CHAPTER 12

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THE HEART

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3 types of damage to valves:
• Damage to collagen
• Calcification
• Fibrous thickening
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• Cardiac myocytes rely exclusively on oxidative phosphorylation to meet energy needs and therefore
are very sensitive to ischemia.
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Causes of cardiovascular dysfunction
• Failure of pump
• Obstruction to flow
• Regurgitant flow
• Shunted flow
• Disorders of cardiac conduction
• Rupture of the heart or major vessel
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CONGESTIVE HEART FAILURE
• The hypertrophied heart will eventually decompensate because capillaries do not increase
proportionally to the muscle mass.
• The increased muscle mass requires increased nutrients so eventually the heart outgrows its blood
supply and decompensates.
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Left-sided heart failure
• Major causes include:
• IHD
• Hypertension
• Aortic and mitral valve disease
• Myocardial disease
• Clinical features:
• pulmonary congestion and edema
• left atrial dilation with atrial fibrillation
• ↓ renal perfusion: salt and water retention, ATN, impaired waste excretion
• hypoxic encephalopathy
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Right-sided heart failure
• Major causes include:
• Left-sided failure
• tricuspid or pulmonary valve disease
• Pulmonary parenchymal diseases
• Pulmonary vascular diseases
• Clinical features:
• RA and RV dilation and hypertrophy
 • edema, esp in dependent peripheral locations with serous effusions (pleural, pericardial,
peritoneal)
• hepatomegaly with centrilobular congestion and atrophy (can lead to centrilobular necrosis and
cardiac cirrhosis)
• Congestive splenomegaly
• renal congestion with hypoxic injury and ATN (more marked on right side than left)
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CONGENITAL HEART DISEASE
• Most arise from faulty embryogenesis from 3 – 8 weeks. Incidence 1%.
• Non-syndromic (gene mutation versus environmental stress) vs syndromic (Down syndrome most
common in this category).
• Most common are VSD, ASD, pulmonary stenosis, patent ductus, tetralogy, coarc.
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Classification of congenital heart disease:
• Left to right shunt (ASD, VSD, PDA)
• If unrepaired can lead to pulmonary hypertension – Eisenmenger syndrome
• Right to left shunt (the 5 t’s)
• Obstructive (coarc, aortic and pulmonary valve stenosis, atresias)
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Defects associated with cyanosis:
• Tetralogy of Fallot: VSD, plum stenosis with RV outflow obstruction, overriding aorta, RVH
• Truncus Arteriosus
• Transposition of the Great Vessels
• Total anomalous pulmonary venous connection
• Tricuspid atresia
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Types of ASD
• Primum
• Secundum – 90% and not associated with syndromes
• Venosus
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Types of VSD
• Membranous
• Muscular
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ISCHEMIC HEART DISEASE
• MI
• Angina
• Heart failure
• Sudden cardiac death
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Chronic atherosclerosis
• A fixed lesion obstructing at least 75% of the lumen is required to produce symptoms
• Obstruction of 90% of the lumen can produce symptoms at rest
• Acute coronary syndromes are most commonly due to plaque rupture
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Consequences of ischemia
• Angina
• Stable
• Prinzmetal – vasospasm
 • Unstable – plaque disruption, preinfarction angina
• Myocardial infarction
• 90% due to coronary artery occlusion due to plaque rupture
• 10% due to:
▪ Vasospasm
▪ Emboli
▪ Other (vasculitis, hematologic – sickle cell, amyloid, dissection, shock – low blood
pressure)
• Permanent damage generally occurs after 2 hours, complete within 6 hours
• Classified as transmural versus subendocardial and global versus regional
• First year mortality 30%
• Chronic IHD – heart failure as a consequence of ischemic myocardial damage
• Sudden cardiac death – unexpected death due to cardiac causes in a person with or without a history
of heart disease occurring within 1 hour of symptom onset or with no cardiac symptoms
• Usually due to lethal arrhythmia, most commonly due to IHD
▪ Congenital abnormalities
▪ Aortic valve stenosis
▪ Mitral valve prolapse
▪ Myocarditis
▪ Cardiomyopathies
▪ Pulmonary hypertension
▪ Hereditary/acquired arrhythmia (WPW, long QT)
▪ Cardiac hypertrophy
▪ Other – metabolic abnormality, drugs, hematologic, catecholamines
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Morphological changes in MI
• 0 – 4 hours: none or pallor and some wavy fibers, necrosis can be highlighted with phenyltetrazolium
chloride
• 4 – 12 hours: dark mottling, early coagulative necrosis, edema, hemorrhage
• 12 – 24 hours: dark mottling, contraction band necrosis, neuts
