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Non-Technical Skills For Surgeons

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Cardiac Surgery

Misc

Porcelain Aorta

Left pericardiotomy for prevention of POAF - Video

- Myocardial protection

Cardioplegia Review

Suboptimal cardioplegia delivery is a problem that results in short and long term cardiac dysfunction, primarily in the septum which is wholly subendocardial. The septum is responsible for about 80% of RV function and a considerable deal of LV function.

Delivery:

Antegrade vs retrograde (suboptimal with coronary stenoses vs unreliable for right protection) in vs mixed

Warm vs cold (vs ischemic protection)

Continuous vs intermittent (optimal protection vs bloodless surgical field)

Hot shot - Controlled reperfusion with 3-5 minutes of warm cardioplegia before releasing clamp, shown to reduce mortality.

Solution:

Blood vs crystalloid (Blood is superior, oxygen delivery, limitation of hemodilution, buffering)

Meta analysis: Decreased Low Output Syndrome (OR 0,54), reduced CKMB release, similary MI and mortality)

Polarizing vs non polarizing

Strategy

Integrated method - Mix of antegrade/retrograde, warm induction -> cold cardioplegia -> Hot shot, intermittent/continuous. Shown to minimize mortality and post op cardiac dysfunction

Warm induction - Active resuscitation for energy depleted hearts before asystole. Seems to lower mortality in marginal hearts

Retrograde cardioplegia - Technique

- CPB

Canula Sizes

Hage - Hypothermic circulatory arrest: >24 degrees is better than below, antegrade or retrograde cerebral perfusion is protective against death and stroke

Cytosorb - 60 patients - Mitral endocarditis, retrospective, Post op sepsis:16,7/39,3%, Sepsis mortality: 0/17,9%, Mortality 10/17,9%,

Anti thrombin 3 for Heparin Resistance - AT3 MOA: Natural anticoagulant, inhibits thrombin and other factors, activity enhanced by heparin.
Heparin resistance = Failure to achieve ACT 600 with 600 U/kg heparin (skv fyrstu greininni). Solved with 500-1000 U of antithrombin III. Antithrombin is present in FFP as well.
Mechanism of heparin resistance: Subnormal AT3 activity due to acquired AT3 deficiency resulting from prior heparin exposure

- Technical

Needle types - Rb-2 (Minni) og V-7 (stærri)

IABP

- Complications

DSWI - 1-3% sjúklinga

Iatrogenic Aortic Dissection: 0,06% of ascending aortic cannulation, 0,6% in femoral cannulation and 0,5% axillary cannulation. Mortality is estimated at 30%.

- Pre op tölur

-Post Operative

ERAS in cardiac surgery

Post operative atrial fibrillation and anticoagulation: New onset POAF after CABG vs NVAF, cohort. Anticoagulation:8,4%/42,9%, Thromboembolism HR: 0,67, thromboembolism risk was similar for postop patients with or without POAF. New onset POAF after CABG does not need anticoagulation.

Postcardiotomy syndrome - Systematic Review: Retrospective studies,

Definition: 2 of 5 criteria (new or worsening pericardial effusion, new or worsening pleural effusion, fever without an alternative cause, pleuritic chest pain, pleural/pericardial rubbing)

Median incidence: 16%, unclear pathophysiology, higher incidence with younger age, lower BMI and history of pericarditis

EACTS perioperative medication guidelines:

Aspirin: Decreased early mortality after CABG (1,3%/4,0%), myocardial infarction (2,8%/5,4%), stroke (1,3%/2,6%), renal failure (0,9%/3,4%)

Rec: Preoperative and early postoperative administration of ASA, continued indefinitely (Clopidogrel is an acceptable alternative)

CABG

EACTS guidelines on myocardial revascularization

Precondition with Levosimendan in low cardiac output (EF>40%) patients (n=54)

48 hour preconditioning, infusion without loading dose. Historic cohort compared with prospective cohort (Simdax arm)

Simdax/Control - Postop low cardiac output (15,4%/61%), shorter ICU LOS (2d/4d)

