EMCrit.org

Acute Coronary Syndromes (ACS)

Best Chest Pain Article

ST depression more than 0.1 mV measured 80 milliseconds from the J point

Initial Approach

Get ekg within 10 minutes.  2 sets biomarkers, last at least 8 hours from sx.  If presenting in less than 6 hours of symptoms, get myoglobin.

History

Nature of Sx, History of CAD, Sex, Age, # of traditional risk factors

HTN, increased chol., cigarettes (not so important, only prognostic), Diabetes (true risk)

Inquire about cocaine use in all patients

Multicenter chest pain study:  22% had sharp, stabbing pain, 13% had pleuritic, 7% had reproducible pain (Arch Int Med 1985;145:65-69)

response to nitroglycerin has no diagnostic role (Am J Card 90:1264, December 1, 2002)

It has a sensitivity of 35% and specificity of 59% (Gibbons RJ  Nitroglycerin: Should We Still Ask? Ann Intern Med. 2003;139:1036-1037 and 979 Henrikson) and (Annals EM 2005;35(6):581)

Neither does response to antacids (Emerg Med J BETs 20:169, March 2003)

Spontaneous coronary artery dissection remains an unusual cause of acute coronary syndrome. It should be included in the differential diagnosis of acute myocardial infarction, especially when it affects young, healthy females

Chest pain of unknown origin:  if patient has abnormal ekg, diabetes, or CAD they have a high rate of adverse events (Annals EM 2004;43:1,p.59)

Goldman Low risk patients have no need of telemetry monitoring (Annals EM 2004;43:1,p.71)

Retrospective study of confirmed MIs:  47% did not present with chest pain, Women and older patients more likely to present without chest pain. (Ann Emerg Med 40(2):180, 2002)

HIV is an independent risk factor treatment; with protease inhibitors is also an independent risk factor for MI (NEJM 2003 Nov 20; 349)

Systemic Lupus

Lupus accelerates atherosclerosis by about 20 years

50 x the ACS risk as age matched controls from the Framingham study (Review Am J Emerg Med 2005;23:696)

Conventional Risk Factors:  At least one, but not necessarily more than one risk factor was present in ~85% of women and 80% of men.  Meaning up to 1/5 had no risk factors. (JAMA 290 (7):891-898, Aug 2003)

Diabetes should no longer be considered a risk factor but instead an equivalent to known CAD (Heart 2005;91(3):388)

GERD symptoms should make you rather than less concerned, a suprising number of MIs were probably initiated by reflux attacks (In J Cardiol 2005;99(1):1-8) (In j Cardiol 2005;104(1):67)

No historical descriptors were good enough to rule out chest pain (JAMA. 2005 Nov 23;294(20):2623-9.)

Pathophy

Pathophys of ACS is not the large clots, but the small clots that tend to cause MI (Tiong AY, Am Heart J 2005; Hannson GK, NEJM 2005; Libby P Circulation 2005)

systemic inflammation plays a huge role

HS-CRP

lupus is a huge risk factor (

HIV (10 years younger), RA, Chronic Kidney Disease, chronic cocaine use as well

plaque composition is most important fibrous cap, lipid core, and lipid core composition

Women c MI at presentation

58% SOB

weakness

Only 20% had chest pain on presentation

(Circulation 108:2619, Nov 25, 2003)

traditional risk factors

Age>65
Male sex
DM
Smoking
FH
HTN
High Chol

New risk factors

DM as independent
Cocaine/Meth
HIV
CRI
SLE

relief with antacids (Emerg Med J 2003;20:170)

TIMI Risk Score

3 0r more of seven variables predicts increased risk of death or MI (JAMA 2000; 284, p. 835)

·        Age>65

·        3 or more Traditional Risk Factors (HTN, DM, Hyperchol, FH, Smoking)

·        Known coronary stenosis of 50% or greater

·        ST-segment deviation on ECG

·        2 or more anginal events in past 24 hours

·        ASA use during past week

·        Elevated Cardiac Enzymes

Can be used for risk stratification (Acad Emerg Med 2006;13(1):13)

of interest, the odds ratio for the 2 or more anginal events in past 24 hrs was 0.95, while all the others were > 1.9

----

In another study (Ann Emerg Med 2006;48:252)

in this study, age>65 fell out.

Presentation c AMI

53% have chest pain, less and less with age or female sex.  SOB in 17%, ABD Pain 2%. Weak and dizzy is a common presentation for elderly AMI (Ann Emerg Med 40(2):180, 2002)

Pts c negative inpatient w/u for ACS with CP 6 months later 11% risk of adverse events (Academic EM 2002:9, p.896-902)

JAMA Rational Clinical Exam for MI (JAMA Oct 14, 1998 280:14)

Meta-analysis showed little utility to signs & symptoms (British Journal of General Practice, February 2008)

Pathophysiology

Patients Discharged without Stress Testing

Prospective study of 1200 patients.  In the group who had stress tests, MI occurred subsequently in 0.9% while those with no imaging had 2.1% MI rate.  Rate of death at 3 months was 0.4% in stress group and 3% in those without imaging. (Am J Card 2003, 91:1410)

Patients Returning after Negative Stress Testing

Negative stress is presumed to clear a patient for 1 1/2 years, 1 year in diabetics

Conclusion: Among patients presenting with chest pain to the ED and a history of
stress testing within the past 2 years, a normal stress test result was associated with
a markedly reduced risk of having a major cardiac endpoint. absolute risk of 7% for death within 30 days or MI.

