Hybrid repair versus conventional open repair for aortic arch dissection
Abstract
This is a protocol for a Cochrane Review (Intervention). The objectives are as follows:
To assess the effectiveness and safety of a hybrid technique of treatment over conventional open repair in the management of aortic arch dissection.
Background
See Appendix 1 for Glossary of terms
Description of the condition
The aorta is the main artery in the body. It originates in the heart and supplies blood to all parts of the body. The aorta consists of three layers: the intima, which is the innermost layer; the media, which is the middle layer; and the adventitia, which is the outermost layer. A dissection of the aorta is a separation or tear of the intima from the media. This tear allows blood to flow not only through the original aortic flow channel (known as the true lumen), but also through a second channel between the intima and media (known as the false lumen). A dissection can then propagate along the artery, secondary to the blood flowing into the space. Aortic dissection is a life‐threatening condition which can be rapidly fatal. It occurs more frequently in men, and uncontrolled blood pressure (hypertension) is a leading risk factor (Nienaber 2004). Predominate risk factors for genetic or familial aortic dissection are connective tissue disorders such as Loeys‐Dietz syndrome, Marfan syndrome, and Ehlers‐Danlos syndrome (Murphy‐Ryan 2010).
According to the reporting standards for thoracic endovascular aortic repair, the aorta is divided into 12 treatment zones, zone 0 to zone 11. Aortic arch dissection occurs between zone 0 and zone 4 (Fillinger 2010). Zone 0 refers to an area between the aortic sinus and the brachiocephalic artery origin; zone 1 is distal to the brachiocephalic artery but proximal to the left common carotid artery origin; zone 2 is distal to the left common carotid artery but proximal to the subclavian artery; zone 3 is within 2 cm of the left subclavian artery without covering it; and zone 4 refers to an area 2 cm or more distal to the left subclavian artery and ends within the proximal half of the descending thoracic aorta (Fillinger 2010).
There are two classification systems for aortic dissection:
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the Stanford classification, which categorises dissection into Type A and Type B (Daily 1970; DeBakey 1966). Type A occurs in the ascending aorta or aortic arch, or both, with possible involvement of the descending aorta. Type B occurs in the descending aorta, beyond the left subclavian artery; and
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the DeBakey classification, which categorises dissection into Type I, Type II, and Type III. Type I involves the ascending and descending aorta (Stanford Type A and B), Type II involves the ascending aorta only (Stanford Type A), and Type III involves the descending aorta only, beginning after the left subclavian artery (Stanford Type B) (Daily 1970; DeBakey 1966).
Aortic dissection is also classified based on the age of the dissection (chronicity), as the mortality rates vary with chronicity (Wong 2008). These classifications are, from the onset of symptoms: less than 24 hours (hyper‐acute); less than 2 weeks (acute); 2 to 6 weeks (sub‐acute); and more than 6 weeks (chronic). As the dissection progresses in chronicity, the separated arterial layers that divide the true and false lumen (the intraluminal septum) increase in rigidity and reduce in elasticity and mobility, causing the septum to become stiff.
Description of the intervention
Aortic dissection that affects the ascending aorta, aortic arch and the descending aorta is a challenging pathology for physicians. Patients with this type of aortic disease pose a surgical challenge and this is an area of continuing development and innovation (Cochennec 2013; Kurimoto 2015; Lu 2013). Treatment of aortic dissection can be via open repair, endovascular repair, or a hybrid repair (Antoniou 2010; Cao 2012; Cochennec 2013; Murphy 2012; O'Callaghan 2014). There is debate on the optimum surgical approach for aortic arch dissection. Patients with ascending aortic dissection have poor rates of survival and to date, open surgical repair (OSR) is regarded as the standard treatment for aortic arch dissection (DeBakey 1966; Suzuki 2003).
Open surgical repair
Current treatment for complex aortic arch dissection involves removal of the ascending portion of the aorta, replacement and open distal anastomosis (connection) with a surgical graft, known as a hemi‐arch replacement. This is carried out under artificially induced circulatory arrest (a method of slowing the blood flow) with varying degrees of hypothermia (cooling of core body temperature), and a selection of cerebral protection techniques, including antegrade or retrograde cerebral perfusion, or deep hypothermia alone. Potential complications of open surgical repair include stroke, cardiac arrhythmia (irregular heartbeat), coagulopathy (failure to clot blood), and hypokalaemia (lower than normal level of potassium in the blood) (Groysman 2011). This type of repair is high risk and carries a mortality risk of 21.6%, due to the utilisation of circulatory arrest and cerebral perfusion techniques (Patel 2011).
