What is the most common complication of myocardial infarction 1 to 3 days after?
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Potential complications from a heart attack can vary widely, from mild to life threatening. Some people experience a "minor" heart attack (although it can still be very serious) with no associated complications. This is also known as an uncomplicated heart attack. Other people experience a major heart attack, which has a wide range of potential complications and may require extensive treatment. An arrhythmia is an abnormal heartbeat and can include: Arrhythmias can develop after a heart attack as a result of damage to the heart muscles. Damaged
muscles disrupt electrical signals that control the heart. Some arrhythmias, such as tachycardia, are mild and cause symptoms such as: Other arrhythmias can be life threatening, including: These life-threatening types of arrhythmia can be a major cause of death during the 24 to 48 hours after a heart attack. However, survival rates have improved significantly since the invention of the portable defibrillator – an external device that
delivers an electric shock to the heart and "resets" it to the right rhythm. Mild arrhythmias can usually be controlled with medicine such as beta-blockers. More troublesome bradycardias that cause repeated and prolonged symptoms may need to be treated with a pacemaker. This is an electric device surgically implanted in the
chest to help regulate the heartbeat. Find out more about sudden cardiac arrest from the charity Sudden Cardiac Arrest UK. Heart failure happens when your heart is unable to effectively pump blood around your body. It can develop after a heart attack if your heart muscle is
extensively damaged. This usually happens in the left side of the heart (the left ventricle). Symptoms of heart failure include: Heart failure can be treated with a combination of medicines and, in some cases, surgery. Find out more about treating heart failure. Cardiogenic shock is similar to heart failure, but more serious. It develops when the heart muscle has been damaged so extensively it can no longer pump enough blood to maintain many of the body's functions. Symptoms include: A type of
medicine called vasopressors (or inotropes) may be used. Vasopressors help squeeze (constrict) the blood vessels, which increases blood pressure and improves blood circulation. Once the initial symptoms of cardiogenic shock have been stabilised, surgery may be required to improve the functioning of the heart. This may include percutaneous coronary intervention
(PCI), alongside the insertion of a small pump, known as an intra-aortic balloon pump. This can help improve the flow of blood from the heart. Another option is a coronary artery bypass graft (where a blood vessel from another part of your body is used to bypass any blockage). A heart rupture is an extremely serious but
relatively uncommon complication of a heart attack where the heart's muscles, walls or valves split apart (rupture). It can happen if the heart is significantly damaged during a heart attack and usually happens 1 to 5 days afterwards. Symptoms are the same as those of cardiogenic shock. Open heart surgery is usually required to repair the damage. The outlook for people
who have a heart rupture is poor; it's estimated that 1 in 2 people die within 5 days of the rupture occurring. Page last reviewed: 28 November 2019 Continuing Education ActivityAcute myocardial infarctions are one of the leading causes of death in the developed world, with prevalence approaching three million people worldwide, with more than one million deaths in the United States annually. This activity reviews the presentation, evaluation, and management of patients with acute myocardial infarctions and highlights the role of the interprofessional team in caring for these patients. Objectives:
Access free multiple choice questions on this topic. IntroductionAcute myocardial infarction is one of the leading causes of death in the developed world. The prevalence of the disease approaches three million people worldwide, with more than one million deaths in the United States annually. Acute myocardial infarction can be divided into two categories, non-ST-segment elevation MI (NSTEMI) and ST-segment elevation MI (STEMI). Unstable angina is similar to NSTEMI. However, cardiac markers are not elevated.[1][2][3] An MI results in irreversible damage to the heart muscle due to a lack of oxygen. An MI may lead to impairment in diastolic and systolic function and make the patient prone to arrhythmias. In addition, an MI can lead to a number of serious complications. The key is to reperfuse the heart and restore blood flow. The earlier the treatment (less than 6 hours from symptom onset), the better the prognosis. An MI is diagnosed when two of the following criteria are met:
EtiologyThe etiology of acute myocardial infarction is decreased coronary blood flow. The available oxygen supply cannot meet oxygen demand, resulting in cardiac ischemia. Decreased coronary blood flow is multifactorial. Atherosclerotic plaques classically rupture and lead to thrombosis, contributing to acutely decreased blood flow in the coronary. Other etiologies of decreased oxygenation/myocardial ischemia include coronary artery embolism, which accounts for 2.9% of patients, cocaine-induced ischemia, coronary dissection, and coronary vasospasm.[4][5] Nonmodifiable Risk Factors
Modifiable Risk Factors
Other Causes of MI
EpidemiologyAmong patients suffering from acute myocardial infarction, 70% of fatal events are due to occlusion from atherosclerotic plaques. As atherosclerosis is the predominant cause of acute myocardial infarction, risk-factors for atherosclerotic disease are often mitigated in the prevention of disease. Modifiable risk factors account for 90% (men) and 94% (female) of myocardial infarctions. Modifiable risk factors include cigarette smoking, exercise, hypertension, obesity, cholesterol, LDL, and triglyceride levels. In contrast, age, sex, and family history are non-modifiable risk factors for atherosclerosis.[6][7] PathophysiologyAtherosclerotic rupture leads to an inflammatory cascade of monocytes and macrophages, thrombus formation, and platelet aggregation. This leads to decreased oxygen delivery through the coronary artery resulting in decreased oxygenation of the myocardium. The inability to produce ATP in the mitochondria leads to the ischemic cascade, and therefore apoptosis (cell death) of the endocardium or myocardial infarction. With some exceptions due to genetic variation, coronary arteries have unique and diagnostic territorial distributions. For example, the left anterior descending coronary artery supplies blood flow to the interventricular septum, anterolateral wall, and ventricular apex. The left circumflex artery supplies blood to the inferolateral wall. The right coronary artery supplies the right ventricle. The inferior wall is supplied either by the left circumflex or right coronary artery.[8] HistopathologyThe histology of myocardial infarction changes over the time-course of the disease. At time 0, there are no microscopic histologic changes. Under light microscopy, within 0.5 to 4 hours, waviness of fibers at the periphery of the tissue is seen. Glycogen is depleted. At 4 to 12 hours, the myocardium undergoes coagulation necrosis and edema. At 12 to 24 hours, the gross specimen becomes dark and mottled. There are contraction band necrosis and neutrophil predominance on histopathology. At 1 to 3 days, there is a loss of nuclei, and at 3 to 7 days, macrophages appear to remove apoptosis cells. At 7 to10 days, granulation tissue appears. At 10 days and onward, there is collagen one deposition. After 2 months, the myocardium is scarred. ToxicokineticsCardiac biomarkers are useful in the diagnosis of acute myocardial infarction, specifically non-ST-elevation MI. Troponin is the most specific lab test and has two isoforms, I and T. Troponins peak at 12 hours and persist for seven days. Creatinine kinase MB is also specific to the myocardium. It peaks at ten hours; however, it normalizes within two to three days. LDH peaks over 72 hours and normalizes over ten to 14 hours. In clinical practice, LDH is not used to diagnose acute MI. Finally, MB has very low specificity for the myocardium and is not used clinically; it quickly rises and normalizes. High-sensitivity troponin has recently been approved for use in the United States after having been heavily studied and utilized in Europe. Although it is more sensitive than conventional troponin, it is also less specific. Thus, potential challenges include numerous false-positive interpretations.[3] History and PhysicalThe history of and physical exam is often inconsistent when evaluating for acute myocardial infarction. The history should focus on the onset, quality, and associated symptoms. Recent studies have found that diaphoresis and bilateral arm radiating pain most often are associated with myocardial infarction in men. Associated symptoms include:
Physical exam, most importantly, should note vital signs and patient’s appearance, including diaphoresis, as well as lung findings, and cardiac auscultation.
