Acute myocardial infarction: types, risk factors, symptoms

He acute myocardial infarction (AMI) consists of the necrosis of cardiac myocytes caused by prolonged ischemia, due to the sudden decrease of the blood flow of the coronary arteries. This creates an imbalance between the contribution and the oxygen demand of the myocardium.

According to WHO, cardiovascular diseases are the leading cause of morbidity and mortality in the world. 80% of these deaths occur in underdeveloped countries. This validates the premise that bad nutrition it represents a fundamental role in the appearance of these pathologies.

Oppressive thoracic pain characteristic of acute myocardial infarction

However, it has been shown that coronary arteries that undergo high-grade stenosis due to atherosclerosis, in a slow way, do not usually trigger an acute myocardial infarction.

This happens because it allows the adaptation of collateral vessels that compensate for the decrease in blood flow. Of the totality of patients with acute myocardial infarction, studies reveal that 50% die before receiving hospital care.

Therefore, the prevention of cardiovascular risk factors and the emphasis on prehospital care adopted a leading role in combating this pathology.

Types

Without ST segment elevation

Acute myocardial infarction without ST segment elevation refers to an area with injury and cell death that was revascularized by physiological mechanisms. That is, the lesion did not reach the epicardium and, therefore, did not appear on the electrocardiogram.

With ST segment elevation

In contrast, acute myocardial infarction with ST segment elevation refers to an area of ​​myocardial tissue that was not reperfused. The lesion occupied the entire thickness of the muscular wall, affected the epicardium and, therefore, is reflected in the electrocardiogram.

Risk factor's

Various studies around the world have been carried out around deciphering the preventable and nonpreventable causes of diseases. Special attention has been paid to acute myocardial infarction due to its high mortality rate.

Among them, the Framingham study is one of the most representative, although it is still under development. These causes are considered risk factors. They are classified as modifiable and not modifiable.

Non-modifiable risk factors

• Age : l Age is considered a risk factor only due to the fact that they are people who have been exposed for a longer time to the rest of the cardiovascular risk factors, increasing this risk considerably after 65 years.
• Biological sex : s e has shown that the male sex is 2 to 3 times more likely to suffer from cardiovascular diseases that culminate in an AMI. However, mortality in women with AMI is almost 50% higher than male mortality.
• Heritage : the The existence of first degree relatives with diagnoses of AMI, HBP and DM are serious factors influencing the risk of suffering from any of the pathologies.

Modifiable risk factors

• Sedentary : sedentary lifestyle contributes to obesity and dyslipidemias.
• Bad nutrition : Hyperlipideal or hyperglycemic diet promotes obesity, the formation of atherosclerotic plaque and the manifestation of cardiac ischemia.
• Smoking : in 1960, the Framingham study showed that nicotine and carbon dioxide facilitates the production of atheromatous plaques. They also affect the respiratory system so that the oxygen supply to the cells decreases. Finally, it favors blood viscosity by increasing systemic blood pressure
• Consumption of drugs : Cocaine, mainly, favors the appearance of ventricular dysfunction, malignant arrhythmias. Similarly, it leads to stenosis of the coronary arteries.
• Bad control of triggering pathologies : poor control of systemic hypertension and diabetes mellitus result in an increased risk of AMI.
• Stress : stress activates the Central Nervous System and the endocrine system. In turn, this encourages the release of adrenalin and activation of the hypothalamic-pituitary-adrenal axis. As a result, the cortisol .

This increases the blood viscosity at the expense of the number of platelets and red blood cells. The heart rate and the contractile force of the myocardium increases. In addition, greater dilatation of the coronary vessels occurs.

This makes the cardiovascular system vulnerable to cardiac ischemia.

symptom

Anxiety or restlessness

Acute myocardial infarction can start with a sensation of anxiety and restlessness The patient may try, without success, to appease the pain by changing position and stretching.

