Percutaneous Closure of Patent Foramen Ovale and Atrial Septal Defect



Percutaneous Closure of Patent Foramen Ovale and Atrial Septal Defect


Ricardo Cigarroa

Ignacio Inglessis



PATENT FORAMEN OVALE CLOSURE


INTRODUCTION

Patent foramen ovale (PFO) is the most common intracardiac shunt encountered in clinical practice. The foramen ovale is an essential component of the fetal circulation, allowing highly oxygenated placental blood to flow directly from the right to left atrium, bypassing the fetal lungs and directly supplying the coronary arteries and fetal brain. A communication between septum secundum and septum primum, the foramen ovale typically closes in most individuals in the first year of life following hemodynamic changes that increase left atrial (LA) pressure and decrease right atrial (RA) pressure. The LA pressure rise is the result of an increase in systemic vascular resistance after interruption of the umbilical cord and rising pulmonary venous return to the LA after lung expansion. In addition, RA pressure falls as a result of reducing blood return to the RA after ductus venosus closure and decreasing pulmonary vascular resistance after lung expansion. The competent valve of the foramen ovale is then pressed to the interatrial limbus, and functional closure of the foramen ovale, without left-to-right interatrial shunt, occurs as a result of LA pressure in excess of RA pressure.






The foramen ovale remains patent in about one-third of the population for unknown reasons, although there is evidence to suggest a genetic predisposition.1 The prevalence of PFO appears to decrease with age, whereas older age is associated with larger PFOs.2 The majority of individuals with a PFO will remain asymptomatic, but a small percentage develop clinically significant pathology from this communication and benefit from percutaneous closure.



DIAGNOSIS


Echocardiography

Echocardiography is the primary modality for diagnosing PFO. Although doppler assessment of the interatrial septum may reveal flow across a PFO (Figure 46.1A), bubble studies are often needed to document communication between the two atria and obtain preliminary data on PFO size based on the timing and number of bubbles that appear in the left atrium (Figure 46.1B). A bubble study is performed by injecting agitated saline through a peripheral IV while visualizing both atria, often in the apical four chamber view on transesophageal echocardiography (TTE). Images should be captured at both rest and with provocative maneuvers, such as Valsalva or cough,
which increase the pressure in the right atrium and more forcefully eject bubbles through a shunt if present. Indicators of a high-quality bubble study include complete opacification of the right atrium and atrial septal shift to the left after release of Valsalva maneuver.3

The most inclusive criteria for a “positive” bubble study include bubbles appearing in the LA within 5 to 7 cardiac cycles following Valsalva release, with earlier appearance (<3 beats) more strongly favoring PFO and later appearance (after 5-7 beats) suggesting extracardiac shunt, such as pulmonary arterialvenous malformation.3,4,5 TEE can diagnose PFO by both doppler ultrasound and bubble study, but is often unnecessary with a well-performed TTE.4 Although TTE shows the presence of bubbles in the LA, TEE (Figure 46.2) and intracardiac echo (ICE) can also directly visualize the atrial septal flap, and thus may be more sensitive than TTE for the detection of PFO.4,6 However, if the PFO is not easily visualized, TEE diagnosis may be hindered by requiring sedation, which both decreases RA pressure and impairs the ability to perform provocative testing.

Transcranial doppler (TCD) is another noninvasive method useful in the initial screening for PFO. TCD measures cerebral blood flow and can identify microbubbles passing through intracranial arteries for the detection of right to left shunt. A recent study by Maffe et al.,7 using TEE as the gold standard, found that both TTE and TCD showed high sensitivity for PFO detection, whereas TTE showed improved specificity when using the appearance of bubbles in the left atrium within 3 cardiac cycles as cutoff for PFO detection (Table 46.1).