EvaluationEarly and rapid ECG testing should be employed in all patients presenting with chest pain. Women often have atypical symptoms such as abdominal pain or dizziness and may present without chest pain at all. Elderly patients more often have shortness of breath as their presenting symptom for myocardial infarction. All of these presentations should prompt ECG testing, as well.[9][10][11] The ECG is highly specific for MI (95% to 97%), yet not sensitive (approximately 30%). Right-sided, posterior lead placement, and repeat ECG testing can increase ECG sensitivity. For example, peaked T-waves on ECG, known as “hyperacute T waves,” often indicate early ischemia and will progress to ST elevation. When present, findings of ST-elevations greater than 2 mm in two contiguous leads on ECG (inferior: leads II, III, aVF; septal equal V1, V2; anterior: V3, V4; lateral: I, aVL, V5, V6) are indicative of an ST-elevation myocardial infarction. Often, there are ST depressions that are visualized in opposite anatomical regions of the myocardium. ECG diagnosis of STEMI can be difficult, particularly in patients with a left bundle branch block and pacemakers. Sgarbosa described criteria that can assist the physician or practitioner in diagnosing STEMI in these patients. Isolated ST-elevations in aVR are indicative of left main coronary artery occlusion in the appropriate clinical setting. Wellens noted deeply biphasic T waves in V2, V3 and found they are often predictive of an impending proximal left anterior descending artery occlusion, which may lead to devastating anterior wall myocardial infarction. Patients that present with myocardial infarction may not have diagnostic ST-elevation ECG abnormalities. Patients with typical chest pain should be investigated for NSTEMI with subtle abnormalities on ECG, including ST-depressions and T wave changes. Serial ECGs can be helpful here as well to look for dynamic changes. ECG without acute changes or any abnormalities is common in NSTEMI. There are diagnostic guidelines that can assist the practitioner in determining whether further testing is useful in identifying patients with NSTEMI. Given the poor sensitivity of ECG for STEMI, troponins are almost universally used for patients with a suspicious clinical history. The HEART score has been validated and popularized. It utilizes the clinician’s suspicion, patient risk factors, ECG diagnostics, and troponin level to determine the “risk level.” Laboratory Features
B-type natriuretic peptide (BNP) should not be ordered as a marker for MI, but it is better used to stratify risk, especially in patients with MI who develop heart failure. Cardiac Imaging Cardiac angiography is used to perform percutaneous coronary intervention (PCI) or determine obstructions in the coronary vessels. An echocardiogram is used to assess wall motion, degree of valve abnormality, ischemic mitral regurgitation (MR), and presence of cardiac tamponade. Treatment / ManagementAll patients with STEMI and NSTEMI require immediately chewed aspirin 160 mg to 325 mg. Furthermore, the patient should have intravenous access and oxygen supplementation if oxygen saturation is less than 91%. Opioids may be used for pain control in addition to sublingual nitroglycerin if the blood pressure is adequate.[12][13][14] Treatment for STEMI includes immediate reperfusion. Preference is for emergent percutaneous coronary intervention (PCI). Before PCI, patients should receive dual antiplatelet agents, including intravenous heparin infusion as well as an adenosine diphosphate inhibitor receptor (P2Y2 inhibitor), most commonly ticagrelor. Furthermore, glycoprotein IIb/IIIa inhibitor or direct thrombin inhibitor may be given at the time of percutaneous intervention. If percutaneous intervention is unavailable within 90 minutes of the diagnosis of STEMI, reperfusion should be attempted with an intravenous thrombolytic agent. NSTEMI in a stable asymptomatic patient may not benefit from emergent percutaneous coronary intervention and should be managed medically with