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

Most recent article again shows signs and symptoms not helpful (Resus 2010;81:281)

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)

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)

(1) Mattu A, et al. Premature atherosclerosis and acute coronary syndrome in systemic lupus erythematosus Am J Emerg Med 2005 Sep;23(5):696-703.
(2) Karrar A, et al. Coronary artery disease in systemic lupus erythematosus: A review of the literature Semin Arthritis Rheum 2001;30(6):436-43.
(3) Mehta PK, et al. Acute coronary syndrome as a first presentation of systemic lupus erythematosus in a teenager: revascularization by hybrid coronary artery bypass graft surgery and percutaneous coronary intervention: case report Pediatr Cardiol 2008;29(5):957-61.
(4) Korkmaz C, et al. Myocardial infarction in young patients (< or =35 years of age) with systemic lupus erythematosus: a case report and clinical analysis of the literature Lupus 2007;16(4):289-97.

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.)

from Cliff at resus.me

 A prospective study of 796 ED patients with suspected cardiac chest pain assessed the value of individual historical and examination findings for diagnosing acute myocardial infarction (AMI) and the occurrence of adverse events (death, AMI or urgent revascularization) within 6 months. AMI was diagnosed in 148 (18.6%) of the 796 patients recruited.

The results may surprise some physicians:

Sweating observed by the ED physician was the strongest predictor of AMI (adjusted OR 5.18, 95% CI 3.02–8.86).

Reported vomiting was also a fairly strong predictor of AMI (adjusted OR 3.50, 1.81–6.77).

Pain located in the left anterior chest was found to be the strongest negative predictor of AMI (adjusted OR 0.25, 0.14–0.46).

Patients who described the pain as being the same as previous myocardial ischaemia were significantly less likely to be having AMI!

Following adjustment for age, sex and ECG changes, the following characteristics made AMI more likely (adjusted odds ratio, 95% confidence intervals):

* pain radiating to the right arm (2.23, 1.24-4.00)
* pain radiating to both arms (2.69, 1.36-5.36)
* vomiting reported (3.50, 1.81-6.77), central chest pain (3.29, 1.94-5.61)
* sweating observed by physician (5.18, 3.02-8.86)

Pain in the left anterior chest made AMI significantly less likely (0.25, 0.14-0.46)
The presence of rest pain (0.67, 0.41-1.10) or pain radiating to the left arm (1.36, 0.89-2.09) did not significantly alter the probability of AMI.

Compare these results with the American Heart Association guidelines which state that “chest or left arm pain or discomfort as the chief symptom reproducing prior documented angina” is associated with a high likelihood of ACS, or the European Society of Cardiology guidelines which state that “the typical clinical presentation of NSTE-ACS is retrosternal pressure or heaviness radiating to the left arm, neck or jaw”, which the authors of this study point out are statements made based on expert opinion for which references are not given.

The authors summarise with a powerful message: ‘Several ‘atypical’ symptoms actually render AMI more likely, whereas many ‘typical’ symptoms that are often considered to identify high-risk populations have no diagnostic value.’

The value of symptoms and signs in the emergent diagnosis of acute coronary syndromes
Resuscitation. 2010 Mar;81(3):281-6

Pathophys

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.

meta-analysis shows accuracy, none is sig. lowerer of post-test (CMAJ 2010;182(10):1039)

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, but no proof in ED pop.

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:

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 elevated troponin:

(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)

CT Angiography of Coronary Vessels

Hollanders cohort of CTA negative pts with no adverse 30 day outcome (Annals of Emergency Medicine Volume 53, Issue 3, March 2009, Pages 295-304)

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

Bare Metal Stents-early stent restenosis

Drug Eluting-late stent thrombosis

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)

1. Goldman L, Cook F, Johnson PA, et al: Prediction of the need for intensive care in patients who come

to emergency departments with acute chest pain. New England Journal of Medicine 1996; 334: 1498-1504

 

Elmhurst Rule-out

 

---

 

In Diabetics, dyspnea is far more ominous for ACS than angina (Eur Heart J 2004;35:543 and NEJM2005;353:1889)

