History and exam
Key diagnostic factors
common
Chest pain
Cardiac chest pain is typically retrosternal sensation of pain, pressure, or heaviness radiating to the left arm, both arms, right arm, neck, or jaw, which may be intermittent or persistent. The pain may occur daily or several times a day, instead of occasionally, or decreasing levels of activity needed to trigger chest pain and may occur at rest.
Other diagnostic factors
common
diaphoresis
Diaphoresis is a common feature due to high sympathetic drive.[79]
Acute coronary syndrome (ACS) 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 ACS. These noncharacteristic presentations are more common in women, older people, and people with diabetes.[1]
dyspnea
Isolated dyspnea can occur, particularly in older patients, women, and patients with diabetes.[1]
nausea and vomiting
Nausea and vomiting are common features. May be the only symptom.
carotid bruit
Indicates preexisting atherosclerotic disease.
diminished or absent peripheral pulses
Indicates preexisting atherosclerotic disease.
uncommon
syncope
The patient may have syncope. This occurs more frequently in older patients, women, and patients with diabetes.[1]
back pain
Be aware that women may present with middle/upper back pain.
arrhythmias
Most commonly sinus tachycardia. Atrial fibrillation and other supraventricular tachycardias are possible. Urgent and immediate angiography with the intent to perform revascularization is indicated if the patient has a life-threatening arrhythmia (ventricular tachycardia or ventricular fibrillation).[1] Waiting for results of troponin testing would delay angiography.[1]
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). A third heart sound indicates compromised left ventricular function and heart failure and is associated with worsened prognosis.
rales
Indicates volume overload and compromised left ventricular function.
Risk factors
strong
smoking
Smoking causes nearly 1 in 5 deaths in the US and is the single most important modifiable risk factor for cardiovascular disease (CVD).[19] 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.[19][20][21]
Smoking increases risk for CAD by direct promotion of atherosclerosis, reduced oxygen delivery in the blood, increased thrombogenesis, and direct coronary artery spasm.[22] 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.[3][7][20][23][24][25] Current use of smokeless tobacco also increases the risk of CAD compared with people who have never used.[7][24][25] Patients who stop smoking reduce their risk of recurrent CVD by about one third compared with patients who do not stop smoking.[26]
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".[27]
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.[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][28][29] Even prehypertension (untreated systolic BP 120-139 mmHg and untreated diastolic BP 80-89 mmHg, or both) increases risk twofold compared with normal levels.[7] 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.[1]
diabetes mellitus
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.[30] The mechanisms are not fully known but they may reflect vascular abnormalities of inflammation, endothelial and smooth muscle function, obesity, hypertension, dyslipidemia, 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 favorable long-term outcomes (death, MI, ACS readmission), with approximately double the risk of long-term mortality from CAD than that of people without diabetes following MI.[2][28]
An HbA1c of <7% (<53 mmol/mol) is the goal of treatment for patients with diabetes.[7][31] However, for patients with CAD, this goal may be less stringent (i.e., <8% [<64 mmol/mol]).[31]
obesity and metabolic syndrome
Estimates suggest that more than half of adults in Western society are overweight or obese.[7][32][33] Adipokines and other hormones secreted by adipose tissue are highly linked to inflammation and atherosclerosis.[34] Obesity is associated with diastolic dysfunction and is a strong stimulus for left ventricular hypertrophy.[35][36] 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][7][33][35][37] Bariatric surgery for weight loss reduces risk of major cardiovascular events (fatal ACS and stroke), incident heart failure and cardiovascular mortality.[38]
sedentary behavior and physical inactivity
Sedentary behavior is associated with an increased risk of cardiovascular disease.[7] Epidemiologic studies suggest a cause-and-effect relationship between physical activity and cardiorespiratory fitness and reduced cardiovascular mortality.[39] 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 BP, and cigarette smoking.[40] Physical activity has antiatherosclerotic, psychologic, antithrombotic, antiischemic, and antiarrhythmic effects that are important in primary and secondary prevention of CAD.[39] Regular exercise increases cardiorespiratory fitness and lowers myocardial oxygen demand.[41] Sustained, regular physical activity lowers BP, reduces lipid levels, reduces adiposity, increases insulin sensitivity, and decreases inflammation, stress, and adrenergic activity.[42] 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.[43][44]
dyslipidemia
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.[45] 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.[46] In postmenopausal women, dysfunctional HDL may mean that high HDL levels (usually considered protective) are also associated with an increased risk of atherosclerosis.[47] Lipid-lowering therapy reduces future ischemic events and limits disease progression.[1][2][48][49] Current guidelines recommend high-dose statin therapy in patients with known coronary artery disease (CAD) or CAD equivalent, irrespective of LDL levels.[1][50][51] 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 chronic kidney disease (CKD).[1][52] Excess cardiovascular diseases (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 ischemic heart disease to arrhythmias and venous thromboembolism.[7] Decreasing glomerular filtration rate is associated with increasing risk of cardiovascular events, including death.[2][53]
atherosclerosis (history of angina, MI, 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.[54] 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.[55] Presence of peripheral arterial disease increases the likelihood of associated coronary atherosclerosis.[2]
family history of premature CAD
Defined as premature coronary artery disease (CAD) in family members (men ages <50 years; women ages <55 years).[56] 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.[57] 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
Acute coronary syndrome (ACS) is more common in older patients; the majority of patients presenting with ACS are age >65 (median age 68).[2] Patients with non-STEMI (NSTEMI) are often older than patients with STEMI; half of patients with NSTEMI are ages 70 years or older, whereas half of those with STEMI are ages 64 years or younger.[10] The mean age of patients presenting with STEMI is 60 years for men, and 71 years for women.[58]
cocaine use
Cocaine accounts for up to 25% of acute MI in people ages 18-45 years.[59] In the hour after cocaine is used, the risk of myocardial infarction is 24 times the baseline risk.[60] 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]
sleep apnea
Untreated moderate to severe obstructive sleep apnea (OSA) has been associated with a 17% increase in relative risk of cardiovascular events compared with risk in patients without OSA.[63] Patients with preexisting OSA are at increased risk of further cardiac events following ACS compared with patients who do not have OSA.[64][65]
elevated C-reactive protein levels
Elevation in C-reactive protein (a marker of inflammation) is associated with increased risk of coronary artery disease and has prognostic value in addition to lipid profile.[66]
weak
migraine
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