What is Medicine – Acute Coronary Syndromes NSTE -ACS ( Unstable Angina and NSTEMI)
ACUTE CORONARY SYNDROMES: NSTE-ACS (UNSTABLE ANGINA AND NSTEMI) ESSENTIAL DESCRIPTION Acute coronary syndromes without ST-segment elevation (NSTE-ACS) include unstable angina (UA) and non-ST-segment elevation myocardial infarction (NSTEMI). ● NSTEMI is defined by the rise and fall of cardiac biomarkers (preferably troponin I or T) with at least one value above the 99th percentile upper reference limit and accompanied by one of the following: symptoms of ischemia, new ST-segment/T-wave changes (such as ST depression or T-wave inversions), development of pathologic Q waves on 12-lead ECG, or noninvasive imaging with evidence of myocardium at risk for ischemia or a new regional wall motion abnormality. The presence of clinical signs of cardiac ischemia (new-onset angina, alteration in the pattern of angina, development of angina while resting, or alteration in the typical anginal equivalent) without signs of myocardial necrosis as shown by normal cardiac biomarkers of injury (troponin) defines UA. There could be ECG alterations such ST segment depression or T wave inversions. EPIDEMIOLOGY New and recurrent MI are estimated to occur 605,000 and 200,000 times per year, respectively. The average age at the onset of MI in the United States is 65.6 years for men and 72.0 years for women (1). Prevalence According to estimates, 16.5 million Americans under the age of 20 have CAD. Mortality: With an overall age-adjusted mortality rate of 98.8/100,000, CAD is the top cause of adult mortality in the United States. Men have a greater death rate. NSTE-ACS is primarily caused by a sharp drop in myocardial blood flow caused by acute plaque rupture or plaque erosion, which results in a partially occluding thrombus. Other mechanisms include (i) dynamic obstruction brought on by a severe spasm of an epicardial coronary artery (prinzmetal angina or coronary vasospasm caused by tobacco use, hyperventilation, magnesium deficiency, cocaine, or methamphetamine use In general, genetic CAD is a complicated, polygenic condition. Age is the biggest risk factor, followed by male sex, prior MI, hypertension (HTN), cigarette use, diabetes mellitus (DM), dyslipidemia, and a family history of premature CAD (defined as age of onset prior to 55 years for men and 65 years for women). Sedentary behaviour, being overweight or obese (metabolic syndrome), inflammation (psoriasis, rheumatoid arthritis), psychosocial variables (anxiety/depression), chronic kidney disease (CKD), obstructive sleep apnea, and environmental contaminants are some of the new or increasing risk factors. GENERAL PREVENTION Quitting smoking, eating a diet low in saturated fat, keeping a normal body mass index, and engaging in regular exercise while managing risk factors: glycemic control for diabetics, blood pressure (BP) control for those with HTN, risk-based statins, and aspirin for those with CAD are all recommended. CONDITIONS OFTEN Associated with Chronic kidney disease and vascular disease DISEASE HISTORY A 10-minute-long tightness or heaviness in the chest that can happen with or without effort. Typically retrosternal in origin, pain or discomfort may radiate to the neck, jaw, interscapular region, upper extremities, or epigastrium. Common adjectives for pain include pressure, tightness, weight, squeezing, or fullness. Palpitations, dyspnea, nausea, diaphoresis, lightheadedness, syncope, or dysphoria are possible accompanying symptoms. Patients, particularly the elderly, diabetics, and women, may present without chest discomfort and with "anginal equivalents" of dyspnea, diaphoresis, and excessive exhaustion. Cocaine or amphetamine usage as CAD risk factors MEDICAL ANALYSIS Note any abnormal vital signs, including tachycardia, bradycardia, HTN, hypotension, tachypnea, fever, and poor dental hygiene. Dysrhythmia, jugular venous distention (JVD), new murmur, rub, or gallop, reduced peripheral pulses, carotid bruits are among cardiovascular symptoms. Tachypnea, difficulty breathing, crackles are respiratory symptoms. Musculoskeletal: It is doubtful that a sharp pain that is reproduced with movement or palpation is cardiac. Skin: xanthomas and xanthelasmas (signs of dyslipidemia), pallor, diaphoresis, and cold skin Cardiac differential diagnoses include: mitral valve disease, aortic dissection, myocarditis, pericarditis, pericardial effusion/cardiac tamponade, heart failure with preserved and reduced ejection fraction, hypertensive emergency Psychiatric: panic attacks, anxiety; musculoskeletal: costochondritis; rib fracture; gastroenterology: gastroesophageal reflux disease; esophageal spasm; esophagitis; esophageal rupture or perforation; hiatal hernia; penetrating or perforating peptic ulcer; biliary or pancreatic pain; pulmonary: pulmonary embolism; pneumot DETECTION & INTERPRETATION OF