Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3913_Библиотеки_им_академика_М_И_Перельмана
.pdf
[71] Igawa G, Ishida K, Matsubara K, Kinugasa Y, Ogura K, Kato M, et al. Right-and left-sided carcinoid heart disease without intracardiac
shunting. J Echocardiogr 2012;10(4):135e7.
[72] Le Me
´
tayer P, Constans J, Bernard N, Roudaut R, Pellegrin J, Lacostet D, et al. Carcinoid heart disease: two cases of left heart involvement
diagnosed by transthoracic and transoesophageal echocardiography. Eur Heart J 1993;14(12):1721e3.
[73] Materazzo C, Meazza R, Stefanelli M, Biasi S. Left valvular involvement in carcinoid: description of a case. G Ital Cardiol 1994;24(4):429e33.
[74] Requile
´
A, Van De Bruaene A, Reenaers V, Dendale P. A case of carcinoid heart disease with desaturation and no liver metastases. Echocar-
diography 2014;31(10):E307e9.
[75] Hastie MJ, Souh J, Ju A, Shanewise JS. Undiagnosed severe pulmonic regurgitation in a carcinoid patient for tricuspid valve replacement and
patent foramen ovale closure. Anesth Analg 2013;116(2):300e2.
[76] Ramos-Levı
´
AM, Dı
´
az-Pe
´
rez JA, Poves C, Bover R. Carcinoid tumor and patent foramen ovale. Endocrinol Nutr 2011;58(4):206.
[77] Thorstensen A, Amundsen T, Jianu C, Vilsvik JS, Soma J. Noe a laere av-En mann i 60-arene med tungpust og hypoksemi. Tidsskrift for den
Norske legeforening 2009;129(3):189.
[78] Pearson AC, Steinberg S, Shah MH, Bloomston M. The complicated management of a patient following transarterial chemoembolization for
metastatic carcinoid. World J Surg Oncol 2008;6(1):125.
[79] Hayashi Y, McGaw DJ, Goldstein J. Urgent transcatheter closure of patent foramen ovale followed by elective right-sided valve surgery for
decompensated carcinoid heart disease. Heart Lung Circ 2008;17(3):259e61.
[80] Rodriguez-Cintron W, Gonzalez JM, Zoghbi W, Stevens PM. An unusual cause of cyanosis in a patient with a carcinoid tumor. South Med J
1997;90(10):1029e31.
[81] Blick DR, Zoghbi WA, Lawrie GM, Verani MS. Carcinoid heart disease presenting as right-to-left shunt and congestive heart failure: success-
ful surgical treatment. Am Heart J 1988;115(1):201e3.
[82] Pitcher D, Fletcher P, Laszlo G, Keen G, Rees JR. Cyanosis attributable to right to left shunt in the carcinoid syndrome. Br Med J 1986;
292(6526):1016.
[83] Bhattacharyya S, Jagroop A, Gujral DM, Hayward C, Toumpanakis C, Caplin M, et al. Circulating plasma and platelet 5-hydroxytryptamine
in carcinoid heart disease: a pilot study. J Heart Valve Dis 2013;22(3):400e7.
[84] Khay K, Arous S, Bentaoune T, Drighil A, Habbal R. Carcinoid heart disease revealed by cyanosis with both right and left valvular involve-
ment: a case report. J Med Case Rep 2018;12(1):23.
[85] Chaudhari PR, Abergel J, Warner RR, Zacks J, Love BA, Halperin JL, et al. Percutaneous closure of a patent foramen ovale in left-sided carci-
noid heart disease. Nat Rev Cardiol 2007;4(8):455.
[86] Marenco J, Naimi S, Hijazi Z, Patel A, Pandian N. Nonsurgical closure of a patent foramen ovale in a patient with carcinoid heart disease and
severe hypoxia from interatrial shunting. Cathet Cardiovasc Interv 2000;51(2):210e3.
[87] Mottram PM, McGaw DJ, Meredith IT, Peverill RE, Harper RW. Profound hypoxaemia corrected by PFO closure device in carcinoid heart
disease. Eur J Echocardiogr 2006;9(1):47e9.
