Cardiovascular disease is the number one cause of death worldwide, accounting for 17.5 million deaths per year. In 2012, the WHO estimated that one third of all deaths globally were attributable to cardiovascular disease, and 7.4 million of those deaths were from ischaemic heart disease.[6] Coronary heart disease mortality is decreasing in many developed countries, but is increasing in developing and transitional countries, partly as a result of increasing longevity, urbanisation, and lifestyle changes. 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.[4][7] 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] Trends from the world's largest database of patients with ACS show that the percentage of patients with a diagnosis of NSTEMI is rising dramatically.[8] This is likely to be due to the advent of more sensitive assays for myocardial injury, earlier pharmacotherapy, and reperfusion (and prevention) of STEMI.[2][8]

Risk factors

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 to 19 years, and in the right coronary artery in more than half of those of this age.[12] Atherosclerosis is typically silent until an acute event occurs (e.g., acute coronary syndrome). 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 NSTEMI. However, they do appear to be important in determining prognosis in acute coronary syndrome and targeting secondary prevention strategies.[1]

Patients with diabetes mellitus are at increased risk of coronary artery disease (CAD). The mechanisms are not fully known but they may reflect vascular abnormalities of inflammation, obesity, hypertension, dyslipidaemia, and hypercoagulability.

Approximately 20% to 25% of all patients with NSTEMI have diabetes and CAD accounts for 75% of all deaths in the diabetic population.[1][13] Diabetes is associated with more extensive CAD, unstable lesions, and less favourable long-term outcomes (death, myocardial infarction, acute coronary syndrome re-admission), as well as with coronary revascularisation, especially percutaneous coronary intervention.[1]

Smoking causes nearly 1 in 5 deaths in the US. 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.[14] Smoking increases risk for CAD by direct promotion of atherosclerosis, reduced oxygen delivery in the blood, increased thrombogenesis, and direct coronary artery spasm.

Smoking results in a two- to threefold increase in cardiac mortality.[7] Exposure to environmental tobacco smoke also significantly increases risk for heart disease.[15] Surprisingly, current smoking is associated with a lower risk of acute death in the setting of acute coronary syndrome.[1] 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.

Cholesterol is a main constituent of advanced atherosclerotic plaques. Western diet, excess calorie intake, and sedentary lifestyle are the strongest contributors to dyslipidaemia. Large epidemiological studies have firmly identified an increased risk of myocardial infarction with serum lipid abnormalities (mainly increased low-density lipoproteins [LDL], elevated triglycerides, and decreased high-density lipoproteins).[16][17] LDL levels have the strongest relationship.

Lipid-lowering therapy reduces future ischaemic events and limits disease progression.[18][19] Lower LDL levels highly correlate with reduction of death from myocardial infarction or recurrent acute coronary syndrome.[20]

Defined as premature CAD in family members (men <55 years; women <65 years). 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. On physical examination, patients may have eruptive xanthomas, lipaemia retinalis (lipid accumulation within retinal vessels), or tendinous xanthomas. In the acute setting of NSTEMI, presence or absence of family history does not help in treatment, but presence of family history increases the probability of NSTEMI, and is associated with an increased risk of 30-day cardiac events in patients with acute coronary syndrome.[1]

Nearly 60% of people admitted to hospital with NSTEMI as the primary diagnosis are >65 years of age.[21] Between 1990-1999, the mean age of NSTEMI patients rose from 65-68 years.[8] Older patients have increased risks of underlying coronary artery disease (CAD) and multiple-vessel CAD. They are at higher risk than younger patients for an adverse outcome.[1]

A major risk factor for poor outcomes in patients with acute coronary syndrome.[1] About 69% of people who have a first myocardial infarction have BP >140/90 mmHg.[7] Hypertension is one of the most prevalent risk factors for coronary artery disease in the US. Approximately 30% of Americans have blood pressure >140/90 mmHg, placing them at greater risk of myocardial infarction.[7] Effective treatment of hypertension dramatically reduces the risk of cerebrovascular events, heart failure, and future myocardial infarction.[7] High blood pressure induces ventricular hypertrophy and endothelial dysfunction/damage, and promotes atherosclerosis, all of which predispose patients to cardiac events.

Estimates suggest that more than half of adults in Western society will become overweight or obese.[22] Excess calorie intake increases low-density lipoproteins, total cholesterol, and triglyceride levels. Obesity and the metabolic phenotype (abdominal obesity with known history of hyperlipidaemia, hypertension, and insulin resistance) predispose to coronary artery disease.[22][23][24] Cardiac output and blood volume increase to supply the vascular-rich adipose tissue. Obesity is associated with diastolic dysfunction and is a strong stimulus for left ventricular hypertrophy.[23] Adipokines and other hormones secreted by adipose tissue are highly linked to inflammation and atherosclerosis.

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.[25] Physical activity has anti-atherosclerotic, psychological, antithrombotic, anti-ischaemic, and anti-arrhythmic effects that are important in primary and secondary prevention of CAD.[26] Regular exercise increases cardiorespiratory fitness and lowers myocardial oxygen demand. This correlates with lower mortality, and reduced risk of CAD and morbidity from NSTEMI. [ Cochrane Clinical Answers logo ] Sustained, regular physical activity lowers blood pressure, reduces lipid levels, reduces adiposity, increases insulin sensitivity, and decreases inflammation, stress, and adrenergic activity.[26]

Cocaine accounts for up to 25% of acute myocardial infarction in people aged 18 to 45 years. The lifetime risk of non-fatal myocardial infarction with cocaine use is 7 times the risk in non-users.[27] In the hour after cocaine is used, the risk of myocardial infarction is 24 times the baseline risk. It 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.[1]

An independent predictor of future myocardial infarction in otherwise healthy people.[28][29]

Stent thrombosis or in-stent restenosis may cause 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.[30]

Patients with chronic kidney disease have increased risk of NSTEMI and worsened prognosis following an NSTEMI.[31]

NSTEMI is a relatively common complication of all types of surgical and non-surgical procedures. Type of surgery, patient risk factors, and prior patient history are important contributors to postoperative NSTEMI. Often this is detected as a rise in cardiac markers in the days following the surgical procedure. Preoperative risk assessment and additional steps to reduce the risk of myocardial ischaemia/stress may prevent this complication or enable early recognition and therapy.[32]

Untreated moderate to severe obstructive sleep apnoea (OSA) has been associated with a 17% increase in relative risk of cardiovascular events compared to risk in patients without OSA.[33]

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