Cardiovascular Pathology-2 Flashcards
What are the 4 clinical syndromes associated with ischemic heart disease?
– Angina pectoris (AP)
– Myocardial infarction (MI)
– Chronic IHD with CHF
– Sudden cardiac death (SCD)
What is the common feature of Angina pectoris and the 3 subtypes?
– Stable (Typical) angina pectoris
– Prinzmetal (Variant) angina
– Unstable (Crescendo) angina pectoris
What is the common features of STABLE
(TYPICAL) ANGINA
stable when extra stress or excertion
What is the common features associated with PRINZMETAL (VARIANT) ANGINA
occurs at rest, vasospasms
What are the common features associated with UNSTABLE (CRESCENDO) ANGINA?
Common feature of Myocardial infarction?
• Indicates the development of an area of myocardial necrosis caused by local ischemia
- occurs at any age
- more males affected than females affected until menopause where the protection affect of estrogen tapers off
What are the Major contributing factors of Myocardial infarction?
- Hypercholesterolemia
- Smoking
- Hypertension
- Diabetes mellitus
What is the pathogenesis of Myocardial infarction?
Pathogenesis: 90% of cases due to acute thrombosis that leads to coronary artery occlusion. • Disruption of a pre-existing plaque which in
– 2/3rd have < 50% stenosis – 85% have < 70% stenosis
Remaining 10% of cases due to
• Vasospasm – isolated, intense and relatively prolonged with or without coronary atherosclerosis • Emboli – from the left sided mural thrombus • Unexplained – Disease of small intramural coronary vessels or Hematological abnormalities
Transmural Infarctions features?
– Involve the full thickness of ventricular wall in the distribution of a single coronary artery (Regional) also called STEM
- Due to total occulsion of the feeding coronary artery and the collaterals cant compensate for that
– Usually associated with acute plaque changes and superimposed, completely occlusive thrombosis.
– Can also occur with Cocaine abuse
Subendocardial infarctions features?
Subendocardial infarctions
– Limited to the inner one third or at most one half of the ventricular wall also called NSTEMI
– Associated with diffuse stenosing coronary atherosclerosis or with prolonged hypotension (Global/Circumferential infarctions)
– May occur due to transient/partial arterial obstruction (Regional) – Less serious than transmural infarction
What are the essential sequence of events in MI ?
Coagulative necrosis
Inflammation then resorption of necrotic myocardium
Formation of granulation tissue
Organization of granulation tissue to form a collagen rich scar tissue
Time sequence of MI
- 1-day-old infarct showing coagulative necrosis and wavy fibers
- Dense polymorphonuclear leukocytic infiltrate in an acute myocardial infarction of a 3 days old
- Removal of necrotic myocytes by phagocytosis (approximately 7 to 10 days)
- Granulation tissue characterized by loose collagen and abundant capillaries
- Healed myocardial infarct, necrotic tissue is replaced by a dense collagenous scar. The residual cardiac muscle hypertrophy
Reperfusion therapy in MI
Is the goal of therapy to salvage maximal amount of ischemic cells
• Achieved by:
– Thrombolysis using enzymes e.g. Streptokinase
or tissue plasminogen activator
– Angioplasty or CABG
• Although it is useful, reperfusion of ischemic tissue can cause rebound myocardial damage which can lead to Reperfusion injury
Mechanisms of Reperfusion Injury ?
• Mitochondrial dysfunction → promote apoptosis
- High extracellular Ca+2 and impaired Ca+2 cycling → myocyte hypercontracture → cytoskeletal damage
- Free radicals are produced within minutes of reperfusion → myocardial damage
• Leukocytes aggregation & platelet activation → microvasculature injury and occlusion → “no reflow” phenomenon
Contraction band necrosis occurs?
– Intense hyper-eosinophilic transverse bands (hypercontracted sarcomeres)
– Induced by high amount of extracellular calcium in restored blood flow which easily crosses the leaky plasma membrane of ischemic myocytes – Actin - myosin interaction in the absence of ATP- the sarcomeres are stuck in this agonal tetanic state
Clinical Features of MI
• Chest pain: – Retrosternal pain, Crushing in nature, May radiate to the neck, jaw, epigastrium, shoulder, or left arm
– The pain is persistent >30 mins (unlike angina)
– Not significantly relieved by vasodilators
(nitroglycerine) or rest
- Dyspnea
- Rapid weak pulse
- Diaphoresis, Nausea & vomiting
What is a silent MI
• Silent MI (neuropathy)
– Occurs in as many as 25% of cases
– Asymptomatic MI that is discovered only by EKG changes and laboratory tests
– Common in elderly patients
– Underlying Diabetes mellitus/ Hypertension
Complication of Ischemic MI
• Extension of the infarction • Reinfarction • Angina
Arrhythmic MI complications?
Factors that can cause arrhythmias following MI:
- Myocardial irritability and conduction disturbances
- Electrolyte imbalance
- Hypoxia Arrhythmias are the most common cause of SCD
Complication of an Embolic MI?
- Wall motion abnormalities endocardial damage → Mural thrombus
- Mural thrombi are common in the left ventricle→ Systemic emboli
- Stroke (most common), limb ischemia, renal infarction or mesenteric ischemia can occur
Mechanical complication of an MI?
-
Contractile dysfunction: • Depend on size, site, thickness of the infarction • Can cause variable range of ventricular failure • If severe → Cardiogenic Shock(10-15% of cases) • Progressive heart failure (chronic
IHD) -
Papillary muscle dysfunction: • Rupture • Ischemia • Fibrosis
→ Mitral Valve Incompetence or → Tricuspid Valve Incompetence -
Myocardial Rupture
• Occurs between 3-10 days when necrosis, neutrophilic infiltration
and myocardial tissue lysis → weakened myocardium
It includes: • Ventricular free wall rupture → tamponade • Ventricular septum rupture → VS
-
Ventricular aneurysm
• Late complication of large transmural infarcts • Scar tissue wall of an aneurysmbulges during systole • Mural thrombus, arrhythmias
and heart failure may occur • Unlikely to rupture due to tough
fibrotic wall
Inflammaotry complications of MI
Pericarditis
2 types can occur following MI:
- Acute fibrinous/ fibrinohemorrhagic: - Due to direct irritation of the pericardium in transmural infarcts. - Usually in day 2 or 3 post MI
- Autoimmune – Dresslers’ syndrome - Occurs 10-14 days post MI - Autoantibodies that target damaged pericardial antigens
What is seen in the EKG of an MI
EKG: Transmural infarct: • ST segment elevation • Q wave: delayed appear after 6 hours of onset
Subendocardial infarct • No specific changes • No ST segment elevation • May show T wave depression
What are the cardiac injury markers seen in MI?
A. Myoglobin
– First biomarker to rise (1-4 hrs)
– Highly sensitive but not specific for the heart
– Rarely used in practice
B. Troponins (I and T)
– Most sensitive and specific marker
– Normally not detectable in circulation
– Rises in 3-12 hrs, peaks at 48 hrs and persists for 5-14 days
C. Creatine Kinase isoenzymes (CK-MB)
– A dimer composed of M & B subunits: MM, MB, BB
– CK-MB: most specific for the heart among the CKs
– Rises in 3-12 hrs, Peaks at 24 hrs and disappears by 72 hrs – Useful for detection of reinfarction
D. Lactate dehydrogenase (LDH)
– Rises in 24 hrs, peaks at 3-6 days and returns to baseline within 8-12 days
