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Flashcards in Path: diseases of myocardium and pericardium Deck (25):

Ischemic heart disease (IHD)

-Ischemia causes insufficient O2/nutrient delivery and removal of waste
-Usually due to luminal narrowing from atherosclerosis
-Most common in elderly, much more in men than women
-Contributing factors: smoking, dyslipidemia, lack of exercise, obesity, diabetes
-Manifestations: MI, angina, sudden cardiac death (SCD), CHF


Pathogenesis of IHD

-75% of vessel narrowing in 1 or more coronary arteries can cause IHD
-Sx depend on the degree of occlusion and any complications of the plaque, including rupture, thrombosis, hemorrhage or enlargement
-Depending on amount of occlusion after thrombosis, there may be unstable angina, MI, or SCD due to arrhythmia
-Coronary artery vasospasms can further reduce coronary blood flow (athersclerotic segments cannot spasm)
-Ischemia exacerbated by: severe hypotension (shock), increased myocardial O2 demand, hemoglobinopathies


Acute MI

-Major risk factors same as atherosclerosis/IHD
-Manifestation: crushing retrosternal chest pain radiating to neck, jaw, left arm not relieved by rest or nitrates
-Most MIs are preceded by episodes of angina
-Other Sx: diaphoresis, SOB, lightheadedness, nausea
-ECGs: T wave inversions, STE, Q waves
-Dx using Tn test, Hx and ECG


Types of MI

-Transmural (most common): usually of the LV and IVS, involving full or close to full thickness of the ventricle wall (worse prognosis)
-Spares the subendocardial myocardium b/c it gets nourished from the blood in the ventricle
-Usually due to LAD infarct
-Subendocardial infarct (less common): often multifocal, inner 1/3-1/2 of ventricular wall (better prognosis)
-Coronary arteries often show diffuse narrowing w/o thrombus


Pathophysiology of MI 1

-Result from sudden near or complete occlusions, necrosis begins 20-30 min after onset of infarction
-Necrosis first of the subendocardial region, the most poorly perfused region
-Then extends to subepicardial region, reaching full size in 3-6 hrs


Pathophysiology of MI 2

-Reperfusion in 20-30 min and changes may be reversible (reperfusion w/in 24 hrs causes contraction bands due to Ca influx)
-No observable changes in myocardium until after 4-12 hrs (then acute inflammation, loss of striation, followed by chronic after 7-10 days)
-If fibrosis is present, pt has survived an MI for at least 2 wks


Complications of MI 1

-Cardiogenic shock: severe hypotension usually in very large infarcts, can lead to mitral regurg, ventricular septal rupture or cardiac tamponade
-Left ventricular failure: due to contractile dysfxn or arrhythmia, may occur acutely or progressively and may be accompanied by pulmonary edema


Complications of MI 2

-Arrhythmias: most common (in first 3 days), includes ectopic beads, sinus brady/tachycardia, atrial or ventricular fibrillation, heart blocks
-Cardiac rupture: mostly in first week before fibrosis, due to weakening of necrotic myocardium
-Includes formation of false aneurysm (btwn epicardium and parietal pericardium), ventricular wall (cardiac tamponase) or IVS rupture (L-R shunt), papillary muscle rupture (acute mitral regurg and subsequent LV failure)


Complications of MI 3

-Pericarditis: fibrinous or hemorrhage exudate in pericardium (may be weeks post MI, may be immunologically driven)
-Progressive extension of MI
-Mural thrombus: may embolize to lung, brain, kidney depending on which ventricle it originated from
-Ventricular aneurysm: thinning of ventricular wall results from stretching of the scar tissue, but usually do not rupture (can cause CHF, thromboembolism, arrhythmias)


Types of angina

-Stable angina: associated w/ exertion, relieved by rest or nitrates
-Variant angina: pain occurs at rest due to vasospasm
-Unstable angina: pain characterized by increased frequency or severity
-UA may precede MI, caused by acute plaque change w/ overlying thrombus, distal embolus, or vasospasm


Pathological features of angina

-Moderate to severe atherosclerosis of coronary arteries
-Dilation of cardiac chambers
-Multiple areas of myocardial fibrosis
-May see hypertrophy of myocardium
-Microscopic: fibrosis, atrophic and hypertrophic myocytes, vacuolation of myocytes


Sudden cardiac death

-Not only cardiac in origin, can also be from PE, Ao aneurysm, infection, CNS d/o
-Usually due to arrhythmias
-Causes: CAD, myocardial disease (cadiomyopathies, myocarditis), valvular diseases, conduction system abnormalities



-A Dx of exclusion, must be made in the absence of systemic or pulmonary HTN, and IHD, congenital or valvular heart disease


Dilated cardiomyopathy (DCM) 1

-Most common, characterized by a heavy, enlarged, flabby heart w/ dilated chambers
-Ventricular hypertrophy precedes DCM
-Ventricles contract poorly leading to heart failure
-Histologically there is irregular atrophy and compensatory hypertrophy of the myocardium
-L sided HF: pulmonary edema leading to DOE, orthopnea, fatigue, rales


