Note: the following material is for personal use only see below for

Other treatment concerns

• 
  Increased Risk of subsequent MI
  

scintigraphy, ventricular ectopy (> 10 PVCs/min)

Note: females have higher mortality in 30 days after MI (various theories)
Follow-up Care

• 
  measure left ventricle EF / submaximal stress test before discharge (> 2 days post MI) /
  

• 
  return to work and resume sexual activity from 6-8 wks
  
• 
  cardiac rehab improves functional status, exercise/activity tolerance / aerobic activity 20-30
  

Other Causes of MI (besides coronary artery disease)

Coronary emboli

aortic or mitral valve lesions, left atrial or ventricular thrombi, prosthetic valves, fat emboli, intracardiac neoplasms, infective endocarditis, and paradoxical emboli
Thrombotic coronary artery disease

oral contraceptive use, sickle cell anemia and other hemoglobinopathies, polycythemia vera, thrombocytosis, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, antithrombin III deficiency and other hypercoagulable states, macroglobulinemia and other hyperviscosity

states, multiple myeloma, leukemia, malaria, and fibrinolytic system shutdown secondary to impaired

plasminogen activation or excessive inhibition

Takayasu’s disease, Kawasaki’s disease, polyarteritis nodosa, lupus erythematosus, scleroderma, rheumatoid arthritis, and immune-mediated vascular degeneration in cardiac allografts

May be associated with variant angina, nitrate withdrawal, cocaine or amphetamine abuse, and angina with "normal" coronary arteries

amyloidosis, connective tissue disorders (such as pseudoxanthoma elasticum), lipid storage disorders and mucopolysaccharidoses, homocystinuria, diabetes mellitus, collagen vascular disease, muscular dystrophies, and Friedreich’s ataxia

aortic dissection, luetic aortitis, aortic stenosis, and ankylosing spondylitis syndromes

Bland-White-Garland syndrome of anomalous origin of the left coronary artery from the pulmonary artery, left coronary artery origin from the anterior sinus of Valsalva, coronary arteriovenous fistula or aneurysms, and myocardial bridging with secondary vascular degeneration

coronary dissection, laceration, or thrombosis (with endothelial cell injury secondary to trauma such as angioplasty); radiation; and cardiac contusion

aortic stenosis, aortic insufficiency, hypertension with severe left ventricular hypertrophy, pheochromocytoma, thyrotoxicosis, methemoglobinemia, carbon monoxide poisoning, shock, and hyperviscosity syndromes

