Acute myocardial infarction

Myocardial infarction . Also called an acute heart attack, it happens when the blood that reaches the heart muscle is reduced or completely cut by the blockage in one or more coronary arteries .

These arteries that surround the heart nourish the heart muscle (myocardium). When it is deprived of its essential oxygen , it dies. If the affected heart muscle area is small, there may be minor permanent damage. Some attacks do not produce symptoms; they are known as silent heart attacks. Anyway, if the damage to the muscle is extensive it can cause death.

Summary

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• 1 Peculiarities of myocardial infarction
  • 1 Concept
  • 2 Manifestation
  • 3 Diagnosis
• 2 Serum markers of myocardial necrosis
• 3 Classification
  • 1 According to the clinical presentation:
  • 2 According to size:
  • 3 According to location:
• 4 Electrocardiogram
• 5 How it is treated
  • 1 Out-of-hospital initial phase
  • 2 Hospital treatment
  • 3 Restoration of coronary flow
  • 4 Out-of-hospital care after myocardial infarction
  • 5 Pharmacological treatment
  • 6 Antihypertensive treatment
• 6 Tips for alarm symptoms
• 7 References
• 8 Related Links
• 9 Source

Peculiarities of myocardial infarction

Concept

Acute myocardial infarction (AMI) is the situation in which there is necrosis of myocardial cells as a consequence of prolonged ischemia. It represents 36% of the cases admitted with the diagnostic suspicion of acute coronary syndrome (ACS) (Antman EM, 2004 ), a clinical picture caused by coronary artery disease in a situation of instability, which is defined from different perspectives related to clinical aspects, electrocardiographic, biochemical and pathological characteristics (Alpert JS, 2000 ; SIGN 94; 2007 ). AMI and unstable angina are its most important diagnostic categories.

Manner of manifestation

The characteristic ischemic symptom is Pain in the center of the Thorax, which is described as something that squeezes or weighs, of severe intensity, with a minimum duration of 20 minutes, which is not modified by muscular, respiratory or posture movements, when that other types of symptoms such as discomfort, discomfort, pain in the epigastrium, arm , wrist , jaw , back or shoulder , as well as dyspnea , sweating, nausea , vomiting , dizziness, can be added. or a combination of all of them (SIGN 94, 2007), appears at rest or during exercise, is rarely sharp or very localized.

There is myocardial necrosis without symptoms or with an atypical presentation, as occurs in diabetics or the elderly. Sometimes the symptoms are not recognized and are confused with other entities such as indigestion or viral syndrome. When pain refers to the abdomen, it is more often associated with nausea and vomiting and it is easier to confuse it with abdominal problems (Alpert JS, 2000). AMI can be a cause of acute lung edema and sudden death.

Diagnosis

A careful clinical evaluation and an electrocardiogram (ECG) should be done. The suspected diagnosis will be made in the presence of the clinical picture described, sometimes associated with a previous history of ischemic heart disease , male sex, advanced age and existence of known cardiovascular risk factors. The situation will be assessed as high risk in the presence of progressive angina, prolonged pain ≥20 minutes, pulmonary edema, hypotension and arrhythmias. The diagnosis of myocardial infarction should be made without delay, early therapy decisively improves the prognosis.

Damage to the myocardium can be estimated through symptoms and additional tests such as: ECG, serum markers of myocardial necrosis, echocardiogram , myocardial perfusion images, and contrast ventriculography (Alpert JS, 2000).

Serum markers of myocardial necrosis

As a result of myocardial necrosis, proteins appear in the bloodstream: Myoglobin, Troponin T, Troponin I, Creatin Phospho Kinase (CPK) and Lactate dehydrogenase (LDH).

The diagnosis of AMI is made when the most sensitive and specific markers of necrosis are raised in blood: cardiac troponins and CPK-MB, which reflect damage to the myocardium but do not indicate its mechanism of appearance, such that a high value without Clinical evidence of ischemia forces us to look for other causes of injury.

