A patient with ischemic cardiomyopathy (LVEF 33%), left bundle branch block, and permanent atrial fibrillation was admitted for implantation of the cardiac resynchronization therapy device (CRT).
During the procedure, after cannulation of the coronary sinus, venography revealed a filling defect in the proximal lateral cardiac vein. The defect varied with the cardiac cycle, which in itself suggested external compression rather than intrinsic stenosis. Unusual was the way of changes of filling defect: more pronounced during diastole and less during systole.
Fluoroscopy demonstrated that the stented circumflex artery crossed the vein precisely at the site of the filling defect (Fig. 1a, b). The stent had been implanted one year earlier. Thus, the artery acted as a mechanical obstacle for venous flow and impeded the passage of the left ventricular (LV) lead.
Several attempts to advance the lead over a coronary guidewire were unsuccessful because the electrode repeatedly deflected into the coronary sinus (Fig. 1c). Finally, by applying gentle pressure with controlled rotational movements, the LV lead was successfully positioned in the lateral cardiac vein (Fig. 1d).
All pacing and sensing parameters were normal at implantation. AV node ablation was performed a few days later.
At the three-month follow-up, all lead parameters remained stable, the patient’s symptoms improved, and the left ventricular ejection fraction increased from 33 % to over 40 %.
Discussion
A filling defect in a cardiac vein is commonly attributed to intrinsic stenosis. However, external compression must also be considered. Typical causes include fibrotic or muscular bands, particularly after cardiac surgery. In this case, the stented circumflex artery represented the compressive substrate—an association not previously described in the literature.
Two key radiologic features suggest external compression:
- Filling defect varying with the cardiac cycle (in our case, greater in diastole and milder in systole).
- Identification of an external structure corresponding to the site of compression (here, the stented artery).
When the compressing structure is a coronary artery, the filling defect tends to worsen during diastole, when the volumen of the heart is greater and the compression of the vein between the heart wall and the artery is stronger—unlike in cases of muscular bridges, where compression occurs during systole. This distinction may aid in the differential interpretation of venograms and help anticipate technical difficulties during LV lead placement.
Conclusion
This case demonstrates that an intersecting stented artery can mechanically obstruct LV lead implantation by compressing the target vein. Recognition of a diastole-dependent filling defect and the presence of a visible anatomical substrate (such as a stent) can support the diagnosis of external venous compression.
In such situations, gentle advancement of the lead with controlled rotational movements may allow successful placement without complications.