Anatomic Characteristics as Prognostic Indicator and Device Selection

Information about the size and anatomic characteristics of PFO determined by echocardiography are important both prognostically—as risk factors for stroke—and for proper device selection and sizing. The number of bubbles that cross into the left atrium can be used as a rough estimate for PFO size, which is an important variable in determining the benefit of PFO closure. Subanalysis of the REDUCE and RESPECT trials did not find a benefit in preventing recurrent stroke with closure versus medical therapy in patients with small shunts (defined as <6 bubbles in the LA within 3 cardiac cycles) or trace to moderate shunts (<20 bubbles in the LA within 3 cardiac cycles), respectively.8,9 Additionally, the CLOSE trial excluded patients altogether who had small to moderate shunts, defined as less than 30 bubbles in the left atrium within 3 cardiac cycles.10 Being able to accurately quantify shunt size on TTE requires high-quality imaging, including well-performed provocative maneuvers.













Another prognostically significant anatomic feature is the presence of an atrial septal aneurysm (ASA), which is an excursion of the septum primum of 10 mm or greater beyond the plane of the atrial septum.1 ASAs are present in 2% to 3% of the general population, are associated with intracardiac shunts,11,12,13 and have increased prevalence in patients with ischemic stroke, possibly by acting as a nidus for thrombus formation and thus a source of embolus in the setting of shunt. Furthermore, PFO with septal aneurysms are thought to be larger than those without an associated ASA, further increasing the risk for paradoxical emboli.13,14,15 In the RESPECT trial, PFO closure in the setting of ASA was found to be significantly protective against recurrent stroke when compared to medical therapy (1.7% vs. 7.6%, hazard ratio [HR] 0.20, P = .005).9 Finally, the presence of an ASA led to subject inclusion in the studies, regardless of PFO size in the CLOSE trial.10


INDICATIONS FOR PATENT FORAMEN OVALE CLOSURE


Cryptogenic Stroke

PFOs are implicated in the pathophysiology of cryptogenic strokes by allowing clot formed in the venous system to cross into the arterial circulation.16,17 However, multiple early investigations failed to show definitive benefit of routine PFO closure for this indication.18,19,20 A diagnosis of cryptogenic stroke may be made when there is clinical and radiologic evidence
of an ischemic stroke and no cause is readily identifiable.21,22 Important etiologies to investigate prior to making the diagnosis of cryptogenic stroke include atrial fibrillation, peripheral artery disease, endocarditis, and hypercoagulable state. Cryptogenic strokes are more common in younger patients who lack risk factors for stroke that accrue with age.23,24

Recently, three large randomized control trials found a significant reduction in recurrent stroke in patients who underwent transcatheter PFO closure when compared with patients who were treated with antiplatelet therapy alone after experiencing cryptogenic stroke8,9,10 (Table 46.2). These trials enrolled patients who were unlikely to have a stroke from reasons other than paradoxical embolus by ruling out atrial fibrillation, hypercoagulable states, and carotid disease prior to closure. Furthermore, older patients and patients with uncontrolled risk factors for stroke were excluded from the studies. Important eligibility criteria included an age limit of 60 years, moderate or large PFO size, and the presence of an interatrial septal aneurysm, which has been associated with recurrent cryptogenic stroke.11


Decompression Sickness

Decompression sickness is a severe illness that affects individuals exposed to increased atmospheric pressures. It is most commonly encountered in scuba divers, although it also can occur during high-altitude or unpressurized air travel.25 This condition occurs when nitrogen dissolved in the blood and tissues by high pressure forms bubbles as pressure decreases. These bubbles may cross into the arterial system through a PFO and lead to stroke. Other symptoms include musculoskeletal pain, rash, confusion, paresthesias, paralysis, and respiratory distress. Severe decompression syndrome requires expedient treatment with hyperbaric chamber therapy. Although there are no large studies to recommend routine closure in divers, one small randomized study found that subjects who underwent PFO closure had less arterial bubbles when compared to those who did not in patients exposed to similar conditions.26 After PFO closure, patients should be counseled that they are at similar risk for decompression sickness (DCS) as those who do not have PFOs and should continue to take routine precautions.