Acute Coronary Syndrome

Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations ranging from those for STsegment elevation myocardial infarction (STEMI) to presentations found in nonST-segment elevation myocardial infarction (NSTEMI) or in unstable angina. In terms of pathology, ACS is almost always associated with rupture of an atherosclerotic plaque and partial or complete thrombosis of the infarctrelated artery. (See Etiology.) 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[1] (See Workup.): Ischemic symptoms Development of pathologic Q waves Ischemic ST-segment changes on electrocardiogram (ECG) or in the setting of a coronary intervention 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.) Attention to the underlying mechanisms of ischemia is important when managing ACS. A simple predictor of demand is rate-pressure product, which can be lowered by beta blockers (eg, metoprolol or atenolol) and pain/stress relievers (eg, morphine), while supply may be improved by oxygen, adequate hematocrit, blood thinners (eg, heparin, IIb/IIIa agents such as abciximab, eptifibatide, tirofiban, or thrombolytics), and/or vasodilators (eg, nitrates, amlodipine). (See Medications.) In 2010, the American Heart Association (AHA) published new guideline recommendations for the diagnosis and treatment of ACS.[2]

Etiology
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). ACS without elevation in demand requires a new impairment in supply, typically due to thrombosis and/or plaque hemorrhage. 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.

Prognosis
Six-month mortality rates in the Global Registry of Acute Coronary Events (GRACE) were 13% for patients with NSTEMI ACS and 8% for those with unstable angina. An elevated level of troponin (a type of regulatory protein found in skeletal and cardiac muscle) permits risk stratification of patients with ACS and identifies patients at high risk for adverse cardiac events (ie, myocardial infarction, death) up to 6 months after the index event.[3, 4] (See Workup.) The PROVE IT-TIMI trial found that after ACS, a J-shaped or U-shaped curve association is observed between BP and the risk of future cardiovascular events.[5] LeLeiko et al determined that serum choline and free F(2)-isoprostane are also predictors of cardiac events in ACS. The authors evaluated the prognostic value of vascular inflammation and oxidative stress biomarkers in patients with ACS to determine their role in predicting 30-day clinical outcomes. Serum F(2)-isoprostane had an optimal cutoff level of 124.5 pg/mL, and serum choline had a cutoff level of 30.5 mol/L. Choline and F(2)-isoprostane had a positive predictive value of 44% and 57% and a negative predictive value of 89% and 90%, respectively.[6] Testosterone deficiency is common in patients with coronary disease and has a significant negative impact on mortality. Further study is needed to assess the effect of treatment on survival.[7] A study by Sanchis et al suggests renal dysfunction, dementia, peripheral artery disease, previous heart failure, and previous myocardial infarction are the comorbid conditions that predict mortality in NSTEMI ACS.[8] In patients with comorbid conditions, the highest risk period was in the first weeks after NSTEMI ACS. In-hospital management of patients with comorbid conditions merits further investigation. Patients with end-stage renal disease often develop ACS, and little is known about the natural history of ACS in patients receiving dialysis. Gurm et al examined the presentation, management, and outcomes of patients with ACS who received dialysis before presentation for an ACS. These patients were enrolled in the Global Registry of Acute Coronary Events (GRACE) at 123 hospitals in 14 countries from 1999-2007. NSTEMI ACS was the most common in patients receiving dialysis, occurring in 50% of patients (290 of 579) versus 33% (17,955 of 54,610) of those not receiving dialysis The in-hospital mortality rates were higher among patients receiving dialysis (12% vs 4.8%; p < 0.0001). Higher 6-month mortality rates (13% vs 4.2%; p < 0.0001), recurrent myocardial infarction incidence (7.6% vs 2.9%; p < 0.0001), and unplanned rehospitalizations (31% vs 18%; p < 0.0001) were found among those who survived to discharge. Outcomes in patients who received dialysis was worse than was predicted by the calculated GRACE risk score for in-hospital mortality (7.8% predicted vs 12% observed; p < 0.05). This suggests that the GRACE risk score underestimated the risk of major events in these patients.[9] In a study that assessed the impact of prehospital time on STEMI outcome, Chughatai et al suggest that total time to treatment should be used as a core measure instead of door-to-balloon time.[10] This is because on-scene time was the biggest fraction of "pre-hospital time. The study compared groups with total time to treatment of more than 120 minutes compared with 120 minutes or less and found mortalities were 4 compared with 0 and transfers to a tertiary care facility were 3 compared with 1, respectively.

