Cardiac Pathology

Congestive heart failure

The heart can no longer eject blood delivered to it by the venous. system

Left sided heart failure

HTN, aortic valve, mitral valve disease, ischemic heart disease (IHD)

Right sided heart failure

left ventricular failure, cor pulmonale, pulmonary valve, tricuspid valve disease

CHF: morphologic findings

• Congestion of venous circulation

• Pulmonary edema

• Systemic venous congestion and soft tissue edema

• Decreased perfusion of kidneys

Left side heart failure in depth

• Pulmonary congestion and edema

• Elevation of pulmonary venous pressure

• Heart failure cells: hemosiderin-laden macrophages in the lungs

• Brown induration of the lungs: fibrosis and hemosiderin deposition

Right sided heart failure in depth

• Congestion of the abdominal viscera

• Soft tissue edema

• Fluid in the pericardial, pleural, and peritoneal cavities

• Chronic passive congestion

• Cardiac cirrhosis: liver cirrhosis due to heart failure

Chronic heart failure (CHF) clinical feature

• Dyspnea

• Orthopnea

• Lung rales

• Pedal edema

Ischemic heart disease

• AKA Coronary heart disease

• Imbalance between myocardial oxygen demand and blood supply

• Most common cause  is a reduction in coronary artery blood supply

• Single most common cause of death (COD) in developed countries

Ischemic heart disease different types:

• Angina pectoris

• Acute myocardial infarct

• Sudden cardiac death

• Chronic ischemic heart disease

Ischemica heart disease

• HTN, D.M., LDL and cholesterol

• Genetics

• Sex

• Age

IHD Pathogenesis

• Greater than 75% reduction in the lumen of the coronary artery

• Changes in plaque morphology often result in ischemic heart disease, aka myocardial infarction. 

• Platelet aggregation within the coronary artery contributes to the narrowing of the lumen 

• Coronary artery thrombosis: lipid-rich plaque debris

• Coronary artery spasm

Angina pectoris

• Chest pain or pressure

• Typical angina pectoris: fixed degree of narrowing

• Prinzmetal’s angina: artery spasm

• Unstable angina pectoris: increased frequency of pain due to plaque change

Typical angina

fixed degree of narrowing P

Prinzmetal”s angina

artery spasm

Unstable angina pectoris

Increased frequency of pain due to plaque change

Myocardial Infarction (MI)

• Myocardial necrosis caused by ischemia

• Most acute MIs are caused by coronary thrombosis

• Disruption of the underlying plaque

• Begin within 20 to 30 minutes of the time of occlusion

• An acute myocardial infarct begins in the subendocardial region

• The location of MI is determined by the site of occlusion

• Left anterior descending coronary artery(LAD): anterior and apex of LV and septum

• Right coronary artery(RCA): posterior and basal LV

• Left circumflex: lateral wall of LV

What determines the size of a myocardial infarct

• Occlusions arising closer to the origin in the aorta cause larger infarcts

• Degree of collateral circulation: the greater the amount of collateral blood vessels results in smaller infarcts

• More distal occlusions cause smaller infarcts

• In older patients, collateral circulation may limit the size of the infarct

MI- morphology

• Appearance is determined by age

1. Coagulation necrosis with neutrophil infiltration

2. Formation of granulation tissue

3. Resorption of necrotic myocardium

4. Organization of granulation tissue to form a scar

One day old MI

• Coagulation necrosis and wavy fibers

• Edema and neutrophils

• Normal myocardium

MI 3-4 days old

• Dense neutrophilic infiltrate

• Continued coagulation necrosis

MI 7-10 days

Removal of necrotic myocytes by macrophages

Granulation tissue in MI

• Replacement of necrotic myocardium by granulation tissue

• Loose collagen and abundant capillaries

Well healed infarct

• Necrotic tissue has been replaced by dense collagenous scar tissue

• Remaining viable myocytes have compensatory hypertrophy

Complications of MI

• Papillary muscle dysfunction and rupture: 3 days post-MI

• Ventricular and septal rupture: 4 to 7 days post-MI

• Mural thrombi: potential for systemic emboli

• Acute pericarditis: 2-4 days post MI

• Ventricular aneurysms: bulging of fibrous myocardium

Clinical feature of MI

• Substernal chest pain

• Radiation into the left arm, neck, and jaw

• Silent MI may occur in DM, HTN

• Complications have associated symptoms

Spontaneous coronary artery dissection (SCAD)

• Results in separation of the arterial wall layers leading to compression of the coronary artery lumen

• The dissection plane is usually seen between the media and the adventitia but may occur within the outer media.