Complete debranching of the aortic arch consists of revascularisation (restoring blood to the vessel) of at least the brachiocephalic artery and the left common carotid artery via a prosthetic bypass from the ascending aorta. After induction of pharmacologic hypotension (inducing state of low blood pressure to reduce blood loss), the ascending aorta is clamped tangentially and the proximal end of a prosthetic graft sutured in an end‐to‐side anastomosis. The left subclavian artery is revascularised through the sternotomy (division of the chest bone) or through an incision above the clavicle (collar bone). Aortic arch branch vessels can be bypassed via a singular, bifurcated (two branches) or trifurcated (three branches) tube graft. Alternatively, cervical debranching can be performed through cervicotomies (incision in the neck) and consists of retro‐oesophageal right common carotid‐to‐left common carotid artery bypass using a Dacron graft. According to surgeon's preference, the left subclavian artery can be ligated (tied up) or revascularised via a transposition into the left common carotid artery or a carotid artery bypass.
Hybrid repair
Hybrid techniques use a combination of endovascular approaches (intervention through the arteries using wires to carry grafts) and open surgical approaches to treat arch pathologies. These methods are designed to be less invasive than conventional, open techniques. The aorta is treated with a surgical graft in combination with the less invasive approach of endovascular implantation of an aortic stent endograft. Purely endovascular implantation of an endograft in the aorta is made via peripheral arterial access sites such as the femoral arteries, with no invasive surgical intervention. However, techniques for total endovascular repair, although promising, are still in their infancy (Nordon 2012), and reports estimate that in anatomical terms only 30% to 50% of patients with Standford Type A aortic dissection are suitable for total endovascular repair with current technologies (Moon 2011; Sobocinski 2011).
Hybrid repair involves surgical arch debranching of the supra‐aortic vessels, thereby creating a proximal landing zone of adequate length, followed by endovascular stent graft insertion in the surgically constructed landing zone within the aortic arch. Specialist thoracic arch‐debranching grafts such as the 'frozen or stented elephant trunk' have been developed for the purpose of a single‐stage hybrid repair. Elephant trunk is a vascular technique used to repair patients with extensive disease in their aorta. It consists of two stages, 1) open surgery to replace a portion of the ascending aorta, leaving a section of graft hanging within the descending aorta, 2) this graft section can then be used to place an endovascular stent (known as stented elephant trunk technique). This technique can also be carried out as a single stage (known as frozen elephant trunk technique).
During hybrid repair the endovascular intervention can be carried out in isolation or concurrently with the surgical intervention. In patients with extensive disease of the thoracic arch and descending aorta, a single‐stage approach under circulatory arrest is more favourable (Moulakakis 2013).
Hybrid approaches are classified into three types according to the extent of the aortic arch lesion and presence of the proximal and distal landing zones (Moulakakis 2013):
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Type I: the debranching procedure consists of brachiocephalic bypass and endovascular repair of the aortic arch. This approach is reserved for patients with isolated disease exhibiting an adequate proximal landing zone in the ascending aorta and a distal landing zone in the descending thoracic aorta (Stanford Type A/DeBakey Type II);
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Type II: an open ascending aorta reconstruction that creates an appropriate proximal landing zone, supra‐aortic vessel revascularisation, and endoluminal dissection coverage. This approach is designed for patients with ascending aortic lesions with a limited extension into the distal arch (Stanford Type A/DeBakey Type I); and
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Type III: an elephant trunk procedure with a complete endovascular repair of the thoracoabdominal aorta. This technique is reserved for patients with extensive aortic lesions that involve the ascending, transverse arch, and descending thoracic aorta (Stanford Type A/DeBakey Type I).