• 1 – 3 days: mottling with yellow center, lot of neuts and necrosis
• 3 – 7 days: yellow and soft centre with a red margin, macs at infarct border; myocyte breakdown
• 7 – 10 days: yellow with red margin, lots of macs with granulation tissue at the periphery
• 10 – 14 days: red-grey, granulation tissue
• 2 – 8 weeks: gray-white, collagen deposition
• 2 months: dense scar
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Consequences and complications of MI
• Contractile dysfunction
• Arrhythmias
• Myocardial rupture syndromes (from most common to least common)
• Free wall
• Septum
• Papillary muscle
• Pericarditis (day 2 – 3) - aka Dressler syndrome
• RV infarct
• Infarct extension and expansion
• Mural thrombus
• Ventricular aneurysm
• Papillary muscle dysfunction
• Congestive heart failure
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HYPERTENSIVE HEART DISEASE
• Concentric LV hypertrophy in the absence of other CV pathology and clinical history of htn
• Clinical consequences:
• None
• IHD
• Renal damage
• Heart failure or SCD
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Etiologies of cor pulmonale
• Diseases of pulmonary parenchyma
• COPD
• Interstitial fibrosis
• CF
• bronchiectasis
• Diseases of pulmonary vessels
• Recurrent PE
• Primary PH
• Vasculitis
• Drug, toxin, radiation
• Tumor embolism
• Disorders affecting chest movement
• Disorders of pulmonary arterial constriction
• Metabolic
• Hypoxemia
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ENDOCARDITIS
• Infective
• Acute
• Subacute
• Normal versus abnormal valve
• Duke criteria: positive blood culture, mass on echo, new regurg
• Microemboli produce Janeway lesions, Osler nodes, Roth spots
• Rheumatic
• Noninfective
• Marantic: veg along closure lines
• Libman-sacks: veg on either side of valve leaflets, assoc with fibrinoid necoriss and inflame
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Complications of Prosthetic valves
• Thrombosis and embolism
• Hemorrhage due to meds
• IE
• Valve degeneration/dysfunction
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CARDIOMYOPATHIES – Heart disease from an abnormal myocardium
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Dilated (impaired systolic fnx)
• Primary
• Genetic, EtOH, peripartum, myocarditis, hemochromatosis, anemia, drugs, sarcoidosis
• Secondary
 • IHD, valvular disease, HHT, congenital heart disease
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Hypertrophic (impaired diastolic fxn)
• Primary
• Genetic, Friedrich ataxia, storage diseases, infants of diabetic mothers
• Secondary
• hypertensive HD, aortic stenosis
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Restrictive (impaired diastolic fxn)
• Primary
• Amyloid, radiation, fibrosis, idiopathic
• Secondary
• Pericardial constriction
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Conditions associated with heart muscle disease
• Infections
• Toxins
• Metabolic
• Neuromuscular
• Storage disorders
• Infiltrative
• Immunological
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Major causes of myocarditis
• Infections
• Viral
• Chlamydia
• Rickettsiae
• Bacteria
• Fungal
• Protozoal (Chagas)
• Helminths (Trichinosis)
• Immune-mediated
• Post viral
• Post-strep (RF)
• SLE
• Drug reaction
• Transplant rejection
• Other
• Sarcoid
• Giant cell myocarditis
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Catecholamine effect
• Foci of myocardial necrosis with contraction bands associated with sparse inflammatory infiltrate,
mostly macs.
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Cardiac amyloidosis
• Systemic, isolated atrial, or senile:
• Senile cardiac amyloidosis due to transthyretin (synthesized in the liver)
• More common in African Americans
• Isolated atrial amyloidosis can occur from deposition of ANP.
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Classification of pericarditis
• Serous, fibrinous, hemorrhagic (most commonly neoplastic), purulent, caseous.
Causes of pericarditis
• Infectious
• Viral (URTI, mumps)
• Bacterial (direct extension form pneumonia, etc)
• TB
• Fungi
• Immunologic
• CTD – RF, SLE, Scleroderma
• Post MI (Dressler)
• Post cardiotomy
• Drugs
• Other
• Uremia
• Neoplasia
• Trauma
• Radiation
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Consequences of pericarditis
• Adhesive pericarditis (usually no clinical consequence)
• Adhesive mediastinopericarditis (parietal layer of myocardium adheres to the mediastinum, strains
cardiac function)
• Constrictive pericarditis
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Cardiac tumors
• Myxoma
• Lipoma
• Papillary fibroelastoma
• Rhabdomyoma
• Sarcoma
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Cardiovascular effects of noncardiac neoplasms
• Direct consequences of tumor
• Mets
• Large vessel obstruction
• Tumor emboli
• Complications of circulating mediators
• NBTE
• Carcinoid heart
• Catecholamine heart
• Amyloidosis
• Effects of therapy
• Chemo and RT
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