Troponin in blood is a very sensitive and very specific indicator of myocardial cell necrosis. It appears in blood within a few hours of AMI, reaches its maximum concentration at 12-48 hours and remains elevated for up to 7-10 days. It should be requested at the time of admission to the emergency department, if the result is negative and there is a high suspicion index, it will be repeated at 6 and 12 hours. To establish the diagnosis, the determination of troponin 12 hours after the onset of symptoms will be assessed.

There is a demonstrated relationship between their blood levels and the size of the infarction (Alpert JS, 2000; SIGN 94, 2007), the normal troponin reference value is zero. If the patient has high levels at the time of admission, we will use the CPK-MB mass for the diagnosis of AMI (SIGN 94, 2007). Troponin may be slightly elevated in patients with pulmonary embolism, heart failure, myocarditis, and renal failure, which may be a reflection of subclinical myocardial injury. The elevation of troponin in the absence of the characteristic clinical picture does not imply the existence of AMI. Other possible causes of noncardiac elevation are sepsis, cirrhosis, and rheumatoid arthritis. Its long plasma half-life limits its possibilities of use as a reinfarction marker.

• CPK-MB

It is less specific for cardiac tissue than troponin, which is why it is not recommended for routine diagnosis. It rises 6-8 hours after the AMI and normalizes between 24 and 48 hours later, its sustained elevation should make us think of a non-cardiac origin. It allows to identify the evolution time of the infarction when the troponin is elevated in the first determination. There is a variability of between 5 and 10 micrograms between the positive and negative results (Alpert JS, 2000; Achar SA, 2005).
A negative enzyme marker result performed 12 hours after symptoms excludes myocardial infarction.

Classification

According to the clinical presentation:

• Non-ST elevation acute coronary syndrome (SCASET).
• Unstable angina .
• Non-ST elevation myocardial infarction (STEMI).
• Most cases of STEMI will be a non-Q wave myocardial infarction (NAMIQ).
• A small proportion will be Q-wave IAM (IAMQ).
• ST-elevation acute coronary syndrome (SCACEST).
• Most of the cases will be a myocardial infarction (STEMI) with Q wave.
• A small proportion will be IAMNQ.

According to the size:

• Microscopic: Focal necrosis.
• Small: Affects an area less than 10% the size of the left ventricle.
• Medium: between 20% and 30% of the left ventricle.
• Large: surface greater than 30% of the left ventricle .

According to the location:

• Anterior, lateral, inferior, posterior, antero septal.
• More than one area may be affected.

Electrocardiogram

Changes in the electrocardiogram (ECG) in relation to AMI can be observed in the record of the 12 leads in the absence of confounding factors such as: known left bundle branch block (LBBB), ventricular hypertrophy, WPW syndrome, and immediate postoperative period of coronary surgery.

ST elevation in ACS is defined by the presence of (SIGN 94, 2007)

• ST≥1mm elevation in two or more contiguous limb leads.
• ST≥2mm elevation in two contiguous precordial leads.
• New or presumably new left bundle branch block.

ST elevation (SCACEST) and newly presented left bundle branch block feel the indication of urgent reperfusion without waiting for the result of the markers, which will later confirm its presence. If the ECG is normal at the time of reception and the clinical picture is highly suggestive, records will be made every 5 ‘to monitor the evolution of the ST segment, in other cases ECG will be done at 6 and 8 hours until the diagnosis (Antman EM, 2004).

In the presence of new BRI in a patient with SCACEST, the following criteria add diagnostic value:

• ST≥1mm elevation in leads with positive QRS complex.
• ST≥1mm depression in V1-V3.
• ST≥5mm elevation in leads with negative QRS complex.

The following findings are suggestive signs of myocardial necrosis (Afilalo J, 2007):

• QR wave in leads from V1 to V3≥30ms (0.03s).
• Abnormal Q wave in I, II, aVL, aVF or V4 to V6 in two contiguous leads and at least 1 mm deep.

A normal ECG does not exclude the diagnosis of AMI in the presence of a characteristic clinical picture.

Given the difficulty in interpreting the ECG in patients with LBBB, it is considered useful that they have previous records or descriptive reports thereof to facilitate clinical evaluation in the event of suffering an ACS (Alpert JS, 2000).

ECG leads in which changes occur in the ST segment help to know the location of ischemia and the affected coronary artery.

