therapy reduces future ischaemic events and limits disease progression.[1][2][43][44] Current guidelines recommend high-dose statin therapy in patients with known CAD or CAD equivalent, irrespective of LDL levels.[1][45][46] Other lipid-lowering treatments can be considered in patients who are contraindicated or intolerant of statins.
Approximately 30% to 40% of patients with ACS have chronic kidney disease (CKD).[1][47] Excess CVD in patients with CKD is caused, at least in part, by higher prevalence of traditional risk factors in this group; there is a very high prevalence of comorbid CVDs in patients with CKD, ranging from ischaemic heart disease to arrhythmias and venous thromboembolism.[10] Decreasing glomerular filtration rate is associated with increasing risk of cardiovascular events, including death.[2][48]
Atherosclerotic heart disease is the underlying mechanism in CAD. It evolves over decades and can begin in childhood. One study found intimal lesions in the aorta in all those aged 15-19 years, and in the right coronary artery in more than half of those of this age.[49] Atherosclerosis is typically silent until an acute event occurs (e.g., ACS). A sedentary lifestyle, excess caloric intake, and cigarette smoking are strongly associated with atherosclerosis.
In an acute setting, the presence or absence of the traditional risk factors for CAD are not specific or sensitive for diagnosing ACS. However, they do appear to be important in determining prognosis in ACS and targeting secondary prevention strategies.[2]
Long-standing angina pectoris is a risk factor for coronary events.[50] Presence of peripheral arterial disease increases the likelihood of associated coronary atherosclerosis.[2]
Defined as premature CAD in family members (men aged <50 years; women aged <55 years).[51] Family history includes a first-degree relative with a history of MI, sudden cardiac death, aortic dissection, percutaneous coronary intervention, or coronary artery bypass graft. Inherited (primary) disorders of lipoprotein metabolism are an important cause, though other genetic variants may also play a role.[52] On physical examination, patients may have eruptive xanthomas, lipaemia retinalis (lipid accumulation within retinal vessels), or tendinous xanthomas. In the acute setting of ACS, presence or absence of family history does not help in treatment, but presence of family history increases the probability of ACS, and is associated with an increased risk of 30-day cardiac events in patients with ACS.[2]
ACS is more common in older patients; the majority of patients presenting with ACS are age >65 (median age 68).[2] Patients with NSTEMI are often older than patients with STEMI; half of patients with NSTEMI are aged 70 years or older, whereas half of those with STEMI are aged 64 years or younger.[9] The mean age of patients presenting with STEMI is 60 years for men, and 71 years for women.[53]
Cocaine accounts for up to 25% of acute MI in people aged 18-45 years.[54] In the hour after cocaine is used, the risk of MI is 24 times the baseline risk.[55] This is probably due to cocaine-induced coronary vasospasm and thrombosis, in addition to a direct effect on heart rate and arterial pressure. Cocaine also has direct myocardial toxic properties.[2]
Untreated moderate to severe obstructive sleep apnoea (OSA) has been associated with a 17% increase in relative risk of cardiovascular events compared with risk in patients without OSA.[58] Patients with pre-existing OSA are at increased risk of further cardiac events following ACS compared with patients who do not have OSA.[59][60]
Elevation in CRP (a marker of inflammation) is associated with increased risk of CAD and has prognostic value in addition to lipid profile.[30]
Use of this content is subject to our disclaimer