9 (2.0%, 95% CI 1.1% to 3.8%) had death or MI if normal biomarkers and non-specific ekg

(Annals EM Supplement 44:4 OCTOBER 2004)

Empiric Treatment

O2

Aspirin

Full adult dose, if contraindication give clopidogrel (Plavix, an adp antagonist-300 mg followed by 75 mg per day, contraindication to CABG, so do not give if possibility)

Clopidogrel

Caprie and CURE trials prove plavix superior to ASA, in post-MI period (Always use if pt gets a stent)

All patients admitted for r/o mi without planned intervention should have plavix started

If patient has history of GI bleeding, aspirin plus a PPI is actually safer than Plavix in terms of bleeding side effects in one well-done RCT (NEJM 2005;352:38)

CURE (Circulation. 2002;106:1622)

PCI-CURE (Lancet 2001;358:527)

CREDO (J Am Coll Cardiology 2005;46(5):761)

Nitroglycerin

oral then IV, increase dose until relief of sx or BP change.  (Not in  24 hrs of Viagra use)

Response to nitro is not sensitive or specific for ACS (Am J Card 90:1264, December 1, 2002)

NTG is contraindicated after use of sildenafil within the previous 24 hours or tadalafil within 48 hours (Circulation, 8/14/07, pg. e186)

Morphine

if still in pain after nitrites

Benzodiazepines

Consider even in non-cocaine chest pain )Journal of Emergency Medicine
Volume 25, Issue 4 , November 2003, Pages 427-437)

B-Blockers

Contraindications:

• HR<60 bpm,
• systolic blood pressure <100 mmHg
• Signs of Heart Failure or low-output state (cardiogenic shock)
• PR-interval on the electrocardiogram >0.24 seconds,
• second- or third-degree heart block,
• active asthma/reactive airways disease.

• Risk factors for cardiogenic shock:

  • age greater than 70 years,

  • systolic blood pressure less than 120 mmHg,

  • sinus tachycardia greater than 110 or

  • heart rate less than 60

Commit trial probably tells us not to use IV b-blocker in the ED, and probably defer oral until pt stabilizes

Lopressor

5 mg IV x 3, then 50 mg PO Q6 shooting for HR<80

Absolute Contraindications:

Marked first-degree AV block (i.e., ECG PR interval [PR] of greater than 0.24 s), any form of second- or third-degree AV block in the absence of a functioning pacemaker, a history of asthma, or severe LV dysfunction with CHF

Relative:

Significant sinus bradycardia (heart rate less than 50 bpm), COPD or hypotension (systolic blood pressure less than 90 mm Hg)

Esmolol

if COPD or another relative contraindication.

0.1 mg/kg/ min with titration in increments of 0.05 mg · kg^-1 · min^-1 every 10 to 15 min as tolerated by the patient's blood pressure until the desired therapeutic response has been obtained, limiting symptoms develop, or a dosage of 0.3 mg · kg^-1 · min^-1 is reached. A loading dose of 0.5 mg per kg may be given by slow intravenous administration (2 to 5 min) for a more rapid onset of action.

B-blockers work by decreasing risk of V. Fib not by controlling heart rate. Give all patients B-blockers except if contraindications

b-blockers worsen FEV1 and airway hyperresponsiveness in asthma, can also have detrimental effects in COPD (Chest 2005;127(3):818)

Diltiazem

if beta-blockers contraindicated and no LV dysfunction

ACEI

in persistent HTN in diabetics, CHF, or LV dysfunction

Give to all ACS pts unless elevated Creatinine

Statins

All ACS, lipitor if ____ elevated  ???, otherwise any statin (ie. Pravachol)

MIRACLE: study-lipid lowering in 24 hrs post-mi

Risk Stratify Based on EKG and History

EKG In ACS:

Use 15 lead-V8 mid scapular, V9 paraspinal, V4R

AMI

Measuring ST elevation:   >1 mm measured .08 (2 boxes) from j point compared to T-P as baseline or PR to J Point in 2 contiguous leads.

<2mm elevation in leads V1-V4 is borderline but can definitely indicate MI

Reciprocal ST depressions

make any st elevation much more likely to represent AMI. From reflections of infarcted area or ischemia.

Posterior gives

Anterior gives

Inferior gives

Lateral gives

Septal

Hyperacute T Waves

hyperkalemia or ami (often broad based and asymmetric as opposed to t of hyper-k which is symmetric and needle-like)

PVCs should have discordant ST, if concordant, suspect AMI 

Q-Waves

Abnormal Qs:

V2:  Any

V3:  Almost any

V4:  If more than 1  mm deep or larger than Q in V5 or > .02 sec wide (0.5 mm)

aVL:  >.04 sec or >50% amplitude of the QRS

III:  Q wave >0.04 sec, depth in this lead is not important

R waves should increase in amplitude from V1-V4, if not abnormal R wave progression

Rs should be >3mm by V3

Abnormal Q waves usually develop within 8 to 12 up to 24 to 48 hours after the onset of symptoms. Abnormal Q waves are at least 30 msec wide and 0.20 mV deep in at least two leads from the combinations listed.

According to the new criteria, an abnormal Q wave was any Q wave in leads V1 to V3 or a Q wave 30 msec in leads I, II, aVL, aVF, or V4 to V6; the Q wave must be present in any two contiguous leads and 1 mm in depth. (See "Diagnosis of an acute myocardial infarction").

Inferior Wall MI

Five Criteria to differentiate between RCA and L Circumflex

1. ST segment elevation in I=LCx

2. ST segment more elevated in II than III=LCx

3. ST segment elevation in aVR=RCA, depression >1 mm=LCX

4. ST elevation in V4R=RCA, depression=LCx

5. ST elevation in V1 with ST depression in V2, Depression in both=LCx

(Chest 122:1, 2002, p.134)

Be extremely wary of labeling STE in the inferior leads as benign.  Even with concave up morphology, this can represent AMI.  BER is not normally seen in this leads in isolation.

Right Ventricular MI

Robalino et al. found that STE greater than 1 mm in V_4R has 100% sensitivity, 87% specificity, and 92% predictive accuracy in detecting acute infarction of the RV resulting from occlusion of the right coronary artery above its first ventricular branch.  Has higher mortality and morbidity than inferior MI alone.

If inferior wall MI, if the greatest st elevation is in III, consider right-sided. also st elev in V1

Lateral MI

any new ST elevation in the lateral leads should be intervened or lysed as often there will not be >1 mm elevation., also since sometimes aVL will be the only lead affected, there is not the normal requirement of two contiguous leads.