Dilated cardiomyopathy (DCM) 2

-R sided HF: JVP distension, bilateral leg edema, ascites, hepatomegaly
-Exam: lateral displacement of apical impulse, M and T regurg, S3/4 audible
-Complications: arrhythmias, thromboemboli, M/T regurg
-Etiologies: idiopathic (mutations involve cytoskeletal proteins), metabolic diseases, toxins (EtOH), neuromuscular (muscular dystrophies), infections, and late pregnancy
-Related to systolic HF


Hypertrophic caridomyopathy (HCM) 1

-Heavy heart w/ very thick ventricular walls and septum (usually septum thicker than walls), may be causing obstruction of outflow tract
-Myocardium is hyper contractile but poorly compliant
-Diastolic filling decreased, diminished chamber size
-Histologically: myocytes are large and hypertrophied, bundles are arranged haphazardly w/ interstitial fibrosis and thickening of vessel walls


Hypertrophic caridomyopathy (HCM) 2

-Sx include DOE due to pulmonary congestion (secondary to HF), edema/hepatomegaly/ascites, anginal pain (hypertrophied muscle prone to focal ischemia), syncope (fainting) due to decreased CO
-Exam: accentuated apical impulse, mid-systolic murmur due to LV outflow obstruction, holosystolic murmur due to mitral regurg, S4
-Complications: arrhythmias, thromboemboli, endocarditis
-Etiology: many cases familial, w/ mutations involving sarcomeric contractile elements (beta-myosin heavy chain)
-Related to diastolic HF


Restrictive cardiomyopathy (RCM) 1

-Ventricular stiffness due to fibrosis or infiltration, poorly compliant ventricles impairs filling w/ elevation of venous and pulmonary pressures
-Myocardium is dense, but walls are close to normal size
-Histologically there is patchy or diffuse interstitial fibrosis, often amyloid deposition (apple-green bifringience)


Restrictive cardiomyopathy (RCM) 2

-Sx: DOE from HF, edema/hepatomegaly/ascites
-Exam: reduced heart sounds, S3/4 most common, mitral regurg present
-Complications: arrhythmias, thromboemboli
-Etiology: amyloidosis most common identifiable cause, idiopathic, familial storage diseases, autoimmune (sarcoidosis)
-Related to diastolic HF


Myocarditis 1

-Diffuse inflammatory infiltrate in the myocardium in the absence of IHD, HTN, congenital or valvular heart disease
-Viral etiology is suspected, but my accompany any infectious/inflammatory process
-Clinical presentation: acute onset of chest pain, palpitations, fever, dyspnea
-Cardiac findings: LV failure, arrhythmias, systolic murmur (mitral regurg), complete heart block
-Tests: can see leukocytosis, elevated ESR, Tn positive


Myocarditis 2

-Pathology, gross: heart is dilated, flabby and pale, scattered petechial hemorrhages
-Path, micro: myocardium is infiltrated w/ lymphocytes, plasma cells, and eosinophils, w/ interstitial edema and myocyte necrosis
-Etiology: viral, bacterial, parasites, autoimmune (RA, SLE, Tx rejection, rheumatic fever), toxins (adriamycin, penicillin rxn), sarcoidosis, idiopathic (giant cell)


Pericarditis 1

-Inflammation of the pericardial surfaces and spaces
-Inflammatory exudate varies w/ cause, can be serous, fibrinous, purulent and hemorrhagic
-Pericardium is infiltrated w/ PMNs and fibrin deposition
-Gross: pericardium is reddened and rough from fibrin, parietal and visceral pericardium lays loosely adherent (bread and butter appearance)


Pericarditis 2

-Hemorrhagic pericarditis due to TB, uremia (!), or metastatic tumor
-Clinical presentation: chest pain (may be pleuritic), pericardial rub
-Lab: Tn elevated, increase in CRP and ESR
-Etiologies: viral (most common- serous), pyogenic bacterial, TB, CT disease (RA, SLE), chronic renal failure (uremia !)


Chronic constructive pericarditis

-Occurs when healing of acute pericarditis or a chronic effusion results in obliteration of the pericardial cavity
-Heart encased in thickened fibrotic pericardium
-Follows a slow, indolent course
-Pericardium constricts the chambers, causing impaired filling, leading to ankle edema, ascites, hepatomegaly, pulm edema
-Mostly caused by irradiation, trauma, chronic inflammatory diseases, CA


Pericardial effusions

-Accumulation of fluid in pericardial space, may be due to inflammation (pericarditis) or non-inflammatory causes (increased hydrostatic pressure)
-Serous: CHF, low albumin, MI
-Serosanguinous: trauma, CA
-Chylous: lymphatic obstruction
-Hemopericardium (may lead to cardiac tamponade): pure blood in pericardial space, due to ruptured Ao aneurysm, rupture of ventricle following MI, trauma
-Cardiac tamponade: blood and other stuff (puss, fluid, gas) in pericardial space