- Technical

OPCAB

MIDCAB LIMA-LAD Video

Coronary endarterectomy technique and postoperative treatment - Video

Total arterial revasc - Technique

LIMA harvesting Video

Radialis harvesting - Technique

Video

Radialis primer

Harvesting of the Gastroepiploic Artery

Intraoperative Graft Patency Validation

TTFM (Flödemätare): Flow: Acceptable >20 mL/min, Pulsatility Index (resistance measure): Ideally <3, acceptable <5

The Use if Intraoperative Transit Time Flow Measurement for CABG - Systematic review & Expert opinion

Pulsatility Index (PI): Delta(peak flow & minimum flow)/Mean graft flow. Represents an estimate of flow resistance
Put probe on the grafts perpendicularly, that is: on a straight graft, without the graft bending
Interpretation of TTFM should happen in the context of what was expected (size of runoff and so on)
Place probe distally if possible
A MGF of >15-20 ml/min and PI <3 (<5 for RCA) Should prompt suspicion of graft malfunction

- Patient Selection

State-of-the-Art Coronary Artery Bypass Grafting - Review

EACTS 2018 guidelines

Gaudino et al - CABG vs PCI - Meta Analysis all RCTs, N: 13 260, follow-up: 5,3 yrs, HR all-cause mortality 1,17, cardiac mortality 1,24

Sabatine et al - CABG vs PCI Left main, all RCTs, N: 4394, 5 year mortality 10,2% vs 11,2%, 0,2% difference per year. Higher risks of repeat revasc or myocardial infarction, no difference in stroke

Left main disease

NOBLE - PCI vs CABG for left main stenosis - at 5 years (2020)

600 vs 600 patients. MACCE 28% vs 19%, mortality 9% vs 9%, Later myocardial infarct 8% vs 3%, repeat revasc 17% vs 10%

EXCEL - PCI vs CABG for left main stenosis - at 5 years (2019)

950 vs 950 patients, low or intermediate complexity. Mortality 13% vs 9,9% (NS), stroke 2,9% vs 3,7% (NS), repeat revasc 16,9% vs 10%

PCI or CABG for left main coronary artery disease: the SWEDEHEART registry - (2023)

Retrospectively, all patients undergoing PCI or CABG for left main stenosis, Sweden 2005-2015 (11 137 pts). IPW analysis, Mortality HR 1,5, MACCE HR 2,8.

EACTS/ECS LM recommendations: Review of NOBLE/EXCEL as well as review of PRECOMBAT/SYNTAX


Multivessel disease

SYNTAX - 1800 patients, RCT, 3 vessel disease and/or left main disease, CABG or PCI with 1st gen DES (MACCE includes repeat revasc)

1 yr follow up (2009) (CABG/PCI): Death (%) 3,5/4,4 (NS), MACCE (%) 17,8/12,4, Stroke (%) 2,2/0,6, Repeat revasc (%) 13,5/5,9

3 yr follow up (2011) (CABG/PCI): Death (%) 6,7/8,6 (NS), MACCE (%) 20,2/28,0, Stroke (%) 3,4/2,0 (NS), Repeat revasc (%) 10,7/19,7

5 yr follow up (2013) (CABG/PCI): Death (%) 9,2/14,6, MACCE (%) 24,2/37,5, Stroke (%) 3,5/3,0 (NS), Repeat revasc (%) 12,6/25,4

10 yr follow up (2019) (CABG/PCI): Death (%) 24/28 (NS)

Freedom trial - RCT, 1900 patients with diabetes and multivessel disease, CABG vs PCI (DES)

2 yr follow up (2012) (CABG/PCI): RCT, N:1900, Median follow-up 3,8 yr. Death (%) 10,9/16,3, MACCE (%) 18,7/26,6, Stroke (%) 5,2/2,4, Later Myocardial Infarction (%) 6,0/13,9

10 year follow-up (FREEDOM Follow-On study) (2019) N: 943, Mortality HR 1,36 , 23,7%/18,7%

FAME 3 - RCT, 1500 pat with 3VD (CABG/FFR guided PCI)

1 year follow-up (2021) Composite (death, myocardial infarction, stroke) 6,9%/10,6% (HR 1,5), Death 0,9%/1,6% (HR 1,7), Stroke 1,1%/0,9% (HR 0,9), Repeat revasc 3,9%/5,9% (1,5)

