Non-ST Segment Elevation Myocardial Infarction (NSTEMI) is one of the three types of Acute Coronary Syndrome (ACS), and

like all ACS, NSTEMI should be considered a medical emergency. NSTEMI is identical to unstable angina except for one thing. In NSTEMI, in contrast to unstable angina, cardiac enzyme blood tests are abnormal, indicating that at least some actual cell damage is occurring to heart muscle cells. Fundamentally, however, in every other way NSTEMI and unstable angina are identical. They both indicate that a plaque has ruptured in acoronary artery, that the ruptured plaque and the associated blood clot are producing partial blockage of the artery, and that the heart muscle supplied by that artery is in grave danger of sustaining irreversible damage. In other words, the imminent risk of a "full" myocardial infarction, with irreversible death of part of the heart muscle, is very high in both NSTEMI and unstable angina. The symptoms, the clinical circumstances, and the treatment of NSTEMI are identical to those of unstable angina.You can read about those aspects of NSTEMI here.

Acute coronary syndrome (ACS) refers to any group of symptoms attributed to obstruction of the coronary arteries. The most common symptom prompting diagnosis of ACS is chest pain, often radiating of the left arm or angle of the jaw, pressure-like in character, and associated with nausea and sweating. Acute coronary syndrome usually occurs as a result of one of three problems: ST elevation [1] myocardial infarction (30%), non ST elevation myocardial infarction (25%), or unstable angina (38%). These types are named according to the appearance of the electrocardiogram (ECG/EKG) as non-ST segment elevation myocardial infarction(NSTEMI) and ST segment elevation myocardial [2] infarction (STEMI). There can be some variation as to which forms of MI are classified under acute [3] coronary syndrome. ACS should be distinguished from stable angina, which develops during exertion and resolves at rest. In contrast with stable angina, unstable angina occurs suddenly, often at rest or with minimal exertion, or at lesser degrees of exertion than the individual's previous angina ("crescendo angina"). New onset angina is also considered unstable angina, since it suggests a new problem in a coronary artery. Though ACS is usually associated with coronary thrombosis, it can also be associated [4] with cocaine use. Cardiac chest pain can also be precipitated by anemia, bradycardias (excessively slow heart rate) or tachycardias (excessively fast heart rate).

Signs and symptoms

The cardinal sign of decreased blood flow to the heart is chest pain experienced as tightness around the chest and radiating to the left arm and the left angle of the jaw. This may be associated with diaphoresis (sweating), nausea and vomiting, as well as shortness of breath. In many cases, the sensation is "atypical", with pain experienced in different ways or even being completely absent (which is more likely in female patients and those with diabetes). Some may report palpitations, anxiety or a sense of impending doom and a feeling of being acutely ill. The description of the chest discomfort as a pressure has little utility in aiding a diagnosis as it is [5] not specific for ACS. [edit]Diagnosis

Classification of acute coronary syndromes. [6]

[edit]Electrocardiogram In the setting of acute chest pain, the electrocardiogram is the investigation that most reliably [7] distinguishes between various causes. If this indicates acute heart damage (elevation in the ST segment, new left bundle branch block), treatment for a heart attack in the form ofangioplasty or thrombolysis is indicated immediately (see below). In the absence of such changes, it is not possible to immediately distinguish between unstable angina and NSTEMI. [edit]Imaging

and blood tests

As it is only one of the many potential causes of chest pain, the patient usually has a number of tests in the emergency department, such as a chest X-ray, blood tests (including myocardial markers such as troponin I or T, and H-FABP and/or a D-dimer if a pulmonary embolism is suspected), and telemetry (monitoring of the heart rhythm). [edit]Prediction

scores

The ACI-TIPI score can be used to aid diagnosis; using 7 variables from the admission record, this score [8] predicts crudely which patients are likely to have myocardial ischemia. For example according to a randomized controlled trial, males having chest pain with normal or non diagnostic ECG are at higher [9] risk for having acute coronary syndrome than women. In this study, the sensitivity was 65.2% andspecificity was 44%. This particular study had an 8.4% prevalence of acute coronary syndrome, which means the positive predictive valueof being a male with chest pain and having coronary syndrome is 9.6% and negative predictive value is 93.2% ( click here to adjust these results for patients at higher or lower risk of acute coronary syndrome). In a second cohort study, exercise electrocardiography was similarly found to be a poor predictor of acute [10] coronary syndrome at follow-up. Of the patients who had a coronary event at 6 years of follow up, 47% had a negative ECG at the start of the study. With an average follow up of 2.21 years the receiver operating characteristic curves gave resting ECG a score of 0.72 and exercise ECG a score of 0.74.