antiplatelet agents. Percutaneous coronary intervention can be done within 48 hours of admission and may lead to improved in-hospital mortality and decreased length of stay. In NSTEMI patients with refractory ischemia or ischemia with hemodynamic or electrical instability, PCI should be performed emergently. Before discharge for acute MI, patients may routinely be given aspirin, high-dose statin, beta-blocker, and/or ACE-inhibitor. If PCI is contemplated, it should be done within 12 hours. If fibrinolytic therapy is considered, it should be done within 120 minutes. Parenteral anticoagulation, in addition to antiplatelet therapy, is recommended for all patients. Differential Diagnosis
PrognosisAcute MI still carries a high mortality rate, with most deaths occurring prior to arrival to the hospital. At least 5%-10% of survivors die within the first 12 months after the MI, and close to 50% need hospitalization within the same year. The overall prognosis depends on the extent of muscle damage. Good outcomes are seen in patients who undergo early perfusion- thrombolytic therapy within 30 minutes of arrival or PCI within 90 minutes). In addition, outcomes are good if the ejection fraction is preserved and the patient is started in aspirin, beta-blockers, and ACE inhibitors. Factors that negatively affect prognosis include:
Complications
Deterrence and Patient Education
Enhancing Healthcare Team OutcomesAcute myocardial infarction is managed by an interprofessional team that is solely dedicated to heart disease. Besides the cardiologist, the team usually consists of a cardiac surgeon, an interventional cardiologist, intensivist, cardiac rehabilitation specialist, critical care or cardiology nurses, and physical therapists. Because many patients die before even reaching the hospital, the key is to educate the patient on symptoms and early arrival to the emergency department. The pharmacist, nurse practitioner, and primary care providers should educate patients on how to take nitroglycerin, and if there is no relief after three doses, then 911 should be called. At triage, the nurse should immediately communicate with the interprofessional team as the time to reperfusion is limited. The cardiologist may consider thrombolysis or PCI, depending on the duration of symptoms and contraindications. All patients need ICU monitoring. Nurses should be vigilant about the potentially life-threatening complications and communicate with the team if there are abnormal clinical signs or laboratory parameters. No patient should e prematurely discharged because complications of an MI can occur up to a week after an MI. After stabilization, patients need thorough education by the nurse on the reduction of risk factors for coronary artery disease. Besides a nurse practitioner, the social worker should be involved to facilitate home care, cardiac rehab, and the need for any support services while at home. The pharmacist should address and provide education concerning appropriate medication dosing and discuss potential side effects. After discharge, the patient needs to enter a cardiac rehabilitation program, eat a healthy diet, discontinue smoking, abstain from alcohol, reduce body weight, and lower cholesterol and blood glucose levels. The patient should be educated on the importance of compliance with medications to lower blood pressure and blood cholesterol. [15][16][17][Level 2] Pharmacists review prescribed medications, check for interactions and provide patient education about the importance of compliance. [Level 5] Outcomes Acute myocardial infarction continues to have high mortality out of the hospital. Data indicate that at least one-third of patients die before coming to the hospital, and another 40%-50% are dead upon arrival. Another 5%-10% of patients will die within the first 12 months after their myocardial infarction. Readmission is common in about 50% of patients within the first 12 months after the initial MI. The overall prognosis depends on the ejection fraction, age, and other associated comorbidity. Those who do not undergo any revascularization will have a poorer outcome compared to patients who undergo revascularization. The best prognosis is in patients with early and successful reperfusion and preserved left ventricular function.