Path Heart I & II (11/12)
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Ischemic Heart Disease (IHD)
- a generic description for a group of related syndromes resulting from myocardial ischemia, which is an imbalance between cardiac perfusion (inadequate supply) & myocardial oxygen need (unfulfilled demand)
- also known as Coronary Heart Disease (CHD)
What is the main cause of IHD?
- decreased coronary blood flow due to obstructive atherosclerotic disease
- this is also the leading cause of death in the US + other industrialized nations
Heart Attack Warning Signs
1. Chest discomfort (can feel like uncomfortable pressure, squeezing, fullness, or pain)
2. Discomfort in other areas of the upper body (eg. pain or discomfort in one or both arms, back, neck, jaw, or stomach)
other signs: breaking out in a cold sweat, nausea, light-headedness
What are some symptoms of a heart attack in people who don't have typical chest discomfort?
some people, especially women, who lack the typical signs may experience shortness of breath, tooth ache, weakness, or feeling very tired
Risk Factors of Coronary Heart Disease
- Systemic hypertension
- Cigarette smoking
- Diabetes mellitus
- Elevated blood cholesterol
- Family History
- Use of oral contraceptives
- Sedentary life habits
- chest pain
- caused by ischemia of the heart muscle due to obstruction or spasm of the coronary arteries (usually due to atherosclerotic narrowing of the coronary arteries)
- ischemia causes pain but not death of the myocardium
Stable (Typical) Angina
- mostly caused by coronary artery narrowing
- usually happens during excessive or strenuous activity but not at rest b/c flow is adequate then
- is the most common form of angina pectoris
- characterized by crushing chest pain that radiates to the left arm/jaw (especially in men)
- treated w/ vasodilator (nitroglycerin)
Variant (Prinzmetal) Angina
- caused by coronary artery spasm & therefore can happen during rest
- arteries can be atherosclerotic or normal
- treated w/ vasodilator or calcium channel blockers
Unstable (Crescendo) Angina
- caused by platelet thrombi → fibrin thrombin → worsening of pre-existing stenosis
- it usually begins as a stable angina but then progresses to attacks occurring more often & lasting longer
- is more unpredictable & may occur during rest or sleep
- is a precursor to more serious, potentially irreversible ischemia
Acute Myocardial Infarction (MI)
- when blood stops flowing properly to part of the heart & the myocardium is injured due to not receiving enough oxygen
- aka ischemia necrosis of a portion of cardiac muscle
- the event is "acute" if it is sudden & serious
Sudden Cardiac Death (SCD)
- results from a lethal arrhythmia without myocyte necrosis; can also be due to tissue damage from MI
- SCD in the setting of MI is most often (80-90% of the time) due to ventricular fibrillation caused by myocardial irritability
Chronic Ischemic Heart Disease (IHD)
- natural death from cardiac causes characterized by abrupt loss of consciousness w/in an hour of the onset of acute symptoms
- there is progressive cardiac decompensation (heart failure) following an MI
Acute Coronary Syndrome (ACS)
- any symptom or group of symptoms caused by obstruction of coronary arteries
- unstable angina, acute MI, & sudden cardiac death are all forms of ACS
Cardiac Referred Pain
- cardial pain is referred to the upper limb because the spinal cord segments of cutaneous nerves T1-T3 are common to both the coronary arteries & the substernal & left pectoral regions to the left shoulder & the medial aspect of the upper limb
How much of a vessel lumen must be occluded for the stenosis to be considered "critical"?
- such occlusion usually only causes symptomatic ischemia (angina) in the setting of increased demand
Although atherosclerotic plaques can be found anywhere in the right & left coronary arteries, where are significant plaques predominantly found?
L coronary artery: the 1st segment of either the anterior interventricular branch or the left circumflex branch
anywhere throughout the length of the right coronary artery
Which coronary artery is dominant in 4/5 people?
- Right dominant is found in 4/5 of people
- the coronary artery (either the R or L) that perfuses the posterior third of the septum is called ‘dominant’
Describe the sequential progression of coronary artery lesion morphology:
Myocardial Infarction (heart attack)
- necrosis of heart muscle caused by ischemia
- major cause of IHD is atherosclerosis
- the frequency of MIs rises progressively w/ increasing age
- risk factors: hyperlipidemia, hypertension, cigarette smoking, diabetes mellitus, age, etc.
