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The Heart


... cognitive abnormalities, facial anomalies Hypoplastic left heart syndrome severe stenosis of atresia ... ASD 25% right aortic arch Clinical ... – PowerPoint PPT presentation

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Title: The Heart

The Heart
Cardiac Structure and Specializations
  • Myocardium
  • Valves
  • Conduction system
  • Blood supply

Effects of Aging on the Heart
  • Table 12-1

Heart disease Overview of Pathophysiology
  • Failure of the pump
  • Obstruction to flow
  • Regurgitant flow
  • Shunted flow
  • Disorders of cardiac conduction
  • Rupture of the heart or a major vessel

Heart Failure
  • Heart is unable to pump blood as a rate
    sufficient to meet the metabolic demands of the
    tissues or can do so only at elevated filling
  • Systolic dysfunction progressive deterioration
    of myocardial contractile function
  • Diastolic dysfunction inability of the chamber
    to expand and fill during diastole
  • Several physiologic mechanisms maintain arterial
    pressure and perfusion of vital organs
  • Frank-Starling mechanism
  • Myocardial adaptations, including hypertrophy
    with/without chamber dilation ventricular
  • Activation of neurohumoral systems
  • Release of norepinephrine increases HR,
    contractility, vascular resistance
  • Activation of the renin-angiotensin-aldosterone
  • Release of atrial natriuretic peptide

Heart Failure
  • Cardiac Hypertrophy Pathophysiology and
    Progression to Failure
  • Left-sided Heart Failure
  • Right-sided heart failure

Cardiac Hypertrophy
  • Increased mechanical work due to pressure or
    volume overload or trophic signals causes
    myocytes to increase in size
  • Increased protein synthesis, increased in DNA
    ploidy, increased number of mitochondria,
    increased size of nuclei
  • Pressure-overload hypertrophy concentric
    increase in wall thickness, sarcomere in parallel
  • Volume-overload hypertrophy ventricular
    dilation sarcomeres in series
  • Oxygen supply to hypertrophied heart is tenuous,
    deposition of fibrous tissue, shift to fetal gene
    expression pattern, heightened metabolic demand
  • Vulnerable to decompensation
  • Physiologic vs pathologic hypertrophy
  • CHF variable degrees of decreased cardiac
    output and tissue perfusion, as well as pooling
    of blood in the venous system

Left-sided Heart Failure
  • Causes
  • Ischemic heart disease
  • Aortic and mitral valvular disease
  • Myocardial diseases
  • Pulmonary edema heart failure cells, Kerley B
  • Clinically cough, dyspnea, orthopnea, PND,
    atrial fibrillation, increased vascular and
    extracellular volume, pre-renal azotemia, hypoxic

Rigth-sided Heart Failure
  • Causes
  • Most common is left-sided failure
  • Cor pulmonale (pulmonary hypertension)
  • Congestion liver and portal system, pleural,
    pericardial, peritoneal spaces, peripheral edema
  • Clinically hepatosplenomegaly,peripheral edema,
    pleural effusions, ascites, hypoxia of CNS

Congenital Heart Disease
  • CHD Abnormalities of the heart or great vessels
    present from birth
  • Most faulty embryogenesis during the 3rd-8th
    week when the CVS form and begin functioning
  • Worst ones dont survive to term
  • Those who do usually have only discrete regions
    of the heart affected e.g. septal defect or
    valvular defect

  • Dx
  • Some when change from fetal to postnatal
  • 50 diagnosed by one year of life
  • Mild forms - adulthood

  • Incidence
  • 1 of all live births
  • CV defects among most common malformations and
    are the most common cause of heart disease in
  • Higher in premies and stillborns
  • Table 12-2
  • VSD most common
  • Tetralogy of Fallot most common cyanotic
  • Many survive into adulthood repairs
  • Common problems
  • Arrhythmias
  • Additional surgery
  • Ventricular dysfunction
  • Use of prosthetics
  • Risk of childbearing