How the intervention might work
Although to date trial results using hybrid repair techniques for aortic arch dissection are promising, opinion is divided on its efficaciousness among the wider vascular surgery community (Kurimoto 2015). The aim of both hybrid repair and OSR is to stop further dissection progression in the aortic artery by covering the dissection entry points and also by promoting false lumen thrombosis; OSR is regarded as the standard for aortic arch dissection. Intervention for aortic arch dissection via a hybrid approach would reduce the incidence of highly invasive surgery when compared to OSR, while duration of cardiopulmonary bypass, hypothermic circulatory arrest and antegrade/retrograde cerebral perfusion can be reduced. Cardiopulmonary bypass is a technique that temporarily takes over the function of the heart and lungs during surgery, maintaining the circulation of blood and oxygen in the body. Hypothermic circulatory arrest temporarily suspends blood flow under very cold body temperatures. Antegrade cerebral perfusion involves sewing a small graft to the axillary/brachiocephalic artery or left common carotid artery. The graft is connected to a heart‐lung machine, and allows blood to flow through the brain during complex surgery of the aorta. Retrograde cerebral perfusion requires cannulation of the vena cava with perfusion pressures not exceeding 25 mmHg. Antegrade perfusion permits blood flow through the arterial system, allowing for varying temperature control. Retrograde perfusion permits blood flow through the venous system. The high associated risks using these methods including mortality (death) (6.6% to 9.9%), stroke (2.7% to 6.6%), paraplegia (18%), cardiac arrhythmia (irregular heartbeat), venous congestion and cerebral oedema would therefore be reduced or negated (Estrera 2003; Kamiya 2007; Okita 2001).
Why it is important to do this review
To date, no Cochrane review has assessed the effectiveness of hybrid repair compared to the standard OSR. There is an agreement that intervention is necessary for aortic arch dissection, however complex open aortic arch repair still carries a high degree of health risks and death due to the use of cardiopulmonary bypass, hypothermic circulatory arrest, and antegrade or retrograde cerebral perfusion during the procedure (Lu 2013; Murphy 2012; Rampoldi 2007; Vohra 2012). Deciding if a patient will undergo a hybrid versus open repair depends on surgical skill and physician preference, the overall quality of the supra‐aortic vessels (the brachiocephalic artery, the left common carotid artery, and subclavian artery) and the ability to clamp them, and whether cerebral perfusion can be maintained adequately.
We are undertaking this review as there is a critical need within the cardiovascular community for a synthesis of high quality evidence to inform decisions on optimal management of aortic arch dissection. Our systematic review will focus on aortic arch dissection treatments (specifically of Stanford Type A, i.e. DeBakey Type I and Type II) using hybrid and open repair. Examining hybrid interventions treating aortic arch dissection will allow us to determine the effectiveness and safety of this technique over standard open repair.
Objectives
To assess the effectiveness and safety of a hybrid technique of treatment over conventional open repair in the management of aortic arch dissection.
Methods
Criteria for considering studies for this review
Types of studies
We will include randomised controlled trials (RCTs) and controlled clinical trials (CCTs) assessing the effects of hybrid repair techniques compared to open surgical repair (OSR) of aortic arch dissection.
Types of participants
We will include all participants with a diagnosis of aortic arch dissection. This will include classifications of dissection according to Stanford Type A (DeBakey Type I and Type II). Diagnosis will be made by relevant diagnostic modalities, i.e. computed tomography (CT) or Magnetic Resonance Imaging (MRI), or both. There will be no limitation on participant gender, age, ethnicity, treatment setting (e.g. elective versus emergency repair), or dissection chronicity (acute or chronic). Patients that required a concomitant aortic valve repair will be excluded.
Types of interventions
We will include the following comparisons:
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Type I hybrid repair versus OSR;
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Type II hybrid repair versus OSR; and
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Type III hybrid repair versus OSR.
Types of outcome measures
Outcomes will be guided and defined by the International Aortic Arch Surgery Study Group (Yan 2014; see also Table 1 for more details).