• Previous face: V2 to V4.
• Septal antero: V1 to V3.
• Apical or lateral: V4 to V6.
• Lower face: II, III and aVF.
• Posterior face: ST depression in V1 and V2 with pointed T waves.

How is it treated

A clinical history, physical examination and ECG will be performed on all patients with chest pain in whom the diagnosis of ACS is suspected. Early diagnosis and urgent transfer are keys to survival. Early therapy decisively improves prognosis.

Out-of-hospital initial phase

Monitoring whenever possible. In the first hours, more than 80% of AMIs present a generally severe arrhythmia such as ventricular fibrillation or pulseless ventricular tachycardia, the main cause of death in these situations. Rapid cardioversion with a defibrillator helps save lives. Thus, monitoring and preparation of the defibrillator should be performed upon receiving the patient (SIGN 94, 2007). Notify the Emergency Coordinating Center (Telephone 061 and 112) requesting a medical ambulance to transfer the monitored patient to the nearest hospital center (Antmann EM, 2004).

Chewed acetylsalicylic acid 250-300 mg (preferably without gastric protection to improve absorption). It should be administered immediately as long as there are no contraindications (active ulcer, aspirin allergy or anticoagulation) (Antmman EM, 2004; Alpert JS, 2000; SIGN 97, 2007; EBM, 2006).

Sublingual nitroglycerin at a dose of 0.4-0.8 mg if the dose needs to be repeated at 5 ‘intervals up to four times. It is suitable for angina and hypertension does not have a significant effect on mortality (NZMJ, 2005). Contraindicated if hypotension exists (TAS <90 mmHg).

Morphic chloride with an initial dose of 2.5-5 mg. IV (or SC if IV is not possible), treatment can be repeated up to 3 times using 2.5-5 mg per dose (Fox KA, 2006). For administration, a 10 mg ampoule (1 cc) can be diluted in 9 cc of saline.

35% oxygen in patients with hypoxia (oxygen saturation <90%) or pulmonary edema. There is no evidence that routine administration of oxygen to all ACS patients improves clinical outcomes and reduces infarct size. In experimental animals, oxygen therapy has been shown to limit myocardial damage and reduce ST elevation (SIGN 94, 2007).

Hospital treatment

Acetylsalicylic acid and Clopidogrel: AMI patients benefit from the association of 300 mg of acetylsalicylic acid with 75 mg of clopidogrel daily. It is more effective than aspirin alone used in the first 12 hours after AMI. Aspirin treatment should be maintained long-term in all ACS patients (SIGN, 2007).

Glycoprotein IIB / IIA receptor antagonists: The use of intravenous administration in the treatment of patients with high-risk ACS has been demonstrated, especially if percutaneous coronary intervention is performed (Antmann AM, 2004).

Low molecular weight heparin: its use is recommended in the first 48 hours, it reduces reinfarction rates in cases of ACS with electrocardiographic changes and elevation of cardiac markers (SIGN, 2007).

Beta-blockers: they are the first-line antianginal agents in the treatment of patients with ischemic heart disease and in secondary prevention. Although its early use after ACS may be associated with a slight benefit in low-risk and hemodynamically stable patients, it has been found that it is better to wait before starting oral use (Van de Werf F, 2008).

Angiotensin-converting enzyme (ACE) inhibitors: the beneficial effect of ACE inhibitors introduced in the first 24 hours after infarction has been demonstrated as long as there are no contraindications, as well as their long-term use in all patients with AMI regardless that they have ventricular dysfunction or heart failure (SIGN, 2007).

Angiotensin receptor blockers (ARBs): indicated in patients who do not tolerate ACE inhibitors due to their side effects. Patients with complicated AMI and left ventricular dysfunction or heart failure should start long-term treatment with ARA II if they do not tolerate ACE inhibitors (SIGN, 2007).

Antialdosteronics: patients with AMI and ventricular dysfunction (ejection fraction ≤40%) in the presence of diabetes or signs of heart failure should initiate long-term treatment with spironolactone (SIGN 94, 2007) or due to its effect on reduction of morbidity and mortality (Van de Werf F, 2008) monitoring in both cases the serum concentration of creatinine and potassium.