Posterior Wall MI

From descending RCA or L circumflex, so suspect in inferior or lateral wall MI

ST Seg depression in V1-V3, or Prominent Positive T

R/S ratio >1 in lead V2

V7-V9 c > 1 mm ST elevation

The precordial ST depression of PMI has a relatively horizontal morphology rather than downsloping ST depression, which is more suggestive of of anterior ischemia. Most PMIs occur in the presence of inferior or lateral MI (Am J EM, 10/07, pg. 966).
 

Early Repolarization

st elevations are highest in V3-V4 usually <3.5 mm

are upwardly concave

show j-point elevation

rarely occur with low voltage QRS
are rarely greater than 1 mm in the lateral precordium (V5, V6)

seldom >2mm in pts >45 y/o

are not seen in aVL

STE c widespread distribution. Notching or slurring of the qrs

Symmetric, concordant large t waves

RBBB

• QRS>120 ms

• Wide S in I, aVL, and/or V6

• Delayed intrinsicoid deflection >40-50 ms

• RSR^' in V1 with the r prime>r or qR

V1-V6 usually with STE and T wave depressions which are discordant, if concordant, suspect AMI

Measure QRS duration in a lead where it is clear, use this to find the ST segment in other leads, compare this to the TP segment

LAFB

Left axis deviation

Deep S in the inferior leads

Small Q waves in I and aVL, small R in II, III, aVF

QRS<100 ms

Late intrinsicoid deflection in aVL

Increased QRS Voltage in the limb leads

No ST elevation

If seen with RBBB then it is a bifasicular block

LPFB

Right Axis Deviation

Narrow Q in inferior leads

Narrow R in aVL followed by a wide S

No ST elevation

LBBB

QRS>120

wide, monophasic R in I

Delayed Intrinsicoid Deflection in V5-6 >40 ms

rS or QS in V1

LAD

Discordant ST deviation and T wave inversion

The Sgarbossa Clinical Decision Rule for the ECG Diagnosis of AMI with LBBB. The electrocardiographic criteria suggesting a diagnosis of AMI according to Sgarbossa et al include the following:

A, STE elevation greater than 1 millimeter, which is concordant with the QRS complex (score of 5);

B, STD greater than 1 millimeter in leads V₁ , V₂ , or V₃ (score of 3); and

C, STE greater than 5 millimeters, which is discordant with the QRS complex (score of 2).

A total score of 3 or more suggests that the patient is likely experiencing an acute infarction based on the electrocardiographic criteria. With a score less than 3, the electrocardiographic diagnosis is less assured, requiring additional evaluation.

Ventricular Pacing

usually right paced producing LBBB.  Appropriate discordance to terminal portion of the QRS (ie. If terminal portion positive, should get st depressions.)

T waves should also be discordant

LVH

QRS must be less than 120 ms in isolated LVH

Limb

R in I + S in III >25 mm

R in aVL > 11 mm

R in aVF >20 mm

S in aVR >14 mm

Precordial

R in V5 or V6 > 25 mm

R in V5 or V6 plus S in V1 >35 mm

Largest R plus Largest S >45 mm

poor r wave progression, discordant changes

Pericarditis

Stage I-STE
Stage II-resolution

Stage III-T wave inversion

Stage IV-return to normal

Pr seg depression.  None in AVR, best seen in V5, V6 and inf leads

no reciprocal changes may be seen

Left Ventricular Aneurysm

Bulges outwards during systole and diastole.  Gives persistent STE

most common in V1-V3

always <4 mm

relatively static when compared to old ekgs

should have deep Qs in the same leads

CNS

deep t wave inversion

Prominent U waves

QT prolongation

WPW

(Bundle of Kent)-Short PRI, Wide QRS, Delta wave

Wellens' Syndrome

angina with t-wave inversion from V2-V4

Wellens' Syndrome (from EMEDhome.com)

The Emergency Physician must be familiar with the characteristic changes of Wellens' Syndrome, first described in 1982 and recognized to represent a critical stenosis of the proximal left anterior descending artery.

This entity is manifested by characteristic biphasic or inverted T waves in V2 and V3 and is a marker for a critical stenosis high in the left anterior descending artery.  Patients exhibiting Wellens' T-wave changes are at a high risk for the development of an extensive anterior wall MI.   This is a subgroup of patients who do poorly with conservative management, even though initially they seem to respond well to treatment.  Two variants of the Wellens' Syndrome exist.   The figure below is from the original paper published by Wellens and colleagues.

      click to enlarge

Reprinted with permission from de Zwaan C, Bar FW, Janssen JH, et .al. Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery.   Am Heart J 1989; 117: pg. 731

On the right, is the more common, more dramatic variant manifested by deeply inverted T waves often extending to leads V4 and V5.   On the left, is the less common pattern which is much more subtle.  This is the pattern exhibited on the EKG of the previous page, and the one often underappreciated by clinicians.   The T waves have a characteristic upsloping then sharply downsloping pattern leading to a symmetric T-wave inversion in leads V2 and V3 (and on occasion V4).  

Wellens' changes are not uncommon.  In the original description, of 145 consecutive patients admitted with unstable angina, 18% exhibited this pattern (1).   The EKG abnormalities – the mechanism of which remains unclear -usually occur when the patient is pain-free and when other evidence of ischemia or unstable angina may be absent.   The importance for the Emergency Physician is to recognize that the patient exhibiting Wellens' changes is at high risk and should undergo urgent angiography as exercise stress tests are relatively contraindicated in the presence of left-main lesions.   It is incumbent upon the Emergency Physician to avoid the following pitfalls when confronted with this entity:

• Discharge the patient home for follow up after "ruling out" for a myocardial infarction in a short stay/observation unit. The patient should undergo timely aniography and a strong case can be made that this should be done upon recognition of the changes, not at a later date given the high risk for development of an extensive anterior MI.  