  • ECM swellings endocardial cushions
  • Future valve development
  • Day 50 4 chambered heart
  • Signaling pathways regulating TFs
  • Wnt
  • VEgf
  • bone morphogenetic factor
  • TGF-beta
  • FGF
  • Notch
  • Heart mechanical organ exposed to flowing
    blood from earliest stages hemodynamic forces
    play a role
  • Specific micro RNAs critical role- patterns and
    levels of TF expression

  • Cardiac Development figure 12-3
  • First heart field
  • TFs TBX5, Hand1
  • Mainly LV
  • Second heart field
  • TF Hand2, FGF10
  • Outflow tract, RV, most of atria
  • Cardiac neural crest
  • Septation of outflow tract, aortic arches

  • AD mutations partial loss of function in one or
    more required factors, TFs usually
  • The main known cause of CHD consist of sporadic
    genetic abnormalities.
  • single gene mutations
  • small chromosome deletions
  • additions or deletions of whole chromosomes
  • Table 12-3

  • Heterozygotes 50 reduction in activity
    deranged cardiac development
  • Factors work together- large protein complexes
    different single gene mutations produce similar
  • Signaling pathways or structural roles
  • NOTCH1 bicuspid AV
  • Fibrillin Marfans

  • DiGeorge Syndrome
  • Small deletion of 22q11.2 in 50
  • 4th branchial arch and 3rd and 4th pharyngeal
  • Thymus, parathyroids, heart
  • TBX1
  • Chromosomal aneuploidies
  • Turner Syndrome
  • Trisomies 13,18, 21
  • 21- most common genetic cause of CHD
  • endocardial cushion defects

  • First-degree relatives of affected patients are
    at increased of CHD subtle forms of genetic
  • Environmental factors?
  • /- genetic factors
  • congenital rubella infection
  • gestational diabetes
  • exposure to teratogens
  • nutritional factors?
  • transient environmental stresses during 1st

  • Clinical features
  • Left-to-right shunts
  • Right-to-left shunts
  • Obstructive lesions
  • Shunt abnormal communication between chambers or
  • Obstruction narrowing (if complete- atresia)

  • R to L
  • Hypoxemia
  • Cyanosis
  • Emboli bypass lungs brain infarction, abscess
    ( paradoxical embolism)
  • Clubbing (hypertrophic osteoarthropathy)
  • Polycythemia

  • L to R
  • Normally low-pressure, low-resistance pulmonary
    circulation now sees high flow volumes and
  • RVH
  • Atherosclerosis of pulmonary vessels
  • medial hypertrophy
  • vasoconstriction
  • irreversible obstructive intimal lesions
  • Pulm pressures reach systemic levels
  • R to L shunt
  • Eisenmenger Syndrome
  • Altered hemodynamics of CHD
  • Dilation, hypetrophy or both
  • Decreased volume and muscle mass hypoplasia
    before birth, atrophy postnatally

  • L to R
  • ASD
  • VSD
  • PDA
  • AV septal defects

  • ASD
  • abnormal, fixed opening in the atrial septum
  • usually asymptomatic until adulthood
  • 3 types
  • Secundum (90) center of the septum
  • Primum (5) adjacent to the AV valves
  • Sinus venosus ( 5) SVC, associated with APVR
  • Clinical
  • L to R
  • Pulmonary blood flow -2-4 times normal
  • murmur from increased pulmonic valve blood flow
  • Surgical or catheter correction low
    mortality, normal long-term survival
  • PVO oval fossa, 80 closed permanently, 20
    potential opening that can become clinically
    important r-to-l

  • VSD
  • Most common congenital anomaly
  • 20-30 isolated finding
  • Most are associated with other cardiac anomalies
  • Classified by size and location
  • 90 membranous
  • Rest are infundibular ( below the PV) or
  • Muscular can be multiple ( Swiss-cheese)
  • Clinical
  • Large problems from birth, RVH, pulmonary
    hypertension, correct before irreversible
  • Smaller well-tolerated

