Download Coronary Artery Disease

Coronary Artery Disease
Dory Roedel Ferraro, DNP, ANP-BC, CBN
College of New Rochelle
Coronary Artery Disease

Heart disease cause by impaired coronary blood flow

Most cases are caused by atherosclerosis

1.6 million Americans have new or recurrent myocardial infarctions (MI)

One third will die within 24 hours (500,000)

Risk factors: smoking, HTN, dyslipidemias, diabetes, advancing age,
abdominal obesity, physical inactivity
Coronary Arteries

Arise from the coronary sinus above the aortic valve

Left coronary artery-supplies the anterior and left lateral portions of the LV


Left anterior descending

Circumflex
Right coronary artery-supplies most of the RV and posterior part of the LV in
most people

Posterior descending artery
Assessment of Coronary Blood Flow and
Myocardial Perfusion

ECG

Exercise stress testing


Echocardiography


Used to visualize the regional distribution of bloodflow
MRI and CT



Tests structure and function of the heart
Nuclear cardiac imaging


Observes cardiac function under stress
MRI quantifies the volume, mass and function of the ventricles
CT assesses coronary artery calcification
Cardiac catheterization

Visualizes lesions within coronary arteries, determines extent of CAD
Pathogenesis of CAD

Fixed or stable plaque which obstructs blood flow

Unstable/vulnerable plaque (high-risk plaque), which can rupture and cause
platelet adhesion and thrombus formation

A sudden surge of sympathetic activity can increase the risk for plaque
disruption

Determinates of plaque vulnerability to disruption




The size of the lipid rich core
The stability and thickness of its fibrous cap
The presence of inflammation
The lack of smooth muscle cells
Acute Coronary Syndrome

Unstable angina

Non-ST segment elevation (non-Q-wave) MI


ST segment elevation MI


Subtotal or intermittent thrombotic coronary occlusion
Complete coronary occlusion
ECG changes

T-wave inversion, ST segment elevation, development of an abnormal Q wave
Unstable Angina/Non-ST-Segment MI

Clinical syndrome of myocardial ischemia

Ranges from stable angina to MI

Dependent on severity of ischemia

ECG pattern


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UA
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ST-segment depression (or transient ST elevation) and T-wave changes
Degree of ST-segment deviation is important measure of ischemia and prognosis
No serum markers for MI
NSTEMI

Serum markers are present
Pathophysiology of UA/NSTEMI: 5 Phases

Development of unstable plaque that ruptures or erodes with superimposed
thrombosis

An obstruction: spasm, constriction, dysfunction, adrenergic stimuli

Sever narrowing of the coronary lumen

Inflammation (inflammatory cells release cytokines)

Any physiological state causing ischemia related to decreased oxygen supply
(fever, hypotension)
Pain of UA/NSTEMI

Characterized by at least one of three features:

Occurs at rest or minimal exertion and lasts for more than 20 minutes

Severe and described as frank pain and of new onset (within 1 month)

More severe, prolonged or frequent than previously experienced
ST-Segment Elevation MI (STEMI)

Ischemic death of myocardial tissue associated with atherosclerosis

Extent of infarct depends on

Location and extent of occlusion

Amount of heart tissue supplied by the vessel

Duration of the occlusion

Metabolic needs of the affected tissue

Extent of collateral circulation

HR, BP and cardiac rhythm
ST-Segment Elevation MI (STEMI)


Transmural

Infarct involves full thickness of the ventricle wall

Involves obstruction of a single artery
Subendocardial

Infarct involves inner 1/3 to ½ of the ventricle wall

Severely narrowed, but still patent arteries
ST-Segment Elevation MI (STEMI)

Conversion from aerobic to anaerobic metabolism

Inadequate production of energy to sustain normal myocardial function

Changes in cell structure develop within several minutes

Changes are reversible if blood flow is restored

Irreversible damage occurs to cells within 40 minutes

Necrosis occurs after 20 to 40 minutes of severe ischemia
Clinical Manifestations of STEMI

Onset is usually abrupt

Pain is significant symptom: severe and crushing

More prolonged than angina and not relieved by NTG

Women experience atypical chest discomfort

GI symptoms are common

Tachycardia, anxiety, restlessness and feeling of impending doom

Pale cool and moist skin
Management of Acute Coronary Syndrome

12-lead ECG

Expeditious implementation of reperfusion therapy within 60 to 90 minutes
for patients with ECG evidence of infarction

Oxygen, ASA, nitrates, analgesics, antiplatelets and anticoagulants, βblockers
Serum Biomarkers

Triponon assays – primary biomarker tests for myocardial damage

Begin to rise within 3 hours of myocardial damage
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May remain elevated for 7-10 days