 

Chest pain protocol validated in (Ann Emerg Med 2006;47(5):427)

 

New ACEP clinical policy (Ann Emerg Med 2006;48(3):270)

 

Are serial ECGs useful during the ED evaluation of patients with suspected acute coronary syndromes?
Level B recommendations
Perform repeat ECG or automated serial ECGs during the ED evaluation of patients in whom the initial ECG is nondiagnostic for injury and who have symptoms consistent with ongoing or recurrent ischemia.
No recommendations can be made in regards to the exact timing of repeat ECGs. Studies suggest that 30 to 60 minutes after baseline may be a reasonable time interval for repeat ECG.
 

Patient Management Recommendations
Level A recommendations
Do not utilize cardiac serum marker tests to exclude non-AMI acute coronary syndromes (ie, unstable angina).

Level B recommendations
Utilize any of the following cardiac serum marker tests to exclude non–ST-segment elevation AMI as defined by the World Health Organization (WHO) or modified WHO criteria (Figure 1):⁎

1 A single negative CK-MB mass, Troponin I, or Troponin T measured 8 to 12† hours after symptom onset.‡

2 A negative myoglobin in conjunction with a negative CK-MB mass, or negative Troponin§ when measured at baseline and 90 minutes in patients presenting less than 8 hours after symptom onset.‡

3 A negative 2-hour delta CK-MB mass in conjunction with a negative 2-hour delta Troponin§ in patients presenting less than 8 hours after symptom onset.‡


 Timing of release of common cardiac markers of necrosis. Peaks A, B, and C respectively demonstrate release of myoglobin, troponin, and CK-MB in acute myocardial infarction as defined by WHO diagnostic criteria. Peak D demonstrates troponin release in troponin positive/CK-MB negative acute coronary syndrome now defined as acute myocardial infarction by ESC/ACC diagnostic criteria.

 

Relationship of reported sensitivities of various serum markers in relationship to time of symptom onset.

Time (h)	CK-MB Mass %	Myoglobin %	cTnT %	cTnI %
0-2	7-49	22-53	11-55	16-47
2-4	12-64	27-84	34-55	36-59
4-6	58-87	55-90	58-73	41-58
6-8	72-94	61-95	78-84	71
8-10	90-98	76-98	87-95	92-93
10-12	97-100	71-98	94-100	88
12-24	89-100	41-66	79-99	83-100

 

 

What are the indications for ED administration of glycoprotein IIb/IIIa inhibitors in patients with non–ST-segment elevation acute coronary syndromes?
Exclusion Criteria
Contraindications for a glycoprotein inhibitor (bleeding disorder, renal insufficiency, etc).

Patient Management Recommendations
Level A recommendations
None specified.

Level B recommendations
Consider administration of glycoprotein IIb/IIIa inhibitors (abciximab, tirofiban, or eptifibatide) prior to percutaneous coronary intervention to patients with positive troponin or ischemic ST-segment depression in whom an early interventional strategy is anticipated.* Studies suggest that benefit is greatest in patients in whom treatment was initiated within 6 hours of symptom onset and in patients in whom there will be a delay in percutaneous coronary intervention.

Level C recommendations
Consider administration of glycoprotein IIb/IIIa inhibitors (tirofiban, or eptifibatide) to patients with positive troponin or ischemic ST-segment depression in whom a non-interventional strategy is planned.⁎

 

---

CONCLUSIONS: Patients who are symptomatic during acquisition of a normal or nonspecific ECG have rates of adverse cardiovascular events similar to those of patients without symptoms. Clinicians should not rely on the absence of ECG abnormalities during symptoms to help exclude ACS. (Acad Emerg Med Volume 13, Number 10 1034-1039,)

 

 

 

 

 

 

Relationship between a Clear-cut Alternative Noncardiac Diagnosis and 30-day Outcome in Emergency Department Patients with Chest Pain

Judd E. Hollander, MD^_*, Jennifer L. Robey, RN, BSN, Maureen R. Chase, MD, Aaron M. Brown, BA, Kara E. Zogby, RN, BSN and Frances S. Shofer, PhD

From the Department of Emergency Medicine, Hospital of the University of Pennsylvania (JEH, JLR, MRC, AMB, KEZ, FSS), Philadelphia, PA

 

^_* Contact for correspondence and reprints: Judd E. Hollander, MD (Email: hollandj@uphs.upenn.edu  ).

