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26 Cards in this Set
- Front
- Back
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Myocarditis
Cardiomyopathy |
Myocarditis
-Active inflammation of the myocardium Cardiomyopathy -chronic pathology of the myocardium --many different possible etiologies -Myocarditis may or may not have been the original insult, but myocarditis ≠ cardiomyopathy |
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Left atrium and cardiomyopathies
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Notice the left atrium is dilated in all of them
Any cardiomyopathy causes ↑LVEDP due to ventricular dysfunction (whether systolic or diastolic) ↑LVEDP causes ↑LA pressure -This causes the LA to dilate making Atrial Fibrillation a lot more likely to occur |
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Nonischemic dilated cardiomyopathy: primary problem
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Systolic dysfunction
-↓Left Ventricular Ejection Fraction (LVEF) -- is almost always the main problem RV function sometimes also abnormal |
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Nonischemic dilated cardiomyopathy: etiologies
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Tachycardia-mediated cardiomyopathy
-Incessant tachycardia can cause cardiomyopathy Excessive alcohol intake -Alcohol is toxic to heart cells Peripartum cardiomyopathy Toxic effect of chemotherapy -Adriamycin in particular Certain infectious etiologies: -Chagas disease -Lyme disease -Rocky Mountain Spotted fever -Rheumatic fever |
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Tachycardia-mediated cardiomyopathy
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NIDCM
Prognosis very good if tachycardia can be eliminated If you: Cure tachycardia and LVEF normalizes -Then you know what you cured, you cured a tachycardia-mediated cardiomyopathy Cure tachycardia and LVEF stays low -You’ll never know what caused the low LVEF -Maybe the tachycardia lasted so long that the effect was permanent or maybe there were two separate problems to begin with -Maybe the tachycardia resulted from the cardiomyopathy “which came first, the chicken or the egg?” |
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Alcoholic cardiomyopathy
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NIDCM
May resolve completely if alcohol intake stops Nearly always involves very heavy drinking -But studies have shown even moderate EtOH does have a transient adverse effect on cardiac function in asymptomatic, healthy people |
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Peripartum cardiomyopathy: etiology
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NIDCM
Clear relationship to recent pregnancy -Symptoms can start during third trimester -Usually start within one to five months postpartum Exact etiology unclear -May be multifactorial --Maternal autoimmune response possibly involved --Inflammation (myocarditis) also possible --Evidence of inflammation on heart biopsy is a good prognostic sign |
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Peripartum cardiomyopathy: risk factors
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Maternal age > 30 years
African descent Twins or triplets Preeclampsia or pregnancy-induced hypertension in this or previous pregnancies Long-term (> 4 weeks) use of tocolytic Tx -Tocolytics prevent premature birth in certain situations Cocaine use |
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Peripartum cardiomyopathy: prognosis
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Prognosis (rough approximation)
-1/3 recover completely -1/3 stabilize – never quite normal again, but stable -1/3 progress (i.e. get worse and worse…) High risk for thromboembolism -Deep Venous Thrombosis -Arterial Thromboembolism – i.e. embolic stroke -pregnancy is a hypercoagulable state – add poor heart function to it and the risk is high |
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Peripartium cardiomyopathy: future pregnancies
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For women with persistent LV dysfunction – i.e. do not have complete recovery:
-High risk of death or permanent worsening of cardiomyopathy with subsequent pregnancy -Advice to patient is clear: --Never get pregnant again! -Surgical sterilization is highly recommended For women with apparently complete recovery – i.e. LVEF returns to normal: -substantial risk of recurrent cardiomyopathy with subsequent pregnancy --may not return to normal the next time -no clear guidelines due to no way to predict outcomes --my take: persistent LV dysfunction: subsequent pregnancy is an unbelievably bad idea presumed complete recovery: subsequent pregnancy is still a very bad idea |
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Peripartum cardiomyopathy: treatment
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Same as any other nonischemic dilated cardiomyopathy
Except: - higher risk of thromboembolism -Anticoagulation is required |
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Viral myocarditis: why is it idiopathic
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NIDCM
-most common cause The period of active inflammation (myocarditis) isn’t recognized -After the fact, patient sometimes remembers “a few months ago I felt really crummy for several weeks, thought I had the flu or something…” The inflammation goes away but leaves behind a cardiomyopathy When you see the patient, all you find is cardiomyopathy, no myocarditis -That’s why it gets labeled “idiopathic” |
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Viral myocarditis: causes
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Coxsackievirus
-MOST COMMON -It is an ENTEROVIRUS Others: -parvovirus B19 -human herpesvirus 6 -Influenza -Adenovirus -Echovirus -Cytomegalovirus HIV -not “idiopathic”, -?whether HIV is causing myocarditis itself, or just allowing other viruses to cause the problem |