• As the lumen is occluded, this leads to ischemia and often myocardial infarcts, which may lead to sudden cardiac death

• Has a wide range of symptoms

• It may be asymptomatic or may result in sudden death

Spontaneous coronary artery dissection (SCAD)-risk factors

• Atherosclerosis

• Peripartum state

• Connective tissue and autoimmune diseases

• Idiopathic origin

Spontaneous coronary artery dissection (SCAD)-atherosclerosis

• Typical risk factors for atherosclerosis: smoking, hypertension, hyperlipidemia

• Plague rupture leads to a defect within the artery with the formation of a false lumen.

• The hemorrhage in the false lumen results in the  dissection of the wall of the vessel

Spontaneous coronary artery dissection (SCAD)-postpartum

• Young age and lack of risk factors for atherosclerosis

• Possible mechanisms include decreased collagen production in combination with increased estrogen and progesterone levels

• The hormonal changes combined with the increased cardiac output result in a weakened artery, which is susceptible to shearing forces 

• Those on oral contraceptives may present with similar pathology

• Shows eosinophilic infiltration in the adventitia 

• Lytic substances such as collagenase, peroxidase, and acid phosphatase may be released from the eosinophils

Spontaneous coronary artery dissection (SCAD)-connective tissue diseases

• Marfan syndrome, Ehlers-Danlos, and autoimmune diseases

• Many have an underlying vasculitis

• This type has cystic medial degeneration due to a loss of smooth muscle and fragmentation of elastic fibers.

• There also may be deposition of mucopolysaccharides.

Spontaneous coronary artery dissection (SCAD)-idiopathic

• No underlying mechanism for development is identified 

• Some associations include cocaine use, vigorous exercise, and blunt trauma to the chest

• No specific genetic predispositions to SCAD have been identified

Chronic ischemic heart disease

• Progressive heart failure due to ischemic myocardial damage

• Most cases involve prior myocardial infarcts or coronary artery interventions

• Often results from decompensation of hypertrophied non-infarcted myocardium

• Hearts usually have areas of hypertrophy and dilation

• Remote healed infarcts are seen as scar tissue

• Mural thrombi may be present on the ventricular wall

Sudden cardiac death

• Unexpected death from cardiac causes without symptomatic heart disease or early after the onset of symptoms

• Usually due to a lethal arrhythmia 

• Acute myocardial ischemia is a common trigger

• Other cardiac pathologies can also cause it, such as valvular and myocardial diseases.

• Some conditions are inherited.

• May have anatomic abnormalities such as cardiomyopathies

• Others are due to electrical disturbances such as prolonged QT syndrome, which do not have an associated anatomic abnormality and are difficult to determine at autopsy

Sudden cardiac death; Channelopathies:

• associated with mutations in genes that encode the ion channels needed for normal cardiac conduction 

• These mutations predispose individuals to conduction abnormalities and possible arrhythmias 

• Postmortem blood and heart samples can be tested for genetic alterations.

The most common cause is ischemic heart disease

• Coronary artery disease

• Myocardial diseases

• Valvular diseases

Chronic ischemic heart disease

• Progressive CHF from long-standing ischemic injury

• Atherosclerosis

• Dilation of the cardiac chambers

• Myocardial fibrosis

• Hypertrophy

Hypertensive heart disease

• Left ventricular hypertrophy with hypertension

• Increased risk of sudden death

• Increased metabolic requirements of the hypertrophied myocardium make the myocardium more prone to arrhythmias

Cor Pulmonale (right sided heart failure)

• Acute: associated with pulmonary embolus(PE)

• Chronic: COPD, interstitial fibrosis

• Right-sided heart disease due to pulmonary disease

Rheumatic fever

• Acute immunologically mediated inflammatory disease

• Follows group A streptococcal pharyngitis aka “strep throat”

• Caused by antibodies directed against streptococci cross-react with tissue glycoproteins in the heart and joints.

Acute rheumatic carditis

• It involves all three layers of the heart

• Aschoff bodies: fibrinoid necrosis surrounded by chronic mononuclear cell inflammation

• Anitschkow cells: large histiocytes with vesicular nuclei and basophilic cytoplasm

Aschoff bodies

• fibrinoid necrosis surrounded by chronic mononuclear cell inflammation

Anitschkow cells

• large histiocytes with vesicular nuclei and basophilic cytoplasm

A 56-year-old man presents to the ER with chest pain that radiates to his left jaw and shoulder. An EKG reveals changes consistent with a myocardial infarct. Which of the following is true of a myocardial

1. It results in necrosis following severe ischemia.

Simple explanation

A myocardial infarction (heart attack) happens when blood flow to part of the heart is blocked. This causes a lack of oxygen (ischemia), which leads to heart muscle cell death (necrosis).