 

Abstract

TOP Abstract Introduction Methods Results Discussion Limitations Conclusions References

 
Background: Accurate identification of patients with acute coronary syndromes (ACSs) in the emergency department (ED) remains problematic. Studies have not been able to identify a cohort of patients that are safe for immediate ED discharge; however, prior studies have not examined the utility of a clear-cut alternative noncardiac diagnosis.

Objectives: To compare the 30-day event rate in ED chest pain patients who were diagnosed with a clear-cut alternative noncardiac diagnosis with the 30-day event rate in the cohort of patients in whom a definitive diagnosis could not be made in the ED.

Methods: This was a prospective cohort study of consecutive ED patients with potential ACS. Data included demographics, medical and cardiac history, laboratory and electrocardiogram results, and whether or not the treating physician ascribed the condition to a clear-cut alternative noncardiac diagnosis. The main outcome was death, acute myocardial infarction (AMI), or revascularization within 30 days, as determined by phone follow-up or medical record review.

Results: The investigators enrolled 1,995 patients in the ED who had potential ACSs. Overall, 77 had a final hospital diagnosis of AMI (4%). Within 30 days, 73 patients received revascularization (4%), and 26 died (1%). There were 599 (30%) patients given a clear-cut alternative noncardiac diagnosis. Comparing the patients with a clear-cut alternative noncardiac diagnosis with those without an obvious noncardiac diagnosis, the presence of a clear-cut alternative noncardiac diagnosis was associated with a reduced risk of an in-hospital triple-composite endpoint (death, MI, and revascularization), with a risk ratio of 0.32 (95% confidence interval [CI] = 0.19 to 0.55) and 30-day triple-composite endpoint with a risk ratio of 0.45 (95% CI = 0.29 to 0.69); however, patients with a clear-cut alternative noncardiac diagnosis still had a 4% event rate at 30 days (95% CI = 2.4% to 5.6%).

Conclusions: In the ED chest pain patient, the presence of a clear-cut alternative noncardiac diagnosis reduces the likelihood of a composite outcome of death and cardiovascular events within 30 days. However, it does not reduce the event rate to an acceptable level to allow ED discharge of these patients.

Key words: myocardial infarction; acute coronary syndrome; complications; risk stratification

---

Go to source: Relationship between a Clear-cut Alternative Noncardiac Diagnosis and 30-day Outcome in Emergency Department Patients with Chest Pain -- Hollander et al. 14 (3): 210 -- Academic Emergency Medicine

 

Myocardial Bridging

Myocardial bridging can be seen as an incidental finding at coronary arteriography. Previous studies have reported its prevalence at 0.5 to 33% of all cases [6]. Myocardial bridging rarely causes myocardial ischemia [7]. Also, it is often considered as a simple variant of the normal anatomy of coronary arteries. But previous reports have demonstrated its pathologic potential. Stable or unstable angina pectoris, acute myocardial infarction, complete atrioventricular block or sudden death associated with myocardial bridges have been described [8,9]. It is well known that the main pathogenesis of acute coronary syndromes consists of atherosclerotic plaque disruption and thrombus formation [10]. However, in muscular bridging there is a temporary coronary luminal narrowing. If a patient has a endothelial injury, acute myocardial infartion may occur. Our patient had a smoking history, and nicotine could have damaged the endothelial structure at the bridged segment. Possible explanation of AMI in our patient could be endothelial injury, severe coronary spasm and finally thrombotic occlusion [11]. Primary percutanous revascularization was planned. However, no atherosclerotic plaque in the major coronary arteries was detected on coronary angiography. There was temporary systolic coronary arterial luminal narrowing at the mid-portion of LAD at LAO view. Therefore, we decided to follow the patient conservatively. We obtained an excellent result with blood transfusion. This is a case of acute myocardial infarction caused by coronary thrombosis in the setting of myocardial bridging. A possible association between myocardial bridging and acute myocardial infarction following excess blood donation could not be excluded. This is a report of a case of acute ischemic complication related to myocardial bridging of the LAD, which was resolved by appropriate blood transfusion, and acetylsalicilic acid, beta-blocker, nytroglicerin.