What are most MIs caused by?
- most MIs are caused by acute coronary artery thrombosis
Sequence of Events in a Typical MI:
1. sudden disruption in a preexisting atherosclerotic plaque (inability to withstand mechanical stress → intra-plaque hemorrhage, erosion, ulceration, fissuring, rupture)
2. platelet adhesion, activation, mediator release, aggregation → form microthrombi
3. mediators trigger vasospasm
4. thrombus formation
5.* occlusion of the lumen of the coronary vessel
Timing of Key Myocardial Infarction Events
*I bet this is important
What early changes does an MI induce?
- loss of ATP and accumulation of lactate
For approximately how long after the onset of even the most severe ischemia is myocardial injury potentially reversible?
- 30 minutes
- however after, there is a progressive loss of viability which is complete by 6-12 hrs
- the benefits of reperfusion are greatest when it is achieved early & are progressively lost as reperfusion is delayed
- involves the full thickness of the wall from the endo to epicardium
- most MIs are transmural involving the full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery
- in an EKG S-T elevation is seen
- an area of ischemic necrosis limited to the inner 1/3 → 1/2 of the ventricular wall
- the subendocardial zone is the most vulnerable to any reduction of coronary flow
- in an EKG S-T elevation is NOT seen in this type of infarct
Myocardial Infarct Appearances Over Time
Timing of reperfusion after myocardial ischemia
• start w/ an "area at risk", aka a region that has experienced ischemia/perfusion defect
• if reperfusion occurs in less than 20 minutes, the majority of tissue can return to normal function except for a small, central part that is viable but has post-ischemic dysfunction: called SALVAGE
• if reperfusion occurs in 2-4 hours, the majority of tissue is viable but has post-ischemic dysfunction except for a small, central part that is necrotic with hemorrhage & contraction bands: called PARTIAL SALVAGE
• if reperfusion never occurs & the occlusion is permanent, all of the tissue becomes necrotic: called COMPLETED INFART
What is this the characteristic appearance of?
ischemic myocardium that has been reperfused - can see myocardial necrosis w/ hemorrhage & contraction bands (visible as dark bands spanning some myofibers where the arrow is)
What molecules can be used as biomarkers for diagnosis of myocardial infarction?
- myocyte proteins such as troponin I, T, or C, creatine phosphokinase, or CKM/CKB (enzymes)
- may be found in the circulation as plasma membranes of necrotic myocytes become leaky
After: Complications of an MI
- Contractile dysfunction
- Arrhythmias (potentially fatal)
- Myocardial rupture
- Pericarditis (inflammatory response)
- Infarct expansion, stretching, thinning, dilation
- Mural thrombus, potential thromboembolism
- Ventricular aneurysm, mural thrombus, arrhythmias,
- heart failure (usually no rupture)
- Papillary muscle dysfunction (valve issues)
- Progressive late heart failure
Congestive Heart Failure (CHF)
- occurs when the heart is unable to provide sufficient pump function to maintain blood flow to meet the body's needs (or can only do so only with filling pressures that are ↑ than normal)
- can result in fluid in the lungs or peripheral tissue (congestion)
- is a frequent end point of many of heart conditions (IHD, hypertensive HD, HD caused by intrinsic pulmonary diseases, valvular HD, primary myocardial disease)
*What is the most common cause of CHF?
- systolic dysfunction: the progressive deterioration of myocardial contractile function, usually due to IHD or hypertension
- another cause of CHF is diastolic dysfunction, which is when the heart contracts normally but relaxes abnormally (seen in aged females w/ hypertension or diabetes mellitus)
- valve failure is another cause
Why might CHF occur suddenly in a normal heart?
if it is suddenly subjected to an abnormal load (eg. fluid or pressure overload)
What are a few of the means by which the heart will try to compensate for reduced myocardial contractility or increased hemodynamic burden?