Acute rheumatic carditis

• Fibrinous pericarditis

• Endocardium: AV, MV, small vegetations along the lines of closure

• Arthritis of large joints

Chronic rheumatic heart disease

• Irreversible deformity of one or more cardiac valves

• Can result in:

1. Regurgitation

2. Stenosis

• Mitral valvulitis :most common cause of mitral stenosis

• Women are affected more than men

• “Fish mouth” deformity

• The valve pathology can cause the left atrium to be dilated and hypertrophied

• Mural thrombi are also seen

Chronic aortic valvulitis

• More common in males

• Often coexists with mitral valvulitis

• Aortic stenosis: valve cusps thick , firm, and adherent to one another

• Left ventricular hypertrophy(LVH)

• Aortic regurgitation: fibrosis and retraction

Calcific aortic stenosis

• Fibrosis of valve leaflets with calcification

• Usually asymptomatic

• Can be associated with left ventricular hypertrophy

Mitral valve prolapse (MVP)

• Women > men,20-40 years old

• MV is soft and enlarged, causing ballooning of leaflets

• Loose edematous tissue in the valve

• Most asymptomatic 

• Palpitations, chest pain, and syncope

• Midsystolic click during heart auscultation

Nonbacterial thrombotic endocarditis

• Aka marantic endocarditis

• Small nodules on the valve

• The valve is free of inflammation and bacteria

• Often associated with cancer

• May resolve spontaneously

• The aortic valve is the  most common valve involved

Infective endocarditis

• Acute and subacute forms

• Infection occurs during bacteremia from various sources 

• Preexisting cardiac abnormalities like rheumatic heart disease(RHD) and MVP can predispose the valves to bacterial infections

• Prosthetic valves also predispose to bacterial infections

• Intravenous drug use predisposes to bacterial infections, especially Staphlococcus aureus, on the tricuspid valve

• Previously damaged valves: strept viridans

• Prosthetic valves: staph. Epidermidis

• Intravenous drug use: staph.Aureus

• Difficult to treat with antibiotics because of the avascular nature of heart valves

• Antibiotic treatment may take weeks or more

Infective endocarditis

• Valvular vegetations contain bacteria or less commonly other organisms

• The aortic valve and mitral valve are commonly involved

• Tricuspid valve in intravenous drug use

• The vegetations can become large and destroy the valve

• Infectious  emboli may travel to other organs

Myocarditis: inflammation of the myocardium

• Coxsackieviruses A and B

• Chaga’s disease: trypanosoma cruzi

• Bacteria: neisseria, borrelia

• Fungi: candida

• Sarcoid

• SLE

Myocarditis

• Heart dilated and soft

• Viral: mononuclear cell infiltrate

• Bacterial: neutrophil infiltrate

• Myocyte degeneration/necrosis

• Giant cell myocarditis is one of the most serious forms

Chagas disease

• Common cause of  myocarditis in South America

• Reports of Chagas disease are beginning to be see in the southern US

• Caused by trypanosoma cruzi  a flagellated parasitic protozoan

• Transmitted by triatomine bugs, aka kissing bugs

Myocarditis

• Asymptomatic to CHF

• In most cases self-limiting

• May have lethal arrhythmias

Dilated cardiomyopathy

• Cardiac hypertrophy, dilation, and contractile dysfunction

• Causes 

1. Viral infection

2. Alcohol abuse

3. Peripartum cardiomyopathy

4. Idiopathic dilated cardiomyopath

• Heart enlarged and flabby

• Dilation and hypertrophy of chambers

• The dilated ventricles cause irregular blood flow ,which can predispose to mural thrombi on the ventricular walls

• Myocyte hypertrophy, interstitial fibrosis

• Develop progressive CHF

hypertrophic cardiomyopathy

• Myocardial hypertrophy, abnormal filling, and ventricular outflow obstruction

• The septum is often thicker than the left ventricle

• Often, in the subaortic region of the left ventricle

• Outflow obstruction causes contact between the septum and the mitral valve

• Microscopic findings include haphazard hypertrophied myocytes

• Inability to fill a hypertrophic left ventricle

• Myocardial ischemia common

• Increased incidence of sudden death especially in young persons

Restrictive cardiomyopathy

• Causes a decrease in ventricular compliance

• Results in an impaired ventricular filling during diastole

• Endomyocardial fibrosis: the most common cause worldwide

• Amyloidosis, hemochromatosis, and radiation injury are other causes

• Thickening of the endocardium and valves

• A stiff ventricle that is filled with great effort

• Fatigue, dyspnea, and chest pain

• Can result in varying degrees of congestive heart failure