[88] Prinzmetal M, Kennamer R, Merliss R, Wada T, Bor N. Angina pectoris I. A variant form of angina pectoris: preliminary report. Am J Med
1959;27(3):375e88.
[89] Hung M-J, Hu P, Hung M-Y. Coronary artery spasm: review and update. Int J Med Sci 2014;11(11):1161.
[90] Bakhle Y. Pharmacokinetic and metabolic properties of lung. Br J Anaesth 1990;65(1):79e93.
[91] Chester AH, Allen SP, Tadjkarimi S, Yacoub MH. Interaction between thromboxane A2 and 5-hydroxytryptamine receptor subtypes in human
coronary arteries. Circulation 1993;87(3):874e80.
[92] Bourgault C, Bergeron S, Bogaty P, Poirier P. A most unusual acute coronary syndrome. Can J Cardiol 2006;22(5):429e32.
[93] Topol EJ, Fortuin NJ. Coronary artery spasm and cardiac arrest in carcinoid heart disease. Am J Med 1984;77(5):950e2.
[94] Eapen DJ, Clements Jr S, Block P, Sperling L. Metastatic carcinoid disease inducing coronary vasospasm. Tex Heart Inst J 2012;39(1):76.
[95] Fenning S, Newby D, Toumpanakis C, Strachan M. Coronary artery spasm secondary to carcinoid syndrome. QJM: Int J Med 2016;109(7):
483e4.
[96] Frullini A, Felice F, Burchielli S, Di Stefano R. High production of endothelin after foam sclerotherapy: a new pathogenetic hypothesis for
neurological and visual disturbances after sclerotherapy. Phlebology 2011;26(5):203e8.
[97] Stephens R, Dunn S. Non-ST-elevation myocardial infarction following foam ultrasound-guided sclerotherapy. Phlebology 2014;29(7):
488e90.
[98] Dao CN, Tobis JM. PFO and paradoxical embolism producing events other than stroke. Cathet Cardiovasc Interv 2011;77(6):903e9.
VI. OTHER CONDITIONS AND PFO
REFERENCES 167
https://t.me/med1917
https://t.me/med1917
CHAPTER
14
Percutaneous PFO Closure: History, Devices,
Techniques, Safety, and Informed Consent
Barbara E. Sta
¨
hli
1
, Fabian Nietlispach
2
, Bernhard Meier
3
1
University Heart Center, University Hospital Zurich, Zurich, Switzerland;
2
Cardiovascular Center Zurich, Hirslanden
Klinik im Park, Zurich, Switzerland;
3
University Hospital Bern, Bern, Switzerland
OUTLINE
Introduction 171
History 172
The Understanding of PFO-related Pathologies 172
Development of Percutaneous Techniques for PFO
Closure 173
Accumulating Evidence for Clinical Applications 174
Devices 176
Double Disc Devices 176
Amplatzer PFO Occluder 176
CardioSEAL Device 179
STARFlex Device 179
Figulla II PFO Occluder 179
Gore HELEX Septal Occluder
179
Gore Cardioform Septal Occluder
179
Nondouble Disc Devices
179
FlatStent Occluder
179
NobleStitch EL Occluder
180
Radiofrequency Fusion
180
Safety
180
Informed Consent
180
Conclusion
181
References
181
INTRODUCTION
The presence of a patent foramen ovale (PFO) has been related with various clinical disorders such as stroke or
transient ischemic attack secondary to paradoxical embolism [1], embolic myocardial infarction, peripheral arterial
embolism, migraine headache [2], sleep apnea [3], platypnea-orthodeoxia syndrome [4], exercise desaturation [5],
high-altitude pulmonary edema, and diver decompression illness [6,7]. Over the past decade, percutaneous PFO
closure has evolved as the treatment of choice with proven safety and efficacy in the realm of secondary stroke pre-
vention in otherwise healthy patients. As a remarkable exception for interventional cardiology, closure techniques
and the most frequently used device (the Amplatzer PFO Occluder [Abbott; Chicago, Illinois]) have remained virtu-
ally unchanged ever since their introduction. Percutaneous PFO closure can safely be performed as an outpatient
procedure with high procedural success and very low complication rates. Accumulating evidence stemming
from observational studies and randomized trials supports clinical benefits of percutaneous PFO closure in the pre-
vention of embolic events (Chapter 5e7) and migraine (Chapter 10 and 11) [8e10]. This chapter gives a historical
perspective and summarizes current devices and technologies for percutaneous PFO closure, highlighting related
aspects of safety and patient education.