[18][19][20] [Level 2] Review QuestionsFigureSpecimen showing myocardial infarction in the left ventricle and the interventricular septum. The asterisk(*) also indicates left ventricular hypertrophy. Contributed by Wikimedia Commons (CC by 4.0) https://creativecommons.org/licenses/by/4.0/  FigureHeart attack (myocardial infarction) warning signs in women. Contributed by U.S. Department of Health and Human Services Office on Women's Health FigureAn ECG showing pardee waves indicating acute myocardial infarction in the inferior leads II, III and aVF with reciprocal changes in the anterolateral leads. Contributed by Wikimedia Commons, Glenlarson (Public Domain-Self) FigureTransesophageal echocardiography, Thrombo embolism, Pulmonary artery, Pulmonary Embolism, Thromboembolic , Right Pulmonary artery, TE, RPA, Acute ECG segment elevation mimicking myocardial infarction in a patient with pulmonary embolism. Contribute by (more...) References1.Nascimento BR, Brant LCC, Marino BCA, Passaglia LG, Ribeiro ALP. Implementing myocardial infarction systems of care in low/middle-income countries. Heart. 2019 Jan;105(1):20-26. [PubMed: 30269080] 2.Barberi C, van den Hondel KE. The use of cardiac troponin T (cTnT) in the postmortem diagnosis of acute myocardial infarction and sudden cardiac death: A systematic review. Forensic Sci Int. 2018 Nov;292:27-38. [PubMed: 30269044] 3.Alaour B, Liew F, Kaier TE. Cardiac Troponin - diagnostic problems and impact on cardiovascular disease. Ann Med. 2018 Dec;50(8):655-665. [PubMed: 30265127] 4.Massberg S, Polzin A. [Update ESC-Guideline 2017: Dual Antiplatelet Therapy]. Dtsch Med Wochenschr. 2018 Aug;143(15):1090-1093. [PubMed: 30060279] 5.Scheen AJ. [From atherosclerosis to atherothrombosis : from a silent chronic pathology to an acute critical event]. Rev Med Liege. 2018 May;73(5-6):224-228. [PubMed: 29926559] 6.Berg DD, Wiviott SD, Braunwald E, Guo J, Im K, Kashani A, Gibson CM, Cannon CP, Morrow DA, Bhatt DL, Mega JL, O'Donoghue ML, Antman EM, Newby LK, Sabatine MS, Giugliano RP. Modes and timing of death in 66 252 patients with non-ST-segment elevation acute coronary syndromes enrolled in 14 TIMI trials. Eur Heart J. 2018 Nov 07;39(42):3810-3820. [PMC free article: PMC6220126] [PubMed: 30239711] 7.Deng D, Liu L, Xu G, Gan J, Shen Y, Shi Y, Zhu R, Lin Y. Epidemiology and Serum Metabolic Characteristics of Acute Myocardial Infarction Patients in Chest Pain Centers. Iran J Public Health. 2018 Jul;47(7):1017-1029. [PMC free article: PMC6119561] [PubMed: 30182001] 8.Haig C, Carrick D, Carberry J, Mangion K, Maznyczka A, Wetherall K, McEntegart M, Petrie MC, Eteiba H, Lindsay M, Hood S, Watkins S, Davie A, Mahrous A, Mordi I, Ahmed N, Teng Yue May V, Ford I, Radjenovic A, Welsh P, Sattar N, Oldroyd KG, Berry C. Current Smoking and Prognosis After Acute ST-Segment Elevation Myocardial Infarction: New Pathophysiological Insights. JACC Cardiovasc Imaging. 2019 Jun;12(6):993-1003. [PMC free article: PMC6547246] [PubMed: 30031700] 9.Alquézar-Arbé A, Sanchís J, Guillén E, Bardají A, Miró Ò, Ordóñez-Llanos J. Cardiac troponin measurement and interpretation in the diagnosis of acute myocardial infarction in the emergency department: a consensus statement. Emergencias. 2018 Oct;30(5):336-349. [PubMed: 30260119] 10.Perera M, Aggarwal L, Scott IA, Logan B. Received care compared to ADP-guided care of patients admitted to hospital with chest pain of possible cardiac origin. Int J Gen Med. 2018;11:345-351. [PMC free article: PMC6128279] [PubMed: 30214268] 11.Riley RF, Miller CD, Russell GB, Soliman EZ, Hiestand BC, Herrington DM, Mahler SA. Usefulness of Serial 12-Lead Electrocardiograms in Predicting 30-Day Outcomes in Patients With Undifferentiated Chest Pain (the ASAP CATH Study). Am J Cardiol. 