Myocardial Infarctions: Symptoms, Diagnosis & Treatment

The incidence of myocardial infarctions is declining in high-income countries but rising in middle- and low-income countries. Within the United States, there are significant differences in incidence of myocardial infarction in different populations. – Myocardial incidence after age 35, from highest to lowest: Black males > Black females > White males > White females. Timing of the first MI tends to be earlier in men than in women by about 10 years. – Some research suggests the earlier age in men may be related to risk factors, such as smoking and hyperlipidemia. Although mortality from myocardial infarctions has declined overall, mortality rates are higher in women than in their male peers. – This is especially true for young and/or minority women. Myocardial infarction is an important cause of heart failure, which is itself a significant cause of death. Risk factors for myocardial infarction include: – Dyslipidemia – Diabetes mellitus – Hypertension – Smoking (possibly including daily use of e-cigarettes) – Obesity – Psychosocial stress – Alcohol consumption – Poor diet (diets low in fruits and vegetables) Unfortunately, many people, especially women, are unaware of the risk factors and symptoms of myocardial infarctions. – Unawareness is a significant obstacle to prevention and treatment of myocardial infraction. Myocardial Infarction is defined as myocardial injury with ischemia. Prodromal symptoms = In the days, weeks, or even months prior to the heart attack. Acute symptoms = Experienced at the time of the event. Silent MI = No noticeable symptoms. Chest Pain, aka, angina, which is variably described as dull, sharp, squeezing, pressure, or simply as discomfort. Some patients experience pain in their arms, neck, jaw, or back, which may radiate from the chest. Although chest pain is a hallmark of myocardial infarction, bear in mind that not all patients experience angina. The absence of chest pain and/or young age of a patient often leads to a missed or delayed diagnosis of myocardial infarction, which is associated with worse outcomes. Gastrointestinal issues, including nausea, vomiting, indigestion, etc., are common. Many patients report feeling extreme fatigue, exhaustion, or sleep disturbances, particularly during the prodromal period. Other common symptoms include headaches, dizziness, lightheadedness, and shortness of breath (dyspnea). Patients may feel unaccountably anxious, or experience a sense of impending doom, prior to and during the heart attack. An ECG should be administered as soon as possible when MI is suspected, and should be re-administrated frequently to observe the evolution of the infarction. ECG distinguishes between ST-segment elevated (STEMI) or Non-ST elevated (NSTEMI) myocardial infarctions, which influences treatment strategies. – Q-wave abnormalities may indicate the size or location of a current MI, or, may indicate a prior MI. ECG can indicate localized ischemia in ST-elevated myocardial infarctions: Lateral infarction is indicated by changes in leads I and aVL; these are often the result of blockage in the left circumflex artery. Apical infarctions are suggested by changes in leads V5 and V6, and are often associated with blockages in the left circumflex or right coronary arteries. Anterior infarctions are indicated by changes in leads V3 and V4; they are associated with blockages in the left anterior descending artery. Anterior septal infarctions are indicated by changes in leads V1 and V2; they are associated with blockages in the proximal left anterior descending artery. Inferior infarctions are indicated by changes in leads II, aVF, and III; they are associated with blockages in the right coronary artery, or, less frequently, the left circumflex artery (approximately 10% of the population is Left dominant). Right ventricular infarctions require additional leads V3R through V6R. Posterolateral infarctions require additional posterior leads V7-V9; these infarctions are often due to blockages in the right coronary artery or left circumflex artery. Review Coronary Arteries Cardiac biomarkers, especially cardiac troponin, are key to diagnosis myocardial infarction. Biomarker values help us distinguish between NSTEMI and unstable angina, because only NSTEMI is associated with falling/rising levels of troponin. In a rough graph representing the pattern of cardiac troponin I and CK-MB, we show that both peak within 24 hours of the myocardial infarction, and fall to normal levels over time. Treatment should begin as soon as possible, ideally even before arrival at the hospital, to reduce the extent of myocardial necrosis. – Administration of oxygen when oxygen saturation is less than 90%. – Patients should also be given aspirin, which has antiplatelet effects, and nitrates for chest pain (if nitrates are ineffective, morphine is also an option). – Vary by severity of infarction, but generally include percutaneous coronary intervention (angioplasty), coronary bypass grafting, or fibrinolytic drugs. – It's generally recommended that patients with STEMI receive emergency PCI. – If PCI is not available, then fibrinolytic drugs must be given as soon as possible. – Patients with unstable, complicated NSTEMI often require immediate PCI or CABG, whereas uncomplicated NSTEMI patients may be able to wait longer (a day or two), and revascularization may not be necessary. Fibrinolytic drugs are generally not recommended for NSTEMI patients because the potential risks outweigh benefits. – Antiplatelets (such as aspirin, clopidogrel, or others). – Anticoagulation drugs (such as unfractionated or low molecular weight heparin). – Beta-blockers (or calcium-channel blockers) – Statins – ACE-inhibitors Long-term treatment focuses on reducing risk factors, and include improved diet and exercise, as well as medications to manage hypertension and hyperlipidemia.

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