Evaluation of stress myocardial blood flow patterns in patients with apical hypertrophic cardiomyopathy
Raffaella Calabretta1,2, Aurora Kokomani3, Carlo Fumagalli4
1Nuclear Medicine Unit, Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy. raffaella.calabretta@meduniwien.ac.at.
Insights
Apical hypertrophic cardiomyopathy (AHCM) shows significant microvascular impairment, particularly in the apex. This apical hypoperfusion suggests ischemia may contribute to the potential aneurysmal changes seen in AHCM patients.
Area of Science:
- Cardiology
- Nuclear Medicine
- Medical Imaging
Background:
- Apical hypertrophic cardiomyopathy (AHCM) is a distinct variant of hypertrophic cardiomyopathy.
- AHCM carries a risk of aneurysmal transformation.
Purpose of the Study:
- To assess myocardial perfusion in patients with AHCM using [13N]NH3-PET/CT.
- To compare apical perfusion in AHCM with septal regions and with a classical septal HCM cohort.
Main Methods:
- 12 patients with AHCM underwent [13N]NH3-PET/CT.
- Assessed regional perfusion, global myocardial blood flow (MBF), and transmural patterns.
- Compared apical, septal, and infero-lateral wall MBF, and transmural gradients.
Main Results:
- 10 of 12 AHCM patients exhibited apical hypoperfusion.
- Significant differences in stress MBF were found across apical, septal, and infero-lateral walls (P < .02).
- Apical MBF was significantly lower than septal and infero-lateral MBF in both epicardial and endocardial layers.
Conclusions:
- Patients with AHCM demonstrate more severe apical microvascular dysfunction compared to septal HCM.
- This impairment suggests ischemia may play a role in the aneurysmal evolution of AHCM.
Background:
Among the other variants, the apical pattern of hypertrophic cardiomyopathy (AHCM) is probably the most important, with possible aneurysmatic evolution.
Methods And Results:
We analyzed 12 patients with AHCM who underwent [13N]NH3-PET/CT. Regional perfusion, stress global myocardial blood flow (MBF), and transmural perfusion patterns were assessed. To evaluate the LV-MBF distribution, we compared the apex with septum and infero-lateral wall. Furthermore, global stress MBF distribution in AHCM patients was compared with a reference septal HCM cohort. Visual regional perfusion analysis demonstrated an apical hypoperfusion in 10 of 12 patients, without correlation with the stress MBF of the whole LV. Significant differences among stress MBF in apical, in septal, and in the infero-lateral walls were recorded (P < .02). The transmural analysis showed a significant difference among the three segment groups for epicardial (P < .003) as well for endocardial MBF (P < .005). In the post hoc analysis, the apical MBF was significantly lower than in septal and infero-lateral walls in epicardium (P < .005) and significantly lower than the infero-lateral MBF in endocardium (P < .001).
Conclusion:
In patients with AHCM, more severe apical microvascular impairment was found as compared to patients with classical septal HCM, supporting the suspicion that ischemia could play a role in the future aneurysmatic evolution of AHCM.
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