• Arrange for exercise stress test for evaluation of the patient's coronary arteries.  Although such evaluation is usually done by a cardiologist, the increased use of observation units often places this responsibility in the hands of the EP.   Again, exercise stress testing is relatively contraindicated.  These patients fare poorly with medical management and often require surgical intervention.

• Interpret the T-wave changes as "non-specific ST-T changes" and not appreciate that the patient is at high risk.

Loss of precordial T-wave balance

tall upright T in V1

TV1

Hyperkalemia

diffuse tented T waves contrasted with the hyperacute Ts of AMI which are localized, bulky, wide

short QT interval when here is no QRS prolongation

AVR

if st elev greater in avr than V1 think proximal left main disease or three vessel disease (Am Heart J;154:71)

ST-segment elevation greater than 1.5 mV worry about LMCA

Yamaji et al [4] attempted to determine the ECG features of acute LMCA in the patient with ACS. The ECGs of 86 consecutive patients who experienced ACS were analyzed. Sixteen patients experienced LMCA obstruction, 46 patients experienced obstruction of the left anterior descending artery, and the final 24 patients were diagnosed with right coronary artery obstruction. In this study group, Yamaji noted the relationship between acute LMCA obstruction and ST-segment elevation greater than 0.05 mV in lead aVR. This electrocardiographic finding was present in 88% of patients with LMCA obstruction, as opposed to 43% of patients with left anterior descending obstruction, and 8% of patients with right coronary artery obstructions. From the study, the sensitivity of ST-segment elevation in lead aVR for predicting LMCA obstruction was determined to be 81% and the specificity to be 80%.

Statistical analysis of this finding revealed a sensitivity of 78%, a specificity of 86%, a positive predictive value of 57%, and a negative predictive value of 95%. This reasonably high sensitivity allows the clinician to “rule-in” LMCA in the ACS patient with lead aVR abnormality.

In addition to aiding in the diagnosis of LMCA involvement in patients presenting with acute coronary syndromes, the finding of ST-segment elevation in lead aVR also has prognostic significance. In his second study on the topic, Kosuge et al [7] examined the admission ECGs and biochemical markers of 333 patients with diagnosed non-AMI acute coronary syndromes. Although Kosuge studied numerous ECG findings and a variety biochemical markers, only ST-segment elevation greater than 0.5 mm in lead aVR on the admission ECG and elevated troponin T levels were determined to be independent predictors of adverse clinical events at 90 days, with an odds ratio of 13.8 and 7.9, respectively. Patients with ST-segment elevation in lead aVR and elevated troponin T levels were also determined to have the highest rates of both LMCA or 3-vessel disease and 90-day adverse outcome (62% and 47%, respectively).

Mattu on the use of aVR

Cardiac Markers

CK/MB-also from trauma, rhabdomyolysis, hyperthermia.  Peak @13, stay 72 hours

Myoglobin 1-4 hours, peaks at 6, stays 24

Troponin seen at 3 hours, peaks at 12-24 hours, stays 1 week

Troponin levels reflect increased risk death/MI regardless of renal dysfunction (N Engl J Med 2002; 346:2047-2052) Troponin I>0.8 is ischemic in nature (Acad Emerg Med 2004 11: 979-981)

(1) Jeremias A, Gibson CM. Narrative review: alternative causes for elevated cardiac troponin levels when acute coronary syndromes are excluded. Ann Intern Med 2005;142: 786-91.

Myeloperoxidase as new marker (Brennan ML, et al. Prognostic value of myeloperoxidase in patients with chest pain. N
Engl J Med 2003;349: 1595-1604.)

CRP as a new Marker?

One set of markers is not acceptable even if the chest pain has been going on for a while (Can J Emerg Med 4(5):322, September 2002)

low level troponin I elevations (1-3.0) ARI of 7% compared to Trop<1.0 in patients with suspected ACS HR of 3.4 (Am Heart J 2004;148(5):776)

PREVALENCE OF ELEVATED TROPONIN I IN END-STAGE RENAL DISEASE PATIENTS RECEIVING HEMODIALYSIS
Click here to hear the Reviewer's comments via MP3.
Donnino, M.W., et al, Acad Emerg Med 11:979, September 2004


BACKGROUND: Patients with end-stage renal disease (ESRD) have high rates of atherosclerotic heart disease. In this population, coronary artery disease is the primary cause of death in 45-50%. Some studies have reported false-positive elevation of markers for acute myocardial infarction (AMI) in ESRD patients. Cardiac troponin I (cTnI) has been reported to be specific for cardiac muscle, and is excreted by the kidneys. Although studies have reported false-positive elevation of cTnI in up to 21% of patients with ESRD, several of these studies included patients with acute illnesses that might be associated with cTnI elevation.

METHODS: The authors, from Henry Ford Hospital in Detroit, measured pre- and post- dialysis cTnI in 113 ESRD patients aged 26-92 with no symptoms of acute coronary syndrome who presented for maintenance dialysis. A cTnI above 0.8ng/dL was considered to be elevated.

RESULTS: Nearly all of the patients (94.5%) had hypertension and just over half (53.2%) were diabetic. No patient had a cTnI level positive for AMI either before or after dialysis. Predialysis levels ranged between 0-0.7ng/dL (mean, 0.13ng/dL), and postdialysis levels ranged between 0-0.5ng/dL (mean, 0.11ng/dL).