[edit]Prevention Acute coronary syndrome often reflects a degree of damage to the coronaries by atherosclerosis. Primary prevention of atherosclerosis is controlling the risk factors: healthy eating, exercise, treatment for hypertension and diabetes, avoiding smoking and controlling cholesterol levels; in patients with significant risk factors, aspirin has been shown to reduce the risk of cardiovascular events. Secondary prevention is discussed in myocardial infarction. After a ban on smoking in all enclosed public places was introduced in Scotland in March 2006, there was a 17 percent reduction in hospital admissions for acute coronary syndrome. 67% of the decrease [11] occurred in non-smokers. [edit]Treatment People with presumed ACS are typically treated with aspirin, Clopidogrel, nitroglycerin, and if the chest [12] [12] discomfort persists morphine. Other analgesics such as nitrous oxide are of unknown benefit. [edit]STEMI Main article: Myocardial infarction If the ECG confirms changes suggestive of myocardial infarction (ST elevations in specific leads, a new left bundle branch block or a true posterior MI pattern), thrombolytics may be administered or primary coronary angioplasty may be performed. In the former, medication is injected that stimulates fibrinolysis, destroying blood clots obstructing the coronary arteries. In the latter, a flexible catheter is passed via the femoral or radial arteries and advanced to the heart to identify blockages in the coronaries. When occlusions are found, they can be intervened upon mechanically withangioplasty and usually stent deployment if a lesion, termed the culprit lesion, is thought to be causing myocardial [13] damage. Data suggest that rapid triage, transfer and treatment is essential. The time frame for door-toneedle thrombolytic administration according to American College of Cardiology (ACC) guidelines should be within 30 minutes, whereas the door-to-balloon Percutaneous Coronary Intervention (PCI) time should be less than 90 minutes. It was found that thrombolysis is more likely to be delivered within the established ACC guidelines among patients with STEMI as compared to PCI according to a case [14] control study . [edit]NSTEMI

and NSTE-ACS

If the ECG does not show typical changes, the term "non-ST segment elevation ACS" is applied. The patient may still have suffered a "non-ST elevation MI" (NSTEMI). The accepted management of unstable angina and acute coronary syndrome is therefore empirical treatment with aspirin, a second platelet inhibitor such as clopidogrel, prasugrel or ticagrelor, and heparin (usually a low-molecular weight heparin such as enoxaparin), with intravenous glyceryl trinitrate and opioids if the pain persists. A blood test is generally performed for cardiac troponins twelve hours after onset of the pain. If this is positive, coronary angiography is typically performed on an urgent basis, as this is highly predictive of a heart attack in the near-future. If the troponin is negative, a treadmill exercise test or a thallium scintigram may be requested. If there is no evidence of ST segment elevation on the electrocardiogram, delaying [15] urgent angioplasty until the next morning is not inferior to doing so immediately.

In a cohort study comparing NSTEMI and STEMI, patients with NSTEMI had statistically [16] similar mortality at one year after PCI as compared to patients with STEMI (3.4% vs 4.4%). However, NSTEMI had significantly more "major cardiac events" (death, myocardial infarction, disabling stroke, or requiring revascularization) at one year (24.0% vs 16.6%). Cocaine associated ACS should be managed in a manner similar to other patients with acute coronary [17] syndrome except beta blockers should not be used and benzodiazepines should be administered early. [edit]Prognosis [edit]TIMI

score
[18]

The TIMI risk score can identify high risk patients [edit]Biomarkers

and has been independently validated.

[19][20]

for diagnosis

The aim of diagnostic markers is to identify patients with ACS even when there is no evidence of heart muscle damage. Ischemia-Modified Albumin (IMA) - In cases of Ischemia - Albumin undergoes a conformational change and loses its ability to bind transitional metals (copper or cobalt). IMA can be used to assess the proportion of modified albumin in ischemia. Its use is limited to ruling out ischemia rather than a diagnostic test for the occurrence of ischemia. Myeloperoxidase (MPO) - The levels of circulating MPO, a leukocyte enzyme, elevate early after ACS and can be used as an early marker for the condition. Glycogen Phosphorylase Isoenzyme BB-(GPBB) is an early marker of cardiac ischemia and is one of three isoenzyme of Glycogen Phosphorylase. Troponin is a late cardiac marker of ACS

[edit]Biomarkers

for Risk Stratification

The aim of prognostic markers is to reflect different components of pathophysiology of ACS. For example: Natriuretic peptide - Both B-type natriuretic peptide (BNP) and N-terminal Pro BNP can be applied to predict the risk of death and heart failure following ACS. Monocyte chemo attractive protein (MCP)-1 - has been shown in a number of studies to identify patients with a higher risk of adverse outcomes after ACS.

