ACUTE MYOCARDIAL INFARCTION: TYPES, RISK FACTORS, SYMPTOMS - MEDICINE - 2025

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

According to the 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 poor diet plays a fundamental role in the appearance of these pathologies.

Crushing chest pain characteristic of acute myocardial infarction

However, it has been found that coronary arteries that undergo high-grade stenosis due to atherosclerosis, slowly, 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 all the 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 pre-hospital care took a leading role in combating this pathology.

Types

No 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. In other words, the lesion did not reach the epicardium and, therefore, did not appear on the electrocardiogram.

With ST segment elevation

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

Risk factor's

Various studies around the world have been conducted to decipher the preventable and non-preventable 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 non-modifiable.

Non-modifiable risk factors

• Age: age is considered a risk factor only because they are people who have been exposed to other cardiovascular risk factors for a longer time, this risk increasing considerably after 65 years of age.
• Biological sex: it has been shown that males are 2 to 3 times more likely to suffer from cardiovascular diseases leading to AMI. However, mortality in women with AMI is almost 50% higher than in men.
• Heredity: the existence of first-degree relatives with diagnoses of AMI, HTN and DM are factors seriously influencing the risk of suffering from any of the pathologies.

Modifiable risk factors

• Sedentary lifestyle: sedentary lifestyle contributes to obesity and dyslipidemias.
• Poor diet: the hyperlipidic 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 facilitate the production of atheroma plaques. They also affect the respiratory system in such a way that the supply of oxygen to cells decreases. Lastly, it promotes blood viscosity by increasing systemic blood pressure
• Drug use: cocaine, mainly, favors the appearance of ventricular dysfunction, malignant arrhythmias. Similarly, it leads to stenosis of the coronary arteries.
• Poor control of triggering pathologies: poor control of systemic arterial hypertension and diabetes mellitus result in an increased risk of suffering from AMI.
• Stress: stress activates the central nervous system and the endocrine system. In turn, this stimulates the release of adrenaline and the activation of the hypothalamic-pituitary-adrenal axis. Consequently, cortisol rises.

This increases blood viscosity at the expense of the number of platelets and red cells. The heart rate and the contractile force of the myocardium are increased. In addition, there is a greater dilation of the coronary vessels.

This makes the cardiovascular system vulnerable to cardiac ischemia.

Symptoms

Anxiety or restlessness

Acute myocardial infarction can start with a feeling of anxiety and restlessness. The patient may try, unsuccessfully, to ease the pain by changing posture and stretching.

Deep chest pain

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

The pain is described as oppressive in nature. The patient inevitably raises his claw-shaped hand to the site of pain, on the left side of the chest.

Most visible symptoms

It is frequently associated with sweating, paleness, cold extremities, nausea, weakness, and a feeling of impending doom. 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 attached if the infarction is anterior and hypotension, and bradycardia if it is inferior.

Its duration is greater than 30 min. This clearly suggests the diagnosis of AMI, unlike angina, whose pain is not persistent. Another difference with angina is that the pain is not relieved by nitrates.

Diagnosis

The diagnosis is clinical, enzymatic, and electrocardiographic.

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

Stage 1

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

Stage 2

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

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 few hours or days.

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

The enzymatic diagnosis is made because necrotized 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 due to 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 infarcts of small extent.

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

Treatment

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 PO.
5. Clopidogrel 300 mg PO.
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 crackles. 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 PO.

References

1. A. Ciruzzi, H. Advanced age and risk factors for acute myocardial infarction. Medicine (B. Aires) vol.62 no.6 Buenos Aires Nov./Dec. 2002. Recovered from: scielo.org.ar
2. Cardiovascular Disease (10-year risk). Framingham Heart Study. Recovered from framinghamheartstudy.org
3. Pabón, JH Clinical-Medical Practice Consultation. 2nd Edition. (2014) Medbook Editorial Médica. Ischemic Heart Disease. Acute Myocardial Infarction. Page 87 - 89.
4. Rodríguez García, L. Diagnosis Medical Treatment. Marbán Books. Green Book. ST-Elevation Acute Coronary Syndrome (STEACS), Pages 95-99.
5. Harrison's Principles of Internal Medicine. 18th Edition. Mcgraw Hill Publishing House. Vol. 2. Chapter 245: ST-segment elevation myocardial infarction, pp. 2021 - 2034.