1- ischaemic heart disease

Question 1

consequences of myocardial ischaemia

Answer 1

Stable angina (Angina pectoris):
Prinzmetal variant angina
Unstable or crescendo angina
Myocardial infarction (MI)
Sudden cardiac death: may be caused by regional myocardial ischaemia that induces a fatal ventricular arrhythmia

Question 2

stable angina

Answer 2

Stable angina ( angina pectoris) results from increases in myocardial oxygen demand that outstrip the ability of stenosed coronary arteries to increase oxygen delivery.

It is usually not associated with plaque disruption.

Stable (typical) angina is the commonest form of angina.

Angina pectoris is characterized by paroxysmal and usually recurrent attacks variously described as a deep, poorly localized pressure, squeezing, or burning sensation (like indigestion) of substernal or precordial chest discomfort caused by transient (15 seconds to 15 minutes) myocardial ischaemia that is insufficient to induce myocyte necrosis.

The pain is likely a consequence of the ischaemia-induced release of adenosine, bradykinin, and other molecules that stimulate sympathetic and vagal afferent nerves.

Usually relieved by rest (decreasing demand) or administering vasodilators, such as nitroglycerin and calcium channel blockers

Question 3

Prinzmetal variant angina

Answer 3

Prinzmetal variant angina : is an uncommon form of episodic myocardial ischaemia; caused by coronary artery spasm.

Although individuals with Prinzmetal variant angina may well have significant coronary atherosclerosis, the anginal attacks are unrelated to physical activity, heart rate, or blood pressure.

Prinzmetal angina generally responds promptly to vasodilators.

Question 4

unstable of crescendo angina

Answer 4

Unstable or crescendo angina: refers to a pattern of increasingly frequent, prolonged (>20 min), or severe angina or chest discomfort that is described as frank pain, precipitated by progressively lower levels of physical activity or even occurring at rest.

In most patients, unstable angina is caused by the disruption of an atherosclerotic plaque with superimposed partial thrombosis and possibly embolization or vasospasm (or both).

In some cases, microinfarcts can occur distal to disrupted plaques due to thromboemboli.

Approximately one-half of patients with unstable angina have evidence of myocardial necrosis; for others, acute MI may be imminent.

Question 5

Myocardial infarction

Answer 5

Myocardial infarction (MI): commonly referred to as “heart attack,” is the death of cardiac muscle due to prolonged severe ischaemia.

MI is often the result of acute plaque change that induces an abrupt thrombotic occlusion, resulting in myocardial necrosis.

Question 6

Pathogenesis of Myocardial infarction

Answer 6

1. Atherosclerosis Formation
   Endothelial Dysfunction: The inner lining of the coronary arteries (endothelium) becomes damaged due to risk factors such as hypertension, smoking, diabetes, hyperlipidemia, and inflammation.

Lipid Accumulation: Low-density lipoprotein (LDL) cholesterol penetrates the damaged endothelium and accumulates in the arterial wall.

Plaque Formation: Inflammatory cells (e.g., macrophages) engulf the LDL cholesterol, forming foam cells. Smooth muscle cells proliferate, and a fibrous cap develops over the lipid-rich core, creating an atherosclerotic plaque.

2. Plaque Rupture or Erosion
   Vulnerable Plaque: Some plaques are unstable due to a thin fibrous cap, a large lipid core, and high inflammatory activity. These are called “vulnerable plaques.”

Plaque Rupture: Physical stress (e.g., high blood pressure) or enzymatic degradation of the fibrous cap (e.g., by matrix metalloproteinases) can cause the plaque to rupture.

Plaque Erosion: In some cases, the endothelial layer over the plaque erodes without frank rupture, exposing the thrombogenic core.

3. Thrombus Formation
   When the plaque ruptures or erodes, the highly thrombogenic lipid core and subendothelial collagen are exposed to the bloodstream.

Platelets adhere to the exposed site, become activated, and aggregate, forming a platelet-rich thrombus.

The coagulation cascade is activated, leading to fibrin deposition and the formation of a stable clot.

The thrombus can partially or completely occlude the coronary artery, reducing or stopping blood flow to the downstream myocardium.

4. Ischemia and Myocardial Injury
   Oxygen Supply-Demand Mismatch: The occlusion of the coronary artery reduces oxygen supply to the myocardium, while demand remains unchanged or increases.

Ischemic Cascade: Within seconds to minutes, the affected myocardium shifts from aerobic to anaerobic metabolism, leading to lactic acid accumulation, cellular acidosis, and impaired contractility.

Reversible Injury: If blood flow is restored promptly (e.g., by thrombolysis or percutaneous coronary intervention), the myocardial cells may recover.

Irreversible Injury: Prolonged ischemia (typically >20-30 minutes) leads to irreversible damage, characterized by cell death (coagulation necrosis).

Question 7

complications of myocardial infarction

Answer 7

Contractile dysfunction. left ventricular failure with hypotension, Pulmonary oedema and respiratory impairment.

Cardiogenic shock

Arrhythmias.

Myocardial rupture. These include:
Rupture of the ventricular free wall (most common), with hemopericardium and cardiac tamponade)
Rupture of the ventricular septum (less common): acute VSD and left-to-right shunting
Papillary muscle rupture (least common): acute onset of severe mitral regurgitation

Ventricular aneurysm.

Pericarditis. A fibrinous or fibrinohaemorrhagic pericarditis usually in day 2 or 3 following a transmural infarct as a result of underlying myocardial inflammation (Dressler syndrome;

Mural thrombus.

Papillary muscle dysfunction results in precipitous onset of mitral (or tricuspid) valve incompetence,

Progressive late heart failure (chronic IHD)