- 1. activation of the neurohumoral systems
- 2. the Frank-Starling mechanism
- 3. myocardial structural changes (hypertrophy)
- SNS stimulation & release of norepinephrine vascular resistance ↑ heart rate & contractility
- activation of the renin-angiotensin-aldosterone system ↑ blood volume
- ANP (atrial natriuretic peptide) leads to vasodilation, natriuresis, & diuresis ↓ blood volume which helps alleviate volume or pressure overload states
The Frank-Starling Mechanism
- cardiac stroke volume is a function of diastolic fiber length; a normal heart will pump whatever volume is brought to it by the venous circulation
- an ↑ EDP → more cardiac muscle fibers stretch → more force generated → stroke volume ↑
- compensated heart failure: dilated ventricle is able to maintain C.O. at a level that meets the needs of the body
- decompensated heart failure: a failing myocardium is no longer able to propel sufficient blood to meet the needs of the body, even at rest
- when there is an increase in the diameter of the individual muscle fiber & the thickness of the ventricular wall increases without an increase in the size of the chamber (walls of the organ are thickened as its capacity or volume is diminished)
- results from pressure overload states (hypertension, valvular stenosis)
- there is an increase in the length of the individual muscle fiber & an increase in both heart size + wall thickness
- results from VOLUME overload (eg. valvular regurgitation, abnormal shunts)
What are some activators of receptor-mediated signaling pathways that bring about a hypertrophic response?
- ANF (atrial natriuretic factor)
- ANG II (angiotensin II)
- HSP-70 (heat shock protein 70)
- IGF (insulin-like growth factor)
- TGF-β (transforming growth factor-β)
Effects of hypertrophy?
- it puts extra demands on the heart & the myocardium becomes vulnerable to ischemic injury
Left-Sided Heart Failure Causes (most common)
- systemic hypertension
- mitral or aortic valve diseases
- primary diseases of the myocardium
What are the morphological & clinical effects of left sided heart failure due to?
- 1. progressive damming of blood within the pulmonary circulation
- 2. diminished peripheral blood pressure & flow (hypoperfusion → organ dysfunction)
How does left-sided heart failure affect the heart?
- mainly by causing ventricular hypertrophy
- especially in the left ventricle, which becomes hypertrophied & dilated
- atrial fibrillation can reduce stroke volume or lead to blood stasis & thrombus formation w/ increased risk of embolic stroke
How does left-sided heart failure affect the lungs?
- rising pressure in the pulmonary veins is transmitted backward into the capillaries & causes pulmonary congestion & edema
- the lungs become heavy & soggy, there's perivascular & interstitial transudate, alveolarseptal edema, intra-alveolar edema, & 'heart failure cells’ (macrophages loaded with hemosiderin from extravasated RBC)
- *the extracardiac effects of left-sided heart failure are MOST prominent in the lungs
Clinical Features of Left-sided Heart Failure
- pulmonary congestion (↑ in hydrostatic pressure)
- dyspnea (breathlessness), usually the earliest & most significant complaint (edema causes poor gas exchange)
- cough (fluid transduction into airspaces)
- orthopnea (dyspnea when recumbent due to ↑ venous return from lower extremities)
- sudden onset of severe respiratory distress at night (paroxysmal nocturnal dyspnea)
- most patients present with BIventricular congestive heart failure (CHF)
What are the most common causes of right-sided heart failure?
1. left ventricular failure: any pressure ↑ in the pulmonary circulation that burdens the L side will ALSO burden the R side (eg. patients w/ chronic pulmonary hypertension or pulmonic or tricuspid valve disease)
2. Cor pulmonale: ‘pure’ right-sided failure in patients w/ 1 of a variety of disorders affecting the lungs, all of which have pulmonary hypertension as their common feature (parenchymal disorders of the lungs, secondary disorders affecting the pulmonary vasculature, recurrent pulmonary thromboembolism, etc.)
How does right-sided heart failure affect the heart?
hypertrophy + dilation of the right ventricle & atrium (effects are generally confined to the right side)
How does right-sided heart failure affect the rest of the body?
- it causes pronounced engorgement of the systemic & portal venous system (distention of neck veins, nutmeg liver, congestive splenomegaly) due to increased hydrostatic pressure
- it also causes peripheral edema + accumulation of fluid in subcutaneous tissue
How does left-sided heart failure affect the lungs?
not as badly as left-sided heart failure - there is minimal pulmonary congestion
How do clinical features of isolated right-sided heart failure manifest themselves?