	AORTIC STENOSIS	MITRAL STENOSIS	MITRAL REGURGITATION	AORTIC REGURGITATION
	Idiopathic calcification of a bicuspid or tricuspid valve Congenital Rheumatic	Rheumatic fever Annular calcification	MVP Ruptured chordae Endocarditis Ischemic papillary muscle dysfunction or rupture CTD LV myocardial diseases	Annuloaortic ectasia Hypertension Endocarditis Marfan syndrome Ankylosing spondylitis Aortic dissection Syphilis CTD
Mechanism	Pressure overload upon the LV with compensation by LV hypertrophy. As disease advances, reduced coronary flow reserve causes angina. Hypertrophy and afterload excess lead to both systolic and diastolic LV dysfunction.	Obstruction to LV inflow increases left atrial pressure and limits cardiac output mimicking LV failure. Mitral valve obstruction increases the pressure work of the right ventricle. Right ventricular pressure overload is augmented further when pulmonary hypertension develops.	Places volume overload on the LV. Ventricle responds with eccentric hypertrophy and dilatation, which allow for increased ventricular stroke volume. Eventually, however, LV dysfunction develops if volume overload is uncorrected.	Chronic increased SV  hyperdynamic circulation, systolic HTN (pressure and volume overload) Compensation (concentric and eccentric hypertrophy) Acute Because cardiac dilation has not developed, hyperdynamic findings are absent. High diastolic LV pressure causes mitral valve preclosure and potentiates LV ischemia and failure.
Symptoms	Angina Syncope Heart failure	Dyspnea Orthopnea PND Hemoptysis Hoarseness Edema Ascites	Dyspnea Orthopnea PND	Dyspnea Orthopnea PND Angina Syncope
Findings	Systolic ejection murmur radiating to neck Delayed carotid upstroke S4 , soft or paradoxic S2	Diastolic rumble following an opening snap Loud S1 RV lift Loud P2	Holosystolic apical murmur radiates to axilla, S3 Displaced PMI	Chronic Diastolic blowing Hyperdynamic circulation Displaced PMI Quincke et al Acute Short diastolic blowing Soft S1
ECG	LAA LVH	LAA RVH	LAA LVH	LAA LVH
CXR	Boot-shaped heart Aortic valve calcification on lateral view	Straightening of left heart border Double density at right heart border Kerley B lines Enlarged pulmonary arteries	Cardiac enlargement	Chronic Cardiac enlargement Uncoiling of the aorta Acute Pulmonary congestion with normal heart size
Echo	Concentric LVH Reduced aortic valve cusp separation Doppler shows mean gradient > 50 mm Hg in most severe cases	Restricted mitral leaflet motion Valve area 1.0 cm2 in most severe cases Tricuspid Doppler may reveal pulmonary hypertension	LV and left atrial enlargement in chronic severe disease Doppler: large regurgitant jet	Chronic LV enlargement Large Doppler jet PHT < 400 msec Acute Small LV, mitral valve preclosure
Cath	Increased LVEDP Transaortic gradient 50 mm Hg AVA < 0.7 in most severe cases	Elevated pulmonary capillary wedge pressure Transmitral gradient usually >10 mm Hg in severe cases MVA < 1.0 cm2	Elevated pulmonary capillary wedge pressure Ventriculography shows regurgitation of dye into left ventricle	Wide pulse pressure Aortography shows regurgitation of dye into LV Usually unnecessary
Medical Treatment	Avoid vasodilators Digitalis, diuretics, and nitroglycerin in inoperable cases	Diuretics for mild symptoms Anticoagulation in atrial fibrillation Digitalis, beta-blockers, verapamil or diltiazem for rate control	Vasodilators in acute disease No proven therapy in chronic disease (but vasodilators commonly used)	Chronic Vasodilators in chronic asymptomatic disease with normal left ventricular function Acute Vasodilators
Indications for Surgery	Appearance of symptoms in patients with severe disease (see text)	Appearance of more than mild symptoms Development of pulmonary hypertension Appearance of persistent atrial fibrillation	Appearance of symptoms EF < 0.60 ESD > 45 min	Chronic Appearance of symptoms EF < 0.55 ESD > 55 min Acute Even mild heart failure Mitral valve preclosure

• 
  valsalva: decreases preload / ↑ HCM, ↓ AS
  

• 
  sustained handgrip: increases afterload (but may enlarge LV cavity) / variable effect on HCM, AS / ↑ AR, MR, MS
  
• 
  squatting: increases venous return and afterload / ↓ HCM / ↑ most murmurs
  
• 
  inspiration: increases flow through right side of heart / ↑ TR
  
• 
  leg raise (decreases HCM, increases AS)
  

Aortic Stenosis

• 
  congenital AS (pediatrics/young adults)
  
• 
  senile calcific AS (50s and older) – most common cause of AS in Western world
  
• 
  bicuspid AS (30-40s)
  
• 
  rheumatic AS (always associated with mitral valve disease) / 20% w/ mitral injury also
  

Sustained, forceful apex beat (not displaced until heart failure occurs)

Medical therapy useful but temporary improvement of heart failure / statins may actually slow progression of valve leaflet calcification

Balloon valvuloplasty only moderate, temporary improvement (used in children)

Aortic valve replacement:

May or may not be able to correct any resultant heart failure

Homograft: no anticoagulation required / donors hard to get

Heterograft (porcine): only lasts about 10 yrs

Mechanical: more durable, coagulation therapy required
Bicuspid Aortic Valve

1-5% overall incidence

Present with AR in 30-40s or AS in 50-70s / ejection click

Mitral Stenosis
Etiology: almost always due to rheumatic heart disease (mostly in women; over ⅔), thrombus, myxoma [similar to endocarditis with fever, chills, embolisms, but negative cultures]

Pathology: elevated LAP leads to pulmonary congestion / 3-5 fold elevated pulmonary arterial pressure leads to RH failure / jet lesions

Symptoms:

• 
  Left heart failure: due to mitral stenosis itself, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea
  
• 
  Right heart failure: edema, ascites, anorexia, fatigue
  
  • 
    High risk of pulmonary hypertension during pregnancy
    
• 
  Hemoptysis: rupture of small bronchial veins
  
• 
  Hoarseness: enlarged left atrium impinges on left recurrent laryngeal nerve [pic]
  

Carotid pulse is brisk but diminished

Pulmonary rales due to pulmonary hypertension

Increased S1: may become reduced late due to incomplete closure

Increased P2 component of S2: due to pulmonary hypertension

Opening snap follows S2: shorter interval from S2 ( < 0.1 sec) means higher LAP and more severe MS [very calcified MS may not have opening snap]

Diastolic rumble: low-pitched apical rumble begins after opening snap (pre-systolic accentuation occurs with atrial contraction when in NSR)

Sternal lift (enlargement of RV due to pulmonary hypertension)

Neck vein distension, edema, hepatic enlargement, ascites (if right heart failure occurs)

• 
  diuretics to control pulmonary congestion (but be careful because MS patients can be very preload dependent and hypovolemia can lead to cardiac collapse)
  
• 
  B-blockers to decrease rate and increase LV filling
  
• 
  if atrial fibrillation present, can use digitalis to control ventricular rate and anticoagulation (warfarin) to prevent systemic embolism
  

Surgical: should be performed prior to pulmonary hypertension (usually regresses if surgery is successful)

• 
  infective endocarditis (see causes)
  
• 
  aortic dissections (retrograde), aneurysm
  
• 
  congenital bicuspid valve
  

Collagen vascular diseases such as SLE, ankylosing spondylitis, relapsing polychondritis

Myxomatous degeneration / weight loss

Congenital: Marfan syndrome (proximal root dilatation or aortic root dissection), Ehlers-Danlos, osteogenesis imperfecta, elastica? something

Course: eccentric dilatation (ESV 40-50, normal 10-15), LVH, decreased ejection fraction, systemic blood pressure ↑↓

• 
  Left ventricular failure:
  

• 
  Syncope:
  
• 
  Angina:
  

Left ventricular impulse displaced left and downward

Diastolic murmur (high pitched, blowing) (increased with squatting and handgrip)

S3 due to rapid filling – okay in young people / suggests surgical correction in older pts

Austin flint murmur – heard best with bell over PMI

Increased total stroke volume and pulse pressure (may be absent in acute AR)

Corrigan’s pulse

Hill’s sign

Pistol-shot femoral pulse

Durozier’s sign

De Musset’s sign

Quincke’s pulse

Labs:

ECG

Echocardiography

Cardiac catheterization

Treatment:

• 
  afterload reduction if LV dilatation is present: ACE inhibitors / nifedipine
  
• 
  periodic echo to evaluate LV function
  
• 
  mildly elevated BP may be due to widened pulse pressure (may not need specific therapy)
  
• 
  antibiotics as needed to prevent endocarditis
  
• 
  valvuloplasty or valve replacement surgery
  

CAD - myocardial infarction of LAD (see ruptured papillary muscle)

Dilated cardiomyopathy

MVP click-murmur syndrome

Rheumatic heart disease

Ruptured chordae tendinae – spontaneous (Marfan’s)

Endocarditis

myxomatous degeneration (including MVP)

Mechanism: LV initially remodels and enlarges eccentrically to compensate, but eventually muscle gives out

Physical signs:

• 
  Murmur: holosystolic, apical, radiates to axilla, frequently has a thrill / increased with squatting (increase venous return and afterload) / high pitch, blowing SEM / murmur may be absent with severe MR / mid-systolic click with MVP / can have diastolic rumble from blood flowing? Shorter duration?
  