Statins: Studies confirm that early initiation of high-dose statin treatment is safe and beneficial in the short term on the prevention of recurrent ischemia and mortality (Van de Werf F, 2008; Afilalo J, 2007; Canon CP) . Patients with ACS before being discharged from the hospital must have started long-term treatment with statins.

Nitrates: The beneficial effect of nitrate use in the initial phase of STEMI has not been demonstrated and is therefore not recommended. Nitrates remain the first-line treatment for angina (Van de Werf F, 2008).

Calcium antagonists: they have not shown benefit in patients with AMI, therefore their routine use is not recommended (SIGN, 2007).
Blood glucose control, diabetic patients with AMI and poorly controlled blood glucose should receive intensive treatment with insulin, it has been shown that adequate control of blood glucose levels reduces mortality compared to standard oral treatment (Van de Werf F, 2008 ; SIGN , 2007 ; Antman EM, 2004 ).

Early psychological intervention: Patients who have suffered an AMI benefit from an early psychological evaluation in order to address erroneous beliefs about their health problem. This is part of the cardiac rehabilitation program and must be a continuous process in the patient’s evolution, providing him and his family with the information they need based on their needs (SIGN, 2007).

Restoration of coronary flow

Pharmacological (fibrinolysis) or mechanical reperfusion by percutaneous coronary intervention (PCI) should be performed during the first 12 hours of the onset of symptoms.

CPI in patients with ACS and ST elevation performed on time in experienced cardiology services is more effective in restoring patency, reducing the risk of reocclusions, improving residual function of the left ventricle and obtaining better clinical results than the fibrinolytic treatment. Stenting in STEMI patients reduces the need for revascularization of the target vessel, but is not associated with a significant reduction in death or reinfarction rates compared to primary angioplasty.

Drug-eluting stents reduce the risk of reoperation compared to uncoated stents, without altering the risk of stent thrombosis, recurrent myocardial infarction, and death (Erne P, 2007; Nordmann AJ, 2007). It has been estimated that the delay time of PCI that can reduce its advantages compared to fibrinolytic treatment varies between 60 and 120 minutes (Van de Werf F, 2008).

After angioplasty, treatment with clopidogrel should be continued for a period of 3 to 6 months, combined with aspirin to prevent thrombosis and restenosis, stent endothelialization is a slow process.

Prehospital thrombolysis is effective and should be done when PCI cannot be performed in the first 90 minutes in patients with STEMI.

Thrombolysis will be evaluated in the following circumstances: Existence of symptoms suggestive of AMI and ECG abnormalities, even without biochemical markers. Expected transfer time to access the hospital greater than 30 minutes. Absence of contraindications. Less than 2 hours from the onset of symptoms. Availability of trained personnel and prior agreement with the reference hospital center.

Absolute contraindications for thrombolysis: hemorrhagic stroke or stroke of unknown origin at any time, ischemic stroke in the preceding 6 months, trauma or neoplasm in the central nervous system during the previous three weeks, gastrointestinal bleeding in the last month, known bleeding disorder, dissection aortic, non-compressible punctures (such as liver biopsy and lumbar puncture).

Relative contraindications: ACVA or TIA in the previous six months, oral anticoagulant treatment, pregnancy or the first week postpartum, refractory hypertension, advanced liver disease, infective endocarditis and active peptic ulcer (Van de Werf F, 2008).

Patients with STEMI within six hours of the onset of symptoms and in whom thrombolysis has failed will be considered rescue ICP. Salvage PCI has been shown to be feasible and relatively safe, reducing the occurrence of events in six months, compared to non-intervention after failed fibrinolysis, has been associated with a significant reduction in heart failure, reinfarction and a tendency to decrease mortality although with an increased risk of acva and bleeding (Van de Werf F, 2008).

Surgical revascularization: the success of fibrinolysis and PCI has led to a considerable decrease in emergency surgery that has been limited to situations in which a reperfusion strategy can be considered in patients with STEMI such as (NZG, 2005): Failure of PCI with persistence of symptoms and hemodynamic compromise. Severe mitral regurgitation due to rupture of the papillary muscles or need for septum rupture repair.
Patients who are not candidates for reperfusion, with ischemia refractory to medical treatment. Presence of cardiogenic shock 36 hours after STEMI, with left trunk injury or severe coronary artery disease of the three vessels in the first 18 hours of shock. Patients with stenosis of 50% of the trunk of the left coronary artery.