Left Ventricular Dysfunction

STICH Trial - RCT, 1212 patients with EF => 35% and CAD (2002-2007) randomized to CABG or medical therapy

5 yr follow up (2011) - Death (%) 36/41 (NS), Cardiovascular death (%) 28/33

10 yr follow-up (2016) - Death (%) 58,9/66,1, Cardiovascular death (%) 40,5/49,3

REVIVED trial - RCT, 700 pts with EF <35%, PCI vs medical therapy

No mortality difference (31,7% vs 32,6% mortality at 41 month follow up)

Completeness of revascularization

Post hoc Syntax Extended Study: PCI vs CABG, more often incomplete revasc in PCI (56,6%/36,8%)

Increased 10 yr mortality with incomplete revascularization with PCI compared with CABG(33,5%/23,7%)

Retrospective, weighted analysis of completeness of revascularization

889/2467 patients (incomplete/complete revasc) - 5 yr survival 82,1% vs 86,5%

Stable Angina

ISCHEMIA trial: RCT, N: 5200, Conservative vs invasive (PCI 75%/CABG 25%) for stable angina, no difference in mortality at 3,2 years follow-up



- Conduits

Conduit selection:

SVG

CABG RCT APT vs DAPT: 1 year SVG failure rate was around 12-14%

Aortocoronary Saphenous Vein Graft Disease - 6/10 year patency of SVG - 75%/60%

No touch versus conventional SVG: RCT, N:2655, Outcome: CT angio occlusion at 12 months (3,7% vs 6,5%, OR 0,56), Recurrence of angina (OR 0,55)

LIMA

LIMA vs SVG: N: 6000, 10 year mortality 93,4%/88 % fyrir 1 vessel disease, 90%/79,5% f 2VD, 82,6%/71,0% f 3VD, RR for mortality 1,61

MIDCAB Technique - Video

BIMA

BIMA (ART trial) - BIMA vs LIMA, N: 1548. Enginn mortality munur vid 10 ar, enginn munur á composite outcome vid 10 ar, Crossover meaning that as-treated analysis showed a HR of 0,81

Radialis

10 yr follow up: a. Radialis compared with SVG, Composite death/Myocardial infarction (HR 0,77), Death (0,73) (Post hoc), myocardial infarction (HR 0,74), repeat revasc (HR 0,62)

RAPCO trial: 394 pat <70 yr randomized between RITA and a. Radialis for second graft and 225 pat <70 yr RA vs SVG

10 year patency (RITA/RA) 80%/89% (HR 0,45 for graft failure), 10 yr survival 83,7%/90,9% (HR 0,53 for 10 yr mortality)

10 year patency (SVG/RA) 71%/85% (HR 0,40 for graft failure), 10 yr survival 65,2%/72,6% (HR 0,76 for 10 yr mortality)

15 year patency (RITA/RA) 15 yr survival 70%/78% (HR 0,69)

15 year patency (SVG/RA) 15 yr survival 37%/48% (HR 0,74)

Radial artery vs SVG: Meta analysis, 1036 patients, mean follow up 5 years, lower risk of occlusion (HR 0,44), myocardial infarction (HR 0,72) and repeat revasc (HR 0,5) but not death (0,9)

Gaudino et al: Meta analysis, N: 1000, median follow up 10 years, Composite OR 0,73, Death HR 0,73

Any Arterial

Rocha et al - Retrospective, prop match, arterial vs SVG: 2132 patient pairs - Óbreytt early mortality, MACCE RR: 0,78, death RR: 0,8, reinfarct RR 0,69

TAG


Velja arterial grafting hja yngri sjuklingum med high grade stenosis (eykur patency a arterial gröftum)


FFR and CABG

FFR should not control graft targets but may be of use in conduit selection. Stenoses with a highly significant FFR gradient are more amenable to arterial grafts than borderline significant stenoses, which should probably receive SVG


Intracoronary stent restenosis - UpToDate

BMS > Usually develops restenosis early, 6-12 months - 12-14% requires reintervention at one year, HR after that 1,7% annually