• 
  S3 from rapid filling of LV by large volume of blood in LA
  
• 
  PMI displaced down and to left, carotid upstroke brisk but diminished
  

• 
  afterload reduction (ACE, nitroprusside)
  
• 
  digoxin for EF and Afib
  
• 
  diuretics for volume overload
  
• 
  anticoagulants for Afib and very low EF
  

• 
  new murmur after MI (acute MR is result of ischemia of posteromedial papillary muscle in 80% of cases; likely from PDA infarct)
  
• 
  murmur peaks in mid-late systole, but usually not holosystolic or short ejection
  

redundant valve leaflets prolapse into left atrium during systole / most common cause of isolated severe MR in U.S. / females (14-30 yrs) / familial inheritance (could be AD)

• 
  can be from connective tissue disorders such as OI, ED, Marfan’s) / redundant leaflets (post>ant) and chordae tendinae, calcifications and annular dilation can cause MR
  
• 
  Others: rheumatic valve disease, cardiomyopathy, CAD, 20% of ostium secundum ASD pts
  

increasing LV size (squatting, B-blockers) delays click-murmur, decreasing LV size (valsalva, hand-grip), advances murmur (and also increases intensity of late systolic component)

Treatment: reassurance +/- B-blockers (empirical relief of CP), abx (for endocarditis prevention), anti-arrhythmics (if this is an issue)

associated w/ other valve disease / drug use and infections of valve

Infective endocarditis, RV failure, rheumatic heart disease, RV infarction

Presentation: similar as RV failure

Physical exam: RV lift, holosystolic murmur at LSB (increases with inspiration), large V wave in

JVP [diagram], pulsatile liver
Acute Rheumatic Fever (ARF)

Epidemiology: overcrowded, undernourished areas / occurs 3-4 weeks after Strep A

pharyngitis in a small percentage of untreated cases 3 yrs and up (average age ~8 yrs) / 20% of

patients have 1^st attack in adulthood (50% of 1^st attack involves heart)

Etiology: Strep (A-T) / Strep A has 80 types of M protein (determines if it causes ARF or PSGN)

Mechanism: molecular mimicry (autoimmune reaction) / familial predisposition: alloantigen on b cell (75% vs. 16% controls)

Note: impetigo causing strep do not cause rheumatic fever, but can cause renal disease

Valvular Involvement: (mitral >> aortic > tricuspid) / mitral only (65-70%) / mitral + aortic

• 
  Arthritis: transient migratory polyarthritis / large joints, hot, red, tender, limitation of movement – no residual deformity / symmetric
  
• 
  Chorea (Sydeham’s): purposeless, involuntary, rapid, emotional lability / can happen 6 months later (as isolated symptom) and is usually transient
  
• 
  Skin Lesions
  
  • 
    erythema marginatum: pea-sized, extensor surfaces, pink with clear centers, serpiginous margins change from morning to evening – trunk and proximal extremities (never on face)
    
  • 
    subcutaneous nodules: firm, painless, freely moving, extensor surfaces of elbows, knees, spine, occiput
    
• 
  Acute Rheumatic Carditis (treat with steroids), focal interstitial, diffuse interstitial, direct injury / migratory polyarthritis, erythema marginatum
  
  • 
    Aschoff nodule: exudative, granulomatous with Aschoff (multinuclear) and
    
  • 
    caterpillar/owl-eye cells, (mononuclear), fibrous scar
    
  • 
    Verrucae – vegetations along lines of closure
    
  • 
    MacCallum’s plaques – sub-endocardial lesions, usually in left atrium
    
  • 
    Prolapse: myxoid replacement of leaflets, chordae tendinae may rupture  severe MR, apical systolic murmur MR, apical mid-diastolic murmur (?Corey-Coombs), basal diastolic murmur aortic regurge, change in previous murmur
    

aspirin 100 mg/kg/day QID (taper down with no heart symptoms)

prednisone 2 mg/kg/day for 2 weeks (taper for 2 weeks), then switch to aspirin with

good response (changes clinical course, but not long-term outcome)

• 
  sharp or tearing pain (often confused for MI), may radiate to back, may persist for long period of time
  
• 
  may have unequal pulses in extremities: involves brachiocephalic artery
  
• 
  AR: involves aortic root and/or pericardial tamponade:
  
• 
  neurological deficits from cerebral compromise (type A  CVA) or acute peripheral neuropathies (type B  peripheral ischemia)
  
• 
  hypotension from pericardial tamponade or exsanguination
  
• 
  MI from coronary occlusion, bowel ischemia (SMA/IMA), ARF (renal arteries)
  