- in systemic & portal venous congestion
- liver: congestive hepatomegaly w/ passive congestion, nutmeg liver, & centrilobular necrosis
- spleen: congestive splenomegaly from portal hypertension
- kidneys: congestion → greater fluid retention &
- peripheral edema
- *distended neck veins
- accumulation of fluid + ascites in pleural, pericardial, & peritoneal spaces
- subcutaneous tissues
- edema of the peripheral & dependent portions of the body, especially ankle & pre-tibia
- mental deficits due to venous congestion & hypoxia of the CNS
Congestive Heart Failure (CHF)
- most patients present w/ biventricular congestive heart failure whether they have right-sided or left-sided heart failure
- is characterized by variable degrees of decreased cardiac output & tissue perfusion, which can lead to pulmonary edema, peripheral edema, or both
- as CHF progresses patients can become cyanotic & acidotic as a result of inadequate tissue perfusion
What are many of the significant clinical features & morphologic changes noted in CHF secondary to?
injuries induced by hypoxia & congestion of tissues distant from the heart
What is backward & what is forward failure?
- backward: pooling of blood in the venous system
- forward: decreased cardiac output & therefore decreased tissue perfusion
Hypertensive Heart Disease (HHD)
- stems from the increased demands placed on the heart by hypertension → pressure overload & ventricular hypertrophy
- most commonly seen in the L heart as the result of systemic hypertension
What can cause right-sided hypertensive heart disease?
pulmonary hypertension (cor pulmonale)
Systemic (Left-Sided) Hypertensive Heart Disease
an adaptive response to pressure overload that can lead to myocardial dysfunction, cardiac dilation, CHF, & in some cases sudden death
What are the diagnostic criteria for systemic (left-sided) hypertensive heart disease?
- a history or extracardiac anatomic evidence of hypertension
- left ventricular (typically concentric) hypertrophy
- an absence of other lesions that cause cardiac hypertrophy
Morphology of Systemic Hypertensive Heart Disease (Left-sided)
- a thickened left ventricle greater than > 2 cm)
- increased heart weight (from 350-500 to >500 mg)
- stiff walls (impairs diastole filling)
- enlarged myocytes + enlarged nuclei
- diffuse interstitial fibrosis
- focal myocyte atrophy & degeneration
- in the long term: left ventricle chamber dilation & wall thinning
What is the cause of death in 1/3 of hypertensive patients?
congestive heart failure
Pulmonary (Right-Sided) Heart Disease, Cor Pulmonale
- caused by pressure overload of the right ventricle, which is often due to pulmonary hypertension (from disorders affecting the lung structure or function)
- it most commonly occurs as a complication of left-sided heart disease of various etiologies
- manifests as R ventricular hypertrophy or dilation
Acute Cor Pulmonale
right ventricular dilation after massive pulmonary embolization
Chronic Cor Pulmonale
- chronic right ventricular hypertrophy (& dilation) secondary to prolonged pressure overload due to disorders in the pulmonary vasculature or parenchyma (eg. emphysema)
- characterized by a markedly dilated & hypertrophic right ventricle w/ a thickened free wall & hypertrophied trabeculae (the shape of the L ventricle can be distorted by the R ventricular enlargement)
Why is right-sided heart disease a relatively common condition?
because chronic obstructive pulmonary disease (COPD) is widespread
a medical condition wherein the heart is enlarged
Which picture, A or B, describes systemic & which describes pulmonary hypertensive heart disease?
- A: systemic (left-sided) b/c L ventricle is enlarged
- B: pulmonary (right-sided) b/c R ventricle is enlarged, distorting the size of the L ventricle
Valvular Heart Disease
- any disease process involving 1 or more of the 4 valves of the heart (the aortic & mitral valves on the left & the pulmonary & tricuspid valves on the right)
- may be caused by Degeneration (calcific aortic stenosis, mitral annular calcification, mitral valve prolapse), Immunological Inflammatory Processes (eg. rheumatic heart disease), or Infection (eg. infective endocarditis)
a failure of a valve to open completely, obstructing forward flow
failure of a valve to close completely, allowing reverse flow
What type of valvular heart disease accounts for the majority (2/3) of cases?
acquired stenoses of the aortic & mitral valves (left)
Of the 3 general causes, what is the most common of all valvular abnormalities?