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Viral myocarditis: mechanism, susceptibility
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Immunologic mechanism
-develops weeks after the original infection. Enhanced susceptibility (animal studies): -Radiation, malnutrition, steroids, exercise, previous myocardial injury Tends to be more aggressive and fulminant in infants and pregnant women |
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Hypertrophic cardiomyopathy: problem
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Abnormal LV hypertrophy
-LV muscle very thick --And not normal: myofibrillar disarray -Not caused by something else --Not caused by aortic stenosis or untreated hypertension Ventricular septum is usually most affected -Called Asymmetric Septal Hypertrophy -But other forms exist: apical HCM, etc… |
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Hypertrophic cardiomyopathy: causes
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Mutations
-Beta myosin heavy chain --The most dangerous one -Troponin T -α-tropomyosin Can be sporadic or familial -Familial form is autosomal dominant |
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Hypertrophic cardiomyopathy: clinical manifestations
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Thickened muscle
-causes poor relaxation = diastolic dysfunction --Inability to relax causes ↑LVEDP --Systolic function is just fine – too good, actually… Myofibrillar disarray -↑risk of dangerous ventricular arrhythmias -what usually kills people |
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Asymmetric septal hypertrophy and HOCM
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Very thick septum can lead to abnormal motion of mitral valve during systole
Mitral valve gets sucked toward the septum, obstructs flow into the aorta “Hypertrophic Obstructive Cardiomyopathy” (HOCM) -causing obstructing of flow into the aorta = obstruction of the LV outflow tract -“Dynamic” because it’s not due to a fixed valvular lesion, only there when the mitral valve swings into the wrong location |
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Dynamic LV outflow obstruction: better/worse
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What makes the obstruction worse:
-↓volume within the LV --Dehydration is bad --Smaller interior dimensions of chamber mean ↑chance of mitral valve getting sucked over to the septum -↑contractility --Strenuous exercise is bad --Positive inotropic drugs are bad What lessens the obstruction: -↑volume within the LV --Hydration is good --Larger interior dimensions of chamber = good -↓contractility --Beta blockers are good --Diltiazem/Verapamil can be good |
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HOCM: Squat to stand, valsalva
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A very important physical exam maneuver
-Commonly done with children before participating in high-level competitive sports Listen with stethoscope while patient squats -Squatting = ↑venous return = ↑LVEDP -HOCM murmur gets softer or disappears Continue listening as patient stands up -Standing = ↓venous return = ↓LVEDP -HOCM murmur gets louder Valsalva Take a breath and contract abdominal muscles -↑intra-abdominal pressure compresses the inferior vena cava = ↓venous return = ↓LVEDP -HOCM murmur gets louder |
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HOCM vs Aortic stenosis: PE
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HOCM:
Dynamic LV outflow obstruction How to get a louder murmur: -↓ venous return / ↓LVEDP more dynamic obstruction = louder murmur -Standing and Valsalva = louder murmur Aortic stenosis Fixed LV outflow obstruction How to get a louder murmur: -↑ venous return / ↑LVEDP -Obstruction doesn’t change --It’s fixed aortic stenosis -But ↑preload means stroke volume and the pressure generated by the LV both increase --Starling’s law -More blood at higher pressure being forced across valve = louder murmur -Squatting = louder murmur |
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HCM/HOCM: sudden death
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Probably never due to obstruction
Ventricular arrhythmias are the problem -Myofibrillar disarray -Beta-Myosin heavy chain mutation is the worst Certain criteria = may need defibrillator (ICD) implant Some patients never have any notable symptoms (or ignore them) and then one day just “drop dead” |
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HCM/HOCM: treatment for obstruction
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Negative inotropes may help
-Beta blockers -Diltiazem / Verapamil Surgical myomectomy -Cut out part of the septum Intentional infarction of the septum -Cardiac cath lab: occlude a septal artery (branch of the LAD) and inject ethanol --Causes infarction of the septum --Reduces septal contraction --May reduce dynamic LVOT obstruction |
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Restrictive cardiomyopathies: etiologies
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Fibrosis or scarring
-Scleroderma Infiltration of myocardium by some other thing -Amyloid -Sarcoid -Cancer (pretty rare) Deposition of something -Hemochromatosis –iron -Glycogen storage diseases |
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Restrictive cardiomyopathies: problem, prognosis
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Systolic function is usually okay
-At least initially -That can eventually change… Primary problem all along is very stiff ventricle due to all that “stuff” in it -Unable to relax = diastolic heart failure -↑LVEDP and ↑RVEDP --Symptoms of Left and Right-sided heart failure Prognosis is poor for most types |
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Arrhythmogenic right ventricular cardiomyopathy: problem
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The primary risk is malignant ventricular arrhythmias
-Sudden cardiac death If certain criteria met, need implantable cardioverter-defibrillator (ICD) No cure |
