History and exam
Key diagnostic factors
common
chest pain
Classically presents with retrosternal, crushing, heavy, diffuse, severe chest pain that can occur at rest or with exertion, is heavy in nature, and is located centrally with radiation to the left arm or jaw. The pain may be described by the patient as '‘pressing’' or ‘'squeezing.’. The pain may be constant or intermittent, or wax and wane intensity, and lasts for at least 20 minutes.[2][74] It is essential to clarify the time of symptoms onset, as this will inform the appropriate reperfusion strategy.[3][86][87]
dyspnea
Dyspnea is a common feature secondary to pulmonary congestion from left ventricular systolic dysfunction.[3]
It can also occur due to other mechanical and electrical complications of acute MI, which occur less commonly in the context of contemporary rapid revascularization, for example:
Left ventricular aneurysm
Ventricular septal rupture
Left ventricular free wall rupture
Acute mitral regurgitation
Papillary muscle rupture
Functional (ischemic) mitral regurgitation
Pericardial effusion
Cardiac tamponade
Supraventricular tachyarrhythmias
Ventricular tachyarrhythmias
Bradycardia and atrioventricular block
pallor
Pallor is a common feature associated with myocardial infarction due to high sympathetic output resulting in peripheral vasoconstriction.
uncommon
cardiogenic shock
Associated with reduced consciousness, profound hypotension, acute shortness of breath, and imminent cardiac arrest. Cardiogenic shock complicates 5% to 10% of STEMI admissions.[89][90] In-hospital mortality remains high (≥50%).[89] There is a bimodal presentation: the majority occur within 24 hours; the remainder occur within the first week.[90][91]
Other diagnostic factors
common
additional heart sounds
Muffled heart sounds could suggest a pericardial effusion or even cardiac tamponade. An audible S3 or S4 on cardiac exam indicates poor cardiac muscle compliance of the infarcted muscle and severe heart failure. A murmur might suggest acute ventricular septal defect, acute mitral regurgitation or underlying chronic valvular heart disease.
nausea and/or vomiting
Common feature associated with myocardial infarction (MI).[3] Nonspecific for MI, but commonly associated with inferior-wall MI due to increased vagal tone, and can be the only indicator of inferior-wall MI.
dizziness or lightheadedness
Feeling lightheaded or weak/lethargic is a common feature associated with myocardial infarction due to cerebral hypoperfusion as a result of hypotension and/or symptomatic bradycardia.
distress and anxiety
Common feature associated with myocardial infarction.
Patients often report a sense of doom or death.
palpitations
Palpitations may be due to:[3][92]
Tachycardia
Common feature associated with myocardial infarction (MI), especially anterior-wall MI, due to high sympathetic output.
Supraventricular tachyarrhythmias such as atrial fibrillation
Ventricular tachyarrhythmias such as ventricular tachycardia
Bradycardia
Sinus bradycardia
Atrioventricular block secondary to inferior STEMI
Atrioventricular block secondary to anterior STEMI
Irregular heart beat
Supraventricular tachyarrhythmias such as atrial fibrillation
Ventricular extrasystoles
uncommon
abnormal breath sounds
Rales, crackles/crepitations or cardiac wheeze on lung exam could suggest heart failure ± pulmonary edema.
reduced consciousness
hypotension
nonclassic location or nature of pain (chest pain-equivalent symptoms)
Pain may be atypical by location (i.e., epigastric, jaw, arm, neck pain) or by nature (i.e., burning, throbbing, uneasiness), and some people present without chest pain as the predominant feature (i.e., with chest pain-equivalent symptoms).[3]
Women, older patients, and patients with diabetes are more likely to present with atypical features.[3][95]
Patients might describe their chest symptoms as burning, throbbing, tight, or a feeling like trapped wind, the patient may even describe indigestion rather than chest pain. In the absence of chest pain, there may be epigastric pain, back (interscapular) pain, neck or jaw pain, or arm pain (typically left-sided). Clinical suspicion is key to making the diagnosis. It is, therefore, vital to make a full assessment based on the history, exam, and serial ECGs.[2][67][96]
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).[13][14] 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.[8][9][13] Smoking increases risk for CAD by direct promotion of atherosclerosis, reduced oxygen delivery in the blood, increased thrombogenesis, and direct coronary artery spasm.[15] 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.[8][9][14][16][17] Current use of smokeless tobacco also increases the risk of CAD compared to people who have never used.[9][14][17]
Patients who quit smoking reduce their risk of recurrent CVD by about one third, compared to patients who do not quit smoking.[18]
Surprisingly, current smoking is associated with a lower risk of acute death in the setting of acute coronary syndrome.[5] 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
Hypertension is 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.[3] 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.[3][5][19][20] Even prehypertension (untreated systolic blood pressure 120-139 mmHg and untreated diastolic blood pressure 80-89 mmHg, or both) increases risk twofold compared with normal levels.[9] 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.[3]
diabetes