 

Which clots rupture

non-significant lesions are actually quite significant (40-60%) these will often stress negative

many cards think only >70% rupture

but we now know it is the smaller clots that rupture

it is clot composition not size

stress test 85 to at best 95% capable of identifying the lesion

thin fibrous cap and large lipid core are unstable

coronary artery remodelling-

 

we do not see the normal group of patients from the cardiology studies

990 of 1000 had no event in 6 months

but of the patients who come back (~10%)

so 100 of the 1000 will come back to the ed with recurrent symptoms

those 10 will most likely be amongst the 100

 

---

 

Patel MR, Chen AY, Peterson ED, et al. Prevalence, predictors, and
outcomes of patients with non–ST-segment elevation myocardial infarction
and insignificant coronary artery disease: results from the can rapid risk
stratification of unstable angina patients suppress adverse outcomes with
early implementation of the ACC/AHA guidelines (CRUSADE) Initiative.
Am Heart J 2006;152:641-647.
We have always assumed that when a patient experiences an acute
myocardial infraction (AMI), it occurs because of a ruptured plaque
followed by coronary thrombosis. Perhaps, the patient can have an AMI
due to vasospasm within clean coronaries or coronaries that have minimal
stenoses—maybe. . .Yet, we assume that is an uncommon event. So if you
the physician are caring for a patient with chest pain that recently had a
bnegativeQ catheterization (ie, clean catheterization or a catheterization with
insignificant stenoses), then you assume that there is almost no chance that
that patient can be having real ACS event. Correct? Or are we making an
incorrect assumption?
Although this study is not groundbreaking, it does reaffirm what many
other studies have indicated: it is very possible, and in fact not infrequent, to
have an AMI even in the setting of minimal or no coronary stenosis. The
authors analyzed 38,301 patients from a registry (the CRUSADE registry) of
patients with non–ST-segment elevation MI who underwent cardiac catheterization
to determine the extent of coronary artery disease. The researchers
found that 8.6% of these AMI patients had binsignificantQ coronary stenoses
(b50% occlusions). This was especially common in women (OR, 2.8),
younger patients (OR, 1.5 for every 10-year drop in age), and nonsmokers
(OR, 1.9). Note that these 3 patient factors are the kind of characteristics that
are very likely to make us discount the coronary artery disease risk.
The in-hospital mortality rate was relatively low (0.65%). One would
also assume that the long-term risk is relatively low in these patients. For
that answer, see the next article. (Mattu's article)

 

---

Bugiardini R, Manfrini O, De Ferrari D. Unanswered questions for

management of acute coronary syndrome: risk stratification of patients with

minimal disease or normal findings on coronary angiography. Arch Int

Med 2006;166:1391-1395.

We now know that patients can present with evidence of an acute

coronary syndrome (ACS) event (ie, electrocardiogram changes and/or

positive cardiac biomarker); these patients are then transferred to the

catheterization laboratory, ultimately with a bnegativeQ catheterization (ie,

the absence of any significant coronary obstructive lesion). Although data

are sparse to support this assertion, the clinician has assumed that these

patients have a normal prognosis. The authors of this study are probably the

first to actually investigate that assertion and determine whether those

patients truly have a normal prognosis.