• 
  Horner’s syndrome: compression of superior cervical ganglion
  
• 
  SVC syndrome: compression of SVC
  

(involves ascending), B (does not involve ascending)

TTE or TEE very important when type A suspected (15% are intimal (non-communicating) and are best diagnosed by TEE

• 
  B-blocker then vasodilator (NP or even Ca blocker)
  
• 
  Labetalol (as single agent)
  
• 
  Trimethaphan camsylate (can be used without B-blocker  bad for COPD, bradycardia, CHF)
  

Heart failure

Clot  10-40% of anterior MI develop clot (risk of embolism)

Sustained VT/VF

False aneurysm: partial rupture of heart, lined by pericardium / echo, LV angiogram, MRI –show narrow discrete communication

usually secondary to cancer, DIC, renal failure, sepsis / fibrin deposition, nidus / marantic

Duke’s major criteria:

1. 
   endocardial involvement: new murmur (not change in murmur) / positive echo
   
2. 
   isolation of typical organisms from 2 separate cultures or persistently positive
   

1. 
   predisposing valvular lesion or IVDA
   
2. 
   fever
   
3. 
   vascular or immune-mediated phenomenon (see above)
   
4. 
   positive blood cultures (not meeting major criteria)
   

• 
  TTE (50% sensitivity, but aorta often not seen well by TTE (you should always speak with the cardiologist who actually read the echo)
  
• 
  TEE (95% sensitivity) (must not have ongoing upper GI problems, bleeding)
  

Elevated WBC with left shift may or may not be present

CBC, ESR, UA, 4 blood cultures over 48 hrs

Tends to cause false positive RPR, SLE and immune reactants in general

		Empiric Rx	Definitive Rx
Community	Strep viridans Enterococcus S. aureus S. pneumonia (1-3%)	amp nafcillin nafcillin/AG	Penicillin/ceftriaxone ampicillin/gentamicin nafcillin + 5 days gentamicin
IVDA	S. aureus (95%) S. non-aureus (5%) Pseudomonas	nafcillin/AG nafcillin/AG? nafcillin/AG +/- ceftazidime
Prosthetic valve (early)	S. epidermidis (50%) S. aureus (50%) Pseudomonas (10%) Fungal (5%)	vancomycin + ceftazidime or anti-pseudomonal AG
Prosthetic valve (late)	S. aureus or MRSA Enterococcus S. epidermidis GNR	vancomycin + gentamicin
Crohn’s	S. milleri
Colon Cancer	S. bovis

Austrian syndrome  pneumococcal pneumonia, meningitis, endocarditis (rapidly progressive)

Antibiotic prophylaxis for endocarditis (also see bone surgery)
Give prophylaxis for the following conditions (all are high-risk unless otherwise stated)

• 
  all prosthetic cardiac valves
  
• 
  previous endocarditis
  
• 
  surgical systemic pulmonary shunts
  
• 
  most congenital heart defects (including ductus arteriosis, coarctation, Marfan’s, others; complex defects are at high risk; except isolated secundum ASD and many of those which have been well surgically corrected)
  
• 
  acquired valve dysfunction (moderate risk)
  
• 
  hypertrophic cardiomyopathy (HCM) (moderate risk)
  
• 
  mitral valve prolapse with regurgitation or thickened leaflets (moderate risk)
  

Low-risk: ASD, post-CABG, AICD or pacemakers, MVP without MR, (surgically repaired ASD, VSD, PDA)

• 
  GI surgeries, biliary tract, ERCP, esophageal sclerotherapy or dilatation
  
• 
  surgery involving respiratory mucosa or rigid bronchoscopy
  
• 
  prostate surgery or cystoscopy
  
• 
  any dental procedure likely to cause bleeding (e.g. dental extraction)
  
• 
  tonsillectomy & adenoidectomy
  

• 
  amoxicillin 2 g PO or cephalexin 2 g PO or clindamycin 600 mg PO or clarithromycin 500 mg PO 1 hour prior to procedure or ampicillin 2 g IV or clindamycin 600 mg IV (make sure infusion ends 30 minutes prior to procedure)
  