| Types of outcome measures | Defined by | Including |
| Primary outcomes | ||
| Mortality | Dissection related and all cause | (Grade V) All deaths at 30 days and 12 months |
| Neurological deficit | Global events | (Grade I ‐ IV) Postoperative agitation, delirium, obtundation, or myoclonic movements, without localised cerebral neurological signs |
| Focal events | (Grade I ‐ IV) Lateralising sensory or motor deficit or focal seizure activity | |
| Spinal neurological events | (Grade I ‐ IV) Paraplegia, paraparesis | |
| Cardiac injury | Myocardial ischaemia | (Grade I ‐ IV) |
| Low cardiac output syndrome | (Grade I ‐ IV) | |
| Arrhythmia | (Grade I ‐ IV) | |
| Pericardial effusion | (Grade I ‐ IV) | |
| Respiratory compromise | Parenchymal complications | (Grade I ‐ IV) Atelectasis, pneumonia, pulmonary oedema, and acute respiratory distress syndrome |
| Pleural complications | (Grade I ‐ IV) Pneumothorax, pleural effusion | |
| Renal ischaemia | Modified RIFLE classification (Bellomo 2004): Risk (I), Injury (II), Failure (III), Loss/End‐Stage Kidney Dysfunction (IV) | (Grade I ‐ IV) Serum creatinine increase, glomerular filtration rate (GFR) decrease, anuria, haemodialysis |
| Secondary outcomes | ||
| False lumen thrombosis | Partial or complete thrombosis | ‐ |
| Mesenteric ischaemia | Gut complications | (Grade I ‐ IV) Ileus or gastric paresis, gut ischaemia manifested as metabolic acidosis or increased lactate |
| Grades as defined by Yan 2014: Grade I: any deviation from the normal postoperative course but self‐limiting or requiring simple therapeutic regimens (including antiemetics, antipyretics, analgesics, electrolytes, and physiotherapy); Grade II: complications requiring pharmacological treatment for resolution; Grade III: complications requiring surgical, endoscopic, or radiological intervention but not requiring regional or general anaesthesia or requiring interdisciplinary intervention; Grade IV: complications requiring surgical, endoscopic, or radiological intervention under regional or general anaesthesia, or requiring new intensive care unit (ICU) admission or ongoing ICU management for > 7 days or hospitalisation for > 30 days, or causing secondary organ failure; Grade V: death caused by a complication. | ||
Primary outcomes
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Dissection‐related mortality and all‐cause mortality at 30 days and 12 months (Grade V)
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Neurological deficit (defined by global, focal and spinal events, Grade I to IV)
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Cardiac injury (defined by myocardial ischaemia, low cardiac output syndrome, arrhythmia, pericardial effusion, Grade I to IV)
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Respiratory compromise (defined by parenchymal and pleural complications, Grade I to IV)
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Renal ischaemia (defined by RIFLE classification Bellomo 2004, Grade I to IV)
Secondary outcomes
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False lumen thrombosis (defined by partial or complete thrombosis)
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Mesenteric ischaemia (defined by gut complications, Grade I to IV)
Search methods for identification of studies
We will apply no restrictions according to language.
Electronic searches
The Cochrane Vascular Information Specialist (CIS) will search the following databases for relevant trials.
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The Cochrane Vascular Specialised Register.
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The Cochrane Central Register of Controlled Trials (CENTRAL) via the Cochrane Register of Studies Online.
See Appendix 2 for details of the search strategy which will be used to search CENTRAL.
The Cochrane Vascular Specialised Register is maintained by the CIS and is constructed from weekly electronic searches of MEDLINE Ovid, EMBASE Ovid, CINAHL, AMED, and through handsearching relevant journals. The full list of the databases, journals and conference proceedings which have been searched, as well as the search strategies used, are described in the Specialised Register section of the Cochrane Vascular module in The Cochrane Library (www.cochranelibrary.com).
In addition, the CIS will search the following trial registries for details of ongoing and unpublished studies.
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ClinicalTrials.gov (www.clinicaltrials.gov).
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World Health Organization International Clinical Trials Registry Platform (www.who.int/trialsearch).
For the purpose of this review, we will also include studies published as abstracts only if we can extract sufficient information. In cases where insufficient data are published, we will first contact the trial authors to access required information. If data remain insufficient after contacting the trial authors, we will exclude the study from our review.
Searching other resources
We will search the reference lists of all included studies.
Data collection and analysis
Selection of studies
Two review authors (EPK and AE) will independently assess the titles and abstracts of each identified study. Both review authors (EPK and AE) will assess full texts of all studies categorised as included or unclear at title/abstract screening. If the review authors disagree on the inclusion or exclusion of a study, the reasons will be discussed. If there is no agreement between the two review authors, then we will discuss with a third reviewer (NH). Reasons for exclusions will be recorded in the 'Characteristics of excluded studies' table. We will describe the selection process in an adapted PRISMA flow chart (Liberati 2009).
Data extraction and management
Full‐text reports of the studies selected will be obtained and two review authors (EPK and AE) will independently extract data using an adapted data extraction form provided by Cochrane Vascular. If there is disagreement between the two review authors, issues will be resolved by discussion with a third review author (NH). For studies with duplicate or multiple publications (or both), we will collate all available data, presenting this as one study dataset.
