History and exam
Key diagnostic factors
common
chest pain
The most common symptom of non-ST-elevation myocardial infarction is chest pain or discomfort. Described as a sensation of tightness, heaviness, aching, burning, pressure, or squeezing.
The pain is most often retrosternal and can often radiate to the left arm but may also radiate to the lower jaw, neck, both arms, back, and epigastrium, where it may mimic heartburn.[7]
diaphoresis
Diaphoresis is a common feature due to high sympathetic drive.[79][105] Non-ST-elevation myocardial infarction (and other acute coronary syndrome) should be suspected in any patient with chest pain, which includes pain in other areas (e.g., the arms, back or jaw), that is associated with nausea and vomiting, marked sweating or diaphoresis, and/or breathlessness, or particularly a combination of these.[79][105]
uncommon
cardiogenic shock
acute heart failure
Urgent and immediate angiography with the intent to perform revascularization is indicated if the patient has left ventricular failure.[86] Waiting for results of troponin testing should not delay angiography.[5] See Acute heart failure.
Other diagnostic factors
common
nausea and vomiting
Nausea and vomiting are common features. May be the only symptom.
Non-ST-elevation myocardial infarction (and other acute coronary syndrome) should be suspected in any patient with chest pain, which includes pain in other areas (e.g., the arms, back or jaw), that is associated with nausea and vomiting, marked sweating or diaphoresis, and/or breathlessness, or particularly a combination of these.[79]
epigastric pain
Patients may present with a range of noncharacteristic symptoms (chest-pain equivalent symptoms), any of which may be the sole presenting symptom. Epigastric pain, indigestion-like symptoms, isolated dyspnea, or syncope can indicate acute coronary syndrome. These noncharacteristic presentations are more common in women, older people, and people with diabetes.[5]
uncommon
arrhythmias
abnormal heart sounds
A new systolic murmur may be present due to ischemic mitral regurgitation, which is associated with a poor prognosis, or a mechanical complication (e.g., papillary muscle rupture or ventricular septal defect).
shortness of breath
Patients may present with a range of noncharacteristic symptoms (chest-pain equivalent symptoms), any of which may be the sole presenting symptom. Epigastric pain, indigestion-like symptoms, isolated dyspnea, or syncope can indicate acute coronary syndrome. These noncharacteristic presentations are more common in women, older people, and people with diabetes.[5][9]
Shortness of breath can also occur secondary to diminished cardiac output, but may also be due to underlying pulmonary congestion.
Frank congestive heart failure, jugular venous distension, pulmonary edema, and cardiogenic shock can be present, and patients who present with these are at high risk for a poor outcome.[2]
syncope
Patients may present with a range of noncharacteristic symptoms (chest-pain equivalent symptoms), any of which may be the sole presenting symptom. Epigastric pain, indigestion-like symptoms, isolated dyspnea, or syncope can indicate acute coronary syndrome. These noncharacteristic presentations are more common in women, older people, and people with diabetes.[5][9]
early morning onset
Events peak at early hours of the morning, presumably due to hemodynamic stress caused by increased serum cortisol, adrenergic hormones, and platelet aggregation.[81]
Risk factors
strong
smoking
Smoking causes nearly 1 in 4 deaths in the US and is the single most important modifiable risk factor for cardiovascular disease (CVD).[22] Cigarette smokers are substantially more likely than nonsmokers to develop coronary artery disease (CAD), to have a stroke, and to develop peripheral vascular disease, and are at increased risk of fatal and nonfatal recurrences of these diseases.[10][22][23]
Smoking increases risk for CAD by direct promotion of atherosclerosis, reduced oxygen delivery in the blood, increased thrombogenesis, and direct coronary artery spasm.[24] 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.[10][23][25][26][27]
Current use of smokeless tobacco also increases the risk of CAD compared to people who have never used.[10][26][27][28] Patients who quit smoking reduce their risk of recurrent CVD by about one third, compared to patients who do not quit smoking.[29] Surprisingly, current smoking is associated with a lower risk of acute death in the setting of acute coronary syndrome.[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 nonsmokers.
hypertension
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 (MI) have blood pressure (BP) >140/90 mmHg.[5] 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 MI, and of poor outcomes in the event of ACS.[2][5][30][31] Even prehypertension (untreated systolic BP 120-139 mmHg and untreated diastolic BP 80-89 mmHg, or both) increases risk twofold compared with normal levels.[10] High BP 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.[5]
diabetes
Patients with diabetes mellitus are at increased risk of coronary artery disease (CAD).[2] They have a two- to fourfold increased risk of cardiovascular disease compared with people who do not have diabetes.[32]
The mechanisms are not fully known but they may reflect vascular abnormalities of inflammation, endothelial and smooth muscle function, obesity, hypertension, dyslipidemia, and hypercoagulability.