• 
  moderate risk  amoxicillin or ampicillin as above / vancomycin 1 g IV if PCN allergic
  
• 
  high risk  give ampicillin 2 g IV + gentamicin 1.5 mg/kg (up to 120 mg) 30 minutes prior to procedure, followed in 6 hours by ampicillin 2 g IV or amoxicillin 2 g PO / if PCN allergic, give vancomycin 1 g IV + gentamicin 1.5 mg/kg (up to 120 mg)
  

tree barking vessels, aneurysms / valves

pericarditis, endocarditis / resembles rheumatoid type / Libman-Sachs

valves, granulomas

fibrotic lesions of aorta

caused by carcinoid tumors / endocardial thickening impairs tricuspid/pulmonic valves

common over 70 yrs / may cause insufficiency

Coxsackie B

CHF from garden-variety CAD

Post-partum cardiomyopathy (more)

Exposure: cobalt, mercury, lead

Endocrine: thyrotoxicosis, hypothyroid, acromegaly (usually reversible)

Metabolic: Fabry’s (hemi), hypophosphatemia, hypocalcemia, thiamine deficiency (wet Beri-beri),

Hemoglobinopathies: sickle cell, thalassemia
CXR: cardiothoracic ratio ( > 0.6 is abnormal) / heart looks wider on expiration (largest effect) and diastole (max 2 cm change)
Obliterative Cardiomyopathy

calcification, thrombi, macrophages

sarcoidosis, amyloidosis, hemochromatosis, carcinoid, idiopathic eosinophilia, endocardial fibroelastosis, endomyocardial fibrosis (Loeffler’s) / also obliterative agents

AD defect in contractile proteins leads to concentric hypertrophy of septum

• 
  ß-blocker, Ca-blocker (to relax ventricle, slow HR and allow more filling)
  
• 
  avoid afterload reducers (similar to AS)
  

• 
  indications for AICD (multiple trials looked at this and decision is not really based on EP study)
  
• 
  check all 1^st degree relatives with echo
  

may occur during last trimester or within 6 months of delivery (most often in 1 month before or after) / African-American, age > 30 / 50% will recovery completely (10-20% mortality)

ball valve obstruction of left atrium (tumor plop sound) / most common adult cardiac

tumor / can mimic PAN / can cause syncope
Rhabdomyoma

hamartoma / vacuolated myocytes / spider cells / most common childhood

Note: there is type I and II for each of the 3 degrees of heart block

type II – His and below / more likely to be anterior MI, permanent, QRS > 0.10

• 
  Type I (Wencheback’s) – cycle (2 to 8) of PR lengthening until beat is dropped / can mimic group beating
  

• 
  Type II – 2:1 (or 3:1 or 4:1) conduction block / here, the problem is in the bundle of His or branches, and therefore, type II is more likely to progress to 3^rd degree block
  

Note: new onset Mobitz II or BBB may signal impending MI (probably PDA from RCA)

Epinephrine  0.25 mg (do not give too much)

DA / isoproterenol (avoid with recent or ongoing ischemia)

Transthoracic pacing (A/P pads)

• 
  Synchronous demand  sends pulse if no R wave is seen in time – may need to change sensitivity to avoid background impulses (big P waves)
  
• 
  Asynchronous  do not do this if they have any inherent pacing (could give you R on T)
  

If no capture  increase current

Get capture then reduce to threshold and then go up to MA of 3 x threshold
DDD senses atrial/ventricular contraction and waits for set PR interval before firing

AV conduction delay

Hypervagotonia (often associated with sinus bradycardia or sinus arrhythmia)

Digitalis

B-Blockers

Ca Channel blockers

Class III antiarrhythmics

CAD

Lenegre’s disease (diffuse fibrosis of the conduction system)

Aortic root disease (syphilis, spondylitis)

Calcification of the mitral and/or aortic annulus

Acute infectious disease

Myocarditis
LBBB or Left Bundle Branch Block
^^ in V5 and V6

• 
  check limb leads / QRS > 0.12 / r/o artifactual QRS widening
  
• 
  cannot rule out MI or LVH in presence of LBBB
  
• 
  can rule in MI if ST changes > than 5 mm in synchronous leads (meaning T wave going same direction as R)