1. PULMONARY VEIN STENOSIS
Cath conference
09/11/12

2. History 2.6 mill people was affected by Afib in the U.S in 2010.
By 2050, >10 mill patients.
Treatment for Afib:
Pharmacological
Non pharmacologic approach:
Surgery
Radiofrequency catheter ablation (RFA)

3. RFA 40000-50000 ablation procedures/year in the US
Ablation procedures for preventing recurrent AF are directed at the following:
. Elimination of the triggers of AF
. Modifying the atrial substrate(s) responsible for the maintenance of AF.
Ablation procedures for preventing recurrent AF are directed at the following:
Elimination of the triggers of AF – Triggers are usually eliminated by disrupting the conduction of electrical activity between the tissues that contain these arrhythmogenic triggers (most commonly the ostial portion of the pulmonary veins), and the atrial myocardium. Less commonly, triggers within the atrial myocardium can be directly ablated.
Modifying the atrial substrate(s) responsible for the maintenance of AF.
Segmental ostial isolation
Circumferential LA ablation

4. Complications of RFA Death (1/1000): Cardiac tamponade (>1%)
Stroke (5.16%)
Atrioesophageal fistula (5.16%)
Cardiac tamponade (>1%)
Catheter entrapment ( %)
Periprocedural embolization
Vascular complications:
Hematoma at the sites of catheter insertion
Pseudoaneurysm
Arteriovenous fistula
Retroperitoneal bleeding
Pulmonary vein stenosis
The types and rates of complications that occur in patients undergoing RFA to prevent recurrent AF vary from series to series and depend upon factors such as the technique being used (eg, segmental versus circumferential procedure), the experience of the operator, and the clinical characteristics of the patients undergoing the procedure. There has been a reduction in complication rates with time presumably reflecting not only operator, institutional, and worldwide experience, but also improvements in equipment and anticoagulation strategies.

5. Pulmonary vein stenosis
Narrowing of PV luminal diameter:
Mild if narrowed by <50%
Moderate if narrowed by 50% to 70%
Severe if the narrowing is more than 70%.
Predictive factors for the development of PV stenosis:
Application of radiofrequency energy inside the veins (associated with a 5.6-fold higher risk of stenosis than ostial ablations) Arentz T et al. European Heart Journal (2003) 24, 963–969
Inappropriately high energy delivery

6. Pulmonary vein stenosis
Mechanism: poor defined
Intense periadventitial inflammation or collagen deposition, which may compromise or occlude the lumen.
The lesion is characterized by intimal thickening, thrombus formation, endocardial contraction, and proliferation of elastic laminae

7. PVS. Frequency and location
Early studies: 38-42%
Recently (improving experience and changes in technique): 1-3%; % requiring intervention
Location:
30% RSPV, LSPV and LIPV
RIPV infrequent
The reported rate of pulmonary vein stenosis depends not only on the factors described above, but also on the definition of stenosis severity and the intensity of screening. Early reports cited rates as high as 38 percent, but more recent studies cite rates for severe stenosis as low as 1.0 to 3.0 percent.
A minority of diagnosed patients appears to develop symptoms and the rate of pulmonary vein stenosis requiring intervention may be as low as 0.1 to 0.3 percent
Qureshi A. et al. Circulation. 2003;108:

8. PVS. Presentation Depending on: The number of PV involved
Lesion severity
The response of the entire pulmonary vasculature to the lesion
The time course to stenosis
Clinical setting
The presence and extent of collaterals

9. PVS. Presentation
Holmes DR. et al. J Am Coll Cardiol Intv 2009;2:267–76

10. PVS. Symptoms Mean onset: 2-5 months Intensity: Degree of obstruction
Inversely to the duration of time to develop stenosis

11. PVS. Symptoms Clinical presentation Qureshi AM et al. (n=19), 2003
Saad EB et al (n=21), 2003
Packer DL et al. (n=23), 2005
Asymptomatic
1 (5%)
8 (38%)
3 (13%)
Cough
17 (89%)
9 (39%)
Flulike symptoms
8 (42%)
Dyspnea on exertion
11 (58%)
11 (52%)
19 (83%)
Dyspnea at rest
7(37%)
7 (30%)
Pleuritic chest pain
6 (29%)
6 (26%)
Hemoptysis
12 (63%)
5 (24%)
Di Biase L et al. (n=16 pts with PVTO), 2006.
. 4 (22%) asymptomatic.
. 4 (22%) mild symptoms: dry cough and NYHA I.
. 4 (22%) moderate symptoms: persitent cough and NYHA II/III
. 3 (17%) severe symptoms: NYHA III/IV, pleuritic chest pain, hemoptysis, fever.

12. PVS. Diagnosis
Diagnostic evaluation for PVS should be performed in patients who develop respiratory symptoms after RFA.
Assessment of the presence and degree of severity of PVS is essential.

13. PVS. Diagnosis Chest X-ray is not diagnostic
Ventilation/perfusion scan
Transesophageal echocardiography
CT and magnetic resonance imaging
(HRS/EHRA/ECAS expert consensus statement of catheter and surgical ablation of atrial fibrillation. Heart Rhythm. 2007;4(6):816.)
V/P scans can be used to characterize the physiology of blood flow within the distribution of a PVS. Under normal conditions, the apparent blood flow of one-third of a lung ranges between 15%-30%. With increasingly severe PVS, local perfusion decreases substantially, particularly with stenoses ≥65% to 75%. With severe stenosis, local blood flow within the affected PV can be decreases to as low as 3% to 4%.
TEE is limited by its inability to image deeply into all 4 PV and is less useful in establishing the extent and location of PVS.
CT and to a lesser extent magnetic resonance imaging provide the best tests for evaluation.

14. PVS. Treatment
The use of angioplasty and/or stent implantation for acquired PVS remains the only available treatment option for severe cases.
PV angioplasty is associated with a significant increase in lung flow and improvement of symptoms.
Restenosis is still an important drawback of this approach.
Angiography should be performed on all patients, even if pulmonary veins appear occluded by other imaging modalities.

15. PVS. Treatment Balloon Stent Restenosis Saad EB et al, 2003, (n=21)
12 (67%)
8 (44%)
4 (33%); 2 ISR
Packer DL et al, 2005 (n=23)
17 (74%)
7 (30%)
13 (57%); 4 ISR
Qureshi AM et al, 2003 (n=19)
30 (81%)
5 (14%)
19 (51%)
Di Biase et al, 2006 (n=16)
7 (44%)
8 (50%)

16. PVS. Treatment
Neumann T et al. J Cardiovasc Electrophysiol Nov;16(11):
12 pts (15 PVS greater than 70% stenosis) were prospectively evaluated.
Within 2 months after primary balloon angioplasty, the PV size parameters were significantly reduced (P < 0.001) with recurrence of PVS in 11 of 15 PVS (73%) after balloon dilation.
Pulmonary vein stenting in 8 patients and 11 PVs resulted in no vein stenosis during 12-month follow-up.

17. PVS. Treatment
Prieto LR et al. J Cardiovasc Electrophysiol Jul;19(7):673-8.
N=34 (55 PVS) 25 months.
Dilation in 39 veins
Stenting in 40 veins (16 primarily, 24 after dilation restenosis).
Acute success and restenosis rates:
42% and 72% for dilation
95% (P < 0.001) and 33% for stenting.
Time to restenosis was greater for stent angioplasty (P = 0.003).
Stents ≥10 mm in diameter had lower restenosis than smaller stents.
Risk factors for restenosis included small reference vessel diameter and longer time from PVI to intervention for PVS.

18. PVS. Treatment De Potter TJR et al. Europace (2011) 13, 57–61
5 pts (8 PVS) were referred for PV DES (7 paclitaxel and 1 zotarolimus DES) with a 2 y FU.
Mean FU was months with TEE control, during which all patients remained asymptomatic.
During FU, Vmax remained stable in three patients and increased moderately in one. Angiography at 3 months confirmed absence of restenosis in the first three patients and moderate (40%) restenosis in one patient.
In one patient, an increase of Vmax back to pre-DES values correlated with a 65% persistent stenosis, treated with a redo DES.
In total, after seven primary DES only one (asymptomatic) proximal margin restenosis required re-stenting.