Out-of-hospital care after myocardial infarction

Secondary prevention is the set of interventions that are recommended to improve survival and quality of life, decrease recurrences and avoid complications in the patient with coronary heart disease (Antmann EM, 2004; Alpert JS, 2000). Between 8 and 10% of AMI patients will have a recurrent heart attack during the first year (Van de Werf F, 2008).

All patients with coronary heart disease are chronic patients who are included in the high-risk group for cardiovascular disease. They should receive individualized recommendations on a healthy diet, weight control, tobacco cessation and the practice of physical exercise.

Diet. A varied diet with fruit, vegetables, cereals, two weekly servings of fish, one of blue fish, lean meat and skimmed dairy products, will be recommended. If there is hypertension, they should reduce their salt intake as much as possible. Decreased overweight if you are looking for a BMI <25, weight loss can improve risk factors related to obesity. Intake of moderate amounts of alcohol has a protective effect on coronary heart disease. Brief interventions are recommended to reduce alcohol consumption in cases of excessive consumption (SIGN 97, 2007).

Tobacco. The snuff has a great protombótico effect. Patients who quit smoking reduce mortality by a third compared to those who continue to smoke (Van de Werf F, 2008).

Physical activity. Physical exercise as part of a coronary rehabilitation program was associated with a 26% reduction in the cardiac mortality rate in patients with coronary heart disease (Van de Werf F, 2009). Physical exercise of moderate intensity is recommended, at least for 30 minutes, 5 days a week (Briffa TG, 2006).

Pharmacotherapy

Acetylsalicylic acid. A daily dose of 75-150 mg should be recommended to all patients with coronary heart disease with or without symptoms, provided there are no contraindications. The highest protection with the minimum risk would be achieved with a dose of 81mg / d (Campell CL, 2007). Clopidogrel, at an equally effective dose of 75 mg / d, will be reserved for cases where there are contraindications to the use of acetylsalicylic acid (Snow V, 2004). The most important side effect is bleeding.

Beta blockers. They reduce morbidity and mortality (Van de Werf F, 2008; Snow V, 2004). Its effect is adequate when the resting heart rate is around 60 bpm. The most indicated are carvedilol, bisoprolol and metoprolol.

Lipid lowering drugs People with established cardiovascular disease should receive lipid lowering treatment preferably with statins. Its use is supported by cost effectiveness studies (Ward S, 2007; Snow V, 2004). The risk / benefit ratio for treatment with high doses will be assessed.

Calcium antagonists. The use of Verapamil and Diltiazem may be indicated when there are contraindications to the administration of beta-blockers, especially if there is COPD. They will be used with caution in the presence of LV dysfunction.

ACEI. Its effect as a vascular protector makes it recommended for all patients who have suffered AMI. Its use will be considered in patients with atherosclerosis but its long-term use is not considered essential in patients with normotensive ischemic heart disease and who do not have heart failure or impaired LV systolic function. ACE inhibitors can be substituted for BRA when there are side effects related to their use.

Nitrates. They have not demonstrated their influence on mortality. They will be recommended as a base treatment in patients with anginal pain (SIGN 94, 2007).

Antihypertensive treatment

If the blood pressure figures are equal to or greater than 140/90, antihypertensive treatment should be added. If there is also diabetes or kidney failure, antihypertensive treatment will be administered with lower values: 130/80.

Tips for alarm symptoms

All patients with coronary heart disease and their families will be trained in the need to recognize the symptoms of acute disease and the measures to be taken. They should have nitroglycerin to use in case of anginal pain, with the recommendation to take a dose when symptoms begin, repeat if necessary after five minutes and if they do not disappear within the next 5 minutes (15 minutes in total) they should ask for help in an emergency department (SIGN 94; 2007; SonW V, 2004). Nitrites will not be administered if PDE5 inhibitors (sildenafil or vardenafil) have been used in the previous 24 hours, 48 ​​hours in the case of tadalafil (see erectile dysfunction guide)