We will aim to describe the studies according to the following:
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trial design;
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diagnosis of aortic arch dissection;
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demographic characteristics of participants;
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type of intervention (hybrid and open repair); and
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frequency of primary and secondary outcomes.
Assessment of risk of bias in included studies
Two review authors (EPK and AE) will independently assess the potential risks of bias in all included RCTs and CCTs using the Cochrane 'Risk of bias' tool (Higgins 2011). Each domain will be judged as low risk, high risk, or unclear risk of bias and we will provide a statement to support each judgment. If there is disagreement between the two review authors, these will be resolved by discussion, and if necessary, discussion with a third review author (NH).
We will assess the risk of bias in the following domains:
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selection bias (random sequence generation and allocation concealment);
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performance bias (blinding of participants and personnel);
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detection bias (blinding of outcome assessors);
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attrition bias (incomplete outcome data);
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reporting bias (selective outcome reporting); and
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other sources of bias.
Measures of treatment effect
Dichotomous data
We will express the results for dichotomous outcomes as risk ratios (RRs) with 95% confidence intervals (CIs), to reflect uncertainty of the point estimate of effects.
Continuous data
We will express the results for continuous scales of measurement as mean differences (MDs), standard deviation (SD) and associated 95% CIs. Where there is a difference in scales for the same outcome, we will use the standardised mean difference with 95% CIs to combine the outcomes.
Time‐to‐event data
Survival analysis will be used to present time‐to‐event data expressed as hazard ratios (HRs) with 95% CIs. Methods used to analyse time‐to‐event outcomes will be guided by those described by Parmar 1998 and Tierney 2007, and as detailed in Chapter 7, section 7.7.6. of the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011).
Unit of analysis issues
We will consider the unit of analysis within each trial to be each participant.
Dealing with missing data
In studies that have incomplete data, we will contact the study authors to seek additional data. For all outcomes, we will carry out analyses, as far as possible, on an intention‐to‐treat basis (i.e. based on the initial treatment assignment and not on the treatment eventually received).
Assessment of heterogeneity
We will evaluate clinical heterogeneity based on participant data, the intervention and outcomes of each study. We will assess the degree of heterogeneity by visual inspection of forest plots and by examining the Chi2 test for heterogeneity. We will use the I2 statistic, Tau2 statistic and Chi2 test to determine statistical heterogeneity among studies, according to the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011).
We will regard statistical heterogeneity as substantial if an I2 is greater than 50% and either the Tau2 is greater than zero, or there is a low P value (less than 0.10) in the Chi2 test for heterogeneity. If we identify substantial heterogeneity, we will explore possible reasons using subgroup analyses.
Assessment of reporting biases
We will address publication bias and other reporting biases (such as multiple publication bias) using funnel plots, as per Cochrane Vascular guidelines, if there are 10 or more included studies (Higgins 2011).
Data synthesis
We will enter the collected data into Review Manager software (RevMan 2014). We will use fixed‐effect meta‐analysis for synthesising data where it is reasonable to assume that trials are estimating the same underlying treatment effect. If there is clinical heterogeneity sufficient to expect that the underlying treatment effects differ between trials, or if substantial statistical heterogeneity is detected, we will use random‐effects meta‐analysis to produce an overall summary where the average treatment effect is clinically meaningful. If we identify clinical, methodological or statistical heterogeneity across included trials sufficient to cause concerns as to the appropriateness of pooling results, we will not report pooled results from the meta‐analysis but will instead use a narrative approach to data synthesis. We will create a forest plot for each treatment effect, as per Cochrane Vascular guidelines (Higgins 2011).
Subgroup analysis and investigation of heterogeneity
If considerable heterogeneity is identified within the included studies, we will carry out subgroup analyses to investigate possible reasons for this heterogeneity. In addition, we will also perform the following subgroup analyses, which will be guided by DISSECT, a mnemonic‐based approach to the categorisation of aortic dissection (Dake 2013).
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Duration of disease (i.e. acute dissection (less than 14 days) versus chronic dissection (14 days or more))
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Intimal tear location (i.e. ascending aorta versus aortic arch)
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Segmental extent of the disease (i.e. DeBakey Type I versus DeBakey Type II)
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Size of the dissected aorta (i.e. maximum diameter less than 5.5 cm versus 5.5 cm or more (Pape 2007))
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Presence or absence of complication
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Thrombosis of aortic false lumen
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Presence or absence of connective tissue disorder
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Gender (Nienaber 2004)
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Age (i.e. less than 70 years versus 70 years or older (Trimarchi 2010)
Sensitivity analysis
We will perform sensitivity analyses on the following:
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High‐quality trials, defined as studies with a low risk of bias for sequence generation and allocation concealment; and
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RCTs compared with CCTs.