Diabetes is associated with more extensive CAD, unstable lesions, and less favorable long-term outcomes (death, myocardial infarction [MI], acute coronary syndrome re-admission), with approximately double the risk of long-term mortality from CAD than that of people without diabetes following MI.[2][30]
An HbA1c of <7% (<53 mmol/mol) is the goal of treatment for patients with diabetes.[10][33] However, for patients with coronary heart disease, this goal may be less stringent (i.e., <8% [<64 mmol/mol]).[33]
obesity and metabolic syndrome phenotype
Estimates suggest that more than half of adults in Western society are overweight or obese.[10][34][35] Adipokines and other hormones secreted by adipose tissue are highly linked to inflammation and atherosclerosis.[36] Obesity is associated with diastolic dysfunction and is a strong stimulus for left ventricular hypertrophy.[37][38] Obesity and the metabolic phenotype (abdominal obesity with known history of hyperlipidemia, hypertension, and insulin resistance) predispose to coronary artery disease, and increase cardiovascular and all-cause mortality.[2][10][35][37][39][40] Bariatric surgery for weight loss reduces risk of major cardiovascular events (fatal acute coronary syndrome and stroke), incident heart failure and cardiovascular mortality.[41]
sedentary behavior and physical inactivity
Sedentary behavior is associated with an increased risk of cardiovascular disease.[10] Epidemiologic studies suggest a cause-and-effect relationship between phyisical activity and cardiorespiratory fitness and reduced cardiovascular mortality.[42] 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 (BP), and cigarette smoking.[43] Physical activity has anti-atherosclerotic, psychologic, antithrombotic, anti-ischemic, and antiarrhythmic effects that are important in primary and secondary prevention of CAD.[42] Regular exercise increases cardiorespiratory fitness and lowers myocardial oxygen demand.[44] Sustained, regular physical activity lowers BP, reduces lipid levels, reduces adiposity, increases insulin sensitivity, and decreases inflammation, stress, and adrenergic activity.[45] 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.[46][47]
dyslipidemia
Elevated low-density lipoprotein cholesterol (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.[48]
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 depend on the baseline risk of cardiovascular events and degree of LDL-cholesterol lowering.[49] In postmenopausal women, dysfunctional HDL may mean that high HDL levels (usually considered protective) are also associated with an increased risk of atherosclerosis.[50]
Lipid-lowering therapy reduces future ischemic events and limits disease progression.[2][5][51][52] Current guidelines recommend high-dose statin therapy in patients with known coronary artery disease (CAD) or CAD equivalent, irrespective of LDL levels.[5][53] Other lipid-lowering treatments can be considered in patients who are contraindicated or intolerant of statins.
chronic kidney disease (CKD)
Approximately 30% to 40% of patients with acute coronary syndrome have CKD.[5][54] Excess cardiovascular disease (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 CVD in patients with CKD, ranging from ischemic heart disease to arrhythmias and venous thromboembolism.[10] Decreasing glomerular filtration rate is associated with increasing risk of cardiovascular events, including death.[2][55]
Patients with CKD have increased risk of non-ST-elevation myocardial infarction (NSTEMI) and worsened prognosis following an NSTEMI.[54]
atherosclerosis (history of angina, myocardial infarction, stroke, transient ischemic attack, peripheral vascular disease)
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 ages 15-19 years, and in the right coronary artery in more than half of those of this age.[56] 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.[2]
Long-standing angina pectoris is a risk factor for coronary events.[57] Presence of peripheral arterial disease increases the likelihood of associated coronary atherosclerosis.[2]
family history of premature coronary artery disease (CAD)
Defined as premature CAD in family members (men <50 years; women <55 years).[58] 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 exam, patients may have eruptive xanthomas, lipemia 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.[2]
age >60 years
The majority of patients presenting with acute coronary syndromes are >65 (median age 68).[2] Patients with non-ST-elevation myocardial infarction (NSTEMI) are often older than patients with ST-elevation myocardial infarction (STEMI); half of patients with NSTEMI are 70 years old or older, whereas half of those with STEMI are 64 years old or younger.[13] The mean age of patients presenting with NSTEMI is 65 in men and 73 in women.[59]
cocaine use
Cocaine accounts for up to 25% of acute myocardial infarction (MI) in people ages 18-45 years.[60] In the hour after cocaine is used, the risk of MI is 24 times the baseline risk.[61] 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]
depression
stent thrombosis or restenosis
Stent thrombosis or in-stent restenosis may cause ST-elevation myocardial infarction, non-ST-elevation myocardial infarction, 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][5]
sleep apnea
Untreated moderate to severe obstructive sleep apnea (OSA) has been associated with a 17% increase in relative risk of cardiovascular events compared to risk in patients without OSA.[64] Patients with preexisting OSA are at increased risk of further cardiac events following acute coronary syndrome compared to patients who do not have OSA.[65][66]
surgical procedures (including intraoperative and postoperative periods)
Non-ST-elevation myocardial infarction (NSTEMI) is a relatively common complication of all types of surgical and nonsurgical procedures. Type of surgery, patient risk factors, and prior patient history are important contributors to postoperative NSTEMI.[2] Often this is detected as a rise in cardiac markers in the days following the surgical procedure.[67] Perioperative acute coronary syndrome is associated with high incidence of subsequent major cardiac events and mortality.[68] Preoperative risk assessment and additional steps to reduce the risk of myocardial ischemia/stress may prevent this complication or enable early recognition and therapy.[2]
weak
migraine
People with migraine are more likely to have acute coronary syndrome and have higher rates of cardiovascular mortality.[69] It is unclear whether this is an independent risk factor for cardiovascular disease, or due to higher prevalence of cardiovascular risk factors in patients with migraine.[69]
adverse pregnancy outcomes
anticholinergic burden
An association between raised anticholinergic burden and increased risk of cardiovascular events has been identified.[72] This means an association between recent use of drugs such as antihistamines, gastrointestinal antispasmodics, and diuretics, with increased risk of acute cardiovascular events.[72]
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