TnI-cardiac specific troponin I

TnT-cardiac specific troponin T

CK-MB-creatinine kinase MB
Pharmacological Management of Acute
Coronary Syndrome
Nitroglycerin
Vasodilator (preload and afterload) myocardial O2 consumption
Relieves pain
Morphine
Anxiety and autonomic nervous system activity
β-Adrenergic
blockers
myocardial O2 demand
Alter resting membrane potentials, life-threatening ventricular
arrhythmias
ASA
Inhibition of platelet aggregation
Promote reperfusion and prevents likelihood of rethrombosis
ACE inhibitors
Reduces LV dysfunction
 CO and SV and pulmonary vascular resistance
Chronic Ischemic Heart Disease

Chronic stable angina

Silent myocardial ischemia

Variant or vasospastic angina
Chronic Stable Angina

Associated with a fixed coronary obstruction that produces an imbalance
between coronary blood flow and metabolic demands of the heart

Only half patients with coronary artery disease experience angina

Usually precipitated by situations that increase the work demands of the
heart: exertion, exposure to cold, emotional stress and relieved with rest or
sublingual nitroglycerin (NTG)

Steady constricting, squeezing or suffocating sensation in the precordial or
substernal chest or back, sometimes radiating to the left shoulder, jaw or
arm
Silent Myocardial Ischemia

Occurs in the absence of anginal pain

Episodes may be shorter and involve less myocardial tissue than those
producing pain

Reason for painless episodes unclear

Defects in pain threshold or pain transmission

Autonomic neuropathy with with sensory denervation (patients with DM)
Variant (Vasospastic) Angina
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“Prinzmetal angina”
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Caused by coronary artery vasospasm
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Usually occurs during rest, minimal exertion, or nocturnally

ECG changes are transient
Diagnosis and Treatment of Chronic
Ischemic Heart Disease

ECG, echocardiography, exercise stress testing, nuclear imaging studies, cardiac
catheterization and coronary arteriography

Treatment directed toward symptom reduction and prevention of MI



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Lifestyle modification
Pharmacologic agents
 Nitrates (vasodilators), beta-blockers ( myocardial oxygen requirements), calcium
channel blockers (coronary and peripheral artery vasodilation)
Percutaneous intervention (balloon angioplasty, stents)
Coronary bypass grafting
Endocardial Disorders
Infective Endocarditis (IE)

Rare, serious, potentially life-threatening infection of the inner surface of the heart and
cardiac valves

Characterized by colonization or invasion of the valves and endocardium by a microbial
agent leading to destruction of underlying tissue

Contributing factors:


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Obvious (dental procedure) or occult infection (oral cavity, gut or SQ injury)
Host factors (structural valvular abnormalities, neutropenia, immunosuppression, DM, ETOH)
Staphylococcal infections are leading cause
Manifested by fever and chills, anorexia, malaise, petechial or splinter hemorrhages under
the nailbeds
Rheumatic Heart Disease

Cardiac manifestation of rheumatic fever (RF)

RF is an immune-mediated, multisystem inflammatory disease that occurs a
few weeks after a group A streptococcal throat infection

Inflammation of all three layers of the heart
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Likely an immunological response
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Causes chronic deformity and impairment of heart valves
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Rare in developed countries
Valvular Disorders
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Most commonly involves valves are the mitral and aortic valves
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Produce abnormal heart sounds (murmurs)
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Two types of mechanical disruption:
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Stenosis-narrowing of the valve which causes turbulent blood flow and increased
workload in the chamber emptying through the narrowed valve
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Regurgitation-caused by a valve which does not close properly, thereby
permitting backflow
Diagnosis and Treatment of Valvular
Disorders


Diagnosis
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Cardiac auscultation
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Echocardiography
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Transesophageal echocardiography
Treatment

Medical management of heart failure
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Surgical repair or replacement
Mitral Valve Disease
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Mitral valve stenosis
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Incomplete opening of the mitral valve during systole
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Left atrial distension and impaired filling of left ventricle  pulmonary congestion
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Symptoms are related to pulmonary congestion (DOE, PND, palpitations, chest
pain, atrial arrhythmias)
Mitral regurgitation
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Incomplete closure of the mitral valve
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Eventually impairs LV function
Mitral valve prolapse (1 to 2.5% of the population)
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Usually asymptomatic and an incidental finding
Aortic Valve Disorders

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Aortic stenosis
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Usually first diagnosed by the presence of a loud, systolic ejection murmur
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Eventually causes angina, syncope and heart failure
Aortic regurgitation

Incompetent aortic valve that allows blood to flow back to the left ventricle during
diastole
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Eventually left ventricular failure develops (exertional dyspnea, orthopnea, PND)
Disorders of the
Pericardium
Acute Pericarditis

Signs and symptoms resulting from pericardial inflammation of less than 2
weeks duration

Infectious or non-infectious etiology (viral, bacterial, mycobacterial,
connective tissue diseases, uremia, neoplasms, radiation, trauma, drug
toxicity)

Viral infection is the most common cause
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Chest pain, auscultatory pericardial friction rub, electrocardiographic
changes
Pericardial Effusion
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Accumulation of fluid in the pericardial cavity usually a result of an inflammatory or
infectious process

Small effusions or large effusions that develop slowly may not produce symptoms

Sudden accumulations may raise intracardiac pressures that significantly limit venous
return to the heart
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Diagnosed by echocardiography
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Treatment