171
PFO Closure for Stroke, Myocardial Infarction, Peripheral Embolism, Migraine, and Hypoxemia
Copyright © 2020 Elsevier Inc. All rights reserved.https://doi.org/10.1016/B978-0-12-816966-7.00014-2
https://t.me/med1917
HISTORY
The Understanding of PFO-related Pathologies
The presence of a PFO has been known since the time of Galen, but the first anatomical description and illustration
of a communicating channel between the atria was made by Leonardo da Vinci in Quaderni d’Anatomia in 1513
(Fig. 14.1) [8e22]. In the 19th century, paradoxical embolism through a PFO was recognized as a potential pathophys-
iological mechanism that could cause devastating clinical events. The first report of a paradoxical embolism has been
attributed to Julius Cohnheim, who described the case of a 35-year-old woman with lower extremity deep venous
thrombosis and consecutive fatal middle cerebral artery embolization in his text Lectures of General Pathology published
in 1877 [12]. The term “paradoxical embolization” was introduced by Zahn who described the case of a woman with
thrombus within the inferior vena cava, multiple systemic emboli, and a branched embolus lodged in a PFO on au-
topsy [13]. Numerous cases were described thereafter and included coronary and peripheral embolizations [23,24].
The mechanistic concept of venous thrombus formation with subsequent paradoxical embolization into the
systemic circulation via a PFO was rapidly adopted, and the diagnosis was later supported by the advent of
advanced imaging modalities such as echocardiography, magnetic resonance imaging, and computed tomography
[25e28]. Contrast echocardiography studies provided the first epidemiological evidence f or a relation between the
presence of PFO and the occurrence of stroke. These studies demonstrated an increased prevalence of right-to-left
shunting in patients with stroke as compared to age- and sex-matched controls, thereby suggesting that paradox-
ical embolism through a PFO may be a more common culprit of embolic stroke than previously thought [1,29].
While other etiologies of stroke are more frequently encountered in elderly patients, the PFO initially was falsely
accepted as a cause of stroke exclusively in younger patients. This was refuted in 2007 [30]; however, s troke clas-
sification as of this writing wrongly neglects the PFO as a separate and equally important cause of stroke, by sum-
marizing it under the misnomer of “cryptogenic stroke.” Therefore, a new stroke classification should be adopted
by the respective international neurological societies, respecting the role of PFO as a separate stroke culprit. While
FIGURE 14.1 Timeline of PFO as a medical entity. Selected milestones in history. CLOSE, PFO Closure or Anticoagulants vs. Antiplatelet
Therapy to Prevent Stroke Recurrence; CLOSURE I, Evaluation of the STARFlex Septal Closure System in Patients with a Stroke and/or Transient
Ischemic Attack due to Presumed Paradoxical Embolism through a PFO; DEFENSE-PFO, Device Closure vs. Medical Therapy for Cryptogenic
Stroke PatientscWith High-Risk PFO; MIST, Migraine Intervention With STARFlex Technology; PC, Clinical Trial Comparing Percutaneous
Closure of PFO Using the Amplatzer PFO Occluder with Medical Treatment in Patients with Cryptogenic Embolism; PREMIUM, Prospective,
Randomized Investigation to Evaluate Incidence of Headache Reduction in Subjects With Migraine and PFO Using the Amplatzer PFO Occluder
to Medical Management; PRIMA, Percutaneous Closure of PFO in Migraine with Aura; REDUCE, Gore Helex Septal Occluder/Gore Cardioform
Septal Occluder and Antiplatelet Medical Management for Reduction of Recurrent Stroke or Imaging-Confirmed Transient Ischemic Attack in
Patients with PFO; RESPECT, Randomized Evaluation of Recurrent Stroke Comparing PFO Closure to Established Current Standard of Care
Treatment.