Data were pooled from 3 large trials of patients with myocardial

infarction (MI). The authors found 7656 patients with non–ST-segment

elevation MI and angiogram results. They then followed those patients for 1

year to evaluate their risk of death, MI, unstable angina requiring

rehospitalization, revascularization, or stroke. The bprimary end pointQ was

if any of these events occurred. The angiogram results showed that 710

(9.1%) of the 7656 patients had nonobstructive coronary artery disease

(CAD), a statistic nearly identical to that noted in the previous article. They

further broke this group down into those patients with completely normal

coronaries (49%) and those with bmildQ (N0% to b50% stenoses) CAD

(51%). For this group of patients with nonobstructive CAD, the primary end

point occurred in 9.4% of patients with normal coronaries and 15.5% of

patients with mild stenoses. Focusing only on the rates of death or MI, 1.2%

of patients with normal coronaries and 3.3% of patients with mild CAD died

or had MI. The probability of an event appeared to correlate with a patient’s

initial TIMI score (a scoring system that is often used by cardiologists to

predict the risk of short-term adverse cardiac events when a patient is

admitted for ACS). The authors state that b. . .[t]hese findings are not in

agreement with the notion that [patients with ACS] with normal or nearnormal

findings on coronary angiography [have a] benign prognosis. . .Q

Consider the above data from our standpoint in the ED: you are working

a shift and see a worrisome patient with chest pain. The electrocardiogram

is nondiagnostic, just as it is in greater than 50% of ACS cases. You are

planning to admit the patient but then find out that the patient had a

bcompletely normal catheterizationQ within the past year. The admitting

physican tells you that the catheterization result means you should not

worry. . .Q send the patient home on an antacid.Q You, the primary treating

physician, have 2 options: (1) discharge the patient from the ED or (2) call

another admitting physician. You, the treating physician, are in the best

position to judge which option is most appropriate—yet, do not rapidly

jump to the conclusion that an new ACS event is not possible simply due to

the cardiac catheterization result.

---

The

recent largest trial (COMMIT) incorporating more than 45,000 patients,

the majority with STEMI, demonstrated no overall benefit to the use of

early BBs [17]! Although intravenous metoprolol reduced reinfarction

and ventricular fibrillation, there was an increased risk of cardiogenic

shock. Therefore, the early use of intravenous BBs is only recommended

in AMI patients after their hemodynamic status has stabilized. In other

words, there is no major time sensitivity. In addition, realize that this

recommendation is based on a study that primarily involved STEMI

patients—there is likely even less use in NSTE-ACS patients.

---

Van Wijk JPH, de Koning EJP, Cabezas MC, et al. Functional and

structural markers of atherosclerosis in human immunodeficiency virus–

infected patients. J Am Coll Cardiol 2006;47:1117-1123.

Stein JH. Cardiovascular risk in patients with human immunodeficiency

virus infection. J Am Coll Cardiol 2006;47:1124-1125. (editorial accompanying

above article)

These 2 articles provide a nice opportunity to remind everyone about

the cardiovascular risks associated with HIV. Prior studies indicate that HIV

infection is associated with bdyslipoproteinemiaQ and premature atherosclerosis.

In general, HIV-positive patients have their first MI 10 years

earlier than age-matched non-HIV counterparts. HIV patients also tend to

have much higher restenosis rates after both balloon angioplasty and

stenting. Just to complicate matters, the standard antiviral therapy is itself

associated with insulin resistance and hyperlipidemia, which further

increases the risk of premature atherosclerosis.

In this study, the authors assessed several indirect markers of early

atherosclerosis in 37HIV-infected patients: flow-mediated vasodilation, aortic

pulse-wave velocity, and carotid intima-media thickness. The authors found

that HIV infection was clearly associated with increased cardiovascular risk,

even in the absence of other metabolic risk factors. It is critically important to

consider ACS in HIV patients with any cardiopulmonary complaints.

 

---

Kosuge M, Kimura K, Ishikawa T, et al. Combined prognostic utility of ST

segment in lead aVR and troponin T on admission in non–ST-segment

elevation acute coronary syndromes. Am J Cardiol 2006;97:334-339.