DIAGNOSIS Initial examinations (lab, imaging) When applicable to both NSTEMI and UA, a 12-lead ECG should be obtained within 10 minutes after presentation. A transmural STEMI of the posterior wall may be indicated by new ST-segment depressions of less than 0.5 mm in two or more adjacent leads and/or T-wave inversions of less than 1 mm in two or more adjacent leads with a significant R wave or R/S ratio of greater than 1. Perform an ECG using the posterior leads (V7-V9). – Perform serial ECGs at intervals of 15 to 30 minutes if the initial ECG is nondiagnostic but symptoms continue and there is a suspicion of ACS. A full blood count and serum biomarkers (which are invariably negative in UA) - The rise in troponin levels occurs 3 to 6 hours after the onset of ischemia symptoms, but it can be postponed for up to 8 to 12 hours (troponin T is not specific in patients with renal failure). - Ultra-high sensitive troponins are more sensitive than conventional assays, but additional validation is necessary. - It has been demonstrated that in post-PCI MI, CK-MB has more specificity than troponins. In 3 to 10 days, the troponin elevation will go away, and in 3 to 4 days, the CK-MB level will return to normal. Repeat biomarkers 8–12 hours after the start of symptoms. A chest x-ray and computed tomography with contrast to rule out any other causes, if necessary. It is advised to undergo transthoracic echocardiography. Tests in the Future & Special Considerations A lipid profile taken while fasting, ideally within 24 hours. TSH, HgbA1c, and activated partial thromboplastin time (aPTT) Urine drug testing in a subset of patients Other/Diagnostic Procedures Consider noninvasive cardiac testing with a standard exercise treadmill test, exercise stress echocardiography, or myocardial perfusion imaging with single-photon emission computed tomography for low- to intermediate-risk patients with improved symptoms and nondiagnostic ECGs with negative biomarkers. In addition, coronary computed tomography angiography can be done on the same demographic of people who are at low to moderate risk. Treatment and general precautions Risk stratify (using the TIMI or GRACE score) to decide whether to use an early invasive approach (coronary angiography within 24 hours of admission) or ischemia-guided therapy; urgent invasive management is needed for very high-risk patients, such as those with hemodynamic instability or cardiogenic shock, persistent chest pain that is resistant to medical treatment, life-threatening arrhythmias or cardiac arrest, mechanical complications, acute heart failure, and recurrent dynamic ST-T wave changes Bed or chair rest with continuous ECG monitoring, keep O2 saturation over 90%, and strictly manage blood pressure. Stop using NSAIDs if at all possible. Promote quitting smoking. Correct K+ and Mg++ electrolyte imbalances. First Line: MEDICATION All patients with NSTE-ACS should receive dual antiplatelet treatment, according to the recommendation. Aspirin, nonenteric coated, first dose of 162–325 mg chewed or crushed for all patients; maintenance dose of 75–100 mg/day forever; reduces mortality and morbidity P2Y12 inhibitors: Ticagrelor, 180 mg PO as a loading dose, followed by 90 mg PO twice daily; avoid in patients with 2nd and 3rd degree heart block; should be given at the time of diagnosis unless invasive approach is planned in a patient with very high bleeding risk. can in some patients lead to dyspnea. Patients with severe liver impairment should not take this medication. A reversal agent can be PB2452, a monoclonal antibody fragment that binds ticagrelor, OR - Prasugrel 60 mg PO, followed by 10 mg PO daily. Indicated in patients under 75 years of age or those with a history of CVA or TIA OR - Clopidogrel, loading dose 300 to 600 mg PO, followed by 75 mg PO daily. Frequently reserved for post-PCI patients treated with coronary stents. In patients with thrombocytopenia and CKD, use with caution. roughly 15% of the general populace are clopidogrel "nonresponders." P2Y12 assay can be used to test for resistance, although routine screening is not currently advised (1). – P2Y12 inhibitors should be given as a loading and maintenance dose to those who cannot take aspirin. - GP IIb/IIIa inhibitors: After PCI, add eptifibatide or tirofiban in some high-risk patients (persistent chest discomfort, significant thrombus burden). If oxygen saturations are below 90% or in patients who are showing signs of heart failure, more oxygen may be administered. Sublingual nitroglycerin 0.4 mg every 5 minutes for a total of 3 doses, and then determine whether IV nitroglycerin is necessary. Avoid if you have hypotension or have taken phosphodiesterase inhibitors. Right ventricular infarction may lessen the hypotension brought on by nitroglycerin. Patients with persistent ischemic chest discomfort should receive morphine sulphate 1 to 