- Degenerative calcific aortic valve stenosis
- occurs usually in people over the age of 70 due to contributory factors such as wear-and-tear, hyperlipidemia, hypertension, inflammation, etc.
- manifests as nodular, rigid calcific subendothelial masses on the outflow surface of the valve → cusp thickening & immobility, preventing complete opening of the cusps → impeding aortic outflow
- end result: concentric L ventricular hypertrophy due to chronic pressure overload
Mitral Valve Prolapse (primary form of Myxomatous Degeneration)
- when 1 or both mitral leaflets are enlarged, myxomatous, & “floppy”
- they balloon back (prolapse) into the left atrium during systole
- there is systolic murmur, midsystolic clicks, & regurgitation
- is typically seen in 20-40 y/o's & in 7 females for every 1 male (female to male ratio = 7:1)
- treat with surgical repair & replacement
- a pathological weakening of connective tissue
- myxomatous mitral valve degeneration is the when the fibrosa layer of the valve shows thinning &
- degeneration w/ mucoid expansion of the middle spongiosa layer
What does mitral valve prolapse increase one's risk of?
infective endocarditic, gradual valvular insufficiency leading to CHF, arrhythmias, & sudden death, although it's usually asymptotic
- an inflammatory disease that occurs a few weeks after a Streptococcus pyogenes infection (eg. streptococcal pharyngitis)
- is caused by antibody cross-reactivity that can involve the heart, joints, skin, & brain
- the rheumatic fever antigen looks similar to heart valve proteins, therefore upon proliferation of anti-Rheumatic fever antibodies to target the bacteria, they go on to damage a patient's heart
What is the most important consequences of Rheumatic Heart Disease (RHD)?
- chronic valvular deformities
- the disease is characterized by diffuse & dense scarring of valves resulting in permanent dysfunction (the most common being mitral stenosis)
- [there is fibrinoid necrosis w/in the cusps or along the tendinous cords + small vegetations (verrucae) over the necrotic foci along the lines of closure]
Which valve is more likely to be affected by Rheumatic Fever?
the mitral & aortic valves are MORE likely to be affected than the tricuspid & pulmonary valves
Acute Phase of Rheumatic Heart Disease
- Aschoff bodies: areas of inflammation of the connective tissue of the heart; have fragmented collagen, foci of fibrinoid necrosis, large myocytes, & occasional multinucleated giant cells
- Inflammatory valvulitis characterized by beady fibrinous vegetations (verrucae) that can contain Aschoff bodies
Chronic Features of Valves Affected by Rheumatic Heart Disease
- fibrous thickening of leaflets (parts of the valve)
- commissural fusion & shortening
- fishmouth or buttonhole stenoses
- thickened, fused, & shortened chordae tendineae
- calcification in the fibrous leaflets
Infective Endocarditis (IE)
colonization of heart valves by microorganisms (eg. extracellular bacteria) which leads to the formation of friable, infective vegetations, frequently causing valve damage
Acute Infective Endocarditis
- caused by highly virulent organisms (Staph. aureus), attacking a previously normal valve, producing necrotizing, ulcerative, & invasive infections
- there is rapid development of fever w/ rigors, malaise, & weakness
- most commonly affects the mitral or aortic valves
- more than 50% of patients die within days - weeks
Subacute Infective Endocarditis
- caused by infection w/ moderate to low virulence organisms (Strep. viridans) seeding an abnormal or previously injured valve
- causes less destruction than in acute IE
- appears insidiously w/ nonspecific malaise, low- grade fever, weight loss, & flu-like syndrome
- vegetations are small & there are fewer embolic complications
- lasts weeks to months w/ most patients recovering after appropriate antibiotic therapy
Nonbacterial Thrombotic Endocarditis (Marantic Endocarditis)
- occurs in settings of cancer or prolonged debilitating
- associated w/ disseminated intravascular coagulation or other hypercoagulable states
- variably sized masses of fibrin, platelets, & other blood components present on cardiac valves
- vegetations are sterile, nondestructive, & small but can embolize systemically or serve as a potential location for bacterial colonization leading to infective endocarditis
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