Overview
Ischemic heart disease refers to a group of syndromes related to myocardial ischemia caused by an imbalance between myocardial oxygen demand and the blood supply. The most common cause is atherosclerosis of the coronary artery which decreases the blood flow to the myocardium. In most cases, the syndromes of IHD are the last manifestations of coronary atherosclerosis accumulated over many years (maybe beginning even in childhood). Clinical manifestations of coronary atherosclerosis may occur at any age but are more common in older adults. Coronary atherosclerosis risk factors are very similar to ischemic heart disease, such as
- Hypertension
- Diabetes
- Smoking
- High levels of low-density lipoprotein cholesterol
The imbalance between oxygen demand and blood supply arises as a complication of pre-existing atherosclerotic occlusion of coronary arteries and new superimposed thrombosis or vasospasm.
Types of ischemic heart disease
Angina pectoris
Angina Pectoris is intermittent chest pain caused by transient and reversible myocardial ischemia. This ischemia is usually a result of stenosis of one or more of the coronary arteries.
Typical or stable angina
Angina refers to chest pain, that is reversible, and the term stable or typical stands for no chest pain at rest instead pain develops with exertion or emotional stress. When there is atherosclerosis in the coronary artery, that reduces the blood flow to the myocardium, but there will be no problem at rest, however, when there is exertion, the coronary artery can not provide sufficient blood to the myocardium, hence there will be a reversible injury to the myocardium resulting in chest pain. Stable angina causes reversible injury to the myocytes and the hallmark of reversible injury is cellular swelling. Stable angina occurs when there is greater than 70% of stenosis in the coronary artery, and less than 70% of stenosis is asymptomatic even with exertion.
Stable angina lasts less than 20 minutes as that is the limit the myocardium can stand with a lack of blood supply, and if this pain lasts more than 20 minutes, the myocardium will undergo irreversible injury and eventually die. patients with stable angina present with pain radiating to the left arm or jaw, diaphoresis or sweating, and shortness of breath.
EKG shows ST-segment depression because the heart has three layers (epicardium, myocardium, and endocardium). The coronary artery begins at the epicardium and eventually submerges to supply blood to all the layers of the heart, and when coronary artery stenosis reduces blood flow, the region below the endocardium (which is most susceptible to ischemic injury) become damaged, which is called subendocardial ischemia, and the key finding of subendocardial ischemia is ST-segment depression on the EKG.
Stable angina is relieved by rest and nitroglycerin which can vasodilate both arteries and veins.
Unstable angina
Unstable angina refers to chest pain that occurs either at rest or with less exertion and it causes reversible injury to the myocardium. It occurs due to the rupture of an atherosclerotic plaque with thrombosis, which leads to the occlusion of the coronary artery. Unstable angina causes subendocardial ischemia, therefore the EKG shows ST-segment depression. It can be relieved with nitroglycerine and has a high risk of progression to myocardial infarction.
Variant or prinzmetal angina
It is caused by vasospasm of the coronary artery and is reversible. It typically occurs at rest and is not associated with exertion. EKG shows ST-segment elevation due to transmural ischemia as the vasospasm completely blocks the blood supply to the entire wall of the epicardium or transmural. Prinzmetal angina is relieved by nitroglycerin and calcium channel blockers, which help ease vasospasm of the coronary artery.
Myocardial infarction (MI)
Myocardial infarction is the necrosis (death) of heart muscle cells (myocytes) as a result of ischemia, therefore, it is an irreversible injury to myocytes. It is the most lethal pattern of heart disease. The incidence progressively increases with age and with atherosclerotic risk factors.
