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Anxiety induced chest pain

Inappropriate myocardial lactate production

calcification, lipofuscin, scarring, nodular stenosis of valves

Withdrawal of short-acting anti-hypertensives (clonidine or propranolol), cocaine, amphetamines, phencyclidine, MAO + tyramine foods, pheochromocytoma, and ANS dysfunction (Guillain-Barré)

Treatment: anti-hypertensive medication / labetalol can cause paradoxical worsening

Alternatives: phentolamine and nitroprusside

Cocaine-associated chest pain  25% ischemia, 75% be musculoskeletal or psychological

Cocaine use may reduce the sensitivity and specificity of CK-MB and myoglobin (8050%) for infarction

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  Thrombosis (increased platelet action)
  
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  Vasospasm (acute)
  
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  Peripheral vasoconstriction (with prolonged adrenergic sensitization)
  
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  Increased heart rate (with prolonged adrenergic sensitization)
  
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  Accelerated atherosclerosis
  

intense pain / may radiate or present as chest, jaw/teeth, left arm (4^th 5^th digit), epigastrum /

Lavine’s sign  clenched fist over midchest / diabetics 20% or more have decreased sensation of pain from peripheral neuropathy / post-cardiac transplant patients also have a decreased sensation of pain

Ddx for MI

Pericarditis  ST elevations / echo

Myocarditis  ST elevations, Q waves / echo

Aortic dissection  ST elevation/depression, non-specific ST/T waves / TEE, chest CT, MRI, aortography

Pneumothorax  new, poor R-wave progression in V1-V6, acute QRS axis shift / CXR

PE  inferior ST elevation, ST shifts V1-V3

Cholecystitis  inferior ST elevation / U/S, radioisotope scan
Subendocardial (non-Q wave)

not occlusive (successful fibrinolysis occurs) / ST depression, flat T-wave

90% occlusive / moves from inner wall, vertically outward / ST elevation, inverted T-wave, wide Q wave is pathognomonic for MI

Anterior vs. Septal vs. Posterior vs. Right Ventricle (determined by ECG)

Note: pre-existing BBB clouds evaluation of ischemia

Early R wave progression (V₁/V₂) suggests posterior MI

CK (CPK) [more]	not selective / rises at 4-8 hrs, peaks at 16-24 hrs, normal by 2-5 days Note: if CK goes up in 7-15 hrs, could be early ‘washout’ (reperfusion)
CK-MB [more]	very selective / rises at 8 hrs, peaks at 16-24 hrs, normal by 3 days / cannot rule out MI when taken 24-48 hrs later CKMB [0-10] / CK-MB to CK fraction [0-2.5] increase within 3 hrs – peaks 10-12 hrs (reperfused infarct – later peak if you don’t reperfuse) – descend – [MM (skeletal > heart), BB (brain), MB (heart >)]
Troponin C	up in 3-5 hrs, normal by 10 days / 20 mins rapid test
Troponin I [< 0.3]	more specific 6-8 hrs after infarction – remains elevated 7-10 days Note: troponins can also be elevated (mildly) in renal failure Note: peak troponin levels 6 hrs after onset of chest pain in unstable angina and non Q MI can predict subsequent more severe MI within 30 days
Troponin T [< 0.1]	more specific 6-8 hrs after infarction – remains elevated 10-14 days
myoglobin	fast and sensitive (also from skeletal muscle damage) / leaks out within 1 hr / 4-6 hr peak normal by 24 hrs / used to monitor thrombolysis / urine myoglobin underestimates level
LD1 [30-80]	not specific, but sensitive / up at 24 hrs / peak at 3 days / normal by 1-2 wks
LD isozymes	LD1 > LD2 / LD flip is more selective

high WBC 12-24 hrs to 2 wks

AST up at 12 h, peak at day 2, normal by day 5 (over 200 means liver damage)

CRP mediator/marker of inflammation

cardiac myosin light chains under investigation

Management of LV Infarct

to prevent clot propagation / risk of major bleed is 2% (½ with subsequent CABG will bleed, but this can be controlled with transfusions)

give with ASA and heparin in pts in whom cath is planned; some cardiologist are more aggressive about giving IIb/IIIa agents (i.e. even if cath not necessarily planned, even if only NSTEMI, still not ruled in, etc)

coronary artery dilation improves blood flow to sub-endocardium

venodilation reduces preload and wall tension
Morphine

Pain, anxiety, decreased work for heart

benefits are seen with early initiation (< 24 hrs) for afterload reduction and to limit ventricular remodeling

shown to decrease mortality (but be careful to make sure patient is hemodynamically stable; overly aggressive b-blockade can worsen acute heart failure)

may have early benefit on vasodilatory tone (so give in early with ACS)