Deep thoracic pain

The most notorious clinical manifestation of an AMI is deep chest pain. This can radiate to epigastrium (which makes some patients think it is indigestion), neck, back, jaw and / or upper limbs, mainly the left upper limb.

Pain is described as oppressive. The patient inevitably takes the claw-like hand to the site of pain on the left side of the chest.

Most visible symptoms

Frequently, it is associated with diaphoresis, paleness, coldness in the extremities, nausea, weakness and imminent death sensation. Similarly, it is related to dyspnea and syncope.

Blood pressure

Blood pressure may be normal in the first hour. But usually tachycardia and arterial hypertension are added if the infarct is in the anterior plane and hypotension, and bradycardia if it is inferior.

Its duration is greater than 30 min. This strongly suggests the diagnosis of AMI, unlike an angina, whose pain is not persistent. Another difference with angina is that the pain does not relieve with nitrates.

Diagnosis

The diagnosis is clinical, enzymatic and electrocardiographic.

The clinical diagnosis will depend on the symptoms referred to above, accompanied by a correctly performed anamnesis. Electrocardiographically, several changes are visualized.

Stadium 1

Changes in the T wave occur. This becomes high and peaked (hyperacute T waves).

Stadium 2

A few moments later, the ST segment elevation begins. At this stage it is less than 50% of the amplitude of the R wave if there is a QRS or RR QRS configuration.

Stage 3

The ST segment elevation is greater than 50% of the R wave. The T wave becomes negative and Q waves appear in the same location in the next hours or days.

If the myocardium reperfers, the ST segment elevation disappears. But the T waves remain inverted. The Q waves may or may not disappear.

The enzymatic diagnosis is made because the necrotic myocytes release proteins into the circulation such as myoglobin, CK, CK-MB, Troponins (I and T), aspartate aminotransferase and lactate dehydrogenase.

Troponins are the ideal biomarkers for their sensitivity and specificity. They can be detected in plasma from 3 - 4 hrs.

Total CK and CK-MB are used as a biochemical marker of myocardial necrosis, but they have low cardiospecificity and sensitivity. Therefore, they can miss small infarcts.

CK-MB is the isoform of CK specific for muscle and cerebral cortex. It may be increased even when the CK is normal.

Treatment

The treatment must be effective and timely to reduce the probability of death in the first 24 hours. The following steps must be followed:

1. Place the patient in the Coronary Care Unit, with a nearby defibrillator if necessary.
2. 12-lead continuous electrocardiographic monitoring.
3. Peripheral venous route.
4. Aspirin 300 mg VO.
5. Clopidogrel 300 mg VO.
6. Sublingual nitroglycerin if there is no hypotension.
7. Morphine 2-4 mg iv slow every 5-30 min up to a maximum dose of 25 mg.

When confirming ST elevation:

1. Enoxaparin at a dose of 1 mg / kg / SC.
2. B-blockers, only use if there are no crackers. In case of crackles, use Furosemide 20-40 mg BID.
3. Reperfusion: Streptokinase at a dose of 1.5 million units in 60 min.
4. Atorvastatin 80 mg VO.

References

1. A. Ciruzzi, H. Advanced age and risk factors for acute myocardial infarction. Medicine (B. Aires) v.62 n.6 Buenos Aires nov./dic. 2002. Retrieved from: scielo.org.ar
2. Cardiovascular Disease (10-year risk). Framingham Heart Study. Retrieved from framinghamheartstudy.org
3. Pabón, J. H. Practical Clinical-Medical Consultation. 2nd Edition. (2014) Medbook Medical Editorial. Ischemic heart disease Acute Myocardial Infarction. P 87 - 89.
4. Rodríguez García, L. Diagnosis Medical Treatment. Marbán Books. Green Book Acute Coronary Syndrome with ST elevation (STEACS), p. 95 - 99.
5. Harrison Principles of Internal Medicine. 18th Edition. Mcgraw Hill. Vol. 2. Chapter 245: Myocardial infarction with ST segment elevation, p. 2021 - 2034.