Pathology Associates Of Lexington, P.A.
Pathology Associates Of Lexington, P.A.
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        AMI Redefined, Newspath May 2001
      
Myocardial Infarction Redefined
[NewsPath, May 2001, Dr. John Carter]
[see April 2002 update of this topic]

 LMC’s Laboratory provided the Midland’s first STAT, 24-hr-available (24/7/365), acute-MI profiling in March ’96.  Experience with that profile, particularly with cardiac troponin results, soon suggested the ability to detect minimal  myocardial injury or micro-infarcts to a much more sensitive degree than with the previous diagnostic profiles (cardiac isoenzymes).  While practice guidelines initially defined cases of acute infarction as those with a peak troponin level >2.5 ng/ml AND defined patients with the AMI profile series of troponin levels (0, 3, 6 hours) remaining <0.5 ng/ml as having “No evidence of infarction”, it became evident that many patients with borderline troponin elevations (0.5-2.5 ng/ml) had some type of myocardial injury or micro-infarcts.  Some of these patients had clinical evidence of unstable angina, congestive heart failure, myocarditis or cardiomyopathy.  The term “Minimal Myocardial Injury” entered the literature and it became evident that patients with borderline  troponin elevations had an overall worse prognosis than patients with no elevation of cardiac troponin levels. 

Now a joint consensus document published by the European Society of Cardiology and the American College of Cardiology (JACC 2000; 36:959-69) verifies this concept of  “Minimal Myocardial Injury” and the sensitivity and clinical importance of laboratory diagnosis and its prognostic implications.  Highlights of this document are outlined below, as are extracts from three other recent and relevant publications.  Copies of this important consensus publication and the other reviewed papers are available on request (791-2413). 

 

JOINT CONSENSUS DOCUMENT SUMMARY 


Cardiac troponin is the preferred biomarker for myocardial damage, reflecting even microscopic areas of myocardial necrosis.  Any amount of myocardial necrosis caused by ischemia should be labeled as an infarct.  [Troponin-I and Troponin-T are essentially equivalent tests with current technology, the choice determined by the analytical system.]
Cases formerly diagnosed as having severe stable or unstable angina might be diagnosed today as having a small AMI.

The resulting increase in the sensitivity of the defining criteria for MI will mean more cases identified…and the fatality rate to fall…thereby allowing appropriate intervention and secondary prevention. 
All elevated cardiac troponin results are associated with a worsened prognosis.
Elevated troponin values should be recorded from two successive blood samples…and related to very recent clinical symptoms…to diagnose AMI (clinical correlation is necessary).
Myocardial infarction as a diagnostic term should be qualified and described as to:
    1) infarct size (based on degree of troponin elevation);
    2) clinical setting (spontaneous, post-op, post-angioplasty, etc.)
    3) timing (acute, or evolving, recent or healing, or healed MI).
Coronary angioplasty: "…the risks of subsequent ischemic complications (death or MI) is related to the extent of cardiac troponin increase, if any" (during or after the procedure).
Each individual laboratory should confirm the reference or “normal” range (99th percentile) of serum troponin values…and the degree of precision (variation) at the abnormal cutoff point. (Study currently in progress at LMC.); Results to be reported in follow-up newsletter.)
 

THE JOINT CONSENSUS DOCUMENT INCLUDES THE FOLLOWING SUMMARIES:

Clinical Presentations -- a description of varied atypical symptoms “in the absence of chest symptoms”. 

Pathophysiology of Acute Infarction -- a brief summary.

EKG and Imaging Studies -- a summary discussion.

Social and Public Policy Implications of Redefining MI -- a brief summary discussion.

 

The Redefined Definitions of Acute Myocardial Infarction :

Documentation of a typical rise (any elevation above normal) and gradual fall of cardiac troponin levels  (or a more rapid rise and fall of CK-MB)  with at least one of the following:            
1) Ischemic symptoms (typical or atypical);
2) Pathologic Q-waves on EKG;
3) Ischemic ST segment elevation or depression; or
4) Coronary artery interventional procedures.
 

Atypical Clinical Presentations of Myocardial Infarction:
1) Atypical pain patterns (without chest symptoms).
2) Unexplained nausea and vomiting.
3) Persistent dyspnea.
4) Unexplained weakness, dizziness, lightheadedness or syncope.

Missed Diagnosis of Acute Coronary Syndromes

H. P. Selker, NE Med Center, Boston

NEJM, April 20 ’00 p.1207-9. 

summary:

The majority of patients with missed AMI diagnosis… were considered to have either unstable angina or a myocardial infarction without ST-segment elevation. 

Myocardial infarction patients who are discharged prematurely without having been diagnosed as AMI have a high mortality rate (25-33%).

Many of these missed diagnoses might be avoided by more careful history taking and EKG evaluation. [And CDU monitoring with laboratory AMI profiling]. 

Physicians are under considerable pressure to cut costs, a strategy that could serve to increase the rate of missed diagnoses…

The accuracy of diagnosis of acute coronary syndromes can be maximized by a careful history and physical examination, risk factor assessment [and AMI profile testing for myocardial injury].