CONCLUSIONS: These findings suggest that cardiac troponin I is a reliable marker of myocardial injury in patients with ESRD on chronic dialysis. 11 references (mdonnino@aol.com)
 

Acute Coronary Syndrome vs Nonspecific Troponin Elevation (Arch Intern Med. 2007;167:276-281. )

Causes of False-Positive Troponin Results

Heterophile antibodies

Human anti-mouse antibodies

Autoantibodies

Fibrin clots

Rheumatoid factor

Microparticles in specimen

Interference by endogenous components in blood (bilirubin, hemoglobin, lipemia)

High concentration of alkaline phosphatase

Immunocomplex formation

Analyzer malfunction

 

 

Discordant MB and Troponin

an elevation of either in the absence of the other was associated with a higher risk of ACS

(Ann Emerg Med 2006;48(6):660)

Likelihood that presentation represents
ACS secondary to CAD (ACC Guidelines 2002)

http://www.acc.org/clinical/guidelines/unstable/unstable.pdf

Vancouver Very Low Risk Patient Identification

in derivation, right now (Annals Emerg Med 2006;47(1):1)

Treatment of UA/NSTEMI

Heparin

All intermediate and high risk ACS

UFH:  60 U/kg loading and then 12 U/kg/hr

Use lovenox unless CABG planned in 24 hours or elevated Creatinine

Lovenox:  1 mg/kg q 12 (Bolus 30 mg IV if STEMI)

2002 guidelines specifically recommend lovenox, heparinization is now Ia

LMH-preferentially bind Xa with decreased effect on platelets

ESSENCE trial supports lovenox over UFH

Not for anticoagulation of mech. Valves (not approved)

Can use during PCI (Am Heart J 144:615 2002)

Same cost as UFH (West J Med 173:138, August 2000)

safe in PCI

Enoxaparin versus Unfractionated Heparin in Elective Percutaneous Coronary Intervention

Conclusions In elective PCI, a single intravenous bolus of 0.5 mg of enoxaparin per kilogram is associated with reduced rates of bleeding, and a dose of 0.75 mg per kilogram yields rates similar to those for unfractionated heparin, with more predictable anticoagulation levels. Target anticoagulation levels were reached in significantly more patients who received enoxaparin (0.5-mg-per-kilogram dose, 79%; 0.75-mg-per-kilogram dose, 92%) than who received unfractionated heparin (20%, P<0.001). (NEJM 2006;355(10):1006-1017
 

LOW MOLECULAR WEIGHT HEPARINS VERSUS UNFRACTIONATED HEPARIN FOR ACUTE CORONARY SYNDROMES
Background
This review aimed to identify randomized controlled clinical trials to determine the relative safety and efficacy of subcutaneous low-molecular-weight heparins (LMWH) versus intravenous unfractionated heparin (UFH) for people with acute coronary syndromes (ACS; unstable angina or non-ST segment elevation myocardial infarction).
Results
Seven studies (n = 11 092) were included. No difference was found in overall mortality between the groups treated with LMWH and UFH (RR 1.0, 95% CI: 0.69 to 1.44). LMWH reduced the occurrence of myocardial infarction (RR 0.83, 95% CI 0.70 to 0.99) and the need for revascularization procedures (RR = 0.88, 95% CI 0.82 to 0.95). A decrease in the incidence of thrombocytopenia (RR 0.64, 95% CI 0.44 to 0.94) was noted in patients who were given LMWH. No evidence was found for difference in occurrence of recurrent angina, or major or minor bleeds.
SOCRATES says
LMWH should be used rather than UFH in ACS. Insufficient data exist to recommend a single form of LMWH.
Magee KD, Sevcik W, Moher D, et al. Low molecular weight heparins versus unfractionated heparin for acute coronary syndromes. In: Cochrane Library, Issue 2. Oxford: Update Software, 2006 .

IIb/IIIa

All going to cath:

Reopro-.25 mg/kg bolus followed by .125 mg/kg/min

All high risk ACS, especially diabetics, elevated troponin, or stuttering pain:

Integrilin 180 mg/kg bolus, 2 mg/kg/min with second 180 mg/kg bolus administered 10 minutes after starting infusion lower infusion to 1 mg/kg/min if cr 2-4, do not use Cr>4    

(UA/NSTEMI guidelines, ACC.  2002  Ia if going to cath, IIa if high risk s cath, IIb if not)

Integrilin Drip Chart

Transfusions

Transfuse elderly with hematocrit <30 (NEJM 345:17)

Associated with worse outcomes in patients with ischemic disease  (JAMA Vol. 292 No. 13, October 6, 2004)

Treatment of STEMI

New STEMI Guidelines 2004 (Summary Annals of EM 2005;45(4):364)

Door to lysis <30, door to cath <90

No nitro if PDE in last 24 to 48 hours

Lyse if ST>1mm or presumably new LBBB if within 12 hours

Lyse posterior if within 12 hours

IIA for lysis at 12-24 hours with continuing symptoms

IIB abciximab + ½ dose tenectaplase or reteplase for prevention of reinfarction

Pulmonary edema or hypotension makes PCI preferable

60 U/kg (max 4000) then 12 U/kg (max 1000) for 50 to 70 (1.5-2)

Pts <75 y/o with normal renal function can get LMWH

Right Ventricular Infarction

10-15 % of anterior wall (R sided leads are not as sensitive in this case)

Increased morbidity/mortality than same MI without R sided involvement

If Lead III’s st elev. > II consider RV involvement.

Up to 10 liters of fluids

May see elevation in V1 and V2

Inferior Wall MI

Fluid load

Careful Use of Nitrites

Consider deleting b-blockes

ACEP Clinical Policy

Annals of Emergency Medicine  (Volume 48, Issue 4 , October 2006, Pages 358-383 )

Level A recommendations
Assess for fibrinolytic therapy in patients with symptoms suggestive of AMI and presenting within 12 hours of symptom onset if ECG reveals:

1 ST elevations greater than or equal to 0.1 mV (1 mm) in 2 or more contiguous limb leads or greater than or equal to 0.2 mV (2 mm) in 2 or more contiguous precordial leads lacking features of non-infarction causes of ST-segment elevation (eg, early repolarization, pericarditis, left ventricular hypertrophy [LVH], incomplete bundle branch block [BBB]).

2 Any type of BBB (right, left, and atypical – new or old) thought to be obscuring ST-segment analysis in patients with clinical presentation strongly suggestive of AMI.