  • PDA
  • DA stays open, allowing L to R shunt from aorta
    to pulmonary artery
  • 90 isolated anomaly
  • machinery-like murmur
  • close as soon as possible to prevent
    irreversible PH
  • Some congenital lesions are ductus dependent
    and there by need to keep the DA open-
  • e.g. aortic atresia, use prostaglandin E

  • AV septal defect
  • Complete atrioventricular canal defect
  • Partial primum ASD with mitral insufficiency
  • Complete large combined AV septal defect and
    a common AV valve all 4 chambers communicate,
    all have hypertrophy
  • 1/3 have Down syndrome
  • Surgically correctible

  • R to L
  • Tetralogy of Fallot
  • Transposition of the Great Arteries
  • Truncus arteriosus
  • Tricupsid Atresia
  • Total Anomalous Venous Connection

  • Tetralogy of Fallot
  • 4 cardinal features
  • VSD
  • Obstruction of the right ventricular outflow
    tract (subpulmonary stenosis)
  • An aorta that overrides the VSD
  • RVH
  • Embryoloigcally anterosuperior displacement of
    the infundibular septum
  • Boot-shaped heart marked apical RVH
  • Sometimes PVS, PV atresia
  • Sometines AV insufficiency, ASD
  • 25 right aortic arch
  • Clinical Classic TOF r-to-l shunt
  • Pink TOF l to r shunt because of mild
    subpulmonary stenosis
  • As child grows obstruction becomes worse
  • Stenosis protects pulmonary arteries from
    overload and RV failure rare because RV
    decompressed by the VSD

  • TGA
  • Ventriculoarterial discord
  • Aorta from RV
  • PA from LV
  • Separation of the systemic and pulmonary
  • circulations incompatible with life unless
    a shunt exists VSD or PFO or PDA or artificial
    shunt balloon atrial septostomy
  • Surgical repair

  • TA
  • Failure of separation into the aorta and PA
  • Single vessel giving rise to the systemic,
    pulmonary and coronary circulation
  • Associated VSD

  • TAPC
  • Pulmonary veins fail to join the left atrium
  • PFO or ASD
  • Aplastic Left atrium
  • LV normal size

  • Obstructive Congenital Anomalies
  • Coartation of the aorta
  • PS and atresia
  • AS and atresia

  • Coarctation of the Aorta
  • Males 2x females
  • Associated with Turner syndrome
  • 2 classic types
  • Infantile
  • hypoplasia of the arch proximal to a PDA,
    symptomatic in early childhood, cyanosis over
    lower half of body, surgical correction
    needed early
  • Adult
  • discrete ridgelike infolding of the aorta,
    just opposite a closed DA (ligamentum
    arteriosus) distal to the arch vessels,
    hypertension in upper extremities, signs of
    arterial insufficiency in lower, notching of
    the ribs due to collateral circulation
  • Clinical
  • murmur with thrill
  • LVH

  • PS and atresia
  • Obstruction of the PV
  • Isolated or part of a more complex anomaly
  • RVH
  • Poststenotic dilation of PA
  • Complete obstruction- need shunt to survive
  • Mild asymptomatic
  • Symptomatic surgical correction

  • AS and atresia
  • Vavular-hypoplastic, dysplastic, decreased
  • Subvalular-dense fibrous tissue below the cusps
  • Supravavular- aortic dysplasia, thickened and
    constricted, deletion on chromosome 7, elastin
    gene, Williams- Beuren syndrome,
  • hypercalcemia, cognitive abnormalities, facial
  • Hypoplastic left heart syndrome severe
    stenosis of atresia underdevelopment of LV
    and aorta endocardial fibroelastosis
  • Clinical systolic murmur, thrill, LVH,
    antibiotic prophylaxis for SBE, avoid strenuous
    activity, sudden death

Ischemic Heart Disease
  • Leading cause of death worldwide for both men and
  • Ischemia oxygen and nutrients insufficiency
  • 90 cause is atherosclerotic lesions in the
    coronary arteries, thus coronary artery disease
  • Other causes emboli, blockage of small
    myocardiql blood vessels, shock

