First off, thank you very much for participating in this great service. I am 26 year old asthmatic athletic male. Recently, I experienced moderate chest pains and numbness in chest following cocaine use and a dose of albuterol asthma inhaler. The following morning I visited hospital, and EKG was taken, which showed Left Anterior Fascicular Block (LAFB). Was discharged, but during second visit after pain persisted, General Practitioner suspected that LAFB could be due either to minor MI (caused by aforementioned activities) or pre-existing congenital structural irregularity. Blood test for CK enzymes came back negative (79 U/L), but test was administered 33 hours after onset of symptoms, which I understand to be tail end of diagnostic window. Troponin I protein test, which apparently has longer diagnostic window, administered 4+ days (102 hrs.) after onset of symptoms also came back negative (<.3 NG/ML). ECHO results came back "normal," with following readings:
- No direct or indirect evidence of any enlargement of the right ventricle.
- No evidence of any prima more secundum atrial septal defect
- Trace mitral and tricuspid regurgitation
- Trace pulmonary insufficiency
- Predicted Peak systolic pulmonary artery pressure 30 mm HG
- Left Ventricular EF: estimated 60%
Stabbing chest pain still occurs intermittently even now (approx. 9 days after initial event), and I have an appointment with cardiologist in coming week. My questions are as follows:
1) Given the above narrative, what do you think the LAFB can be attributed to? Putting aside MI for a moment, my GP suspected possible ASD, but ECHO produced no evidence of such irregularity. What other structural problems/underlying conditions are there with which LAFB may be associated? Which are serious and which are not?
2) Along similar lines: How dangerous/common is an LAFB? I have inconsistent answers to this question. On one hand, GP and cardiologist friend of mine say that LAFB in 26 year old male is extremely uncommon and potentially problematic. However, online medical fora and advise columns (including this one) consistently state that LAFB in isolation should not be cause for concern, is relatively common, and long-term prognosis for patients whose EKGs show LAFB is no different than normal individual. One column even stated that nearly 14% of all EKGs show evidence of LAFB. Can you please provide nuanced answer to resolve this apparent discrepancy? How common is it for 20-something male to have LAFB? Is it more likely that the condition exists in isolation, or is attached to more serious defect?
3) Could LAFB be attributed to the trace MR, TR, and PI that showed up on my ECHO? If so, would this make the LAFB cause for concern? Is there any way to correct LAFB?
4) Will Troponin I levels remain elevated in blood following minor MI 102 hrs. (approx. 4 days) after onset of symptoms? I've heard diagnostic window is 5-7 days for cTNI (& up to 2 weeks for cTNT), but is this just for diagnosis of ACUTE MI? That is, was Troponin I test administered within diagnostic window given a minor MI?
5) If I missed diagnostic window for blood tests used to diagnose MI (CK, Troponin), are there more sensitive tests that can be administered to detect low-level MI/"microinfact." My GP says cardiologist will likely administer nuclear stress tests. Can heart cath./thalium stress test/MUGA detect evidence of minor myocardial muscle/cell damage when blood work comes back negative? Are there cases in which it is simply indeterminable whether patient has in fact suffered MI?
6) In related vein, is it possible for someone to suffer minor MI and experience virtually no myocardial injury? If this is possible, does the possibility that the individual experiences future cardiac event/MI nevertheless increase even though first event inflicted no damage?
Obviously, these concerns are giving me a great deal of anxiety. I apologize for length of questions, and greatly appreciate your consideration and response.
1) What do you think the LAFB can be attributed to?
A: It's most likely congenital and not associated with any structural abnormality.
2) Along similar lines: How dangerous/common is an LAFB?
A: I wouldn't call it dangerous but it's not normal either. Think of there being 3 bundles of nerve conduction tissue in your heart. One of them is not working entirely normaly. This places you at slightly higher risk of needing a pacemaker in the future but no other "bad" things.
3) Could LAFB be attributed to the trace MR, TR, and PI that showed up on my ECHO? Is there any way to correct LAFB?
A: No and no.
4) Will Troponin I levels remain elevated in blood following minor MI 102 hrs. (approx. 4 days) after onset of
A: Probably not in a young person with normal kidney function.
5) If I missed diagnostic window for blood tests used to diagnose MI (CK, Troponin), are there more sensitive
tests that can be administered to detect low-level MI/"microinfact."
6) In related vein, is it possible for someone to suffer minor MI and experience virtually no myocardial injury? If
this is possible, does the possibility that the individual experiences future cardiac event/MI nevertheless increase
even though first event inflicted no damage?
A: Yes it is possible to do very little damage. The risk for further events is not increased. Of course the individual would be wise to avoid further cocaine use due to the problems it may cause.
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