Patients with diabetes mellitus are at increased risk of coronary artery disease (CAD).[5] They have a two- to fourfold increased risk of cardiovascular disease compared with people who do not have diabetes.[21]
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.[5] Diabetes is associated with more extensive CAD, unstable lesions, and less favorable long-term outcomes (death, MI, acute coronary syndrome readmission), with approximately double the risk of long-term mortality from CAD than that of people without diabetes following MI.[5][19]
An HbA1c of <7% (53 mmol/mol) is the goal of treatment for many patients with diabetes, but targets should be individualized based on duration of diabetes, age/life expectancy, and other factors.[22]
obesity and metabolic syndrome
Estimates suggest that more than half of adults in Western society are overweight or obese.[9][23][24] Adipokines and other hormones secreted by adipose tissue are highly linked to inflammation and atherosclerosis.[25] Obesity is associated with diastolic dysfunction and is a strong stimulus for left ventricular hypertrophy.[26][27] It is also associated with accelerated atherosclerosis, through several mechanisms including insulin resistance and inflammation.[28] 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.[5][9][24][26][29] Bariatric surgery for weight loss reduces risk of major cardiovascular events (fatal acute coronary syndrome and stroke), incident heart failure, and cardiovascular mortality.[30]
sedentary behavior and physical inactivity
Sedentary behavior is associated with an increased risk of cardiovascular disease.[9] Epidemiologic studies suggest a cause-and-effect relationship between phyisical activity and cardiorespiratory fitness and reduced cardiovascular mortality.[31] 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.[32] Physical activity has antiatherosclerotic, psychologic, antithrombotic, anti-ischemic, and antiarrhythmic effects that are important in primary and secondary prevention of CAD.[31] Regular exercise increases cardiorespiratory fitness and lowers myocardial oxygen demand.[33] Sustained, regular physical activity lowers BP, reduces lipid levels, reduces adiposity, increases insulin sensitivity, and decreases inflammation, stress, and adrenergic activity.[34] 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.[35][36]
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.[37]
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.[38]
In postmenopausal women, dysfunctional HDL may mean that high HDL levels (usually considered protective) are also associated with an increased risk of atherosclerosis.[39]
Lipid-lowering therapy reduces future ischemic events and limits disease progression.[3][5][40][41] Current guidelines recommend high-dose statin therapy in patients with known coronary artery disease (CAD) or CAD equivalent, irrespective of LDL levels.[3][42] Other lipid-lowering treatments can be considered in patients who are contraindicated or intolerant of statins. Reduction of lipoprotein levels, with drugs such as alirocumab, reduces risk of cardiovascular events following acute coronary syndrome.[43]
chronic kidney disease
Approximately 30% to 40% of patients with acute coronary syndrome have chronic kidney disease (CKD).[3][44] 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 CVDs in patients with CKD, ranging from ischemic heart disease to arrhythmias and venous thromboembolism.[9] Decreasing glomerular filtration rate is associated with increasing risk of cardiovascular events, including death.[5][45]
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.[46] 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.[5]
Longstanding angina pectoris is a risk factor for coronary events.[47] Presence of peripheral arterial disease increases the likelihood of associated coronary atherosclerosis.[5]
family history of premature CAD
Defined as premature coronary artery disease in family members (men <50 years; women <55 years).[48] Family history includes a first-degree relative with a history of MI, sudden cardiac death, aortic dissection, PCI, or coronary artery bypass graft. Inherited (primary) disorders of lipoprotein metabolism are an important cause, though other genetic variants may also play a role.[49] 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.[5]
age >60 years
Acute coronary syndrome (ACS) is more common in older patients; the majority of patients presenting with ACS are >65 years (median age 68 years).[5] Patients with NSTEMI are often older than patients with STEMI; half of patients with NSTEMI are 70 years old or older, whereas half of those with STEMI are 64 years old or younger.[50] The mean age of patients presenting with STEMI is 60 years for men and 71 years for women.[51]
cocaine use
Cocaine accounts for up to 25% of acute myocardial infarction (MI) in people ages 18-45 years.[52] In the hour after cocaine is used, the risk of MI is 24 times the baseline risk.[53] 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.[5]
depression
stent thrombosis or restenosis
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.[3][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.[56] Patients with preexisting OSA are at increased risk of further cardiac events following acute coronary syndrome compared to patients who do not have OSA.[57][58]
weak
migraine
People with migraine are more likely to have acute coronary syndrome and have higher rates of cardiovascular mortality.[59] 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.[59]
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