Ischemic Heart Disease
  • Angina Pectoris
  • Myocardial Infarction
  • Chronic IHD ischemic cardiomyopathy
  • Sudden cardiac death

Ischemic Heart Disease
  • Peak in mortality in 1963, fallen by 50 since
    then due to prevention, diagnostic and
    therapeutic advances
  • The dominant cause of the IHD syndromes is
    insufficient coronary perfusion relative to
    myocardial demand, due to chronic, progressive
    atherosclerotic narrowing of the epicardial
    coronary arteries, and variable degrees of
    superimposed acute plaque change, thrombosis, and

Ischemic Heart Disease
  • Fixed lesion obstructing gt 75 of the lumen leads
    to Symptomatic ischemia precipitated by exercise
  • Obstruction of 90 leads to symptoms even at rest
  • May lead to formation of collateral vessels over
  • Clinically significant stenotic lesions tend to
    predominate in the first several centimeters of
    the LAD and LCX and along the entire length of
    the RCA

Angina Pectoris
  • Paroxysmal and usually recurrent attacks of
    substernal or precordial chest discomfort cause
    by transient myocardial ischemia that fall short
    of inducing myocyte necrosis
  • Three overlapping patterns
  • Stable or typical angina
  • Prinzmetal variant angina
  • Unstable or crescendo angina

Myocardial Infarction
  • Death of cardiac muscle due to prolonged severe
  • Sequence of events in typical MI
  • Sudden change in an atheromatous plaque
  • Platelets adhere, become activated, release their
    granule contents, and aggregate to form
    microthrombi when exposed to subendothelial
    collagen and necrotic plaque contents
  • Vasospasm is stimulated by mediators released by
  • Tissue factor activates the coagulation pathway,
    adding to the bulk of the thrombus
  • Frequently within minutes, the thrombus evolves
    to completely occlude the lumen

Myocardial Infarction
  • Myocardial response
  • Cessation of aerobic metabolism within seconds
    leading to inadequate high-energy phosphates and
    accumulation of lactic acid
  • Severe ischemia induces loss of contractility
    within 60 seconds
  • Ultrastructural changes potentially reversible,
    develop within a few minutes
  • Myofibrillar relaxation
  • Glycogen depletion
  • Cell and mitochondrial swelling

Myocardial Infarction
  • Table 12-4 Approximate time of onset of key
    events in ischemic cardiac myocytes
  • Key feature in the early phases of myocyte
    necrosis disruption of the integrity of the
    sarcolemmal membrane allowing intracellular
    macromolecules to leak out of cells into the
    cardiac interstitium and ultimately into the
    microvasculature and lymphatics in the region of
    the infarct

Myocardial Infarction
  • In most cases of acute MI, permanent damage to
    the heart occurs when the perfusion of the
    myocardium is severely reduced for an extended
    interval (usually at least 2-4 hours). This delay
    in the onset of permanent myocardial injury
    provides the rationale for rapid diagnosis in
    acute MI to permit early coronary intervention,
    the purpose of which is to establish reperfusion
    and salvage as much at risk myocardium as

Myocardial Infarction
  • Precise location, size, and specific morphologic
    features of an acute MI depend on
  • Location, severity, and rate of development of
    coronary obstruction
  • Size of the vascular bed perfused by the
    obstructed vessels
  • Duration of the occlusion
  • Metabolic/oxygen needs of the myocardium at risk
  • Extent of collateral vessels
  • Presence, site, severity of coronary arterial
  • Other factors HR, rhythm, blood oxygenation

Myocardial Infarction
  • Typically
  • LAD apex, anterior wall of LV, anterior 2/3 of
    ventricular septum
  • The coronary artery that perfuses the posterior
    third of the septum is called dominant ( either
    the LCX or RCA)
  • Right dominant circulation (4/5 of population)
  • LCX lateral wall of the LV
  • RCA entire RV free wall, posterobasal wall of
    the LV, posterior third of the septum

