CVS

Heart - Pathology

Ischemic Heart Disease Hypoxemia (diminished transport of oxygen by the blood) less deleterious than ischemia Also called coronary artery disease (CAD) or coronary heart disease IHD =Syndromes late manifestations of coronary atherosclerosis Cause => 90% of cases, coronary atherosclerotic arterial obstruction

Heart - Pathology

Ischemic Heart Disease Classification = mainly 4 types Myocardial infarction (MI) Sudden cardiac death Angina pectoris Chronic IHD with heart failure Acute Coronary syndromes important predisposing factor -Plaque disruption or Acute plaque change Acute myocardial infarction Unstable angina Sudden cardiac death

Heart - Pathology

Ischemic Heart Disease75% stenosis = symptomatic ischemia induced by exercise90% stenosis = symptomatic even at restPathogenesis↓ coronary perfusion relative to myocardial demandRole of Acute Plaque Change (Erosion/ulceration, Hemorrhage into the atheroma, Rupture/fissuring, Thrombosis)Role of InflammationT cell, Macrophages (MMPs), CRPRole of Coronary ThrombusThe most dreaded complicationRole of Vasoconstriction (VC)Platelet & Endothelial factors, VC substances

Heart - Pathology

Heart - Pathology
Ischemic Heart DiseaseAngina PectorisChest discomfort = prolonged, recurrent, different qualitiesCause = transient myocardial ischemia( seconds to minutes)PatternsStable = 75% vessel block, transient ( <15 minutes), aggravated by exertion, relived by rest & Nitroglycerin (VD)Prinzmetal = coronary spasm, episodic, Typical EKG change – ST elevation, Relived by VD but not restUnstable = 90% vessel block or Acute plaque change ( superimposed thrombus), prolonged ( >15 min.), not relived by rest, VD, Pre-infarction Angina

MI - Types

Transmural Full thickness Superimposed thrombus in atherosclerosis Focal damage
Sub-endocardial Inner 1/3 to half of ventricular wall Decreased circulating blood volume( shock, Hypotension, Lysed thrombus) Circumferential


Heart - Pathology
Ischemic Heart DiseaseMI= Also called Heart attackIncidence = disease of old elderly (45% in 65 yrs. old) young ( 10% in 40yrs. Old), Sex = Male > FemaleEthnic = same in African & AmericanRisk factorsMajor modifiable- DM, HTN, Smoking, HypercholesterolemiaHRT for Postmenopausal females – will not protect the heart

Heart - Pathology

Ischemic Heart DiseaseMIPathogenesis Coronary vessel occlusionAtherosclerosis with thrombus = MC cause ( 90% cases)Others = vasospasm (10%)Most important mechanism = dynamic changes in the plaque (rather than plaque size), Plaque disruption PLTS aggregation thrombus and VC (happens in minutes)Irreversible changes = after 30 minutes of ischemia ATP < 10% of normalMechanism of cell death = necrosis ( Coagulative)

Heart - Pathology

Ischemic Heart Disease TTC

Heart - Pathology

Ischemic Heart DiseaseMI -Morphologylight microscopyFirst 12 hrs. after MI – no changeUp to 3 days = Coagulative necrosis, neutrophils1-2 weeks = Granulation tissue≥ 3 weeks = fine scar≥ 2 months = dense scarEM – membrane disruption and Mitochondrial densitiesSpecial stain = TTC ( Triphenyl Tetrazolium chloride), Detects and stains Mahogany brown with Lactate dehydrogenaseUnstained area = infarctionMahogany brown = viableWhite, glistening= scarMost common and nonspecific change in ischemia = sub-endocardial myocyte vacuolization

MI- Microscopic features

One-day-old infarct
coagulative necrosis
wavy fibers
Up to 3 days duration
Neutrophilic infiltrate
1 -2 weeks
Granulation tissue
Scar
>3 weeks

Heart - Pathology

Ischemic Heart DiseaseMI –ReperfusionMechanismsIntrinsic Extrinsic = Thrombolytic drugs = < 1hr. After onset of MITarget = clot lysis and restoration of blood flowPost- reperfusion changes =Contraction bands = hyper contracting myocytes, Stunned myocardium = transient, protective dysfunctionReperfusion damage = mostly apoptosis by free radicals ( unlike MI)

Heart - Pathology

Ischemic Heart Disease

Heart - Pathology

Ischemic Heart DiseaseMI = ClinicalSilent MI = DM, Elderly, Cardiac transplantation recipients,Typical features = Rapid, weak pulse and sweating profusely (diaphoretic), Dyspnea, chest painLab= Diagnostic Best markers = Troponins ( T & I), both sensitive and cardio – specificNext best – CK-MBPredictiveCRP- >3mg/l – highest risk

Heart - Pathology

Ischemic Heart DiseaseMI –ComplicationsIn 75% of Patients with MIPoor prognosis in = elderly, females, DM, old case of MI, Anterior wall infarct – worst, posterior –worse, Inferior wall – best 1. Arrhythmia = Ventr. Fibrillation – MC arrhythmia lead to sudden death in MI patients, before they reach hospital2. pump failure – LVF, cardiogenic shock, if >LV wall infarcts, lead to death ( 70% of hospitalized MI patients)3.Ventricular rupture = Free or lateral LV wall – later cause false aneurysm, 4.True aneurysm = rupture is very rare5.Pericarditis6.Recurrence

Heart - Pathology

Ischemic Heart DiseaseSudden cardiac death = unexpected death in one hour due to cardiac causes with or without clinical symptomsCause – Atherosclerosis ( 90%), others (10%)Romano- Ward syndrome – Long Q-T syndrome ( K+, Na+ channel defects)Mechanism- Most likely due to arrhythmias ( VF)Patients – young athletes, with Pul. HTN, IHDMorphology Prominent finding – increased heart massVacuolations in Sub – endocardial myocardium

Heart - Pathology

Ischemic Heart Disease Chronic IHD = also called ischemic cardiomyopathy Patients = post heart transplant receipts, previous MI or CABG pts Cause =compromised ventricular function Morphology =vacuoles, Myocyte Hypertrophy Diagnosis= by exclusion