14. PERCUTANEOUS PFO CLOSURE172
VII. SAFETY, TECHNICAL ASPECTS TO PFO CLOSURE, AND FUTURE OUTLOOK
https://t.me/med1917
the prevalence of a PFO is estimated to be about 25% in the general population [31], it was found in up to 50% of
cryptogenic stroke patients [1,29,32]. Despite unprecedented advances in therapeutic strategies, stroke remains
associated with a substantial health care and economic burden, representing the second leading cause of death
worldwide [33]. Given an annual stroke incidence of about 800,000 per year in the United States with 15% of
them considered to be due to paradoxical embolization mediated by a PFO [30,33,34], the combination of stroke
and a PFO occurs in over 107,000 patients each year in the United States.
Paradoxical embolism through a PFO may produce devastating and potentially lethal complications other than
stroke, such as myocardial infarction and visceral or limb ischemia (Fig. 14.2) [24,35,36]. Furthermore, the presence
of a PFO is considered to represent a risk factor for neurological decompression sickness in divers, which is caused
by nitrogen bubble formation in supersaturated tissues during diving ascent and subsequent paradoxical emboliza-
tion into the systemic circulation [7].
In the 1990s, the first observational studies pointed toward a possible link between PFO and migraine, particu-
larly when aura is present. Studies demonstrated an increased prevalence of right-to-left shunting in patients
suffering from migraine with aura as compared to patients with migraine without aura and healthy controls
[37e41]. In a transesophageal echocardiography study, nearly half of patients who had migraine with aura were
shown to have right-to-left shunting due to PFO, with larger shunt size in migraineurs than in controls [37].In
line with these findings, an increased prevalence of migraine was reported in patients with known PFO [42].
Although the pathophysiological mechanisms underlying this relation remain to be further determined, paradoxical
microembolizations into the vertebrobasilar territory and, more plausibly, the passage of metabolites such as sero-
tonin into the systemic circulation, which are normally metabolized within the pulmonary vasculature, are consid-
ered to be principally involved [43,44].
Over the past 20 years, the PFO has been related to various clinical disorders and is therefore increasingly being
recognized as a therapeutic target, particularly in the era of transcatheter treatments.
Development of Percutaneous Techniques for PFO Closure
Experimental closure of atrial septal defects was first attempted in dogs in 1947 [45], and the first surgical closure
of an atrial septal defect was performed in a 12-year-old boy in 1948 by suturing together the anterior and posterior
atrial walls in the septal plane [46]. Surgical techniques were then further developed and advancements resulted in
the first direct closure of an atrial septal defect with the use of cardiopulmonary bypass in 1953 [47]. Thus, atrial
septal defect closure paved the way for modern heart surgery [48]. Given the ease of transvenous access of the atrial
FIGURE 14.2 Selected clinical disorders related to PFO.
VII. SAFETY, TECHNICAL ASPECTS TO PFO CLOSURE, AND FUTURE OUTLOOK
HISTORY 173
https://t.me/med1917
septum, substantial efforts have been undertaken to develop percutaneous strategies for the closure of atrial septal
defects and PFOs. The first closure of an atrial septal defect with a dedicated device was performed by Hufnagel and
Gillespie in an experimental surgical model in 1951, and further technical refinements then led to the design of a
double disc device, with a disc placed on each side of the atrial septum [49]. In 1975, having successfully performed
preclinical studies in dogs using an umbrella device, King and Mills for the first time closed an atrial septal defect via
a percutaneous approach in humans [14]. The automatically opening umbrella device was then further refined to the
clamshell double-umbrella device, which had the advantage of being recapturable or removable up to the final step
of the procedure [14]. Using this device, the first patients with PFO-associated stroke were treated in the early 1990s
[50]. Due to the occurrence of late fractures of the metal arms of the umbrellas [50], the device was withdrawn from
clinical trials and re-engineered to the subsequent CardioSEAL and STARFlex devices (NMT Medical Inc, Boston,
Massachusetts) [17,51,52]. In the mid-1990s, the first Amplatzer Septal Occluder (Abbott, Chicago, Illinois) was
designed as a self-expandable, fully retrievable double disc device made of nitinol wire [53]. The Amplatzer PFO
Occluder was a derivative of it, specifically designed for PFO closure with a smaller left than right atrial disc. It
was first implanted on September 10, 1997 by Bernhard Meier in the presence of Kurt Amplatz in Switzerland
(Fig. 14.3) [15]. It has become the most widely investigated and used device for percutaneous PFO closure or atrial
septal closure in general, as PFO closure is the most common form of atrial septal defect closure [18,19,54]. An over-
view of dedicated devices for percutaneous PFO closure is given below.
