IHD 2025 PDF - Libyan International Medical University

Libyan International Medical University Faculty Of AMS 2rd year (2024-2025) Block : CVS Week II IHD and Pericardial effusion Dr. Warda Musbah 1  Intended learning outcomes By the end of this session you will...

Libyan International Medical University Faculty Of AMS 2rd year (2024-2025) Block : CVS Week II IHD and Pericardial effusion Dr. Warda Musbah 1  Intended learning outcomes By the end of this session you will be able to:  Define Angina pectoris & outline the three patterns of Angina  Describe pathogenesis of myocardial infarction.  Summarize complications of myocardial infarctions.  Outline the evolution of the morphologic changes in myocardial infarction  Outline classification and morphology of aneurysms  Classify pericardial effusion and enumerate causes of the different forms of pericarditis. Angina pectoris This term refers to the pain resulting from myocardial ischemia. It typically occurs in the substernal portion of the chest and may radiate to the left arm, jaw and epigastrium  Stable angina  Unstable or Crescendo Angina  Prinzmetal or Variant or Vasospastic Angina Stable angina: It is the most common and is also known as typical angina pectoris occurs when myocardial oxygen demand increases with increased physical activity or emotional excitement. It takes place when the coronary artery is occluded >75%. Stable angina is characterized by pain on exertion , ranges from 1 to 15 minutes which is relieved on taking rest or taking vasodilators like nitrates. There is neither any plaque disruption nor any plaque associated thrombus. Unstable or Crescendo Angina: It is induced by atherosclerotic plaque disruption with superimposed partial thrombosis or vasospasm or both of them. It is characterized by more frequent onset of pain of prolonged duration and occurring often at rest. Consequence: May progress to myocardial infarction and is also referred to as preinfarction angina Prinzmetal or Variant or Vasospastic Angina Uncommon Occurs at rest generally during sleep Caused by Large Coronary Artery Spasm Usually associated with atheromatous disease.. It is characterized by ST segment elevation on the ECG (due to transmural ischemia).  Myocardial Infarction It is the necrosis of cardiac muscle due to prolonged ischemia.  Pathogenesis of MI  Coronary Atherosclerosis Coronary artery occlusion in 90% of cases, myocardial infarction is due to atherosclerotic narrowing of one or more coronary arteries.  An atheromatous plaque is eroded or disturbed  Platelets adhere, aggregate, and are activated releasing thromboxane A2, adenosine diphosphate (ADP), and serotonin— causing further platelet aggregation and vasospasm.  Activation of coagulation by tissue factor  Within minutes, the thrombus can evolve to completely occlude the coronary artery lumen  Complete occlusion results in ischemic coagulative necrosis of the area supplied by the particular coronary artery.  Pathogenesis of MI  Nonatheromatous Causes In about 10% of cases, MI occurs without atherosclerosis of the coronary vessels. It may be due to: Vasospasm with or without coronary atherosclerosis, perhaps in association with platelet aggregation or due to drug ingestion (e.g., cocaine or ephedrine). Emboli Uncommon causes of MI without atherothrombosis include vasculitis, hematologic abnormalities (e.g., sickle cell disease), lowered systemic blood pressure (e.g., shock).  The progression of ischemic necrosis in the myocardium Irreversible injury of ischemic myocytes first occurs in the sub endocardial zone. Prolonged ischemia, a cell death moves through other regions of the myocardium, driven by progressive tissue edema and myocardial-derived reactive oxygen species and inflammatory mediators Infarcts have been classified in a number of ways by the physicians and the pathologists: According to the degree of thickness of the ventricular wall Involved. Transmural: is the most common type, and is considered to have occurred when ischemic necrosis involves more than 50% of myocardial wall. It is associated with regional vascular occlusion by thrombus. Subendocardial: is considered to have occurred when ischemic necrosis involves less than 50% of myocardial wall. It is associated with hypoperfusion due to shock.  Common locations and the regions of involvement in myocardial infarction In the case of a myocardial infarction, the anatomy of the vessel is important. The left anterior descending artery (LAD) is involved in 45% of cases; infarcts involving the anterior wall of left ventricle near the apex; the anterior portion of ventricular septum; and the apex circumferentiall the right coronary artery (RCA) is involved in 35% of cases; infarcts involving the inferior/ posterior wall of the left ventricle; posterior portion of ventricular septum; and the inferior/posterior right ventricular free wall in some cases the left circumflex coronary artery (LCA) is involved in 15% of cases. %): infarcts involving the lateral wall of the left ventricle except at the apex  Common locations and the regions of involvement in myocardial infarction Atherosclerotic narrowing can affect any of the coronary)— singly or in combination.  The evolution of the morphologic changes in Myocardial Infarction Areas of damage progress through a highly characteristic sequence of morphologic changes from coagulative necrosis, to acute and then chronic inflammation, to fibrosis lack of staining by triphenyltetrazolium chloride in areas of necrosis.  Complications of MI The risk of complications depends on: (1) Infarct size (2) Location (3) Thickness of myocardium involved (subendocardial or transmural). 