Level B recommendations
Assess for fibrinolytic therapy in patients with symptoms suggestive of AMI and presenting within 12 hours of symptom onset if ECG reveals:

1 ST elevations greater than or equal to 0.1 mV (1 mm) in 2 or more contiguous precordial leads lacking features of non-infarction causes of ST-segment elevation (eg, early repolarization, pericarditis, LVH, incomplete BBB).

2 New or presumably new left bundle branch block (LBBB).

3 LBBB with concordant ST-segment deviations greater than or equal to 0.1 mV (1 mm) towards the major QRS deflection or discordant ST-segment deviations greater than or equal to 0.5 mV (5 mm) away from the major QRS deflection in 2 or more contiguous leads.

4 ST depressions greater than or equal to 0.2 mV (2 mm) with upright T-waves in 2 or more contiguous anterior precordial leads (V1 to V4) in patients with clinical presentation suggestive of AMI involving the posterior left ventricular wall.

Level C recommendations
Assess for fibrinolytic therapy in patients with symptoms suggestive of AMI and presenting within 12 hours of symptom onset if ECG reveals:

1 New or presumably new right bundle branch block (RBBB).

2 RBBB, atypical BBB, or ventricular paced and concordant ST-segment deviations greater than or equal to 0.1 mV (1 mm) towards the major QRS deflection or discordant ST-segment deviations greater than or equal to 0.5 mV (5 mm) away from the major QRS deflection in 2 or more contiguous leads.

 

PCI Vs Lytics

C-Port (Jama 287 (15))  Hospitals s cardiothoracic still had better outcomes than lytics

Thrombolysis

Class I

1. ST elevation (greater than 0.1 mV, two or more contiguous leads),  time to therapy 12 hours or less, age less than 75 years.
2. Bundle branch block (obscuring ST-segment analysis) and history suggesting acute MI.

Class IIa

1. ST elevation, age 75 years or older.

Contraindications:

Hemorrhagic Stroke

Other cerebrovascular events within one year

Known intracranial neoplasm

Active Internal Bleeding (not menses)

Suspected Aortic Dissection

Cautions

BP >180/110

Distant history of CVA

INR>2 or bleeding diatheses

Recent Trauma

Noncompressible vascular punctures

Pregnancy

History of severe hypertension

Thrombolytics not indicated for patients >75 (3/2002 Archives of Internal Medicine)

EKG signs of reperfusion

st segment elevation will usually worsen and then resolve with reperfusion

Terminal t wave inversion will usually occur within 90 minutes

ST resolution is the best marker of successful reperfusion

If original STE was > 4 mm and there is neither >50% recovery nor terminal T wave inversion at 60 minutes, consider rescue PCI

Relief of chest pain often with transient preceding increase is an excellent sign, continued chest pain is not necessarily bad

Erlanger Chest Pain Evaluation Protocol

Erlanger Six Step Accelerated Protocol:

1.      Initial EKG diagnostic of ACS

2.     CK-MB>10 or >5% of CK or Trop I >2

3.     Evolving Injury on Serial EKGs

4.     Increase in CK-MB>1.5 or in Trop I>.2 at 2 hours

5.     Clinical DX

Sens/Spec for AMI at 2 hrs 93.2/93.9 LR + 15.3/LR- 0.07

At this point risk stratify: 

Category

II-intermediate to high risk of ACS, admit or get repeat enzymes by standard practice,

III-Low Risk send to stress test,

IV-Very Low Risk, send patient home.

6.     Reversible Perfusion Defect on stress vs. resting nuclear scan

Sensitivity for 30 day ACS was 99.1%/spec 87.4% LR+ 7.9/LR - 0.07

 (Annals Emerg Med 2002; 40:6, 584)

Stress Tests

There are many limitations to a standard Bruce Protocol stress test. The most familiar have to do with the amount of workload achieved. The workload is measured in METs. The sensitivity of the test will be influenced by the amount of METs, the duration of exercise greater than 6–12 min, as well a heart rate at 85% of predicted [1, 2, 3, 4 and 6]. Exercise capacity itself shows a linear relation to adverse cardiac outcomes; the greater the METs achieved, the lower the relative risk of events [5]. The sensitivity of a standard ETT is thought to be approximately 66%, ranging from 40% to 90%, depending on the severity of disease when compared to the gold standard of coronary angiography, whereas specificity is approximately 84% [6]. The sensitivity is influenced by the severity of disease (multivessel vs. single vessel), the work load or exercise level, and antiischemic drugs such as beta-blockers [6]. Interpreting the results of any stress test must be applied to Bayes' Theorem, i.e., one must consider the pretest probability of coronary disease in the patient population you are screening.

Adding nuclear imaging to a standard ETT may improve the sensitivity and specificity. Planar Tc99m sestamibi imaging increases the sensitivity to 84%, whereas specificity is 83% [6]. Single photon emission computed tomography (SPECT) with Tc99m sestamibi can increase both the sensitivity and specificity to 90% and 93%, respectively [6]. It is a well-known phenomenon that the sensitivity of a nuclear stress test is limited by motion artifact, diaphragmatic attenuation, and "balanced" 3-vessel disease or left main disease [7 and 8]. This is due to the inability of a SPECT scan to detect subendocardial blood flow [10]. The overall sensitivity of a standard Tc-99 MIBI SPECT is approximately 60–70% in patients with multivessel disease [7 and 9]. Additional modalities added to the standard SPECT study, such as echocardiogram or adding pharmacologic agents like dipyridamole, can increase the sensitivity to 82% and 76%, respectively [7 and 9]. However, this is not routinely done. Therefore, in patients with a high pretest likelihood of severe CAD like the patient discussed, the interpretation of a "negative" imaging stress test should not necessarily end the workup.

test characteristics (NEJM 2001;344(24):1840)

Misc. Syndromes

Cocaine

Can cause vasospastic ST elevations

true mi (6% of cocaine chest pain)

can also result in aortic dissection

Get tox screen if young patient c chest pain

benzos to block central norepinephrine release.  Consider bicarb for dysrhythmias.  Benzos not b-blockers for tachycardias