DES > 1st gen restenosis rate 13-16% at 5 years, 2nd gen restenosis rate 5-6,3% at 5 years


Endoscopic vs conventional SVG - Ekki significant munur á primary outcome né fótasýkingum

Mechanisms of graft failures

Vein mapping of the Saphenous Vein - Technique

- Prognosis

Aortic valve

- Technical

Aortic Root Enlargement - Nicks/Manougian

Aortic annular enlargement - Y incision (modified Nicks)

David Aortic root reconstruction - Incl how to make the coronary buttons

Video

- Patient selection

Asymptomatic severe aortic stenosis - Intervention of conservative care - RCT, N:145, asymptomatic patients with very severe aortic stenosis

Minna mortality með aðgerð en conservative, 6 ára follow up, Mortality 7% vs 21%, favouring surgery

Severe aortic stenosis, RCT, Intermediate risk patients(4-8% 30d mortality) (Partner 2, sponsored by TAVI company):

More crossover in surgery group (7,5%vs 1,7%)

2 year: (sAVR/TAVI%): Death 18/16,7, stroke 8,9/9,5, Aortic valve reintervention 0,5/0,7, A fib 27,5/11,5

5 year: (sAVR/TAVI%): Death 42,1/46, stroke 12,5/15,3, Aortic valve reintervention 0,8/3,2, A fib 30,4/15,8

Severe aortic stenosis, RCT, low-risk patients (<4% 30d mortality) (Partner 3, sponsored by Edwards)

1000 patients, TAVR vs sAVR, 8,6% withdrawal from sAVR group, 1,4% from TAVR group, concomitant procedures in 26,4% sAVR group, 7,9% TAVR group, mean age 73 years, STS score 1,9%

1 year: (sAVR/TAVR%): Death 2,5/1,0 (NS), Stroke 3,1/1,2 (NS), Death or disabling stroke 3,1/1,0, composite endpoint (death, stroke, rehospitalization) 15,1/8,5

2 year: (sAVR/TAVR): Death 3,2/2,4 (NS), Stroke 3,6/2,4 (NS), Death or disabling stroke 3,8/3,0 (NS), composite endpoint (death, stroke, rehospitalization) 17,1/11,5

Study outcome variables are diverging, The Mean gradient is statistically but not clinically significant (11,8/13,6), favoring surgery, PVL 2,3/26,0

5 year: (sAVR/TAVR): Death 8,2/10 (NS), Stroke 6,4/5,8 (NS), Death or disabling stroke Not reported?, composite endpoint (death, stroke, rehospitalization) 27,2/22,8 (NS)

Severe Aortic Stenosis, RCT, Low-risk patients (Evolut Low Risk). STS score 1,9-2. 1400 patients

4 year: (sAVR/TAVR): Death 12,1/9,0 (NS), Stroke 3,8/2,9 (NS), Composite (Death/Stroke) 14,1/10,7

Severe aortic stenosis, STS Registry, Low-risk patients, 42 500 patients, 8 year follow-up

Same inclusion criteria as Partner 3/Evolut Low Risk. 1, 3, 5, 8-year mortality (2,6%, 4,5%, 7,1%, 12,4%). Dramatically less than industry-sponsored RCTs

Severe aortic stenosis, RCT sAVR/TAVI, intermediate-risk patients (STS 4,5±1,6%, 79,8±6,2 years), N: 1660 (SURTAVI)

2 year follow-up: Mortality 11,6%/11,4% (NS), Stroke 8,4%/6,2% (NS)

5-year follow-up: Presented at TCT 2021, Mortality 30,8%/31,3% (NS)

Severe aortic stenosis, RCT, >69 years, all-comers (Notion): TAVI/sAVR, 280 patients, 79,1±4,8 years old, STS score 3±1,7%

1 year follow-up: Mortality 4,9%/7,5% (NS), Stroke 2,9%/4,6% (NS)

5-year follow-up: Mortality 27,6%/28,9% (NS), Stroke 9%/7,4% (NS), Lower gradients in TAVI group, 8,2% developed moderate/severe AI vs none in surgical group, more pacemakers in TAVI group, more atrial fibrillation in sAVR group