Summary of findings
We will prepare a 'Summary of findings' table according to the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011). We intend to use GRADE profiler software to create the tables (GRADEproGDT 2015). For each comparator, we will include all primary and secondary outcomes as described in theTypes of outcome measures section. We have included an example table in this protocol (Table 2). Using the GRADE approach, we will assess the quality of the body of evidence for each outcome as high, moderate, low or very low, based on the criteria of risk of bias, inconsistency, indirectness, imprecision and publication bias (Atkins 2004; GRADE Working Group 2014, Guyatt 2008a, Guyatt 2008b; Schünemann 2006).
| Summary of findings for the main comparison: Hybrid repair versus conventional open repair for aortic arch dissection | ||||||
| Patient or population: patients with a diagnosis of aortic arch dissection Settings: hospital Intervention: hybrid repair Comparison: open repair | ||||||
| Outcomes | Illustrative comparative risks* (95% CI) | Relative effect | Number of Participants | Quality of the evidence | Comments | |
| Assumed risk | Corresponding risk | |||||
| Open repair | Hybrid repair | |||||
| Mortality, Follow up: median N (months) | Study population | HR N (N to N) | N | ⊕⊝⊝⊝ ⊕⊕⊝⊝ ⊕⊕⊕⊝ ⊕⊕⊕⊕ | ||
| N per 1000 | N per 1000 | |||||
| Neurological deficit, Follow up: median N (months) | Study population | RR N (N to N) | N | ⊕⊝⊝⊝ ⊕⊕⊝⊝ ⊕⊕⊕⊝ ⊕⊕⊕⊕ | ||
| N per 1000 | N per 1000 | |||||
| Cardiac injury, Follow up: median N (months) | Study population | RR N (N to N) | N | ⊕⊝⊝⊝ ⊕⊕⊝⊝ ⊕⊕⊕⊝ ⊕⊕⊕⊕ | ||
| N per 1000 | N per 1000 | |||||
| Respiratory compromise, Follow up: median N (months) | Study population | RR N (N to N) | N | ⊕⊝⊝⊝ ⊕⊕⊝⊝ ⊕⊕⊕⊝ ⊕⊕⊕⊕ | ||
| N per 1000 | N per 1000 | |||||
| Renal ischaemia, Follow up: median N (months) | Study population | RR N (N to N) | N | ⊕⊝⊝⊝ ⊕⊕⊝⊝ ⊕⊕⊕⊝ ⊕⊕⊕⊕ | ||
| N per 1000 | N per 1000 | |||||
| False lumen thrombosis, Follow up: median N (months) | Study population | RR N (N to N) | N | ⊕⊝⊝⊝ ⊕⊕⊝⊝ ⊕⊕⊕⊝ ⊕⊕⊕⊕ | ||
| N per 1000 | N per 1000 | |||||
| Mesenteric ischaemia, Follow up: median N (months) | Study population | RR N (N to N) | N | ⊕⊝⊝⊝ ⊕⊕⊝⊝ ⊕⊕⊕⊝ ⊕⊕⊕⊕ | ||
| N per 1000 | N per 1000 | |||||
| *The basis for the assumed risk (e.g. the median control group risk across studies) is provided in footnotes. The corresponding risk (and its 95% confidence interval) is based on the assumed risk in the comparison group and the relative effect of the intervention (and its 95% CI). | ||||||
| GRADE Working Group grades of evidence | ||||||
| Types of outcome measures | Defined by | Including |
| Primary outcomes | ||
| Mortality | Dissection related and all cause | (Grade V) All deaths at 30 days and 12 months |
| Neurological deficit | Global events | (Grade I ‐ IV) Postoperative agitation, delirium, obtundation, or myoclonic movements, without localised cerebral neurological signs |
| Focal events | (Grade I ‐ IV) Lateralising sensory or motor deficit or focal seizure activity | |
| Spinal neurological events | (Grade I ‐ IV) Paraplegia, paraparesis | |
| Cardiac injury | Myocardial ischaemia | (Grade I ‐ IV) |
| Low cardiac output syndrome | (Grade I ‐ IV) | |
| Arrhythmia | (Grade I ‐ IV) | |
| Pericardial effusion | (Grade I ‐ IV) | |