First treat with nitrites and diltiazem, if ST segments persist go to cath or if not available, thrombolyis

Beta-blockers

are actually IIA (negatives are based on one trial)

Comment(s)
Beta blockade for cocaine induced myocardial infarction has been advocated in some quarters. At first sight it would seem to make sense as many of these patients will be hypertensive and suffering the effects of an adrenergic drive. However, it must be remembered that cocaine affects both alpha and beta receptors and that by giving a beta blocker the effects of alpha blockade on the heart may become unopposed. These trials seems to confirm this concern with a decrease in myocardial blood flow and coronary vasoconstriction. In a patient with myocardial ischaemia this could result in an even lower coronary blood flow thereby worsening the ischaemia. However, we must remember that this is a small study in an experimental setting with patients receiving very small amounts of cocaine (much less than the typical recreational user). It therefore makes the interpretation of these findings difficult.
On balance, in light of the feasible pathophysiological argument against the use of beta blockers, and the findings of these limited studies it appears sensible not to advocate the use of beta blockers in acute myocardial pain secondary to cocaine use.

CLINICAL BOTTOM LINE
Beta Blockers should not be used in the treatment of cocaine induced myocardial ischaemia.

Lange RA, Cigarroa RG, Flores ED, et al. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Annals of Internal Medicine 1990 Jun 15;112(12):897–903.
 

in pts with cocaine urine tox positive, b-blockers may reduce mortality (Ann Emerg Med 2008;51:117) which does not mean we should use them for cocaine induced chest pain, perhaps just -associated

0 and 6 hour and 12 hr enzymes, then safe to D/C for out-pt stress testing (NEJM 348:6 2003)

If multiple lesions found on cath in a young player, consider endocarditis

Give 1 mg of ativan with every nitro, more effective than nitro alone (Am J Emerg Med 21:1, 2003)

A majority of those that rule in for MI will have coronary artery blockage (not vasospastic) while a huge majority of those that rule out will have no structural disease. (J Emerg Med 24:1, 2003)

A 9-12 hour observation period with 2 sets negative is probably sufficient if follow-up can be arranged. (N Engl J Med 348(6):510, February 6, 2003)

Methamphetamines

FREQUENCY OF ACUTE CORONARY SYNDROME IN PATIENTS PRESENTING TO THE EMERGENCY DEPARTMENT WITH CHEST PAIN AFTER METHAMPHETAMINE USE Turnipseed S.D., et al, J Emerg Med 24(4):369, May 2003
high risk of acs in these patients

Syndrome X

Angina, positive exercise stress but no lesions on cath.  More common in women than men.

Tietze’s syndrome

20 to 30 y/o’s, fusiform swelling of costal cartilage

Pleuritic chest pain can sometimes be relieved by holding breath at deep expiration

Post-Stent Complications

Acute Thrombosis of Stent

Life threatening, soon after cath

Plavix reduces risk

Stent Restenosis

Occurs at either end of stent (candy wrapper)

Coated stents help, may need brachytherapy

Other Post Complications

Post-MI Complications

Left Ventricular Aneurysm

caused by fibrosis of necrotic myocardium

Presents with heart failure, dysrhythmias, mural thrombus formation

Persistent ST elevations at site of MI

Can cause chest pain for weeks after the MI,

Can lead to thrombus formation: Although a mural thrombus adheres to the endocardium overlying the infarcted myocardium, superficial portions of it can become detached and produce systemic arterial emboli. Although estimates vary based on patient selection, about 10% of mural thrombi result in systemic embolization (2).

Left Ventricular Free Wall Rupture

1-8% of AMI patients, but responsible for 8-24% of deaths

90% occur in the first two weeks

Acute Tearing Chest Pain

Volume Expansion, Afterload Reduction, Pericardiocentesis

Acute Ventricular Septal Defect

acute chest pain, weakness, mental status changes

Hypotension, new murmur,

Afterload reduction, volume expansion, intra-aortic balloon pump

Acute Mitral Regurgitation

papillary muscle rupture or dysfunction

75% of ruptures are at the posterior papillary muscle as this has lone blood supply (RCA or Circ)

acute onset of SOB, Pulmonary edema, hypotension, shock

Tachycardia, tachypnea, rales, and new murmur

Volume expansion, afterload reduction, intra-aortic balloon pump

Pericarditis

can happen immediately following MI 12 hours to 10 days, this is PostInfarction Pericarditis (PIP)

Give high dose aspirin 650 mg four - six times per day

Dressler's is an autoimmune response involving the myocardium

7-11 weeks after MI

WBC and ESR will be elevated

chest pain is worse when lying down

Post-Cath Complications

Insertion of vascular sheaths may produce groin or retroperitoneal hematomas:

Groin hematomas

may present with localized pain, leg edema due to femoral vein compression, or lower-extremity neurologic symptoms due to compression of the femoral nerve. Palpation of localized swelling or tenderness in the area, or loss of sensory or motor function, is highly suggestive of hematoma. The diagnosis can be confirmed by ultrasonography or computed tomography.
 

Retroperitoneal hematoma

Unexplained low blood pressure or drop in crit.  Can present with back, flank or abdominal pain.  Dx with CT scan of ABD/Pelvis.  Most retroperitoneal hematomas can be treated conservatively with discontinuation or reversal of anticoagulation and antiplatelet therapy, and with blood transfusions alone when necessary; approx. 1 in 8  patients require surgery. Indications for surgical intervention include persistent hypotension, decreasing hematocrit despite transfusion, or femoral neuropathy (due to nerve compression).
 

After the vascular sheath is removed from the femoral artery, a femoral pseudoaneurysm can form.


