Acute Coronary Syndrome

In some instances, however, stable coronary artery disease (CAD) may result in ACS in the absence of plaque rupture and thrombosis, when physiologic stress (eg, trauma, blood loss, anemia, infection, tachyarrhythmia) increases demands on the heart. The diagnosis of acute myocardial infarction in this setting requires a finding of the typical rise and fall of biochemical markers of myocardial necrosis in addition to at least 1 of the following [2] (See Workup.):

The terms transmural and nontransmural (subendocardial) myocardial infarction are no longer used because ECG findings in patients with this condition are not closely correlated with pathologic changes in the myocardium. Therefore, a transmural infarct may occur in the absence of Q waves on ECGs, and many Q-wave myocardial infarctions may be subendocardial, as noted on pathologic examination. Because elevation of the ST segment during ACS is correlated with coronary occlusion and because it affects the choice of therapy (urgent reperfusion therapy), ACS-related myocardial infarction should be designated STEMI or NSTEMI. (See Workup.)

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Acute coronary syndrome (ACS) is caused primarily by atherosclerosis. Most cases of ACS occur from disruption of a previously nonsevere lesion (an atherosclerotic lesion that was previously hemodynamically insignificant yet vulnerable to rupture). The vulnerable plaque is typified by a large lipid pool, numerous inflammatory cells, and a thin, fibrous cap.

Elevated demand can produce ACS in the presence of a high-grade fixed coronary obstruction, due to increased myocardial oxygen and nutrition requirements, such as those resulting from exertion, emotional stress, or physiologic stress (eg, from dehydration, blood loss, hypotension, infection, thyrotoxicosis, or surgery).

The major trigger for coronary thrombosis is considered to be plaque rupture caused by the dissolution of the fibrous cap, the dissolution itself being the result of the release of metalloproteinases (collagenases) from activated inflammatory cells. This event is followed by platelet activation and aggregation, activation of the coagulation pathway, and vasoconstriction. This process culminates in coronary intraluminal thrombosis and variable degrees of vascular occlusion. Distal embolization may occur. The severity and duration of coronary arterial obstruction, the volume of myocardium affected, the level of demand on the heart, and the ability of the rest of the heart to compensate are major determinants of a patient's clinical presentation and outcome. (Anemia and hypoxemia can precipitate myocardial ischemia in the absence of severe reduction in coronary artery blood flow.)

A syndrome consisting of chest pain, ischemic ST-segment and T-wave changes, elevated levels of biomarkers of myocyte injury, and transient left ventricular apical ballooning (takotsubo syndrome) has been shown to occur in the absence of clinical CAD, after emotional or physical stress. The etiology of this syndrome is not well understood but is thought to relate to a surge of catechol stress hormones and/or high sensitivity to those hormones.

Despite their smaller coronary vessels and higher risk profile, women with STEMI appear to respond just as well as men to primary PCI and stenting, according to the Optical Coherence Tomography Assessment of Gender Diversity in Primary Angioplasty (OCTAVIA) study. [13] OCTAVIA, which was designed to examine gender differences at the time of primary PCI, included 140 STEMI patients at 14 Italian centers, matched by age and risk factors, who received an everolimus-eluting stent. [13]

Educate patients about the dangers of cigarette smoking, a major risk factor for coronary artery disease (CAD). The risk of recurrent coronary events decreases 50% at 1 year after smoking cessation. Provide all patients who smoke with guidance, education, and support to avoid smoking. Smoking-cessation classes should be offered to help patients avoid smoking after a myocardial infarction. Bupropion increases the likelihood of successful smoking cessation.

Treatment for acute coronary syndrome includes medicines and a procedure known as angioplasty, during which doctors inflate a small balloon to open the artery. A wire mesh tube called a stent may be permanently placed in the artery to keep it open. In hospitals not equipped to do angioplasty quickly, doctors may administer drugs to dissolve blood clots. View an illustration of coronary arteries(link opens in new window).

Acute coronary syndrome refers to a group of diseases in which blood flow to the heart is decreases. Some examples include ST-elevation myocardial infarction, non-ST elevation myocardial infarction, and unstable angina. This activity reviews the evaluation and treatment of patients with acute coronary syndrome, and highlights the role of the interprofessional team in caring for these patients.

Objectives:Identify risk factors for acute coronary syndrome.Identify how a patient with acute coronary syndrome might present, and describe the evaluation that should be done.Describe the treatment of acute coronary syndrome.Describe the importance of well-coordinated interprofessional teamwork in caring for patients with acute coronary syndrome.Access free multiple choice questions on this topic.