| Respiratory compromise | Parenchymal complications | (Grade I ‐ IV) Atelectasis, pneumonia, pulmonary oedema, and acute respiratory distress syndrome |
| Pleural complications | (Grade I ‐ IV) Pneumothorax, pleural effusion | |
| Renal ischaemia | Modified RIFLE classification (Bellomo 2004): Risk (I), Injury (II), Failure (III), Loss/End‐Stage Kidney Dysfunction (IV) | (Grade I ‐ IV) Serum creatinine increase, glomerular filtration rate (GFR) decrease, anuria, haemodialysis |
| Secondary outcomes | ||
| False lumen thrombosis | Partial or complete thrombosis | ‐ |
| Mesenteric ischaemia | Gut complications | (Grade I ‐ IV) Ileus or gastric paresis, gut ischaemia manifested as metabolic acidosis or increased lactate |
| Grades as defined by Yan 2014: Grade I: any deviation from the normal postoperative course but self‐limiting or requiring simple therapeutic regimens (including antiemetics, antipyretics, analgesics, electrolytes, and physiotherapy); Grade II: complications requiring pharmacological treatment for resolution; Grade III: complications requiring surgical, endoscopic, or radiological intervention but not requiring regional or general anaesthesia or requiring interdisciplinary intervention; Grade IV: complications requiring surgical, endoscopic, or radiological intervention under regional or general anaesthesia, or requiring new intensive care unit (ICU) admission or ongoing ICU management for > 7 days or hospitalisation for > 30 days, or causing secondary organ failure; Grade V: death caused by a complication. | ||
| Summary of findings for the main comparison: Hybrid repair versus conventional open repair for aortic arch dissection | ||||||
| Patient or population: patients with a diagnosis of aortic arch dissection Settings: hospital Intervention: hybrid repair Comparison: open repair | ||||||
| Outcomes | Illustrative comparative risks* (95% CI) | Relative effect | Number of Participants | Quality of the evidence | Comments | |
| Assumed risk | Corresponding risk | |||||
| Open repair | Hybrid repair | |||||
| Mortality, Follow up: median N (months) | Study population | HR N (N to N) | N | ⊕⊝⊝⊝ ⊕⊕⊝⊝ ⊕⊕⊕⊝ ⊕⊕⊕⊕ | ||
| N per 1000 | N per 1000 | |||||
| Neurological deficit, Follow up: median N (months) | Study population | RR N (N to N) | N | ⊕⊝⊝⊝ ⊕⊕⊝⊝ ⊕⊕⊕⊝ ⊕⊕⊕⊕ | ||
| N per 1000 | N per 1000 | |||||
| Cardiac injury, Follow up: median N (months) | Study population | RR N (N to N) | N | ⊕⊝⊝⊝ ⊕⊕⊝⊝ ⊕⊕⊕⊝ ⊕⊕⊕⊕ | ||
| N per 1000 | N per 1000 | |||||
| Respiratory compromise, Follow up: median N (months) | Study population | RR N (N to N) | N | ⊕⊝⊝⊝ ⊕⊕⊝⊝ ⊕⊕⊕⊝ ⊕⊕⊕⊕ | ||
| N per 1000 | N per 1000 | |||||
| Renal ischaemia, Follow up: median N (months) | Study population | RR N (N to N) | N | ⊕⊝⊝⊝ ⊕⊕⊝⊝ ⊕⊕⊕⊝ ⊕⊕⊕⊕ | ||
| N per 1000 | N per 1000 | |||||
| False lumen thrombosis, Follow up: median N (months) | Study population | RR N (N to N) | N | ⊕⊝⊝⊝ ⊕⊕⊝⊝ ⊕⊕⊕⊝ ⊕⊕⊕⊕ | ||
| N per 1000 | N per 1000 | |||||
| Mesenteric ischaemia, Follow up: median N (months) | Study population | RR N (N to N) | N | ⊕⊝⊝⊝ ⊕⊕⊝⊝ ⊕⊕⊕⊝ ⊕⊕⊕⊕ | ||
| N per 1000 | N per 1000 | |||||
| *The basis for the assumed risk (e.g. the median control group risk across studies) is provided in footnotes. The corresponding risk (and its 95% confidence interval) is based on the assumed risk in the comparison group and the relative effect of the intervention (and its 95% CI). | ||||||
| GRADE Working Group grades of evidence | ||||||