Ca channel blockers are in general ?frowned upon for CAD patients (but I haven’t read the studies)

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  Thrombolysis (see thrombolytics/contraindications)
  

(RPA + Reapro) slightly better outcome than (RPA alone)

tPA or rPA (increased half-life, action / studies ongoing)

expect idioventricular “reperfusion” rhythm (“accelerated idioventricular” rhythm)  don’t be alarmed if rate drops to 45~ (often 60-110 bpm; wide-complex escape rhythm)

reperfusion is almost assured with resolution of chest pain / 5% get acute re-occlusion

Prognosis: 30 day mortality only 2% with 60% post-thrombolysis reduction in ST segment elevation (7% otherwise) / mortality also better with flip T at 2 hrs post-MI

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  PCA (with stenting) (cardiac cath)
  

CURE  add plavix along with ASA in pts w/ UA/NSTEMI in whom PTCA planned (duration from 1–9 months)

PCI-CURE  start plavix x 1 mo s/o PTCA

Note: hold plavix 5-7 d prior to surgery in planned CABG

SIRIUS study showing dramatic reduction in restenosis rates using drug-eluting stents (especially for DM patients)
General outcomes for elective stenting: 1% mortality, 2-5% incidence of nonfatal MI, 1-3% need for emergency CABG / clinical restenosis rate of 10-20% in discrete lesions
low-risk  ASA before, heparin during

mod-risk  ?

high-risk  2b3a inhibitors before, during, after
TIMI risk score (0 to 14)

one point each for:  3 CAD risk factors; prior angiographic evidence; ST

changes;  2 anginal events last 24 hrs; use of ASA in last 7 days; increased

troponins, time to reperfusion therapy > 4 hrs

two points: age > 65, HR > 100, Killip class II to IV

three points: SBP < 100 mm Hg, age > 75 yrs
Risk of event increases linearly for TIMI 0/1 to 6/7 (4 to 41%)

30-day mortality (1 to 36%) / 1 yr mortality (those surviving 1^st 30 days) (1 to 17%)

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  TACTICS-TIMI 18  TIMI  3 benefited from early invasive
  
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  PRISM-PLUS  TIMI  4 benefited from 2b3a in addition to heparin
  
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  TIMI 11B, ESSENCE  benefit of Lovenox over heparin for  4 and  5 respectively
  

key is not to lose LV preload

give IVF as needed

avoid NTG, morphine (use with caution)

still give antiplatelet and anticoagulation agents
Complications of MI

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  Arrhythmias (1st COD post-MI; most often < 1 hr post-MI; must monitor closely first 24 hrs)
  

Ventricular arrhythmias (NSVT, sustained VT (> 30s requires treatment), VF)

Note: females with MI more likely to develop cardiac arrest or shock (males  VT)

Bradycardia/heart block

1^st degree AV block – every P followed by QRS

2^nd degree AV block

Mobitz I (inferior MI)

Mobitz II (large anterior MI, needs pacer)

3^rd degree AV block (needs pacer)

Indications for temporary AV pacing

Asystole, 3^rd degree block, Mobitz II AV block, sinus brady or Mobitz II w/

hypotension and refractory to atropine, new trifascicular block, alternating

BBB, 3^rd degree block w/ inferior MI complicated by RV infarction, incessant VT

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  CHF w/ pulmonary edema
  

II - bibasilar rales – 80% survival

III - rales, low BP – 60%

IV - rales, low BP, poor perfusion – 20% (cardiogenic shock)

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  Shock
  
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  Acute pericarditis (3-5 days) vs. Dressler’s autoimmune pericarditis (weeks to months)
  
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  Mural thrombosis
  
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  Rupture of papillary muscle (1%; 2-7 days)
  
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  VSD (1 to 4%; 3-7 days)
  
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  Cardiac tamponade
  
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  Ventricular aneurysm (rupture of infarct) (5-10 days)