1.Left ventricular failure and cardiogenic shock. 2.Arrhythmias. 3.Myocardial rupture: Most frequent during 3 to 7 days after transmural infarcts.  Rupture of the ventricular free wall : result in hemopericardium.  Rupture of the ventricular septum: It is less common and lead to an acute VSD and left-to-right shunt.  Rupture of papillary muscle: leads to acute severe mitral regurgitation. c. Left ventricular free wall Rupture of the ventricular septum Rupture of papillary muscle 4. Ventricular aneurysm. 5. Mural thrombus. 6. Pericarditis:  Early pericarditis: A transmural myocardial infarction can involve the pericardium cause fibrinous or fibrinohemorrhagic pericarditis. Usually develops on second or third day.  Delayed form of pericarditis (postmyocardial infarction syndrome/ Dressler syndrome): Develops 2 to 10 weeks after infarction— probably immunologically mediated. recurrent pericarditis, pericadical effusion, pleural effusion, Fever. 7. Progressive late heart failure mural thrombus Large apical left ventricular aneurysm (arrow  ANEURYSMS localized, abnormal, permanent dilation of a blood vessel or the heart.  Classification Depending on the composition of the wall of the aneurysm. Depending on gross appearance (shape and size) Classification of aneurysm by etiology. Depending on the composition of the wall of the aneurysm: True aneurysm is composed of all the layers of thinned arterial wall (intima, media and adeventia) or attenuated ventricular wall of the heart. False aneurysm (or pseudoaneurysm) is a defect in the vascular wall with a hematoma which freely communicates with the intravascular space (“pulsating hematoma”). Depending on gross appearance (shape) Fusiform aneurysm Saccular aneurysm Cylindrical aneurysm: It has parallel dilatation. Arterial dissection/dissecting hematoma: It develops when blood enters/dissects between the layers of the arterial wall. Just like a hematoma it separates the layers of the arterial wall. Classification of aneurysm by etiology: 1. Congenital. 2. Atherosclerotic: are the most common type 3. Syphilitic: Found in the tertiary stage of the syphilis. 4. Dissecting:(Dissecting haematoma) in which the blood enters the separated or dissected wall of the vessel. 5. Mycotic: resulting from weakening of the arterial wall by microbial infection. 6. Traumatict  Atherosclerosis *It is the most common cause of true aneurysm in aorta *The most commonly affected vessel is the abdominal aorta (below the origin of renal artery and above bifurcation into common iliac artery). Morphology Usually positioned below the renal arteries and above the bifurcation of the aorta AAA can be saccular or fusiform as large as 15 cm in diameter, and as long as 25 cm.  Syphilis *The thoracic aorta is involved in tertiary stage of syphilis *Endarteritis of vasa vasorum results in patchy ischemia of tunica media. This is responsible for the often seen “tree barking” appearance of the thoracic aorta. *Aortic valve insufficiency can also occur which may result in cardiac hypertrophy. The increase in the size of heart is called as cor bovinum/cow heart tree barking” appearance of the thoracic aorta.  AORTIC DISSECTION Definition: Aortic dissection develops when blood from the aortic lumen enters into the aortic wall and travels along the layers of the media to form a blood-filled channel within the aortic wall. Older term “dissecting aneurysm” is replaced by aortic dissection. It is fatal, if the dissection ruptures through the adventitia → results in hemorrhages into adjacent spaces. Etiology: Occurs mainly in two groups: 1) men between 40 to 60 years, with hypertension or 2) Younger patients with connective tissue disease of the aorta, e.g. Marfan syndrome. Aortic dissection. (A) An opened aorta with a proximal dissection originating from a small, oblique intimal tear (identified by the probe) associated with an intramural hematoma. (B) Histologic preparation : the dissection and intramural hematoma (\Aortic elastic layers are black, and blood is red in this section.  Pericardial fluid accumulation Normally, the pericardial sac contains less than 50 ml of thin, clear, straw-colored fluid.  Accumulation of fluid in the pericardial sac may be watery or pure blood. Accordingly, it is of 2 types: Hydropericardium (pericardial effusion) 1. Serous effusions. 2. Serosanguineous effusion. 3. Chylous effusion. 4. Cholesterol effusion. Haemopericardium.  Hydropericardium 1. Serous fluid (pericardial effusion) – Congestive heart failure. – hypoalbuminemia of any cause 2. Serosanguineous: – Blunt chest trauma – malignancy. 3. Chylous: – Mediastinal lymphatic obstruction 4. Cholesterol effusion. There is presence of cholesterol crystals such as in myxoedema.  Haemopericardium The causes of haemopericardium are as under: i) Rupture of the heart through a myocardial infarct. ii) Rupture of dissecting aneurysm. iii) Bleeding diathesis such as in scurvy, acute leukaemias, thrombocytopenia. iv) Trauma following cardiopulmonary resuscitation or by laceration of a coronary artery.  Pericarditis Primary pericarditis Secondary pericarditis Based on the morphologic appearance, pericarditis is classified into: Acute type chronic type Primary pericarditis is uncommon. It is typically due to viral infection (often with concurrent myocarditis), although bacteria, fungi, or parasites may also be involved Secondarypericarditis o Dressler’s syndrome (post myocardial infarction syndrome) o Radiation to the mediastinum o Pneumonia or pleuritis o Uremia is the most common systemic disorder associated with pericarditis. o Less common secondary causes include systemic lupus erythematosus, and metastatic malignancies