Causes of MI
- Rupture of an atherosclerotic plaque with complete occlusion of coronary artery
- Coronary artery vasospasm (prinzmetal angina)
- Embolus
- Vasculitis (If there is vasculitis in the coronary artery, inflammation damages the endothelium and expose subendothelial collagen and tissue factor and eventually leading to developing a thrombus)
Symptoms of MI
- Severe crushing chest pain lasts more than 20 minutes and radiates to the left arm or jaw
- Unconsiousness or fainting
- Diaphoresis or sweating
- Dyspnea (due to the inability of the heart to pump blood well results in pulmonary congestion and edema which results in dyspnea)
Symptoms are not relieved by nitroglycerine. The most common artery involved in myocardial infarction is the left anterior descending artery. Complete occlusion of this artery infarcts the anterior wall of the left ventricle and the anterior portion of the intraventricular septum. The second most commonly affected coronary artery is the right coronary artery and complete occlusion of this artery results in infarction of the posterior wall along with the intraventricular septum. The third artery that can be involved in Myocardial infarction is the left circumflex and occlusion of this artery results in left ventricular lateral wall infarction.
The initial involvement phase of myocardial infarction is the subendocardium region underneath the endocardium, which represents less than 50% of the myocardial thickness. The most distal part from the beginning of the coronary artery is the endocardium which is the first to become necrotic hence, initial cell death of MI occurs in the subendothelial region, known as subendothelial necrosis.
Types of MI
Based on the size of the involved vessel and the degree of collateral circulation, MI has three patterns and they may not have any electrocardiograph changes.
- Transmural infarct (regional MI)
Ischemic necrosis involves the entire thickness of the epicardium or transmural
- Subendocardial infarct
Involves no more than the inner one-third thickness of the myocardium
- Microscopic infarcts
Small vessel occlusions. May not show any diagnostic ECG changes
Diagnosis of MI
- Clinical history of ischemic chest pain lasting for more than 20 minutes
- Changes in serial ECG tracings
- Myocardial enzymes present in the serum (Troponin I and CK-MB)
When MI occurs, myocardial cell membranes are damaged, and eventually, enzymes inside the membrane are leaked into the blood. The most specific and sensitive marker enzymes are Troponin I and creatine kinase-MB (CK-MB).
Complications of MI
The risk of developing complications
and the prognosis after MI depend on the infarct size, site, and type.
- Arrhythmias
Arrhythmia is the most common complication because they make the conduction tissue involved, which can lead to sudden death. The risk of arrhythmias is greatest in the first hour and decreases thereafter.
- Rupture of heart
Cell necrosis leads to the inflammatory phase. In the inflammatory phase, the Neutrophils phase is followed by the macrophages phase, and the macrophages absorb all dead cells that lead to the weakened wall of the heart, and eventually, that wall may rupture. It occurs only in 1-5% of myocardial infarction cases but is usually lethal. When the left ventricular free wall involves in infarction and then ruptures, blood eventually flows to the pericardium and begins to compress the heart, resulting in cardiac tamponade.
- Pericarditis
If a person had a transmural infarction, which means that the entire wall is dead and eventually, neutrophils inflame the entire wall, and some part of that inflammatory exudate will leak into the pericardium which surrounds the epicardium and results in pericarditis. pericarditis gives a villus-like heart appearance.
- Papillary muscle dysfunction
This is infrequent and it can lead to papillary muscle fibrosis and shortening
- Mural thrombus
Many layers of thrombus are formed on the infarcted myocardium, this can detach from the myocardium and emboli distal organs such as the brain, kidney, etc.
- Ventricular aneurysm
After 1-3 weeks of infarction, granulation tissue will begin to repair the myocardial wall by the formation of the scar because myocytes can not be regenerated but the scar is not strong as the myocardium hence it creates a balloon-like structure called an aneurysm.
Morphologic changes in myocardial infarction
Treatments of MI
- Aspirin or heparin (reduce additional thrombosis formation)
- Nitrates (vasodilate both arteries and veins)
- Supplemental oxygen (minimize ischemia)
- ACE inhibitor (block the production of angiotensin II)
- Beta-blockers (slow the heart rate and decrease the oxygen demand)
Chronic ischemic heart disease
Refers as poor function of the heart due to chronic ischemia. Chronic ischemia slowly damages the myocardium with or without infarction and eventually progresses to congestive heart failure.
Sudden cardiac death
Unexpected death due to cardiac disease. Generally asymptomatic or less than one hour of symptom and usually due to arrhythmia. The most common cause is acute ischemia.