Accumulating Evidence for Clinical Applications
The high prevalence and the substantial morbidity and mortality associated with paradoxical embolization fueled
the search for interventional therapeutic strategies in these patients. Although percutaneous PFO closure offers a safe,
technically feasible, and effective procedure, which can be performed in less than 15 minutes, indications for percuta-
neous PFO closure have been the subject of ongoing debate since its introduction in the 1990s [50]. Over the last years, a
plethora of data favoring PFO closure over medical therapy have been published and they paved the way for expan-
sion of indications for PFO closure. The most compelling data have so far been obtained from studies for secondary
prevention of stroke (Chapter 5e7) and as a potential therapy for migraine headache, particularly migraine with aura
(Chapter 10 and 11).
The 3 initial randomized trials, published in 2012 and 2013, showed only non-significant reductions in the
recurrence of stroke with PFO closure as compared with medical management in their intention-to-treat analyses
FIGURE 14.3 Kurt Amplatz (left) and Bernhard Meier (right) on September 10, 1997. The occasion was the world’s first PFO closure with a
dedicated device, the Amplatzer PFO Occluder.
VII. SAFETY, TECHNICAL ASPECTS TO PFO CLOSURE, AND FUTURE OUTLOOK
14. PERCUTANEOUS PFO CLOSURE174
https://t.me/med1917
(Chapter 6). Among the 909 patients enrolled in CLOSURE I (Evaluation of the STARFlex Septal Closure System in
Patients with a Stroke and/or Transient Ischemic Attack due to Presumed Paradoxical Embolism through a PFO),
PFO closure did not offer a significant benefit over medical therapy alone for the prevention of recurrent stroke
or transient ischemic attack [17]. Similarly, PC (Clinical Trial Comparing Percutaneous Closure of PFO Using the
Amplatzer PFO Occluder with Medical Treatment in Patients with Cryptogenic Embolism) could not prove superi-
ority of percutaneous PFO closure over antithrombotic therapy in significantly reducing rates of death, recurrent
stroke, transient ischemic attack, or peripheral embolism [18], and the primary endpoint of early RESPECT (Ran-
domized Evaluation of Recurrent Stroke Comparing PFO Closure to Established Current Standard of Care Treat-
ment) was also not met in the intention-to-treat analysis. However, the prespecified per-protocol and as-treated
analyses of RESPECT demonstrated significant between-group differences in the recurrence rates of stroke in favor
of PFO closure at a median follow-up of 2.1 years [19]. Consistent with these findings, an exploratory analysis of the
long-term RESPECT data (median 5.9-year follow-up) demonstrated a significant benefit of PFO closure over med-
ical therapy even in the intention-to-treat analysis [20]. In line with the observed numerically lower rates of events in
the PFO closure arm of these initial, underpowered trials (based on lower than expected stroke rates in the medical
therapy arms), several meta-analyses then showed superiority of PFO closure over medical therapy in reducing the
risk of recurrent vascular events. An accumul ating benefit of PFO closure can be expected over time because the rate
of recurrent stroke must be expected to accrue by at least 1% per year unde r medical treatment only (Chapter 6)
[54e58]. In 2017, CLOSE (PFO Closure or Anticoagulants vs. Antiplatelet Therapy to Prevent Stroke Recurrence)
and REDUCE (Gore Helex Septal Occluder/Gore Cardioform Septal Occluder and Antiplatelet Medical Manage-
ment for Reduction of Recurrent Stroke or Imaging-Confirmed Transient Ischemic Attack in Patients with PFO) pro-
vided further evidence to support benefits of PFO closure in patients with PFO-associated stroke [9,22]. In CLOSE,
enrolling patients with stroke and a PFO with an associated atrial septal aneurysm or large interatrial shunt, the rate
of stroke recurrence was lower in the PFO closure group as compared to the antiplatelet therapy group (P <.001); the
5-year number needed to treat was 20 [9]. The goal of REDUCE was to determine the efficacy of PFO closure in com-
parison to antiplatelet therapy for the prevention of recurrent ischemic stroke or clinically silent brain infarction
detected on cerebrovascular imaging [22]. During a median follow-up of 3.2 years, rates of ischemic stroke (1.4%
vs. 5.4%, P ¼ .002) and new brain infarction (5.7% vs. 11.3%, P ¼ .04) were lower in the PFO closure group as
