LVOT gradient 234 mmHg at rest. A 15 mm septum.
Would you call this HCM?
Two patients with severe dynamic LVOT obstruction despite modest septal thickening. One presented with exertional dyspnoea and presyncope. The other reported no symptoms at rest, but developed dyspnoea during low-workload exercise testing.
These cases raised several questions:
• Is the high-velocity Doppler signal truly LVOT flow rather than mitral regurgitation?
• Does the overall picture favour HCM, or could age- and hypertension-related remodelling explain it?
• What does cardiac MRI add to the diagnosis and assessment of fibrosis?
• How should we interpret a TNNT2 variant of uncertain significance in one patient and a negative genetic panel in the other?
A high gradient establishes the severity of obstruction. Understanding its cause requires a broader assessment.
Link to echo loops, pictures and MRI findings in the first comment.
What would carry the most weight in your assessment?
#Echocardiography #HypertrophicCardiomyopathy #CardiacMRI #cardiology
@DrMarthaGulati IMO it’s not risk scores vs CAC — it’s a sensible, individualized decision using all the risk factors AND CAC. A CAC of zero doesn’t nullify risk, and a high CAC in a seemingly healthy, ‘risk-free’ person should ring alarm bells. Judicious use of every tool, not one vs the other.
Stenting asymptomatic disease doesn't prevent MI, but CAC isn't a stent referral — it's risk reclassification. A CAC of 400 in a borderline-risk patient changes statin/PCSK9 decisions, and statins in primary prevention have RCT-proven MI and mortality benefit. The test isn't the intervention.
@afshineemrani Is this how you also practice cardiology? Your patients are doomed. I am pretty sure that you know they are speaking Arabic and Hebrew and not Persian, so why are you spreading misinformation?!
@jpcostabel Had a patient like this, from Myanmar with severe MS, on Apixaban for 10 years. No clots or stroke. Although I don’t endorse it, it makes you wonder.