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] 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. 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 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 The severity and duration of coronary artery obstruction, the volume of myocardium affected, the level of demand, and the ability of the rest of the heart to compensate are major determinants of a patient's clinical presentation and outcome. A patient may present to the ED because of a change in pattern or severity of symptoms. Typically, angina is a symptom of myocardial ischemia that appears in circumstances of increased oxygen demand. It is usually described as a sensation of chest pressure or heaviness that is reproduced by activities or conditions that increase myocardial oxygen demand. A new case of angina is more difficult to diagnose because symptoms are often vague and similar to those caused by other conditions (eg, indigestion, anxiety). However, not all patients experience chest pain. They may present with only neck, jaw, ear, arm, or epigastric discomfort. Some patients, including some who are elderly or who have diabetes, present with no pain, complaining only of episodic shortness of breath, severe weakness, light-headedness, diaphoresis, or nausea and vomiting. Elderly persons may also present only with altered mental status. Those with preexisting altered mental status or dementia may have no recollection of recent symptoms and may have no complaints. In addition, evidence exists that women more often have coronary events without typical symptoms, which may explain the frequent failure of clinicians to initially diagnose ACS in women. A summary of patient complaints is as follows: Palpitations Pain, which is usually described as pressure, squeezing, or a burning sensation across the precordium and may radiate to the neck, shoulder, jaw, back, upper abdomen, or either arm Exertional dyspnea that resolves with pain or rest Diaphoresis from sympathetic discharge Nausea from vagal stimulation Decreased exercise tolerance Stable angina involves episodic pain lasting 5-15 minutes, is provoked by exertion, and is relieved by rest or nitroglycerin. In unstable angina, patients have increased risk for adverse cardiac events, such as myocardial infarction or death. New-onset exertional angina can occur at rest and is of increasing frequency or duration or is refractory to nitroglycerin. Variant angina (Prinzmetal angina) occurs primarily at rest, is triggered by smoking, and is thought to be due to coronary vasospasm. Physical examination results are frequently normal. If chest pain is ongoing, the patient will usually lie quietly in bed and may appear anxious, diaphoretic, and pale. Physical findings can vary from normal to any of the following: Hypotension - Indicates ventricular dysfunction due to myocardial ischemia, infarction, or acute valvular dysfunction Hypertension - May precipitate angina or reflect elevated catecholamine levels due to anxiety or to exogenous sympathomimetic stimulation Diaphoresis Pulmonary edema and other signs of left heart failure Extracardiac vascular disease Jugular venous distention Cool, clammy skin and diaphoresis in patients with cardiogenic shock

In addition, a third heart sound (S3) may be present, and frequently, a fourth heart sound (S4) exists. The latter is especially prevalent in patients with inferior-wall ischemia and may be heard in patients with ischemia or systolic murmur secondary to mitral regurgitation A systolic murmur related to dynamic obstruction of the left ventricular (LV) outflow tract may also occur. It is caused by hyperdynamic motion of the basal left ventricular myocardium and may be heard in patients with an apical infarct. A new murmur may reflect papillary muscle dysfunction. Rales on pulmonary examination may suggest LV dysfunction or mitral regurgitation. Patients who present to the ED with chest pain who have a low short-term risk of a major adverse cardiac event must be identified to facilitate early discharge in order to avoid lengthy and costly hospital stays.[11] The ASPECT study tested a 2-hour, accelerated diagnostic protocol (ADP) that included the use of a structured pretest probability scoring method, electrocardiography, and a point-of-care biomarker panel that included troponin, creatine kinase MB, and myoglobin levels. The study suggests that ADP can identify patients at low risk for a short-term major adverse cardiac event who may be suitable for early discharge; such an approach could be used to decrease the overall observation periods and admissions for chest pain and has the potential to affect health-service delivery worldwide. Complications of ischemia include pulmonary edema, while those of myocardial infarction include rupture of the papillary muscle, left ventricular free wall, and ventricular septum.