Acute coronary syndrome (ACS) refers to a group of conditions that include ST-elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina. It is a type of coronary heart disease (CHD), which is responsible for one-third of total deaths in people older than 35. Some forms of CHD can be asymptomatic, but ACS is always symptomatic.[1][2][3]

ACS is a manifestation of CHD (coronary heart disease) and usually a result of plaque disruption in coronary arteries (atherosclerosis). The common risk factors for the disease are smoking, hypertension, diabetes, hyperlipidemia, male sex, physical inactivity, family obesity, and poor nutritional practices. Cocaine abuse can also lead to vasospasm. [4][5][6]A family history of early myocardial infarction (55 years of age) is also a high-risk factor.

The first step of evaluation is an ECG, which helps differentiate between STEMI and NSTEMI unstable angina. American Heart Association guidelines maintain that any patient with complaints suspicious of ACS should get an ECG within 10 minutes of arrival. Cath lab should be activated as soon as STEMI is confirmed in a percutaneous coronary intervention (PCI) center. Cardiac enzymes especially troponin, CK-MB/CK ratio is important in assessing the NSTEMI versus myocardial ischemia without tissue destruction. A chest x-ray is useful in diagnosing causes other than MI presenting with chest pain like pneumonia and pneumothorax. The same applies for blood work like complete blood count (CBC), chemistry, liver function test, and lipase which can help differentiate intraabdominal pathology presenting with chest pain. Aortic dissection and pulmonary emboli should be kept in differential and investigated when the situation warrants. [7][8][9]

Beta-blockers, statin, and ACE inhibitors should be initiated in all ACS cases as quickly as possible unless contraindications exist. Cases not amenable to PCI are taken for CABG (coronary artery bypass graft) or managed medically depending upon comorbidities and patient choice.

Coronary heart disease and acute coronary syndrome remain widely prevalent and still is the top cause of death in people over 35 years of age. It is essential that providers all over the world maintain a high degree of suspicion and vigilance while assessing patients with possible ACS. Along with this, public education and recognition of symptoms are crucial. Another important aspect of controlling this disease is public education about lifestyle modification and making people aware of healthier life choices. A critical aspect of STEMI and ACS timely treatment depends on adequate emergency medical services availability and training. Another crucial step of ACS control and prevention is education about lifestyle modification including smoking cessation, regular physical activity, and dietary modifications. Only through this multi-prong approach can practitioners control this high mortality disease.

Acute coronary syndrome is a term for a group of conditions that suddenly stop or severely reduce blood from flowing to the heart muscle. When blood cannot flow to the heart muscle, the heart muscle can become damaged. Heart attack and unstable angina are both acute coronary syndromes (ACS).

You feel a tight band of pain around your chest. The pain moves from your chest to your arms, shoulder, and neck. What could your pain mean? Could it be a heart attack, could it be the big one? Heart attacks are caused by interruption of blood supply to part of the heart. If the blood flow is blocked, your heart is starved of oxygen and heart cells die. A hard substance called plaque can build up in the walls of your coronary arteries. This plaque is made up of cholesterol and other cells. A heart attack can occur as a result of plaque buildup or the rupture of one of these plaques. We're not sure why heart attacks occur when they do. You may have a heart attack when you are resting or asleep, or after a sudden increase in physical activity, when you are outside in cold weather, or after a sudden, severe emotional or physical stress, including an illness. So, how is a heart attack treated? If you go to the hospital for a suspected heart attack, a doctor or nurse will listen to your chest with a stethoscope. You will have a blood test to look for heart damage. A coronary angiography test can show your doctor how well blood is moving through your heart. If blood moves slowly, or not at all through your coronary arteries, you have either a narrowed, or blocked artery. Other tests can look at the valves and chambers of your heart and check for abnormal heart rhythms. If you've had a heart attack, doctors can do an emergency procedure called angioplasty. This surgery or procedure can open narrowed or blocked blood vessels. Usually they'll place a small, metal mesh tube, called a stent, in your artery to help keep it open. You may also receive drugs to break up the clot in your artery. Sometimes, doctors will do heart bypass surgery to get blood flowing to your heart muscle again. After you are treated in the hospital for a heart attack, you may need to take medicines to thin your blood, to protect your heart, or to improve your cholesterol levels. You may need to take these medicines for the rest of your life. Most people who have had a heart attack also need cardiac rehabilitation. This will help you slowly increase your exercise level and learn how to follow a healthy lifestyle. After you have a heart attack, your chance of another is higher. How well you do after a heart attack depends on the damage to your heart and where the damage is, and what steps you take to prevent another one. If your heart can no longer pump blood to your body as well as it used to, you may have heart failure and will need lifelong treatment. Usually a person who has had a heart attack can slowly go back to normal activities, but you will need to take steps to prevent another heart attack. 2351a5e196