compared with antiplatelet therapy, while the incidence of silent brain infarction did not differ among groups
[22]. The number needed to treat to prevent 1 stroke within 24 months in REDUCE was only 28 [22]. In 2018,
DEFENSE-PFO (Device Closure vs. Medical Therapy for Cryptogenic Stroke Patients With High-Risk PFO) demon-
strated superiority of closure of high-risk PFOs including those with atrial septal aneurysm, hypermobility, or
size 2 mm, over medical management in reducing rates of stroke, vascular death, or Thrombolysis In Myocardial
Infarctionedefined major bleeding at a 2 year follow-up (Chapter 7) [8]. In addition to the reduction of recurrent
ischemic events observed in these trials, PFO closure obviates the need for lifelong anticoagulant therapy in patients
with left circulation thromboembolism deemed related to the PFO, thereby avoiding the risk of devastating bleeding
events. As shown in a subgroup analysis of RESPECT, only lifelong oral anticoagulation yields comparable protec-
tion from recurrent stroke as PFO closure does, while antiplatelet therapy was inferior [19]. Therefore, the only alter-
native to PFO closure is lifelong oral anticoagulation with its inherent bleeding risk (risk for major bleeding 2%e5%
per year). It should be emphasized that the risk of bleeding rises with increasing age and comorbid burden, and is
highly dependent on the duration of anticoagulation/antiplatelet therapy. Percutaneous PFO closure obviates spe-
cific inherent challenges related to drug therapy such as drug intolerance, overdosing, drug interactions, poor
compliance, or the need to stop blood thinners prior to procedures and surgeries.
Besides the benefits reported in stroke patients, observational studies pointed toward beneficial effects of percuta-
neous PFO closure in patients with migraine [6]. In 2000, Wilmshurst et al. for the first time reported symptomatic ben-
efits in patients with migraine, who had undergone percutaneous PFO closure for other reasons [6]. Numerous case
series similarly suggested improvement in both frequency and severity of migraine headaches after percutaneous PFO
closure [59e62]. Given the observed association between PFO and migraine and the promising data obtained from
observational studies (Chapter 10) [6,59e63], randomized trials were then designed to investigate whether percuta-
neous PFO closure beneficially affects migraine symptoms (Chapter 11). The prospective, sham-controlled study
MIST (Migraine Intervention With STARFlex Technology), published in 2008, was the first randomized trial to inves-
tigate percutaneous PFO closure for the treatment of migraine with aura. In MIST, device closure had no effect on the
primary efficacy measure, the cessation of migraine headache 91e180 days after the procedure. However, PFO closure
resulted in a greater reduction in total migraine days [16]. Although this trial was limited by the rather small sample
size and short follow-up duration, the robust sham-controlled design of the study served as a model for the evaluation
of novel interventions in outcome trials. The PRIMA (Percutaneous Closure of PFO in Migraine with Aura) trial,
VII. SAFETY, TECHNICAL ASPECTS TO PFO CLOSURE, AND FUTURE OUTLOOK
HISTORY 175
https://t.me/med1917
published in 2016, randomly allocated a total of 107 migraine patients to either treatment with the Amplatzer PFO
Occluder or control with medical management. In this trial, PFO closure significantly reduced migraine days, migraine
with aura attacks, and days per month with complete migraine cessation [10]. PREMIUM (Prospective, Randomized
Investigation to Evaluate Incidence of Headache Reduction in Subjects With Migraine and PFO Using the Amplatzer
PFO Occluder to Medical Management), published in 2017, randomized patients with migraine to medical therapy
with a sham procedure, versus medical therapy plus percutaneous PFO closure with the Amplatzer PFO Occluder;
the study found a significant reduction in monthly migraine days [21]. In 2018, 2 meta-analyses including these
3 randomized trials both demonstrated superiority of PFO closure over medical management in terms of number
of migraine attacks and migraine days, but not complete resolution of migraine attacks (Chapter 11) [64,65]. The results
of the pooled analyses, along with the positive signals observed in the randomized trials, are encouraging.