A pseudoaneurysm is a communication between the femoral artery and the overlying fibromuscular tissue, resulting in a blood-filled cavity. Groin tenderness, a palpable pulsatile mass, and/or new bruit in the groin area should prompt examination by Doppler flow imaging. Smaller pseudoaneurysms are usually followed clinically. Most larger pseudoaneurysms can be treated with ultrasound-guided compression, ultrasound-guided thrombin injection, or surgical repair. An emerging alternative therapy is percutaneous polytetrafluoroethylene-covered stent-graft deployment at the site of the pseudoaneurysm.

An arteriovenous (AV) fistula can result from sheath-mediated communication between the femoral artery and femoral vein. An AV fistula may be suggested by the presence of a systolic and diastolic bruit and confirmed by Doppler ultrasonography. AV fistulae can be treated with conservative therapy (careful observation) in most patients or with ultrasound-guided compression, surgical repair, or percutaneous implantation of covered stents if necessary.

The incidence of stroke following PCI ranges from less than 0.1% to 0.38%. Approximately half of PCI-related strokes are hemorrhagic, and half are nonhemorrhagic. Factors associated with increased risk for stroke include older age, presence of diabetes, saphenous vein graft interventions, and placement of an intra-aortic balloon pump (placed either prophylactically or for intraprocedural complications). In-hospital mortality rates are high in such patients.

Many arterial access sites are "sealed" after the procedure with percutaneous vascular closure devices. These devices can percutaneously place one or more sutures in the femoral artery or deliver a procoagulant, such as collagen or collagen and thrombin, through a sheath to stimulate local hemostasis. Physicians should be aware that hemostasis success rates are less than 100% and that these devices are associated with a risk for vascular complications. These complications include pseudoaneurysm, bleeding and hematoma, infection, arterial stenosis or occlusion, and venous thrombosis. Several reports in the surgical literature suggest that vascular closure devices are associated with a higher incidence of large pseudoaneurysms and pseudoaneurysms not amenable to ultrasound compression therapy, greater loss of blood and need for transfusions, higher incidence of arterial stenosis or occlusion, more extensive surgical repair, and higher incidence of groin infections compared with manual compression. Thus, the possibility of vascular complications should be considered at least as seriously in patients treated with vascular closure devices as in those treated with manual compression.
(EMEDhome.com)

Can We Send Home Low Risk Patients with 2 Troponins Negative

American J EM 19:2, March 2001

Picked a group who were admitted, but deemed low risk (<7% by validated risk stratification mechanism), no signs heart failure, hypotension, or arrhythmia. 

9.4% had a positive troponin and 2.6% clinically deteriorated during the first 12 hours.

Therefore, 88% met the criteria for expedited discharge, these patients were kept in the hospital and monitored during the study.  21.8% of this cohort had either a stress test showing ischemia/infarction, and/or an angiogram showing significant CAD.  A further 11.6% had a history of prior revascularization or q waves on their presenting ecg. 

Conclusion:  It might be ok to send home low risk patients after 12 hours, but only if follow up for stress testing or cath can be guaranteed in a timely (24-48 hour) manner.

Decision rule for young patients

Young adults with chest pain decision rule (Acad Emerg Med 2005;12(1):26)
Less than 40 y/o c absence of cardiac risk factors and cocaine report
normal markers (shifty, post hoc addition to the rule)
normal ekg can replace no cardiac risk factrs 0.14% risk ofa ami
 

Most Recent UA update

(Annals EM 2005;46(2):187)

original AHA http://www.acc.org/clinical/guidelines/unstable/unstable.pdf

Deep symmetrical T-wave inversion across the precordial leads may indicate a critical stenosis of the left anterior descending coronary artery (Wellen's phenomena).

Patients with suggestive histories and ST changes in the anterior precordial leads and/or I and L should have posterior leads recorded to detect possible posterior ST-elevation events.

Troponin elevations in the critically ill

elevatins represent myocardial death but do not necessarily need to be treated as MI (Curr Opin Crit Care 2004;10:342)

Review of other conditions with elevated trops (Chest 2004;125(5):1877) and (Ann Intern Med 2005;142:786)

Silent MI and mortality was predicted by elevated troponins in ICU patients at high cardiac risk (Crit Care Med 2005;33:1281)

Goldman Risk Score

Figure 1. Derivation of the Four Initial Risk Groups on the Basis of Data Available at the Time of Presentation in the Emergency Department.

Myocardial infarction (MI) was suspected if the electrocardiogram (ECG) showed ST-segment elevation of 1 mm or more or pathologic Q waves in two or more leads, and these findings were not known to be old. Ischemia was suspected if the ECG showed ST-segment depression of 1 mm or more or T-wave inversion in two or more leads, and these findings were not known to be old. Risk factors included systolic blood pressure below 110 mm Hg, rales heard above the bases bilaterally on physical examination, and known unstable ischemic heart disease, defined as a worsening of previously stable angina, the new onset of postinfarction angina or angina after a coronary-revascularization procedure, or pain that was the same as that associated with a prior myocardial infarction. The difference between each adjacent pair of risk groups was significant (P<0.001).

* Modification to Goldman's prediction rule: Left bundle-branch block not known to be old was also considered evidence of ischemia on ECG.
†Unstable ischemic heart disease was defined as a worsening of previously stable angina, the new onset of postinfarction angina or angina after a coronary revascularization procedure, or pain that was the same as that associated with a prior MI.
‡Cardiology consultation in the ED (for possible admission to the coronary care unit) was recommended for patients stratified as high risk, which included patients who had experienced a major complication in the ED (eg, cardiogenic shock). Modification to Goldman's prediction rule: Cardiology consultation for possible coronary care unit admission was also recommended for 2 subgroups of patients: (1) patients stratified as moderate risk by the original prediction rule because they had acute pulmonary edema or ongoing angina despite maximal medical therapy in the ED, and (2) patients presenting with unstable angina within 2 weeks of acute MI or within 6 months of coronary revascularization. Patients stratified as moderate risk who also had a high probability of significant coronary artery disease (using the Diamond and Forrester criteria²⁵) were recommended for cardiology consultation.

(JAMA Vol. 288 No. 3, July 17, 2002)