Here is yet another study demonstrating that lead aVR actually deserves

considerable attention in patients with NSTEMI. The authors evaluated 333

patients with NSTEMI, correlating their ECG findings, TN-T levels,

catheterization results, and outcomes. ST-segment elevation in lead aVR

(OR, 13.8) and increased TN-T (OR, 7.9) were the only independent

predictors of death or MI at 90 days. Notice that ST-segment elevation in

lead aVR had a much higher or even an elevated TN. They also found that

patients with the combination of ST-segment elevation in lead aVR plus

elevated TN-T had the highest rates of left main or 3-vessel coronary

disease (62%) and 90-day adverse outcomes (47%; this finding also

includes death, MI, or need for urgent revascularization). Remember that

left main coronary artery (LMCA) disease as well as 3-vessel disease rarely

responds to medical therapy, so these patients should be referred emergently

for invasive therapy, preferably at an institution that can perform CABG.

In patients with an ECG that demonstrates ischemia, the additional

presence of ST-segment elevation in lead aVR is important because:

! ST-segment elevation in leads aVR and aVL indicates an acute

LMCA occlusion;

! ST-segment elevation in lead aVR and V1 indicates either a

proximal LAD or LMCA occlusion;

! But if the ST segment elevation in lead aVR is greater than the STsegment

elevation in lead V1, then a LMCA occlusion is likely; and

! ST-segment elevation in lead aVR greater than 1.5 mm is associated

with a 75% mortality.

It is important to realize that patients with ACS with occlusions of the

LMCA have a 70% mortality, and there are no medical therapies that have

been proven to decrease mortality. The only therapy that has been shown to

decrease mortality in the presence of a LMCA occlusion is immediate

invasive therapy. It is also important to realize that the mortality only drops

to 40%. The only predictor of survival is time to invasive therapy.

 

---

approximately 50% of patients with acute inferior wall MI will not have precordial ST-depression or reciprocal change (JEM, Article In Press, OnLine 11/19/07).
 

---

 

from best chest pain article
ACS Without Chest Pain
Chest 2004;126:461-469
• Global Registry Study (GRACE)
• 20,881 patients with ultimately suspected ACS
• 8.4% (1783 pts.) had no chest pain, only “atypical symptoms”
• ¼ of the patients without C.P. did not have ACS initially suspected
• Mortality much higher if no C.P.: 13% vs. 4.3% (p < 0.0001)



Was it:
- tearing or ripping?
- start at maximal intensity?
- Radiate to back, abdomen and legs?
questions for dissection



• You must have at least one set, drawn at least 6 hours post
onset of CP


Early Discharge Without Stress Testing
Ann Emerg Med 2006;47:427-435
Evaluates sending home low risk patients who can then safely get stress testing at a later date.
This article should be carefully studied if its conclusions are to be used.
“for patients with chest pain and low risk for short-term cardiac events, outpatient stress testing
is feasible, safe...With an evidenced based protocol physicians can identify patients at low risk…”
All patients had:
1) ECG
2) Enzymes (Both CK-MB and Troponin at least 6 hours after onset of CP)
3) Had risk stratified by detailed algorithm
PLEASE Look at the Algorithm. NOTE the key questions
• If a patient has extracardiac disease (CVA, PVD, Bruits) ? No D/C
• If a patient has 2-3 Risk Factors ? No D/C
• If a patient has Diabetes ? No D/C
• If a patient has history of prior similar CP diagnosed as angina, MI, or PCI ? No D/C
And finally most importantly: Chest or left arm pain or discomfort as chief symptom
(if clearly not cardiac wall pain), GERD or Pleurisy ? No D/C


The Slovis Method of ETT Testing Without a Treadmill
• Only used After you decide to discharge a low risk patient
• Calculate maximal HR (220-Age)
• Calculate target HR: 75-80% of max HR
• Run patient at bedside till target HR obtained
• Repeat 12 lead ECG
If Chest Pain or New ST Changes; admit!!
If No Chest Pain and No New ST Changes;
Refer for Outpatient Follow-up.