Physicians should be familiar with atypical presentations of acute coronary syndromes.

Laboratory data should be interpreted relative to timing of sample in relation to time of onset of symptoms.  [e.g. negative markers (CK-MB and/or troponin) and a negative EKG in a patient continuously symptomatic for 12-18 hours might be truly negative.  The same negative results shortly after symptom onset require immediate follow-up testing.] 

EKG changes and enzyme elevations may be absent soon after the onset of symptoms.  [Warranting CDU observation and follow-up AMI profile testing]

Patients thought to be at low risk for acute myocardial infarction warrant careful assessment of this “low risk” determination, especially if multiple risk factors are present. [Gender, age, hypertension, lipid abnormalities, atypical pain patterns, atypical or “angina-equivalent” symptoms]

 

Braunwald’s, HEART DISEASE, 5th edition,1997 

(Page 1-7)

As physicians attempt to utilize their time more efficiently by delegating responsibility for history-taking to a physician’s assistant or even by limiting the history to a questionnaire…an undesirable trend.

History taking is the most valuable technique available for determining whether or not the symptoms are caused by heart disease.

Anginal equivalent symptoms include dyspnea; discomfort or pain in atypical radiation patterns; GI symptoms of gas, belching, nausea, “indigestion”; dizziness, diaphoresis [and a general feeling of critical but unexplained illness]. 

(Pages 1198-1200)

Atypical presentations of AMI include:
1) New-onset or worsening congestive heart failure.


2) Classic angina symptoms


3) Atypical pain (or discomfort) radiation patterns. 


4) CNS debility due to sudden decrease in cardiac output.


5) Apprehension and nervousness.


6) Sudden mania or psychosis.


7) Syncope


8) Overwhelming weakness


9) Acute indigestion complaints


10) Peripheral embolization lesions

 

“Pandora’s Box…”

Editorial by: A. S. Jaffe, M. D. (Mayo Clinic)

The American Heart Journal, July ’99, p. 9-11.

Many years of traditional CK-MB testing made us familiar with its imperfections and added to our ability to ignore elevations of CK-MB when we believed they did not make clinical sense.

Troponin elevations should be completely specific for cardiac damage and are more sensitive for detection of cardiac injury than CK-MB.

Troponin elevations occur in up to 33% of patients with unstable angina when CK-MB remains within the normal range.

Troponins are elevated for a longer period after cardiac damage than CK-MB.

Need to attribute each troponin elevation to some type of myocardial injury.

Troponin elevations, whether explained or unexplained, are associated with an adverse outcome over time.

Acute myocardial infarction is not the only source of elevated serum troponin levels. A significant number of patients with unstable angina, cardiomyopathy, myocarditis, congestive heart failure, ventricular remodeling, adriamycin therapy, etc., can present with low to intermediate, sub-infarction elevations of serum troponin, [a finding that reflects Minimal Myocardial Injury in these patients].

The possibility of whether minimal troponin elevations might reflect normal myocardial cell turnover has not been resolved but more likely reflects a variety of subtle myocardial disease processes -- even minor elevations may have physiologic significance.

SUMMARY:
This re-definition of diagnostic criteria for acute myocardial infarction is a concept that we've long suspected and anticipated.  The publication of an international consensus document is very welcome and will go far to improve health care for cardiac patients. 


Medical staff assimilation of these guidelines is important as, while the NEJM paper states a 25-33% mortality rate for missed MI diagnosis, recent publications (JAMA, Dec. 2000, p.3131 & 3138) evaluating coronary interventional procedures suggest a 95+% survival for AMI patients who are diagnosed and treated.  The survival advantage is very significant, as is the hazard of "failure to test" and a missed diagnosis.  


LMC's Pathologists and Laboratory Team will assist in the assimilation of these redefined diagnostic guidelines with follow-up newsletter publications, the first in SC verification of troponin reference ranges and analytic variability and clinical-laboratory correlations as necessary and appropriate.  Medical staff comments and suggestions are welcome.  

New ("RE-DEFINED") Recommendations for
Laboratory Diagnosis of Acute MI:

1) Patients with acute or recent (within hours) onset of ischemic or atypical but clinically suspect symptoms:

  • Acute MI profile* at 0, 3 and 6 hours; (Repeat @ 12 hrs if clinical suspicion persists.)

  • Any sustained (repeated) elevation of troponin reflects myocardial injury/infarction.

 2) Patients with persistent (>12-24 hrs) atypical symptoms who present in CMC's or physician office or     routine emergency setting.

  • Cardiac troponin level and EKG:

  • Normal results (of these two tests) offers documentation that the atypical symptoms do not reflect myocardial injury. 

  • Abnormal results reflect myocardial injury and a need for prompt and appropriate clinical intervention. 

 *    The Acute MI profile at LMC still includes cardiac troponin-I and CK-MB -- only one of these is charged.  CK-MB will be dropped from the profile as medical staff familiarity with interpretation of troponin-I results progresses. [see Jan. 2008 memo]

(posted Dec. 2001; update 19 January 2008)   

 
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