Patient Education

Patient education of risk factors is important, but more attention is needed regarding delays in door-toballoon time, and one major barrier to improving this delay is patient education regarding his or her symptoms. Lack of recognition of symptoms may cause tremendous delays in seeking medical attention. 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. Diet plays an important role in the development of CAD. Therefore, prior to hospital discharge, a patient who has had a myocardial infarction should be evaluated by a dietitian. Patients should be informed about the benefits of a low-cholesterol, low-salt diet. In addition, educate patients about AHA dietary guidelines regarding a low-fat, low-cholesterol diet. A cardiac rehabilitation program after discharge may reinforce education and enhance compliance. The following mnemonic may useful in educating patients with CAD regarding treatments and lifestyle changes necessitated by their condition: A = Aspirin and antianginals B = Beta blockers and blood pressure (BP) C = Cholesterol and cigarettes D = Diet and diabetes E = Exercise and education For patients being discharged home, emphasize the following: Timely follow-up with primary care provider Compliance with discharge medications, specifically aspirin and other medications used to control symptoms Need to return to the ED for any change in frequency or severity of symptoms

Definition
By Mayo Clinic staff Acute coronary syndrome is a term used for any condition brought on by sudden, reduced blood flow to the heart. Acute coronary syndrome can describe chest pain you feel during a heart attack, or chest pain you feel while you're at rest or doing light physical activity (unstable angina). Acute coronary syndrome is often diagnosed in an emergency room or hospital. Acute coronary syndrome is treatable if diagnosed quickly. Acute coronary syndrome treatments vary, depending on your signs, symptoms and overall health condition.

Symptoms
By Mayo Clinic staff Many acute coronary syndrome symptoms are the same as those of a heart attack. And if acute coronary syndrome isn't treated quickly, a heart attack will occur. It's important to take acute coronary syndrome

symptoms very seriously. Get medical help right away if you have these signs and symptoms and think you're having a heart attack: Chest pain (angina) that feels like burning, pressure or tightness and lasts several minutes or longer Pain elsewhere in the body, such as the left upper arm or jaw (referred pain) Nausea Vomiting Shortness of breath (dyspnea) Sudden, heavy sweating (diaphoresis) If you're having a heart attack, the signs and symptoms may vary depending on your sex, age and whether you have an underlying medical condition, such as diabetes. Some unusual heart attack symptoms include: Abdominal pain Pain similar to heartburn Clammy skin Lightheadedness, dizziness or fainting Unusual or unexplained fatigue Feeling restless or apprehensive When to see a doctor If you're having chest pain and you believe it's an emergency situation, seek medical help immediately. Whenever possible, get emergency medical assistance rather than driving yourself to the hospital. You could be having a heart attack. If you have recurring chest pain, talk to your doctor. It could be a form of angina, and your doctor can help you decide the best course of treatment.

Causes
By Mayo Clinic staff Acute coronary syndrome may develop slowly over time by the building up of plaques in the arteries in your heart. These plaques, made up of fatty deposits, cause the arteries to narrow and make it more

difficult for blood to flow through them. This buildup of plaques is known as atherosclerosis. Eventually, this buildup means that your heart can't pump enough oxygen-rich blood to the rest of your body, causing chest pain (angina) or a heart attack. Another medical term closely related to acute coronary syndrome is coronary artery disease. Coronary artery disease refers to the damage to your heart arteries from atherosclerosis. If one of the plaques in your coronary arteries ruptures, it can cause a heart attack. In fact, many instances of coronary artery syndrome develop after a plaque ruptures. A blood clot will form on the site of the rupture, blocking the flow of blood through that artery.

Risk factors
By Mayo Clinic staff The risk factors for acute coronary syndrome are similar to those for other types of heart disease. Acute coronary syndrome risk factors include: Older age (older than 45 for men and older than 55 for women) High blood pressure High blood cholesterol Cigarette smoking Lack of physical activity Type 2 diabetes Family history of chest pain, heart disease or stroke

Treatments and drugs

By Mayo Clinic staff Treatment for acute coronary syndrome varies, depending on your symptoms and how blocked your arteries are. Medications It's likely that your doctor will recommend medications that can relieve chest pain and improve flow through the heart. These could include:

Aspirin. Aspirin decreases blood clotting, helping to keep blood flowing through narrowed heart arteries. Aspirin is one of the first things you may be given in the emergency room for suspected acute coronary syndrome. You may be asked to chew the aspirin, so it's absorbed into your bloodstream more quickly. If your doctor diagnoses your symptoms as acute coronary syndrome, he or she may recommend taking aspirin daily.

Thrombolytics. These drugs, also called clotbusters, help dissolve a blood clot that's blocking blood flow to your heart. If you're having a heart attack, the earlier you receive a thrombolytic drug after a heart attack, the greater the chance you will survive and lessen the damage to your heart.

Nitroglycerin. This medication for treating chest pain and angina temporarily widens narrowed blood vessels, improving blood flow to and from your heart.

Beta blockers. These drugs help relax your heart muscle, slow your heart rate and decrease your blood pressure, which decreases the demand on your heart. These medications can increase blood flow through your heart, decreasing chest pain and the potential for damage to your heart during a heart attack.

Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs). These drugs allow blood to flow from your heart more easily. Your doctor may prescribe ACE inhibitors or ARBs if you've had a moderate to severe heart attack that has reduced your heart's pumping capacity. These drugs also lower blood pressure and may prevent a second heart attack.

Calcium channel blockers. These medications relax the heart and allow more blood to flow to and from the heart. Calcium channel blockers are generally given if symptoms persist after you've taken nitroglycerin and beta blockers.

Cholesterol-lowering drugs. Commonly used drugs known as statins can lower your cholesterol levels, making plaque deposits less likely. The goal of statin therapy is to reduce the low density lipoprotein (LDL, or "bad") cholesterol levels to under 100 milligrams per deciliter (mg/dL).

Clopidogrel. The medication clopidogrel (Plavix) can help prevent blood clots from forming by making your blood platelets less likely to stick together. However, clopidogrel increases your risk of bleeding, so be sure to let everyone on your health care team know that you're taking it, particularly if you need any type of surgery. Surgery and other procedures If medications aren't enough to restore blood flow through your heart, your doctor may recommend one of these procedures:

Angioplasty and stenting. In this procedure, your doctor inserts a long, thin tube (catheter) into the blocked or narrowed part of your artery. A wire with a deflated balloon is passed through the catheter to the narrowed area. The balloon is then inflated, compressing the deposits against your artery walls. A mesh tube (stent) is usually left in the artery to help keep the artery open. Angioplasty may also be done with laser technology.

Coronary bypass surgery. This procedure creates an alternative route for blood to go around a blocked coronary artery.

Tests and diagnosis

By Mayo Clinic staff If you have signs and symptoms of acute coronary syndrome, your doctor may run several tests to see if your symptoms are caused by a heart attack or another form of chest pain. If your doctor thinks you're having a heart attack, the first two tests you have are: Electrocardiogram (ECG). This is the first test done to diagnose a heart attack. It's often done while you are being asked questions about your symptoms. This test records the electrical activity of your heart via electrodes attached to your skin. Impulses are recorded as "waves" displayed on a monitor or printed on paper. Because injured heart muscle doesn't conduct electrical impulses normally, the ECG may show that a heart attack has occurred or is in progress. Blood tests. Certain heart enzymes slowly leak into your blood if your heart has been damaged by a heart attack. Emergency room staff will take samples of your blood to test for the presence of these enzymes. Your doctor will look at these test results and determine the seriousness of your condition. If your blood tests show no markers of a heart attack and your chest pain has gone away, you'll likely be given tests to check the blood flow through your heart. If your test results reveal that you've had a heart attack or that you may be at high risk to have a heart attack, you'll likely be admitted to the hospital. You may then have more-invasive tests, such as a coronary angiogram. Your doctor may also order additional tests, either to figure out if your heart's been damaged by a heart attack, or if your symptoms have been brought on by another cause: Echocardiogram. If your doctor decides you haven't had a heart attack and your risk of having a heart attack is low, you'll likely have an echocardiogram completed before you leave the hospital. This test uses

sound waves to produce an image of your heart. During an echocardiogram, sound waves are directed at your heart from a transducer, a wand-like device, held on your chest. The sound waves bounce off your heart and are reflected back through your chest wall and processed electronically to provide video images of your heart. An echocardiogram can help identify whether an area of your heart has been damaged by a heart attack and isn't pumping normally. Chest X-ray. An X-ray image of your chest allows your doctor to check the size and shape of your heart and its blood vessels. Nuclear scan. This test helps identify blood flow problems to your heart. Small amounts of radioactive material, such as thallium, are injected into your bloodstream. Special cameras can detect the radioactive material as it flows through your heart and lungs. Areas of reduced blood flow to the heart muscle through which less of the radioactive material flows appear as dark spots on the scan. Computerized tomography (CT) angiogram. A CT angiogram allows your doctor to check your arteries to see if they're narrowed or blocked. In this minimally invasive test, you'll change into a hospital gown and lie on a table that's part of the CT scanning machine. You'll receive an injection of a radioactive dye, and the doughnut-shaped CT scanner will be moved to take images of the arteries in your heart. The images are then sent to a computer screen for your doctor to view. This test is usually only done if your blood tests and electrocardiogram don't reveal the cause of your symptoms. Coronary angiogram (cardiac catheterization). This test can show if your coronary arteries are narrowed or blocked. A liquid dye is injected into the arteries of your heart through a long, thin tube (catheter) that's fed through an artery, usually in your leg, to the arteries in your heart. As the dye fills your arteries, the arteries become visible on X-ray, revealing areas of blockage. Additionally, while the catheter is in position, your doctor may treat the blockage by performing an angioplasty. Angioplasty uses tiny balloons threaded through a blood vessel and into a coronary artery to widen the blocked area. In most cases, a mesh tube (stent) is also placed inside the artery to hold it open more widely and prevent renarrowing in the future.