 

 

Right Ventricular Infarction

A Unique Complication of RV Infarction

A unique complication of a right ventricular myocardial infarction is the development of a right-to-left shunt through a patent foramen ovale.  RV infarction causes reduced right ventricular myocardial compliance with increased RV end diastolic and right atrial pressures. In patients with an interatrial septal defect, a right-to-left shunt may develop when the right atrial pressure exceeds the left atrial pressure. Such a situation should be suspected in a patient who exhibits significant hypoxemia that is not responsive to the administration of oxygen.

Patent foramen ovale is not uncommon.  Autopsy series and transesophageal studies report an age-dependent prevalence of PFO ranging from 9% to 34%, with a mean of approximately 27% (5).


References:
(1) Bassi S, et al.  Right ventricular infarction complicated by right to left shunting through an atrial septal defect: successful treatment with an Amplatzer septal occluder  Heart  2005; 91(4):e28.
(2) Kinch JW, et al. Right Ventricular Infarction NEJM  1994; 330:1211.
(3) Laham RJ, et al: Right ventricular infarction complicated by acute right-to-left shunting Am J Cardiol 1994;74:824-6.
(4) Sanchez-Ramos J, et al.  Right-to-left interatrial shunt secondary to right ventricular myocardial infarction: a novel therapeutic approach Intensive Care Med 2001; 27: 323-4.
(5)  Khairy p, et al. Transcatheter Closure versus Medical Therapy of Patent Foramen Ovale and Presumed Paradoxical Thromboemboli: A Systematic Review  Annals Int Med  2003; 139: 753-760.

 

More articles on sending folks home

short term risk after initial obs (JEM 2003;25(4):357)

 

Outcome after troponins negative (JEM 2004;26(4):401)

0.34% had ACE-30 no deaths, both NSTEMI

 

 

90 minute rule-out protocol

 

 

In NSTEMI, does waiting to the next day for PCI cause increased cell death--NO (JAMA. 2009;302(9):947-954.)

Our clinical gestalt is pretty good, if you felt they were low-risk 2.2% event rate, 1.8% in pts deemed non-cardiac (Acad Emerg Med 2009;16:740)

Hyperoxia

 

Am Heart J. 2009 Sep;158(3):371-7. Epub 2009 Jul 15. Links

Systematic review of studies of the effect of hyperoxia on coronary blood flow.

Farquhar H, Weatherall M, Wijesinghe M, Perrin K, Ranchord A, Simmonds M, Beasley R.

Medical Research Institute of New Zealand, Wellington, New Zealand.

BACKGROUND: International guidelines recommend the routine use of oxygen in the initial treatment of myocardial infarction, yet it is uncertain what effect this might have on physiologic and clinical outcomes. METHODS: We undertook a systematic search of Medline, Cochrane Database of Systematic Reviews, EMBASE, and CINHAL using the key words "oxygen," "coronary blood flow," "hyperoxia," and "coronary circulation" to identify human studies involving a measure of coronary blood flow while breathing oxygen and room air. The primary outcome measure was coronary blood flow; secondary outcomes included coronary vascular resistance and myocardial oxygen consumption. RESULTS: From 2,072 potential publications, there were 6 studies from 4 publications that met the inclusion criteria, with 6 healthy subjects and 61 subjects with cardiac disease. It was not possible to undertake a meta-analysis due to methodological limitations. In the 6 studies, high-concentration oxygen therapy resulted in hyperoxia, with a range in mean Pao(2) of 273 to 425 mm Hg. Hyperoxia caused a significant reduction in coronary blood flow (mean change -7.9% to -28.9%, n = 6 studies). Hyperoxia caused a significant increase in coronary vascular resistance (mean change 21.5% to 40.9%, n = 4 studies) and a significant reduction in myocardial oxygen consumption (mean change -15.3% to -26.9%, n = 3 studies). CONCLUSIONS: Hyperoxia from high-concentration oxygen therapy causes a marked reduction in coronary blood flow and myocardial oxygen consumption. These physiologic effects may have the potential to cause harm and are relevant to the use of high-concentration oxygen therapy in the treatment of cardiac and other disorders.

 

 Home   |   Disclaimer   |   Contact   |   Podcast