Myocardial Infarction
  • Transmural vs subendocardial infarction
  • Most MIs are transmural full thickness in the
    distribution of a single artery, ST elevation
  • Subendocardial area of necrosis limited to
    inner 1/3 to1/2 of ventricular wall, non-ST
    elevation, normally the least perfused area of
    the myocardium, most vulnerable to ischemia

Myocardial Infarction
  • Infarct modification by reperfusion
  • Reperfusion most effective way to rescue
    ischemic myocardium
  • May trigger deleterious complications
  • Arrhythmias
  • Myocardial hemorrhage with contraction bands
  • Irreversible cell damage superimposed on the
    original ischemic injury (reperfusion injury)
  • Microvascular injury
  • Prolonged ischemic dysfunction (myocardial

Myocardial Infarction
  • Appearance of reperfused myocardium
  • Hemorrahagic
  • Irreversibly injured myocytes contraction bands
  • Reperfusion not only salvages reversible injured
    cells but alters the morphology of lethally
    injured cells

Myocardial Infarction
  • Consequences and Complications
  • Contractile dysfunction
  • Arrhythmias
  • Myocardial rupture
  • Pericarditis
  • Right ventricular infarction
  • Infarct extension
  • Infarct expansion
  • Mural thrombus
  • Ventricular aneurysm
  • Papillary muscle dysfunction
  • Progressive late heart failure

Morphologic Changes in Acute Myocardial Infarction
Early Risk of Arrhythmia Time Gross
½-4 hours None None, variable waviness of fibers at border
4-12 hours Occasional dark mottling Early coagulation necrosis, edema, hemorrhage
12-24 hours Dark mottling Ongoing coagulation necrosis, pyknosis of nuclei, myocyte eosinophilia,contraction band necrosis, early neutrophilic inflitration
1-3 days Mottling with yellow-tan infarct center Coagulation necrosis with loss of nuclei and striations Brisk interstitial neutrophil infiltration
Middle Risk of Myocardial Rupture Time
Gross LM
3-7 days Hyperemic border central yellow-tan softening Beginning disintegration ofdead myofibers, dyingneutrophils, early phagocytosis by macrophages
7-10 days Maximally yellow-tan and soft, with depressed margins Well-developed phagocytosis of dead cells early formation, of granulation tissue at margins
10-14 days Red-gray depressed infarct borders Well- established granulation tissue

Late Risk of Ventricular Aneurysm
Time Gross LM
2-8 weeks Gray-white scar, progressive from border toward core of infarct Increased collagen with decreased cellularity
gt2 months Scarring complete Dense collagenous scar
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Serum Enzyme changes in Acute MI
Time CK-MB Troponin I (most sensitive and specific) LDH
6 hours Weakly positive Weakly positive
12-16 hours Strongly positive Strongly positive
24 hours__ 2 days____ 3 days____ 4-7 days Peaks____ Persists___ Negative__ Peaks____ Persists___ Persists___ Persists Peaks____ Persists
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Sudden Cardiac Death
  • Usually the consequence of a lethal arrhythmia
  • Acute myocardial ischemia is the most common
    trigger for fatal arrhythmias
  • Nonatherosclerotic causes
  • Congenital structural of coronary arterial
  • AS
  • MVP
  • Myocarditis
  • Dilated or hypertrophic cardiomyopathy
  • Pulmonary hypertension
  • Hereditary or acquired arrhythmias
  • Cardiac hypertrophy of any cuase
  • Other miscellaneous

Hypertensive Heart Disease
  • Systemic (Left-sided) hypertensive heart disease
  • LVH (concentric usually) in absence of other CV
  • History of pathological evidence of hypertension
  • Pulmonary (Right-sided) hypertensive heart
    disease (Cor pulmonale)
  • Table 12-6 -disorders predisposing to cor