5 mg IV, followed by increments of 2 to 8 mg repeated every 5 to 30 minutes. In patients without evidence of heart failure, cardiogenic shock, or other contraindications to -blockade (second or third degree heart block without a pacemaker, active asthma), oral -blocker medication should be started within 24 hours. Metoprolol tartrate 25 to 50 mg every 6 to 12 hours is the recommended dosage. Patients with severe ischemia may want to explore IV treatment. Metoprolol succinate, carvedilol, and bisoprolol are suggested -blockers in individuals with concurrent ACS, stabilised heart failure, and diminished systolic function (LVEF 40%). Lipid-lowering therapy: Regardless of the patient's baseline LDL level, begin or continue high-intensity statin medication with atorvastatin 80 mg daily or rosuvastatin 20 to 40 mg daily (preferred due to nonlipid benefit on vascular function). In statin-intolerant patients or as an adjunctive therapy, ezetimibe, omega-3 fatty acids, PCSK9 inhibitors (evolocumab, alirocumab), and/or fibrates may be investigated. All ACS patients should take an ACE inhibitor (ACEi), especially if they also have diabetes, LV dysfunction, or heart failure. Patients with NSTEMI who are on a therapeutic dose of ACEi/ARB and -blocker and have LVEF 40%, DM, or heart failure are advised to take an aldosterone antagonist (spironolactone or eplerenone) if they do not have substantial renal impairment or hyperkalemia. Start anticoagulant therapy with fondaparinux, enoxaparin, unfractionated heparin (UFH), or bivalirudin. Lower bleeding risk has been linked to bivalirudin. Next Line Verapamil or diltiazem, a non-dihydropyridine calcium channel blocker (CCB), to lower myocardial oxygen demand when beta-blockers are contraindicated and the left ventricular ejection fraction is normal. Use oral long-acting CCB only following complete use of -blockers and nitrates. When treating individuals with epicardial or microvascular coronary artery spasm, long-acting CCBs are advised. Avoid around those who have heart blocks. Long-term nitrate therapy for recurrent angina; sublingual nitroglycerin as needed for angina Ranolazine, 500 to 1,000 mg twice daily, is recommended for the treatment of persistent angina that is unresponsive to other drugs. Patients who have cocaine/methamphetamine intoxication should take benzodiazepines. Patients who use cocaine or methamphetamine should avoid -blockers. QUESTIONS FOR REFERENCE Consultation with a cardiologist is advised for NSTE-ACS. A cardiologist will need to closely monitor patients. Prior to hospital release, referral to an exercise-based cardiac rehabilitation programme is linked to lower morbidity and death. It should be thought about referring someone to a dietician. SURGICAL AND OTHER PROCEDURE Coronary reperfusion techniques include CABG surgery and PCI with stenting. Patients with refractory shock should get mechanical circulatory support. CONSIDERATIONS FOR ADMISSION, THE INPATIENT, AND NURSING Admit patients who have NSTE-ACS suspicions. Special populations are taken into account - Elderly population (75 years) - Early invasive management benefits the elderly - Older population Pharmacotherapy needs to be tailored based on a patient's weight, pre-existing conditions, and comorbidities. - Pregnancy: Preeclampsia/eclampsia, gestational diabetes, and advanced maternal age are specific risk factors for ACS during pregnancy. In evaluating pregnant women with ACS, spontaneous coronary artery dissection and thromboembolism should be taken into account. Statins, ACEi, and ARBs should not be used. CONTINUING CARE AFTERCARE RECOMMENDATIONS Within 72 hours of being discharged, patients with low-risk suspected ACS who have normal serial ECGs and cardiac troponins may undergo a treadmill ECG, stress myocardial perfusion imaging, or stress echocardiography. 2 to 6 weeks of follow-up (low risk) and 14 days (high risk) are recommended. Patients who have an LVEF below 40% are more likely to experience ventricular arrhythmias. One to three months after discharge, perform a second LVEF test to assess function and decide if an ICD should be implanted. DIET The link between diet and coronary artery disease (CAD) is complicated; patients should follow a fiber-rich, sodium- and trans-fat-free diet. Patient education on nutrition, exercise, quitting smoking, and changing one's lifestyle. After an outpatient reevaluation, it is safe for asymptomatic patients to resume exercise and sexual activity. Encourage vaccination against influenza and pneumococci. Patients with UA/NSTEMI had lower in-hospital mortality than STEMI patients, but their long-term prognosis is the same or worse. COMPLICATIONS Depression (increases mortality risk), acute thromboembolic stroke, pericarditis/Dressler syndrome, dysrhythmia, cardiogenic shock, and heart failure
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