Considering these findings and accounting for the collateral benefit of eliminating the source for paradoxical embolism
when closing a PFO for migraine relief, migraineurs should be offered this therapy.
In addition, closure of a PFO has been shown to exert beneficial effects in observational studies on decompression
illness (Chapter 13), particularly ischemic brain lesions in divers [66], high-altitude pulmonary edema [67], obstructive
sleep apnea [68], as well as platypnea-orthodeoxia syndrome and exercise desaturation (Chapter 12) [4,5]. PFO has
been further associated with worse outcomes in high-risk situations for paradoxical embolism, such as any major sur-
gical procedure or in patients with pacemaker or implantable cardioverter defibrillator [69]. Consequently, PFO closure
can be advocated in many other high-risk clinical situations that are associated with venous thrombosis (e.g., frequent
travelers, pilots, pregnancy) or activities with frequent Valsalva maneuvers (e.g., brass musicians, bodybuilders).
Besides the assessment of feasibility, sa fety, and efficacy, cost analysis is important to estimate the overall benefit
of an intervention. Percutaneous PFO closure as a one-time minimally invasive procedure has proven to be cost-
effective as compared with lifelong medical thera py. Assuming costs of $20 000 per PFO closure, it has been shown
that cost-effectiveness (<$50 000 per quality-adjusted life-year gained) is achieved 2.7 years after the procedure
[70,71,72]. In a recent analysis, PFO closure as compared with medical therapy was associated with an incremental
net monetary benefit of over $50 000 at 15 years [73]. However, it is difficult to incorporate the social and economic
consequences of lifelong disability and loss of productivity due to recurrent stroke events into the cost analysis,
along with long-term adverse events of medical therapy; it is conceivable that PFO closure may be even more
cost-effective than estimated in cost-modeling studies.
In conclusion, investigations of the past years have proven the superiority of PFO closure over medical therapy in
the prevention of recurrent ischemic cerebral events after an index cryptogenic stroke, and support the use of PFO
closure for the prevention of numerous other clinical conditions. Research efforts have culminated in the first Euro-
pean position paper for rational PFO management in left circulation thromboembolism, published in 2018 [74].
While recommendations for PFO closure were rather stringent, chang es in treatment recommendations based on
the most recent data are expected in the updated versions of current stroke prevention guidelines [75e77], which
will then give PFO closure the high priority it deserves for the treatment of patients with a prior stroke. A more pro-
gressive and proactive approach on PFO closure, to take advantage of the collateral bene fits between indications, has
been suggested by the authors [34,78].
DEVICES
Several dedicated devices have been developed for the catheter-based therapy of PFO (Table 14.1)
[8,10,16e22,63,79e83]. The choice of the occluder should be based on the available evidence for each device [74].
Most data have been gathered for the Amplatzer PFO Occluder, and the GORE HELEX, and Gore Cardioform septal
occluders (W.L. Gore and Associates; Flagstaff, Arizona) [74].
Double Disc Devices
Amplatzer PFO Occluder
The Amplatzer PFO occluder, consisting of a nitinol wire mesh and polyester, is a self-expanding double-disc de-
vice with a smaller left and a larger right atrial disc (except for the 30 mm version, where the right and the left disc
each comprise 30 mm) and a central waist. The Amplatzer PFO Occluder was the first dedicated PFO occluder and is
the most widely investigated and used device for percutaneous PFO closure, with approximately 100,000 devices
implanted worldwide (Fig. 14.4) [18,19,54]. Procedural success rates are close to 100%, and effective closure rates
VII. SAFETY, TECHNICAL ASPECTS TO PFO CLOSURE, AND FUTURE OUTLOOK
14. PERCUTANEOUS PFO CLOSURE176
https://t.me/med1917
TABLE 14.1 Devices for Percutaneous PFO Closure.