2018 Aug 01;122(3):374-380. [PubMed: 30196932] 12.Larson EA, German DM, Shatzel J, DeLoughery TG. Anticoagulation in the cardiac patient: A concise review. Eur J Haematol. 2019 Jan;102(1):3-19. [PubMed: 30203452] 13.Bath PM, Woodhouse LJ, Appleton JP, Beridze M, Christensen H, Dineen RA, Flaherty K, Duley L, England TJ, Havard D, Heptinstall S, James M, Kasonde C, Krishnan K, Markus HS, Montgomery AA, Pocock S, Randall M, Ranta A, Robinson TG, Scutt P, Venables GS, Sprigg N. Triple versus guideline antiplatelet therapy to prevent recurrence after acute ischaemic stroke or transient ischaemic attack: the TARDIS RCT. Health Technol Assess. 2018 Aug;22(48):1-76. [PMC free article: PMC6139477] [PubMed: 30179153] 14.Adamski P, Adamska U, Ostrowska M, Navarese EP, Kubica J. Evaluating current and emerging antithrombotic therapy currently available for the treatment of acute coronary syndrome in geriatric populations. Expert Opin Pharmacother. 2018 Sep;19(13):1415-1425. [PubMed: 30132731] 15.Aeyels D, Seys D, Sinnaeve PR, Claeys MJ, Gevaert S, Schoors D, Sermeus W, Panella M, Bruyneel L, Vanhaecht K. Managing in-hospital quality improvement: An importance-performance analysis to set priorities for ST-elevation myocardial infarction care. Eur J Cardiovasc Nurs. 2018 Aug;17(6):535-542. [PubMed: 29448818] 16.Schwaab B. [Cardiac Rehabilitation]. Rehabilitation (Stuttg). 2018 Apr;57(2):117-126. [PubMed: 29216666] 17.El Hajj MS, Jaam MJ, Awaisu A. Effect of pharmacist care on medication adherence and cardiovascular outcomes among patients post-acute coronary syndrome: A systematic review. Res Social Adm Pharm. 2018 Jun;14(6):507-520. [PubMed: 28641999] 18.Stone GW, Ellis SG, Gori T, Metzger DC, Stein B, Erickson M, Torzewski J, Williams J, Lawson W, Broderick TM, Kabour A, Piegari G, Cavendish J, Bertolet B, Choi JW, Marx SO, Généreux P, Kereiakes DJ., ABSORB IV Investigators. Blinded outcomes and angina assessment of coronary bioresorbable scaffolds: 30-day and 1-year results from the ABSORB IV randomised trial. Lancet. 2018 Oct 27;392(10157):1530-1540. [PubMed: 30266412] 19.Lopes RD, de Barros E Silva PGM, de Andrade Jesuíno I, Santucci EV, Barbosa LM, Damiani LP, Nakagawa Santos RH, Laranjeira LN, Dall Orto FTC, Beraldo de Andrade P, de Castro Bienert IR, Alexander JH, Granger CB, Berwanger O. Timing of Loading Dose of Atorvastatin in Patients Undergoing Percutaneous Coronary Intervention for Acute Coronary Syndromes: Insights From the SECURE-PCI Randomized Clinical Trial. JAMA Cardiol. 2018 Nov 01;3(11):1113-1118. [PMC free article: PMC6583055] [PubMed: 30264159] 20.Choi AR, Jeong MH, Hong YJ, Sohn SJ, Kook HY, Sim DS, Ahn YK, Lee KH, Cho JY, Kim YJ, Cho MC, Kim CJ., other Korea Acute Myocardial Infarction Registry Investigators. Clinical characteristics and outcomes in acute myocardial infarction patients with versus without any cardiovascular risk factors. Korean J Intern Med. 2019 Sep;34(5):1040-1049. [PMC free article: PMC6718753] [PubMed: 30257551] What is the most common complication of a myocardial infarction in the first 24 hours after it occurs?About 90% of patients who have an acute myocardial infarction (AMI) develop some form of cardiac arrhythmia during or immediately after the event. In 25% of patients, such rhythm abnormalities manifest within the first 24 hours.
What are 3 common complications of a myocardial infarction?These complications include arrhythmias and heart block (due to injured or ischemic conduction system tissue), and hypotension and congestive heart failure (due to ischemic or injured muscle tissue, resulting in abnormal filling {"diastolic dysfunction"} or abnormal emptying {"systolic dysfunction"}).
What is the most common early complication of a myocardial infarction?The most commonly encountered mechanical complications are acute mitral regurgitation secondary to papillary muscle rupture, ventricular septal defect, pseudoaneurysm, and free wall rupture; each complication is associated with a significant risk of morbidity, mortality, and hospital resource utilization.
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