Epidemiology
Cardiovascular disease (CVD) is the number one cause of death worldwide, accounting for 17.9 million deaths per year.[5] 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.[2][6]
The incidence and mortality of ischaemic heart disease has fallen over the last 30 years in Europe and is also decreasing in many developed countries, which may be due to better control of risk factors such as hypertension, diabetes, high cholesterol, and smoking.[7] However, mortality is increasing in developing and transitional countries, with more than 75% of CVD deaths occurring in developing countries.[5] These trends reflect changes in population longevity, urbanisation, and lifestyle changes.[5] 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]
The incidence of STEMI has been steadily declining over the past 20 years. In England, Wales, and Northern Ireland, there were around 86,000 cases of MI between April 2021 and March 2022. There was a 16% increase in total MI cases compared with 2020-21 when admissions were substantially affected by COVID-19.[9]
MI affects both men and women, but tends to occur at a younger age in men.[10] The average age of a person having a first MI is 65.6 years for men and 72 years for women.[10] The incidence in women increases after the menopause. Women aged under 60 years with STEMI have higher 30-day mortality rates from STEMI than men under 60 years, even after adjusting for medications, primary percutaneous coronary intervention, and other co-existing comorbidities.[10][11]
About 90% of patients with coronary heart disease report at least one major risk factor for coronary artery disease, including cigarette smoking, dyslipidaemia, hypertension, diabetes, and abdominal obesity.[12]
Risk factors
Smoking causes 1 in 4 deaths from cardiovascular disease in the US and is the single most important modifiable risk factor for cardiovascular disease.[14] 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.[7][14][15] Smoking increases risk for CAD by direct promotion of atherosclerosis, reduced oxygen delivery in the blood, increased thrombogenesis, and direct coronary artery spasm.[16] 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.[7][15][17][18][19] Current use of smokeless tobacco also increases the risk of CAD compared with people who have never used.[15][18][19]
Patients who stop smoking reduce their risk of recurrent cardiovascular disease by about one third compared with patients who do not stop smoking.[20] Surprisingly, current smoking is associated with a lower risk of acute death in the setting of acute coronary syndrome.[21] 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 acute coronary syndrome (ACS), and for poor outcomes in patients with ACS. About 69% of people who have a first myocardial infarction have BP >140/90 mmHg.[2] Hypertension is one of the most prevalent risk factors for coronary artery disease in the US; approximately 30% of Americans have BP >140/90 mmHg, placing them at greater risk of myocardial infarction, and of poor outcomes in the event of ACS.[2][21][22][23] 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.[15] 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 myocardial infarction.[2]
Patients with diabetes mellitus are at increased risk of coronary artery disease (CAD).[21] They have a two- to fourfold increased risk of cardiovascular disease compared with people who do not have diabetes.[24] 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.[21] Diabetes is associated with more extensive CAD, unstable lesions, and less favourable long-term outcomes (death, myocardial infarction, acute coronary syndrome re-admission), with approximately double the risk of long-term mortality from CAD than that of people without diabetes following myocardial infarction.[21][22]
An HbA1c of <53 mmol/mol (<7%) is the goal of treatment for patients with diabetes.[15][25] However, for patients with coronary heart disease, this goal may be less stringent (i.e., <64 mmol/mol [<8%]).[25]
Estimates suggest that more than half of adults in Western society are overweight or obese.[15][26][27] Adipokines and other hormones secreted by adipose tissue are highly linked to inflammation and atherosclerosis.[28] Obesity is associated with diastolic dysfunction and is a strong stimulus for left ventricular hypertrophy.[29][30] Obesity and the metabolic phenotype (abdominal obesity with known history of hyperlipidaemia, hypertension, and insulin resistance) predispose to coronary artery disease, and increase cardiovascular and all-cause mortality.[15][21][27][29][31] Bariatric surgery for weight loss reduces risk of major cardiovascular events (fatal acute coronary syndrome and stroke), incident heart failure, and cardiovascular mortality.[32]
Sedentary behaviour is associated with an increased risk of cardiovascular disease.[15] Epidemiological studies suggest a cause-and-effect relationship between physical activity and cardiorespiratory fitness and reduced cardiovascular mortality.[33] The relative risk of coronary artery disease (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.[34]
Physical activity has anti-atherosclerotic, psychological, antithrombotic, anti-ischaemic, and anti-arrhythmic effects that are important in primary and secondary prevention of CAD.[33] Regular exercise increases cardiorespiratory fitness and lowers myocardial oxygen demand.[35] Sustained, regular physical activity lowers blood pressure, reduces lipid levels, reduces adiposity, increases insulin sensitivity, and decreases inflammation, stress, and adrenergic activity.[36] 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.[37][38]
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.[39]
There is a linear relationship between reduction in LDL-cholesterol and risk of myocardial infarction 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.[40] In postmenopausal women, dysfunctional HDL may mean that high HDL levels (usually considered protective) are also associated with an increased risk of atherosclerosis.[41]
Lipid-lowering therapy reduces future ischaemic events and limits disease progression.[2][21][42][43] Current guidelines recommend high-dose statin therapy in patients with known coronary artery disease (CAD) or CAD equivalent, irrespective of LDL levels.[2][44][45] Other lipid-lowering treatments can be considered in patients who are contraindicated or intolerant of statins.
Approximately 30% to 40% of patients with acute coronary syndrome have chronic kidney disease (CKD).[2][46] Excess cardiovascular disease 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 cardiovascular diseases in patients with CKD, ranging from ischaemic heart disease to arrhythmias and venous thromboembolism.[15] Decreasing glomerular filtration rate is associated with increasing risk of cardiovascular events, including death.[21][47]
Atherosclerotic heart disease is the underlying mechanism in coronary artery disease (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.[48] Atherosclerosis is typically silent until an acute event occurs (e.g., acute coronary syndrome [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.[21]
Long-standing angina pectoris is a risk factor for coronary events.[49] Presence of peripheral arterial disease increases the likelihood of associated coronary atherosclerosis.[21]
Defined as premature coronary artery disease in family members (men aged <50 years; women aged <55 years).[50] Family history includes a first-degree relative with a history of myocardial infarction, 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.[51] On physical examination, patients may have eruptive xanthomas, lipaemia retinalis (lipid accumulation within retinal vessels), or tendinous xanthomas. In the acute setting of acute coronary syndrome (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.[21]
Acute coronary syndrome (ACS) is more common in older patients; the majority of patients presenting with ACS are age >65 years (median age 68 years).[21] Patients with non-STEMI (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.[52]
Cocaine accounts for up to 25% of acute myocardial infarction in people aged 18-45 years.[53] In the hour after cocaine is used, the risk of myocardial infarction is 24 times the baseline risk.[54] 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.[21]
Stent thrombosis or in-stent restenosis may cause STEMI, non-STEMI (NSTEMI), or unstable angina. Both stent thrombosis and restenosis have complex causes, triggers, pathophysiology, and risk factors. Of importance, premature cessation of antiplatelet agents in patients with stents (drug-eluting and bare-metal) may trigger an acute coronary syndrome.[2][21]
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.[57] Patients with pre-existing OSA are at increased risk of further cardiac events following acute coronary syndrome compared with patients who do not have OSA.[58][59]
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