Pharmacotherapy/Treatment Of Acute Myocardial Infarction

Acute Myocardial Infarction (Heart Attack)

Acute myocardial infarction (AMI) is a medical condition popularly called heart attack. AMI is coined from Latin words of which "myocardial" is the muscular tissue of the heart. The "infarction" means death of tissues due to blockage of blood to the tissue.

AMI occurs when blood flow to the heart muscle is blocked abruptly. A part of the heart muscles start to die called cardiac ischemia causing in most cases angina pectoris (pain in the chest). When the tissue of part of the heart affected completely dies, it is called heart attack. Silent ischemia occurs in about 25 percent of attacks but can be detected in ECG. Silent ischemia is common in diabetes patients.

Cause Of Acute Myocardial Infarction

The left anterior descending coronary artery supplies blood flow to the interventricular septum, anterolateral wall, and ventricular apex of the heart. 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.

Read Also: Pharmacotherapy of angina pectoris

In AMI, any of the coronary arteries can be blocked by plaque buildup from cholesterol or cellular waste and products and secondly by spasm of the artery. Cholesterol buildup is called atherosclerosis.

Pathophysiology Of AMI

Atherosclerosis is caused by fat and cholesterol in the arteries. Low density lipoprotein (LDL), saturated fat and trans fat come together and form small and big plaque on the walls of the arteries. Blood platelets may stick to the plaque and buildup over time. The cover is hard while the inside is soft. This restricts blood flow through.

During a heart attack, a plaque can rupture and spill cholesterol and other substances into the bloodstream. Atherosclerotic 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. If the clot is large, it can block blood flow through the coronary artery, starving the heart of oxygen and nutrients (ischemia).

There are two types of blockage. They are a complete or partial blockage of the coronary artery. A complete blockage means you've had an ST elevation myocardial infarction (STEMI) why a partial blockage means you've had a non-ST elevation myocardial infarction (NSTEMI). Diagnosis and treatment might be different depending on the type.

Another cause of a heart attack is a spasm of a coronary artery that shuts down blood flow to part of the heart muscle. Using tobacco and illicit drugs, such as cocaine, can cause a life-threatening spasm.

Symptoms Of AMI

1. The major symptom is chest pain more severe and long lasting than angina pectoris not relieved by nitroglycerin

2. Shortness of breath

3. Pressure or tightness in the chest

4. Pain radiating to the back, jaw and other areas of the upper body that last more than a few minutes. In some cases, it goes away and comes back especially after rest.

5. Sweating

6. Nausea and Vomiting

8. Anxiety

9. Cough

10. Dizziness

11. Fast heart beat

Symptoms In Women

Sometimes, most women have symptoms that may include;

1. Jaw pain

2. Upper back pain

3. Lightheadedness

4. Flu like symptoms

The pain of heart attack is likened to a fiat fist enclosing and squeezing the chest. If it is mild, it is mistaken for a heartburn or angina. Belching or antacid consumption may offer limited relief giving false interpretation as indigestion symptom. The pain may be constant or intermittent. Angina is one of the major early signs.

Risk Factors

1. Hypertension which damage arteries

2. High cholesterol

3. High triglycerides

4. Diabetes

5. Obesity

6. Smoking

7. Age (above 55 for women and above 45 for men)

8. Family history

9. Stress

10. Lack of exercise

11. Drugs (cocaine)

12. History of preeclampsia

13. Autoimmune disease like rheumatoid arthritis

Complications

1. Heart failure

2. Arrhythmias

3. Stroke

4. Cardiac arrest

Diagnosis Of AMI

Cardiac 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 myocardium and is not used clinically; it quickly rises and normalizes. High-sensitivity troponin has recently been approved for use in the United States 

The electrical activity is measured using an electrocardiogram. Others are hypertension, heartbeat, stress test, angiogram with coronary catheterization which is used to look for blockages in the arteries or echocardiogram that help identify areas of the heart that are not working.

AMI is diagnosed when two of the following criteria are meant;

1. Symptoms of ischemia

2. New ST segment changes or a left bundle branch block (LBBB)

3. Presence of pathological Q waves of the echocardiogram (ECG)

4. Imaging study following new regional wall motion abnormality

5. Presence of an intracoronary thrombus at angiopathy or altetophy

Pharmacotherapy/Treatment Of Acute Myocardial Infarction

All patients with STEMI and NSTEMI require immediately chewed aspirin 160 mg to 325 mg. Furthermore, the patient should have intravenous (IV) access and oxygen supplementation (2 L by nasal cannula) if oxygen saturation is less than 91%. This should be used with continuous single-lead ECG monitoring. Opioids may be used for pain control in addition to sublingual nitroglycerin if the blood pressure is adequate and IV drip.

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 (75-81 mg daily), 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.

Dose

Clopidogrel should be given 300-600mg orally once daily

Pragugrel is 600mg daily

Ticagrelar given 180mg once daily

Management Of Heart Attack

Angioplasty is inserting a balloon into a blocked artery and then inflating it to the right size. To allow blood flow through, the balloon is removed after inserting a stent.

Coronary artery bypass graft (CABG) is another method used. It involves rerouting veins and arteries that are good to and out of the heart so that blood can flow around the blocked arteries. This is important immediately or after some few days.

Prognosis

Recovery is difficult as the heart doesn't recover fully. It can lead to poor blood circulation to other parts of the body, arythnisasis, cardiac arrest or sudden cardiac death, cardiogenic shock, death.

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Acute MI still carries a high mortality rate, with most of the 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:

1. Diabetes

2. Advanced age

3. Prior MI, peripheral vascular disease (PVD), or stroke

4. Delayed reperfusion

5. Diminished ejection fraction (the strongest predictor)

6. Presence of congestive heart failure (CHF)

7. Elevated C-reactive protein and BNP levels

8. Depression

Adapted from Mechanic OJ, Grossman SA. Acute Myocardial Infarction. [Updated 2020 Nov 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan.