• The absolute risk of suffering DCI in the presence of PFO is very low 5:10, 000 vs 1:10, 000 (without PFO)
• the risk of suffering a major DCI parallels PFO size.
• Transoesophageal echocardiography (TOE) is considered the imaging procedure of choice – “gold standard”. However sedation can make the vasalva manoeuvre more difficult.
• The identification and quantification ie.“sizing” of PFO is not standardised. These variables introduce error in diagnosis, and need to be addressed
  • Criteria for determination is different. therefore depending on the criteria of number of bubbles, different “size” of PFO can be determined.
  • Angle of visualisation. some angles are better than others
  • The anatomy of your heart and which vein that the contrast agent is administered can influence diagnosis due to differing blood flow patterns
  • for a given PFO, the amount of right-to-left contrast shunting is a matter of expiratory pressure during the Valsalva manoeuvre. So the harder you force it to open the more bubbles go through
  • that in any PFO right-to-left shunting varies considerably and that the magnitude of contrast shunting does not necessarily correlate with the true anatomical size of the PFO.

• Assessing efficacy of percutaneous PFO closure for each device has been troublesome given the case series nature of existing studies, lack of randomised controlled trials, as well as a lack of defined and clinically meaningful end points for comparison. This is largely due to a lack of: (1) neurologist–cardiologist–primary physician teamwork and coordination of goal and effort; (2) modern precise definition of ischaemic neurologic outcome; (3) data to generate realistic hypotheses and sample size requirements; (4) referring physician and investigator motivation to enrol all candidate patients into randomised expert care; (5) industry based sponsorship of a sufficiently sized trial to adequately address power concerns; and (6) a ‘‘tipping point’’ mentality that CS + PFO is a true and highly morbid disease, requiring study and relief.
• My commentary: You could substitute above with Diving specialist for neurologist in #1 and #2 could be substituted with standardisation of DCS diagnosis and outcome.
• Proposed ‘‘high risk’’ PFO features include: atrial septal aneurysm, spontaneous right-to-left shunting, and ‘‘tunnellike’’ appearance.
• previously symptomatic or high volume divers with ANEs (asymptomatic neurological event) or with ‘‘high risk’’ anatomic PFO features, who wish to continue diving may warrant closure in centres maintaining closure registries or participation in trials.
• Intervention for low volume sports divers with PFO without ANEs or symptoms of DCS, regardless of anatomic concerns, remains unfounded at the present

• PFO as the culprit is often just the least unlikely of a number of possibilities,
• When considering treatment of an incriminated PFO, the risks of the treatment have to be weighed against the risk of recurrence, lest the cure is worse than the disease.
• PFO closure entails a finite procedural and post-procedural risk. Ongoing learning curves and device refinement make it difficult to define these risks.
• Major complications are in the order of 1%. [compare the risk of DCI event of 0.05%]
• [Keeping in mind this is primarily aimed at non-divers.] Suggested criteria for eligibility for interventional PFO closure: 1–4 required

1. Preceding ischaemic neurologic event with probable embolic aetiology

2. Age under 60 years and absence of overt atherosclerotic disease (for example, history of myocardial infarction) or more than one atherosclerotic risk factor

3. Exclusion of other cardiac (for example, atrial fibrillation, endocarditis, tumour) or vascular (carotid stenosis, spontaneous carotid or vertebral dissection, aortic atheromatosis) embolic sources

4. PFO with more than minimal inducible or spontaneous right-to-left shunt, in particular in the presence of an atrial septal aneurysm

5. Contraindications against or unwillingness to undergo anticoagulation

• The description of the implantation technique is accurate (from my memory of my procedure) J. I couldn’t summarise it properly here; if you want to know then you’ll have to read the article.
• A description of atrial septal aneurysm (ASA):
  • The septum secundum positioned towards the aorta is usually a robust, wedge-like structure. The caudad septum primum may be paper thin and extremely mobile. An atrial septal aneurysm is usually diagnosed when the septum primum moves more than 10 mm into each atrium during certain phases of the cardiac cycle. Aneurysm is a misnomer as it merely describes the mobility of the non-muscular part of the septum primum. Nevertheless, the presence of a highly mobile septum primum has been identified as an important risk factor for paradoxical embolism.
• Pitfalls
  • Most devices (with the exception of Amplatzer and Helex) have to be completely removed outside the body and usually a new one used if deployment fails the first time. Amplatzer and Helex by the nature of their designs can be easily recaptured and redeployed.
  • The Amplatzer and Helex devices are the only ones to conform to funnel shaped PFOs. The others are unable to do so because of the fixed length connector between the disks.

• Complications
  • Embolisation
  • Other serious complications occurring in less than 1% of cases are infection, erosion into the pericardium or aorta at the rim of the device, a new ASD caused by the lower rim tearing the thin septum primum, or paroxysmal or persistent atrial fibrillation.
  • Thrombosis on the device has been found in about 6% of devices used for PFO closures at the one month transoesophageal echocardiographic control in 1000 patients, except for the Amplatzer PFO occluder where it was found in less than 1%. A recent study reported thrombosis on five of 23 CardioSEAL devices checked at one month but in none of 20 Amplatzer PFO occluders.