Week 3: diseases of myocardium and pericardium Flashcards
Compare transmural and subendocardial types of MI.
- Transmural infacts-most frequent
- mostly affect LV
- usually involves full thickness of ventricle, sparing only thin band of subendocardial myocardium, nourished by ventricular chamber
- thrombus if major coronary artery present in most cases
- LAD and R coronary most commonly involved - Subendocardial infarct
- multifocal often. inner 1/3 to 1/2 of LV myocardium
- diffuse narrowing of coronaries but no superimposed thrombus
Describe the pathologic events that underlie acute myocardial infarction.
- most acute MIs from sudden near or complete occlusions
- in 60s, anaerobic glycolysis, increased lactic acid, loss of contractility
- in mins: mitochondrial swelling
- necrosis in 20-30 mins of O2 deprivation
- necrosis starts in subendocardial (most poorly perfused), spreads to mid and sub epicardial region
Describe the sequential changes in MI seen microscopically.
-0-12 hr usually nothing. beginning of coagulation necrosis, edema, and hemorrhage @~12hr
-12-24hr: coagulation necrosis, pyknosis, myocyte hypereosinophilia, contraction band necrosis (repercussion of muscle, though to be Ca2+ influx), PMN infiltrate begins
-1-3 days: coagulation necrosis, loss of nuclei and striations, interstitial infiltrate of PMNs
-3-7 days: disintegration of dead myofibers, dying PMNs, early phagocytosis of dead cells by macrophages at border
-7-10days: phagocytosis of dead cells, early formation of fibrovascular granulation tissue at margins
-10-14 days: granulation tissue established, new blood vessels, collagen deposition
2-8 weeks: increased collagen, with decreased cellularity
2 mos.: dense collagenous scar
List the general incidence and associate sequelae for eight potential complications of myocardial infarctions in surviving patients.
- cardiogenic shock: 5-15%. heart damaged so can’t adequately pump blood->hypotension. mostly result of large infarcts. may be caused by acute severe mitral regurg, v. septal rupture, cardiac tamponade. mortality 60-80%.
- Left ventricular failure: 60%, acute or progress over years, varying degrees of CHF
- Arrhythmias: 75-95%, in first 3 days (esp 1st 24 hrs). may lead to sudden death
- Cardiac rupture syndromes: occur in 1st week. subacute rupture can lead to aneurysm, rupture of ventricular wall, IV septum, papillary rupture.
- Pericarditis: 10-20% in patients with transmural infarct. first few days. usually self limiting.
- Progressive extension of infarct: 10%, first 1-2 weeks. weakening of necrotic myocardium may cause dilation of infarcted area.
- Mural thrombi: up to 50%. most likely in first 1-2 weeks.
- Ventricular Aneurysm: 10% of transmural infarcts.
List 5 risk factors for the development of an MI
- smoking
- hypercholesterolemia
- lack of exercise
- diabetes
- obesity
Discuss causes, gross and microscopic appearance, and clinical features of dilated cardiomyopathy.
- causes: idiopathic, genetic, metabolic diseases, ethanol, toxic, neuromuscular, infectious, late pregnancy
- Gross: heavy, large, flabby heart with dilation of all chambers
- microscopic: irregular atrophy and compensatory hypertrophy of myocardial cells. variable degree of fibrosis.
- clinical: 20-60 yrs, present with slowly progressive CHF. Left heart failure-pulmonary congestion, edema, dyspnea, orthopnea, fatigue, rales. Right heart: jugular venous dilation, leg edema, ascites, hepatomegaly.
- cardiac exam: lateral displacement of apical impulse, mitral and/or tricuspid regurg murmurs due to dilation of valvular rings
Discuss causes, gross and microscopic appearance, and clinical features of hypertrophic cardiomyopathy.
- cause: mostly genetic
- gross: heavy heart, thickened ventricular walls and septum. banana shaped LV. Decreased diastolic filling.
- microscopic: large myocytes, myocyte bundles and contractile elements are haphazard, interstitial fibrosis, thickened vessel walls
- clinical: asymptomatic to severe. Exertional dyspnea, blood flow obstruction into aorta, anginal pain, syncope,
- cardiac exam: accentuated apical impulse, may have two systolic murmurs, holosystolic blowing murmur due to mitral regurg, 4th heart sound
Discuss causes, gross and microscopic appearance, and clinical features of restrictive cardiomyopathy.
- cause: idiopathic, amyloidosis, familial storage diseases, autoimmune e.g. sarcoidosis, radiation, metastatic tumor
- ventricular stiffness due to fibrosis or infiltration, impairment of diastolic filling due to poor compliance.
- gross: myocardium firm, ventricular walls are either normal or thickened.
- microscopic: patchy or diffuse interstitial fibrosis.
- clinical: exertional dyspnea, elevated systemic and pulmonary pressure may result in heart failure
- cardiac exam: heart sounds may be reduced. 3rd and 4th heart sounds common. may have mitral regurg.
Define myocarditis.
-diffuse inflammatory infiltrate in the myocardium associated with myocyte damage and occurring in the absence of IHD, HTN, congenital and valvular heart disease
What is the clinical presentation of myocarditis?
- Acute onset: chest pain, palpitations, fever, dyspnea
- cardiac findings: left ventricular failure can occur. Arrhythmias, systolic murmur (mitral regurg if ventricular dilation), complete heart black from inflammation and edema
- lab findings: leukocytosis, elevated ESR, elevated creatine kinase, troponin, LDH, aspartate transaminase due to necrosis of myocardial fibers
What are the gross and microscopic findings of myocarditis?
- gross: heart is dilated, flabby and pale
- microscopic: myocardium infiltrated with lymphocytes, plasma cells, eosinophils
- interstitial edema separates myocytes
- individual myocyte necrosis present throughout
- cause is usually viral/immune, therefore mononuclear cells instead of PMNs
discuss cause and pathogenesis of myocarditis.
- bacterial, fungal, parasitic: myocardial damage from toxicity of organism
- viral: indirect immune reaction causes damage
- infectious agents: viruses, particular Coxsackie A and B, bacterial such as Rickettsiae, Lyme, Diptheria, Neisseria Meningococcus
- parasitic: Chagas, Trichinella spiralis, toxoplasma
- autoimmune: rheumatoid arthritis, SLE, rheumatic fever, systemic sclerosis, dermatomyositis
- toxic: from drugs, hypersensitivity reaction
- sarcoidosis, radiation, idiopathic giant cell
Describe the pathology of acute pericarditis.
- pericardium infiltrated with PMNs and deposition of fibrin
- “bread and butter” appearance-visceral and parietal pericardial layers are loosely adherent and peel apart like bread and butter
- inflammatory exudate varies with cause
What is the clinical presentation of acute pericarditis?
- fever
- chest pain: may be pleuritic, or stead and constricting, with radiation into arms, mimicking MI chest pain
- pericardial friction rub
- lab findings: troponin and creatine kinase may be elevated, less so than MI, leukocytosis, increased C-reactive protein and ESR
- sequelae: most resolve with minimal scarring of pericardium
- unless caused by TB, can have major scarring and fibrous obliteration of pericardial space
What is the etiology of acute pericarditis?
- Viral infections- most common, e.g. Coxsakievirus B, EBV, influenza, mumps
- pyogenic bacteria: from spread from lung or pleura
- TB
- connective tissue disease: SLE, rheumatoid arthritis
- myocardial infarct
- chronic renal failure (uremia)
- acute rheumatic fever
- radiation therapy
- metastatic tumor
