Characterization of Coronary Heart Disease
Insufficient delivery of oxygenated blood to myocardium (ischemia) because of atherosclerotic coronary arteries (CAD)
Coronary Heart Disease Can Lead To:
Angina pectoris (chest pain)
Myocardial infarction (tissue death)
Dysrhythmias
Heart failure
Sudden cardiac death
Etiology of Coronary Heart Disease
Atherosclerosis causes narrowing of arterial lumen and can lead to cardiac ischemia
Plaque accumulates causes vessels to spasm
Lack of open space
Cause of Coronary Artery Disease
Atherosclerosis
Apoproteins
transport lipids through blood
Lipoproteins
Greater risk of atherosclerosis
Atherosclerotic plaque formation is initiated by
Injury to coronary artery endothelium
Lipoproteins contain:
Triglycerides
Phospholipids
Cholesterol
Protein
Types Of Lipoproteins
High density lipoprotein (HDL)
Intermediate density lipoprotein (IDL)
Low density lipoprotein (LDL)
Very low density lipoprotein (VLDL)
Chylomicrons
Produced by intestine
Packaged with dietary lipids
Transport dietary lipids to hepatic and peripheral cells
Hyperlipidemia
Elevated concentration of lipids in blood
Major plasma lipids
Total cholesterol
Triglycerides
Risk factors of hyperlipidemia (primary)
Genetic predisposition for CHD
Cigarette smoking
Elevated total cholesterol
Decreased HDL cholesterol
Elevated triglycerides
Increasing age
Male gender
Risk factors of hyperlipidemia (secondary)
Lack of exercise
Obesity
Stress
Elevated lipoprotein, homocysteine, intermediate density lipoproteins
Renal failure
Mechanism of Coronary Atherosclerosis
Vulnerable plaques may rupture
Clot formation is stimulated on plaque
Vulnerable plaque have
Large lipid core
Thin cap
High shear stress
If there is not fibrous cap...
Atherosclerosis is not stable
Pathophysiology of Ischemia
Local, temporary deprivation of the coronary blood supply
Oxygen supply is insufficient to meet metabolic demands
Factors for meeting cellular demands for oxygen
Rate of coronary perfusion
Myocardial workload
Coronary perfusion can be impaired by
Large, stable atherosclerosis plaque
Acute platelet aggregation and thrombosis
Vasospasm
Failure of autoregualtion by microcirculation
Poor perfusion pressure
Myocardial work load depends on
Heart rate
Preload
Afterload
Contractility
Chronic coronary syndrome
slow progression due to chronic obstruction from stable atherosclerotic plaques
Acute coronary syndrome
acute changes in plaque morphology and thrombosis (plaque is unstable)
Angina pectoris (chronic coronary syndrome)
intermittent myocardial ischemia
chest pain
inefficient cardiac pumping causing pulmonary congestion and shortness of breath
Unstable angina (chronic coronary syndrome)
No exertion
Disruption of plaque
Ischemia
Thrombosis
Pre warning for infarction
Treatment of Angina (chronic coronary syndrome)
Dietary/lifestyle modifications
Cholesterol lowering drugs
Aspirin/platelet inhibitors
Decrease in demand for oxygen (beta and calcium channel blockers)
Increase vasodilation
Angioplasty, stenting, bypass surgery
Acute Coronary Syndrome
Plaque rupture with acute thrombus development
Unstable Angina (Acute Coronary Syndrome)
Occlusion is partial
Myocardial Infarction (Acute Coronary Syndrome)
Occlusion is complete
Extended obstruction of myocardial blood supply
Drop in CO2, triggering compensatory response
SNS causes increased workload which increases (Acute Coronary Syndrome)
Heart rate
Contractility
Blood pressure
Treatment of MI (Acute Coronary Syndrome)
Repercussion the heart (does not restore necrotic or dead fiber, only reversibly injured ones)
Anticoagulants
ACE inhibitors (helps to reduce workload)
Biomarkers
Cardiac troponin T and I
Myoglobin
CK-isoforms
Troponin C (Bind and Location)
Binds to calcium
Found in heart and skeletal muscle
Troponin T (Bind and Location)
Binds tropomyosin
Cardiac specific
Troponin I (Bind and Location)
Inhibit binding of myosin to actin
Cardiac specific
What regulates muscle contraction?
Troponin complex
Calcium
Tropomyosin
What helps diagnose MI?
Troponin
Myoglobin Location
Cardiac and Skeletal Muscle
Change in myoglobin concentration is seen in
MI
Renal failure injury
Trauma
Skeletal muscle disease
Creatine Kinase (CK)
Cytosolic enzyme involved in the transfer of energy in muscle metabolism
Subunits of CK
Brain form (B)
Muscle form (M)
CK Isoenzyme
CK-BB (blood - brain barrier)
CK-MM (activity in skeletal system)
CK-MB (activity in the heart)
Sudden Cardiac Death
Unexpected death from cardiac causes within 1 hour of symptom onset
Non-Atherosclerotic Sudden Cardiac Death (Diseases)
Congenital coronary artery disease
Aortic stenosis
MVP
Myocarditis
Cardiomyopathy
Chronic Ischemic Cardiomyopathy
Heart failure develops insidiously due to progressive ischemic myocardial damage
Supply does not meet demand overtime
Damage to endocardium and valves caused by:
Inflammation and scarring
Calcification
Congenital malformations
Stenosis
Failure for a valve to open completely
Backflow
Extra pressure work
for heart due to high resistance of narrow valve opening
Regurgitation
Inability of a valve to close completely results in
extra volume work
for the heart
Does not prevent back flow
Mitral Valve Prolapse (MVP)
Degeneration of mitral valve (regurgitation)
Valve bulges into left atrium during ventricular systole
Connective tissue disorder
Clinical Features of Mitral Valve Prolapse
Asymptomatic
Mid-systolic "click"
Holosystolic murmur if regurgitating (between S1 and S2 noises)
Chest pain, dyspnea
Manifestations of MVP
Dizziness
Light headed
Shortness of breath
Fatigue
Mechanical valve
Carbon material
Attract clots/thrombosis
Xenograft Valve
Animal
Not at risk for clotting
Rheumatic fever
inflammatory disease caused by a delayed immune response to infection
type 2 hypersensitivity
Febrile illness
Inflammation of the joints, skin, nervous system, and heart
Jones Criteria
C: carditis
A: migratory polyarthritis
N: nodules
C: Sydenham chorea
ER: erythema marginatum
Rheumatic heart disease
acute inflammatory disease that follows infection
Infective endocarditis
Invasion and colonization of endocardial structures by microorganisms with resulting inflammation
Colonize on valves
Acute Infective Endocarditis
Usually have something abnormal with heart to begin with
Bacteria of Infective Endocarditis
Strep
Staph
Who does acute infective endocarditis effect?
IV drug users
Endocarditis
Inflammation of endocardium
Causes Of Endocarditis
bacteria
viruses
fungi
rickettsia
parasites
Pathogenesis of endocarditis
Colonization occurs on valves (become calcified)
Blood-borne microorganism adherence
Proliferation of the microorganisms
Myocarditis
inflammatory disorder
Dilation of all four chambers
Left ventricle dysfunction
Characterizations of myocarditis
necrosis and degeneration of myocytes
Cardiomyopathy
Noninflammatory disorder
Characterization of cardiomyopathy
Genetic or acquired
Causes of myocarditis
Microbial agents
Immune-mediated diseases
Physical agents
Etiology of myocarditis
Virus (Coxsackie B), bacteria, parasites
Inflammatory disease (SLE)
Toxins (drugs and radiation)
Causes of cardiomyopathy
Hypertension
Inflammatory
Autoimmune
Muscular dystrophy
Genetic disorder
Drugs
Viral myocarditis
Aortic regurgitation
Mitral regurgitation
Primary cardiomyopathy
no known cause
Secondary cardiomyopathy
known cause
Dilated cardiomyopathy
cardiac failure associated with dilation of one or both ventricular chambers
heart is big and flabby
Causes Of Dilated Cardiomyopathy
Alchohol toxicity
Pregnancy
Postviral myocarditis
Genetic abnormality
Precursor of dilated cardiomyopathy
Myocarditis
ETOH
Dilated cardiomyopathy found in
Pregnant women
Drug users
Alcoholics
Hypertrophic cardiomyopathy
thickened walls
ventricles can't relax
Causes of hypertrophic cardiomyopathy
Genetic abnormality
Increased pulmonary resistance
Pulmonary hypertension
Left heart failure and lung disease
Pulmonic valve stenosis
Sarcomere proteins related to genetic abnormality of hypertrophic cardiomyopathy
Beta-myosin heavy chain
Troponin T
Alpha-tropomyosin
Myosin binding protein C
Pathology of hypertrophic cardiomyopathy
Massive hypertrophy
Asymmetric septum
Disarray of myocytes
Interstitial fibrosis
Clinical aspects of hypertrophic cardiomyopathy
Decrease in chamber volume
Decrease in stroke volume
Decrease in diastolic filling
Restrictive cardiomyopathy (rare)
Idiopathic disease where walls become restricted but chamber size and wall thickness are normal
Decrease in ventricular compliance
Affects diastole
Decreased cardiac output and left-sided heart failure
Tamponade
Severe restriction of heart
Venous congestion, JVP, distant heart sounds
Accumulate fluid in pericardial sac
Squeezes heart causing pressure
Back flow into systemic veins (swelling)
Treatment of Tamponade
Relieving the pericardial pressure by aspirating the offending fluid
Acute Pericarditis
Idiopathic
Pleuritic chest pain
Pericardial rub
Causes of acute pericarditis
Infection: virus, TB, bacteria
Connective tissue disease: lupus, rheumatoid arthritis
Drugs
Cancer
Renal failure
Radiation
Trauma
MI
Congenital Heart Diseases
Abnormality of heart that is present from birth
Etiology of congenital heart disease
Oxygenated blood shoot across right atrium to left atrium and bypass lungs
Septum doesn't always develop all the way
Causes of congenital heart disease
Maternal rubella
Exposure to cardiac teratogens
Genetic influences
Shunt
Abnormal path of blood flow through the heart or great vessels
Obstruction
Interference with blood flow leading to increased workload of affected chamber
Atrial Septal Defect
Abnormal opening between the atria
Shunts go right to left because blood bypasses lungs
Ventricular Septal Defect
Abnormal communication between ventricles
Shunts left to right or right to left