10-year follow-up: Mortality 62,7%/64,0% (NS), Stroke 9,7%/16,4% (NS) More severe SVD in SAVR group (10% vs 1,5%), more PVL in TAVI (18% vs 5,2%). Same IE risk, 7,3%

Meta analysis of 6 RCTs, >6 000 patients, TAVI/SAVR

Lower 1 year mortality, HR 0,85

Superior results after 40 months, for SAVR. HR 1,31 (40-60 months)

- Prosthesis/Technique selection

mAVR/bAVR in non-elderly - Minnkað life expectancy með báðum týpum

bAVR - Mortality risk: 2,39%/year, reintervention: 1,82%/year, structural valve deterioration 1,59%/year, thromboembolism 0,53%/year, endocarditis: 0,48%/year,

mAVR - Mortality risk: 1,55%/year, thromboembolism: 0,9%/year, major bleeding:0,85%/year, non-structural valve deterioration: 0,49%/year, endocarditis: 0,41%/year, reintervention: 0,51%/year

Expected durability of biological aortic valves:

Structural valve deterioration: A gradual process of dysfunction secondary to stenosis (40%), insufficiency (30%) or a combination (30%). No universal definition but basically a new severe stenosis (calcification and pannus) or insufficiency (Leaflet tear)

Pericardial valves have a tendency to develop stenosis, porcine valves insufficiency

Risk factors for SVD: Younger age at implantation, hypercalcemia, hyperphosphatemia, renal failure, arterial hypertension, PPM (increased stress on valve), larger BSA, diabetes, smoking,

Surgical bioprosthesis freedom from SVD: 10 year 90,2%, 15 year 73,7%, 20 year 60%

Operative risk for aortic valve replacement reoperation is between 5,8-12,8%,

Valve in valve TAVI after SVD: 1 year mortality of 15%, 30 day at 8%, 95% success rate

Aortic valve sparing vs composite: Mean follow-up 5,8 ár

Same early mortality, bleeding, MI, thromboembolism

Significantly less late mortality with AVS (RR 0,68), Thromboembolism/Stroke (0,36) and bleeding (0,21)

ON-X Valves - Reduced Anticoagulation regiment: RCT, N=190 usual Warfarin regiment (2-3), N=185 INR 1,5-2,0 + 81 mg Aspirin

3,82 years of mean follow-up, major bleeding 3,26/1,48%/pt-yr, minor bleeding 3,41/1,32%/pt-yr, stroke 0,74/1,12%/pt-yr (NS), TIA 1,33/0,79%/pt-yr (NS)

Aortic Valve Repair Techniques

Concepts of Bicuspid Aortic Valve Repair

- Prognosis

PPM - Aukið renal failure, stroke og late mortality með moderate og severe PPM (x1,5 og x2,5)

PPM review - PPM er algengt og hættulegt, líklega hættulegast early post op þegar vi slegill er viðkvæmastur

Bicuspid aortic valve - Heritability ca 10% i 1° ættingjum, ca 10x líklegra í nánum ættingjum, 0,5-2,0% almennri population

Woldentorp et al - Syst review/Meta analys of TAVI patients - 3456 patients, 11,5% had subclinical valve thrombosis, that group had 3x the risk of stroke

Reop after TAVR - 123 patients, retroactive series on TAVR patients surgically reoperated - Mortality 17,1%, Observed mortality was higher than predicted STS score mortality

Pannus occurence on mechanical valves - Retrospective, 862 pat,
Incidence: 10 yr:0,3%, 20 yr: 5%, 25 yr: 9,9%
Risk factors: Small prosthesis (HR 0,74), Young age (HR 0,94), concomitant mitral valve replacement (HR 3,863)

Ross procedure outperforms mechanical and biologic valves

Left ventricular remodeling after aortic valve surgery: N:211, 63% AS/37% AI, -> SAVR -> Echo follow-up 1,2 and/or 5 yrs
Both groups showed left ventricular mass regression, mostly by 1 year

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Mitral Valve

Anatomy

10 Commandments of Mitral Valve Surgery

5 tips for mitral surgery - Video

Guiraudon Atriotomy

Operative approaches to the left atrium and mitral valve

MitraClip - A Guide For Surgeons

- Patient selection

Functional Mitral Regurgitation

AHA/EACTS Guidelines:

