Ischemic Heart Disease

Study guide:

Definitions:  

  • Ischemic heart disease is a disease in which the blood supply is reduced toward heart tissue causing it to infarct.

Pathophysiology:

Narrowing of coronary arteries can be by several risk factors (see Figure 1).

Dyslipidemia considered one of the most common cause of angina.

High cholesterol level in the blood is transferred by LDL, Low-Density Lipoprotein, and attached to endothelium of blood vessels, and by attachment, cholesterol enters the tunica intima layer of blood vessel to form a plaque and causes atherosclerosis that will reduce blood flow and decrease perfusion of heart tissues, ischemia (see Figure 1.2).

A
B

Figure 1.2 A. Monocytes transferred to tunica intima to phagocytize cholesterol and become Foam cells. Foam cells necrotized and released many growth factors that lead to migration and growth of smooth muscles in which will lead to formation of plaque. B. Histological appearance of blood vessels shows narrowed lumen due to plaque formation.

Figure 1.1 Traditional risk factors is most common in patients with CAD. Non-Traditional factors are less likely to be found in patients with CAD.

Classification :

  1. Stable Angina: The plaque is still intact. The pain induced by exertion and relived with rest and nitroglycerin.​

  2. Prinzmetal Angina: angina that does not have a link with physical activates rather it has been linked with vasospasm with stable angina, and it happens usually while sleeping and at night, and triggered by alcohol, cocaine, and nicotine.

  3. Unstable Angina: the plaque rupture causing thrombus formation that blocks the artery. The pain will not be relieved by rest but could improve with nitroglycerin, and it could lead to Myocardial Infarction (MI) (see Figure 2).

Figure 2. Showing different stages and levels of plaque development until rupture.

Classification :

  1. Stable Angina: The plaque is still intact. The pain induced by exertion and relived with rest and nitroglycerin.​

  2. Prinzmetal Angina: angina that does not have a link with physical activates rather it has been linked with vasospasm with stable angina, and it happens usually while sleeping and at night, and triggered by alcohol, cocaine, and nicotine.

  3. Unstable Angina: the plaque rupture causing thrombus formation that blocks the artery. The pain will not be relieved by rest but could improve with nitroglycerin, and it could lead to Myocardial Infarction (MI) (see Figure 2).

Clinical Presentation

          -Severe Pain: sudden and pressure-like pain in the chest that usually radiate to the back, shoulders, neck, and jaw.

          -Tachypnea, Dyspnea, and Sweeting: decrease oxygen reaching the heart muscles leads to activation of sympathetic nervous                system.

          -Gaining Weight: a sign indicates decrease in physical activities due to exertional pain with physical effort.

          -Nausea and Vomiting

          -Weakness and Dizziness

Clinical Presentation

          -Severe Pain: sudden and pressure-like pain in the chest that usually radiate to the back, shoulders, neck, and jaw.

          -Tachypnea, Dyspnea, and Sweeting: decrease oxygen reaching the heart muscles leads to activation of sympathetic nervous                system.

          -Gaining Weight: a sign indicates decrease in physical activities due to exertional pain with physical effort.

          -Nausea and Vomiting

          -Weakness and Dizziness

Diagnosis

  • ECG: it is highly sensitive within 6 hours of angina that will demonstrate many details that show in ST segment.                             It’s divided into:

       1-ST-Segment Elevation Myocardial Infarction (STEMI): indicates complete occlusion of artery and transmural infarcts.

       2-Non ST-Segment Elevation Myocardial Infarction (NSTEMI): indicates partial occlusion and sub-endocardial infarcts.

          See Figure 3.1 to more details

Figure 3.1 Coronary arteries moves in epicardial layer, and partial blockage on one of them leads to decrease supply to the distal area, which is sub-endocardial, and utilizes oxygen and nutrition by the proximal areas. In case of fully occlusion, all the layer will be infarcts, it called transmural infarcts.

-Echocardiogram: Echo could show some muscle wall abnormality while contracting due to infarct areas.

-Stress Echo and ECG: used with stable angina patients by recording and imaging their heart beats while performing a physical           effort.

-Coronary Angiography: used to detect which artery is affected and considered as the gold standard for all angina patients.

-Lab tests: are done to look for protein markers released after the infarction

  1. Troponin I: unique marker for heart muscles, released after 4 hours and reaches its peak in about 24 hours. Also presents for 7-10 days after the attack.

  2. CK-MB: specific to cardiac muscles, raised after 6-12 hours reaching its peak in 24 hours and stay about 48 hours. Used to indicate reinfarction.

       See Figure 3.2 for more details

Figure 3.2 showing the peak of both Troponin I and CK-MB in relation to the onset of MI

ECG Localization of ST Segments Changes:

  • Complications

       - Arrhythmia: happens after 24 hours of Myocardial Infarction (MI) due to interruption of cardiac conduction

       -Pericarditis: in 1-3 days due to inflammatory mediators that are released by neutrophils.

       - Myocardial rupture: between 3-14 days by the macrophage degenerative enzymes that are released to clean the infarcted area.

       -Heart Failure: after several months because of heart inability to decompensate to restore the tissue damage that leads to failure.

  • Management

The aim of treatment is reestablish blood supply as soon as possible.

1-Urgent management: MONA and several other drugs are used

    -Morphine: relief the pain

    -Oxygen: improves the patient even though the lungs are not affected.

    -Nitroglycerin: vasodilator.

    -Aspirin:  antiplatelet agent decrease post MI mortality. Also, it shows high efficacy when combined with clopidogrel.

    -Beta-Blockers: to decrease heart rate and decrease its blood needed.

    -Anti-arrhythmic drugs

2-Surgical and Procedural intervention: aims to reopened the occluded artery guided by diagnostic tools

    -Angioplasty: intervention used to dilate the artery by balloon.

    -Percutaneous coronary intervention: used to put a stent to hold the artery physically opened.

3-Prevention: the aim at that level is to inhibit any reinfarction

    -Statin: lower cholesterol level has shown to decrease mortality.

    -Antithrombotic and anticoagulation drugs: could lead to bleeding tendency, but it prevents further               thrombosis.

    -Control blood pressure: risk factor for bleeding and thrombose formation.

    -Control glucose levels

    -Smoking cessation: due to its highly linked to blood pressure and inducing vasospasm.

References:

- First Aid USMLE STEP 1 – Section III. Cardiovascular

- First Aid Basic Science, 2nd Edition – Chapter 1. Cardiovascular

- Gray’s Anatomy, 3rd Edition – Chapter 3. Thorax

- Range and Dale’s Pharmacology, 7th Edition – Section 3, Chapter 21. The Heart

- Risk Factor of Coronary Artery Disease by F Brian Boudi - https://emedicine.medscape.com/article/164163-overview

- Pathogenesis of Atherosclerosis - http://sphweb.bumc.bu.edu/otlt/MPH-Modules/PH/PH709_Heart/PH709_Heart3.html

- Figure 2 - https://www.dreamstime.com/stock-illustration-atherosclerosis-formation-healthy-artery-unhealthy-arteries-showing-step-step-how-plaque-developing-very-detailed-image51911629

First author:   Abdulrahman Alhassan


Reviewed by:  Osama Wadaan


Format Editor:  Noura Alsubaie 

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