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Phamacotherapy: diuretics, NSAIDs, corticosteroids
Pericardiocentesis
Cardiac Tamponade

Compression of the heart due to accumulation of fluid or blood in the
pericardial sac
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Life-threatening condition

Key diagnostic finding: pulsus paradoxus (10mm or more fall in systolic BP
that occurs with inspiration)

Treated with closed or open pericardiocentesis
Cardiomyopathies
Primary Cardiomyopathies

Genetic, mixed, or acquired
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Hypertrophic (HCM) - massively hypertrophied LV with disproportionate thickening of the
ventricular septum, abnormal diastolic filling, cardiac arrhythmias, intermittent LV outflow
obstruction
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Dilated (DCM) – characterized by progressive cardiac dilation and systolic dysfunction

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common cause for heart failure and leading indication for heart transplant
frequently familial
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Restrictive – ventricular filling is restricted due to excessive rigidity
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Inflammatory (myocarditis)- usually caused by a viral infection
Secondary Cardiomyopathies
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Heart muscle disease in the presence of a multisystem disorder
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Cardiomyopathies associated with drugs, DM, muscular dystrophy,
autoimmune disorders, and cancer treatment agents
Heart Disease in Infants and Children


Congenital

Most congenital defects arise between the 4th and 7th week of gestation when the
major development of the fetal heart occurs
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Thought to be multifactorial: environmental, genetic and chromosomal influences
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1 in 125 children are born with a congenital heart defect
Acquired

Kawasaki disease

Cardiomyopathy

Rheumatic fever
Fetal and Perinatal Circulation

Fetal circulation if anatomically and physiologically different from the postnatal
circulation

Fetus is maintained in a low oxygen state (PO2 30-35) and fetal CO is higher

Oxygenation of the blood occurs:


Through the placenta before birth
Through the lungs after birth
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40% of the blood moves from the right atrium through the foramen ovale into the left
atrium
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90% of the blood ejected into the pulmonary artery gets diverted through the ductus
arteriosus into the into the ascending aorta
Postnatal Circulation

Foramen ovale closes
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Ductus arteriosus usually closes within 24-72 hours

Factors affecting postnatal pulmonary vasculature development:

Alveolar hypoxia
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Prematurity
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Lung disease
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Congenital heart defects
Congenital Heart Defects
Patent Ductus Arteriosus

Persistence of the fetal ductus beyond the prenatal period
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Persistent patency: open > 3 months

Ductal closure delayed in very premature infants and infants with congenital
heart defects
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Contributing factors:
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Infant hypoxia
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Fall in endogenous levels of prostaglandins and adenosine

Release of vasoactive substances
Atrial Septal Defects

Opening in the atrial septum persists as a result of improper septal
formation

Single or multiple

Small to large

Most common is the ostium secundum defect

Most children are asymptomatic
Ventricular Septal Defect

An opening in the ventricular septum that results from incomplete
separation of the ventricles during early fetal development

Most common form of congenital defect

Signs and symptoms range from asymptomatic murmur to congestive heart
failure

Approximately 1/3 small defects close spontaneously

Large defects cause shunting of blood with eventual development of
symptoms (tachypnea, diaphoresis and failure to thrive)
Endocardial Cushion Defects
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2% of all congenital heart defects
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Seen in 30% of children with Down syndrome

Partial or complete

Abnormalities similar to atrial and ventricular septal defects
Pulmonary Stenosis

Obstruction of blood flow from the right ventricle to the pulmonary
circulation
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10% of all congenital heart defects
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Produces some impairment of the pulmonary blood flow an dincreases
workload of right side of the heart
Tetralogy of Fallot

Most common cyanotic congenital heart defect
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Four associated defects:

Ventricular septal defect
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Dextroposition (aorta overrides the RV and is in communication with the septal
defect)
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Obstruction or narrowing of the pulmonary outflow channel (pulmonic valve
stenosis, decrease in pulmonary trunk)

Hypertrophy of the RV
Transposition of the Great Arteries

Aorta arises from the RV
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Pulmonary artery arises fro the LV
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More common in mothers with DM

Two to three times more common in boys
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Cyanosis is most common presenting symptom

Ventricular septal defects are present in 50% of infants
Coarctation of the Aorta

Localized narrowing of the aorta

Frequently associated with other congenital heart defects

Classic sign: Disparity in pulsations and blood pressures in the arms and
legs; pulsations are weak or delayed in lower extremities

Functional Single Ventricle
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Only one functional ventricle

Surgical palliation with a series of operations

Long-term outcomes uncertain
Kawasaki Disease

Acute vasculitis with potential for involvement of the coronary arteries

Occurs predominantly in young children (80% < 5 years old)

Leading cause of acquired heart disease

Triphasic

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Acute febrile phase (7-14 days): fever, conjunctivitis, redness and swelling of
hands and feet, strawberry tongue
Subacute phase (10-24 days): desquamation of the skin on fingers and toes,
arthritis and GI manifestations
Convalescent phase: until symptoms subside