I am 30 and my LGE is 32% already, should I be worried?

@punctual451
I am not faimiar with LGE%. Are you talking about ejection fraction (EF).

I have had a EF of 25-30 for over 10 years now. I exercise 1-2 hours 6 days a week. I have been doing Sprint Triathlons since 2017.

Were you told you have heart failure (HF)? If you were what was the cause? The biggest thing with HF is treating it. Great new medication out there. Regarding you mentioned ICD. My HF was caused by a virus or infection not cardiovascular disease or heart attack called Cardiomyopathy.

Thus my cardiologist, heart failure and electrophysiologist wanted me to have a ICD/Pacemaker. Until I got that device to help with my electrical issues of my heart and this team changed my medications (Mayo) my EF was going lower and lower. After my device implant and new medications my EF has been the same for over 10 years.

Sorry for not being clear on what the LGE I am referencing is - I am talking about the Late Gadolinium Enhancement in Cardiac MRI that helps to identify scar tissue. Most resources online say that anything above 15% is considered a risk and they should have an ICD implanted, and I don't have one yet. I was just curious if there are any others who have similar levels of scarring, and how their outlook/symptoms have been?

I am talking about something a little different - but this information is still very helpful! It's great to hear how a combination of help from doctors/meds/ICD can help people have a better outlook on life. I appreciate you commenting, and hope everything continues to go well with you!

sounfs like a great conversation needs to be had with your cardiololigist of COE cant stress it enough Center of Excellence

@punctual451
Thanks, very helpful. Not heard of LGE.

When I was diagnosed with HF and cardiomyopathy per my Catherizations I did not have cardiovascular disease but scar tissues causing PVCs and electrical issues from what they think was caused by an infection or virus in heart causing scar tissues.

I do know that having many Holter monitor tests that my EP could determine where my PVCs were coming from which is an electrical issue. I did have on ablation on RV which worked but he wants to try medication for the LV PVCs because I have 3 areas. So we are trying medications. The one I am on now has cut my PVCs in half and now for a year no tachycardia.

I have had a ICD/Pacemaker since 2006.

Welcome to Mayo Clinic Connect @punctual451.
I found this on the National Library of Medicine that you may find interesting:
https://pmc.ncbi.nlm.nih.gov/articles/PMC10888577/
And here is an excerpt from the above article specific to HCM:

2.3. Hypertrophic Cardiomyopathy
CMR significantly helps to distinguish the different subtypes of the heterogeneous group of diseases with a hypertrophic phenotype, which previously could only be clarified by biopsy. The classic phenotype of hypertrophic cardiomyopathy (HCM) is an asymmetric, septal hypertrophy with (HOCM) or without obstruction of the outflow tract, caused by an autosomal dominant mutation in the sarcomere genes with a prevalence of about 1:350 [33]. CMR is especially important in the detection of midventricular or apical variants of HCM, in which echocardiographic evaluation has limitations [34]. In addition, CMR can detect myocardial crypts [35] and papillary muscle abnormalities [36], which may be a subclinical marker of HCM, and depict apical aneurysms with and without thrombus formation, which is considered a major risk factor in the American College of Cardiology/American Heart Association (ACC/AHA) [37] and ESC [2] guidelines, leading to recommendations for implantable cardioverter-defibrillator (ICD) implantation.

LGE in HCM signifies replacement fibrosis, and its prognostic significance is well-established. It is detected in over 50% of HCM patients, typically manifesting as a mid-mural pattern within the most hypertrophied segments [38] and on right ventricular insertion points (Figure 1D and Figure 2D). In the advanced stages of the disease, LGE with transmural extension may be observed, carrying a poorer prognosis, because the extent of LGE consistently correlates with an increased incidence of sudden cardiac death [39]. In a pivotal multicenter study, the presence of LGE exceeding 15% of the left ventricular (LV) mass was associated with a more than two-fold risk of SCD in patients initially classified as low risk by conventional tools, compared to patients without LGE [38]. Consequently, the presence of “extensive LGE” (≥15% of total LV mass) is considered a high-risk parameter and it has been incorporated in both guidelines mentioned above. Recent findings indicate that HCM patients exhibiting non-extensive LGE, the involvement of subendocardium, rather than the extent of LGE, is linked to unfavorable outcomes [40]. For HCM patients without a defibrillator, CMR should be repeated every 3–5 years to monitor the progression of LGE and reassess strategies for preventing SCD [37].

All this is information, and learning as much as you can is good. We can only share our experiences with you, but not medical advice. But we can share that if you have questions about the results of your CMR, 100% ask your cardiologist! Do not hesitate to make an appointment and ask questions. This is your life, and you are only 30 years old with a lot of runway in front of you!
Did your cardiologist go over the results of this test with you?