Valvular Heart Disease
  • Valvular degeneration associated with
  • Calcific aortic stenosis
  • Calcific stenosis of congenitally bicuspid aortic
  • Mitral annular calcification
  • Mitral Valve Prolapse (Myxomatous degeneration of
    the mitral valve)
  • Rheumatic Fever and rheumatic heart disease
  • Infective endocarditis
  • Noninfected vegetations
  • Nonbacterial thrombotic endocarditis
  • Endocarditis of systemic lupus erythematosus
    (Libman-Sacks disease)
  • Carcinoid heart disease
  • Complications of artificial valves

Valvular Heart Disease
  • Stenosis pressure overload
  • Insufficiency (regurgitation) volume overload
  • Acquired stenosis of the aortic and mitral valves
    account for 2/3 of all cases of valve disease
  • Most frequent
  • AS calcification of normal or bicuspid valve
  • AI dilation of ascending aorta
  • MS RHD
  • MI MVP
  • Table 12-7 Major etiologies of acquired lesions

Mitral Valve Prolapse
  • One or more of the leaflets are floppy and
    prolapse into the left atrium during systole
  • Myxomatous degeneration
  • Most patient are asymptomatic
  • Midsystolic click
  • Chest pain, dypsnea, fatigue
  • Complications
  • Infective endocarditis
  • MI
  • Stroke
  • Arrhythmias

Rheumatic Fever and Rheumatic Heart Disease
  • Rheumatic fever
  • Acute, immunologically mediated, occurs a few
    weeks after an episode of group A strep
  • Antibodies and T cell-mediated reactions
    against M proteins cross-react with heart self-
  • Jones criteria
  • Major migratory polyarthritis of large joints,
    pancarditis, subcutaneous nodules, erythema
    marginatum, Sydenham chorea
  • Minor fever, arthralgia, elevated acute-phase
  • 2 major or 1 major and 2 minor evidence of a
    preceeding strep infection

Rheumatic Fever and Rheumatic Heart Disease
  • RF Aschoff bodies, caterpillar cells, Mac
    Callum plaques
  • RHD leaflet thickening, commissural fusion and
    shortening, thickening and fusion of the
    tendinous cords

Infective Endocarditis
  • Colonization or invasion of the heart valves or
    the mural endocardium by a microbe
  • Vegetations thrombotic debris and organisms,
    destruction of the tissue
  • Acute infection of a previously normal heart by
    a virulent organism, S. Aureus
  • Subacute insidious infection of deformed valves
    with less virulent organisms, S viridnas, HACEK,
    S. epidermidis
  • Table 12-8 Diagnostic criteria for IE

  • Dilated cardiomyopathy
  • Arrhythmogenic right ventricular cardiomyopathy
  • Hypertrophic cardiomyopathy
  • Restrictive cardiomyopathy
  • Myocarditis
  • Other causes of myocardial disease

  • Table 12-10 Cardiomyopathy and Indirect
    Myocardial Dysfunction
  • Table 12-11 Conditions associated with Heart
    Muscle disease
  • Figure 12-32 Causes and consequences of Dilated
    and Hypertrophic Cardiomyopathy
  • Table 12-12 Major Causes of Myocarditis

Other Causes of Myocardial Disease
  • Cardiotoxic drugs
  • Catecholamines
  • Amyloidosis
  • Iron overload
  • Hyperthyroidisn
  • Hypothyroidism

Pericardial Disease
  • Pericardial effusion and hemopericardium
  • Cardiac tamponade
  • Pericarditis Table 12-13 - causes
  • Acute pericarditis friction rub, fever, pain
  • Chronic or healed pericarditis adhesive,
  • Heart disease associated with rheumatologic

Tumors of the heart
  • Primary cardiac tumors
  • Myxoma most common in adults, ball-valve
    obstruction. Carney complex
  • Lipoma
  • Papillary fibroelastoma
  • Rhabdomyoma most commonin children, TS
  • Sarcoma
  • Cardiac effects of noncardiac neoplasms Table

Cardiac Transplantation
  • Rejection resembles myocarditis
  • Graft arteriopathy silent Mis
  • 1-year survival - 70-80, 5-year - gt60