Device Principle Occluder Material Framework Material Sizes
Randomized
Controlled Trials
CardioSEAL/
CardioFLEX (NMT
Medical)
Double square disc
device
Dacron Nickel-cobaltebased
alloy (MP35n)
17, 23, 28, 33, 40 mm e
STARFlex (NMT
Medical)
Double square disc
device (structurally
identical to the
CardioSEAL device)
Dacron Nickel-cobaltebased
alloy (MP35n)
23, 28, 33, 38 mm CLOSURE-1 [17]
MIST [16]
Amplatzer PFO
Occluder (Abbott
Vascular)
Double disc device Polyester Nitinol wire mesh 18, 25, 30, 35 mm PC trial [18], RESPECT
[19], DEFENSE-PFO [8],
PRIMA [10],
PREMIUM [21]
Gore Helex occluder
(Gore Medical)
Single spiral wire ePTFE Nitinol frame 15, 20, 25, 30, 35 mm REDUCE [22]
Gore Cardioform
septal occluder (Gore
Medical)
Double disc device ePTFE Nitinol frame REDUCE [22]
Continued
VII. SAFETY, TECHNICAL ASPECTS TO PFO CLOSURE, AND FUTURE OUTLOOK
DEVICES 177
https://t.me/med1917
TABLE 14.1 Devices for Percutaneous PFO Closure.dcont’d
Device Principle Occluder Material Framework Material Sizes
Randomized
Controlled Trials
Figulla II PFO occluder
(Occlutech)
Double disc device Polyester Nitinol wire mesh Left/right disc: 16/18,
23/25, 27/30, 31/
35 mm
e
BioSTAR (NMT
Medical)
Double square disc
device
Acellular collagen
matrix
Alloy MP35n 23, 28, 32 mm
Heart Stitch (Heart
Stitch Inc.)
Suture Polypropylene suture eee
FlatStent occluder
(Corherex Medical)
Occluder placed within
the PFO tunnel
Polyurethane foam,
radiopaque tantalum
markers
Nitinol-based wire
framework
13, 19 mm e
ePTFE, expanded polytetrafluoroethylene.
CardioSEAL/CardioFLEX, StarFLEX - From Nugent AW, Britt A, Gauvreau K, et al. Device closure rates of simple atrial septal defects optimized by the STARFlex device. J Am Coll Cardiol. 2006;48(3):538e544. Amplatzer - Amplatzer
is a trademark of Abbott or its related companies. Reproduced with permission of Abbott, © 2019. All rights reserved. Gore Helex Occluder e From Thomas K. Jones et al. Results of the U.S. Multicenter Pivotal Study of the HELEX Septal
Occluder for Percutaneous Closure of Secundum Atrial Septal Defects, J. Am. Coll. Cardiol. 2007;49;2215e2221, Gore Cardioform septal occluder - Courtesy of W. L. Gore & Associates Inc. Occlutech Figulla Flex II PFO Occluder - Used
with permission from Occlutech, BioSTAR - From Gian Paolo Ussia et al. Percutaneous closure of patent foramen ovale with a bioabsorbable occluder device, Catheterization and Cardiovascular Interventions, 74(4), 2009, 607e614; Heart
Stitch - Used with permission from Heart Stitch Inc.; FlatStent occluder - From Horst Sievert et al. Initial Clinical Experience with the Coherex FlatStentTM and FlatStentTM EF PFO Closure System for In-tunnel PFO Closure: Results
of the Coherex-EU Study, Catheterization and Cardiovascular Interventions 83:1135e1143 (2014).
VII. SAFETY, TECHNICAL ASPECTS TO PFO CLOSURE, AND FUTURE OUTLOOK
14. PERCUTANEOUS PFO CLOSURE178
https://t.me/med1917
Соседние файлы в папке Библиотека им академика М.И. Перельмана