Class I: Surgery is indicated in patients undergoing CABG and with EF <30%, with severe functional MI

Class IIa: Surgery should be considered in patients with symptomatic, severe secondary MI and who have an indication for revascularization as well as evidence of viable myocardium

Class IIb: Surgery may be considered in patients without indication for revascularization, with symptomatic, secondary MI and EF<30%, as well as low risk for surgery

Tricuspid valve

Diagnosis and management of tricuspid disease

Concomitant tricuspid repair, with mitral surgery

RCT, 400 pat, MMVP vs MVP/TVP in patients with MI and either moderate TI or anular dilatation

Lower 2 yr mortality, HR 0,69

Pulmonary Artery/Valve

Pulmonary artery aneurysms - No guideline recommendations, treat as aortic

PA reconstruction


Techniques

Subaortic stenosis

Modified Konno and myectomy

Konno video

Aortic Surgery

- Pathophysiology

  • At the end of ventricular ejection, the pressure in the aorta falls much more slowly than in the left ventricle because the large central arteries, and particularly the aorta, are elastic and thus act as a reservoir during systole, storing some of the ejected blood, which is then forced out into the peripheral vessels during diastole (Windkessel effect).

  • Both ventricles of the heart contract together during a phase called ventricular systole, ejecting close to 140 mL of nearly incompressible blood from the adult human heart. This volume must be taken up by an expansion of the remainder of the circulatory system. Therefore, by necessity, the vasculature must be compliant to avoid rupture

- Aneurysm

Natural evolution of aortic aneurysms

Mean annual growth rate 0,1 +- 0,01 cm/yr. Rarely over 0,2 cm/yr

10 yr survival free from Adverse Aortic Events: <4 cm(97,8%), <4,5 cm (98,2%), <5 cm (97,3%), <5,5 cm (84,6%), <6 cm (80,4%), >6 cm (70,9%)

- Techniques

Linear Reduction Aortoplasty: Technique & results. (716 patients, retrospective)

No good data, retrospective data shows 3% redilatation rate, acceptable long term results, less mortality

Recommendations: Asc aorta <6cm, reduce to under 3,5cm, isolated aneurysm in asc, no patients with connective tissue disorders, patients with stenosis (CTD more likely with AI), if wrapped with Dacron graft -> anchor graft, ideal for patients who would not tolerate a longer operation

Open Repair of Thoracoabdominal Aortic Aneurysm

FET, FET2

Neurological Complications: N:3154. Spinal ischemia 4,7%, 7,6% stroke, 8,8% operative mortality. A stent lenght of greater than 10 cm is a risk factor

- Aortic Dissection

2021 AATS Aortic Dissection Guidelines

Early mortality in ATAAD: 1996-2018, Surgical mortality at 48 hours, 4,4% (1% died before operation), 48 hour mortality with conservative treatment was 23,7% (,5% per hour)

Prognostic Factors:

Operative mortality 30%

Malperfusion presents in 16-33% of patients, pat with malperfusion and severe acidosis have a mortality rate of 92%

Mesenteric malperfusion syndrome (malperfusion with indicators of end-organ ischemia) has an operative mortality of 60% or higher, many groups delay definitive treatment until after perfusion has been restored (endovascularly) with good results (89% op mortality vs 25%)

Cerebral malperfusion occurs in 7-15% of patients with a type A dissection -> Higher mortality and risk of stroke. The best strategy is probably early intervention and deficits have been shown to reverse postoperatively.

Hemorrhagic conversion of cerebral ischemia occured in only 5% of patients

Presenting with coma is not indicative of a worse neurologic outcome (although mortality is higher)

Prior cardiac surgery does not seem to be protective from tamponade and rupture risk

Resuscitation longer than 15 minutes increases mortality by a factor of 8,27

Non-A Non-B Dissection (Aortic arch eða type B með retrograde involvement of arch) - 14% 30D mortality með medical treatment, 3,6% með intervention og stroke 2,8%

Technique


Mechanical assist

LVAD

Left Ventricular Assist Device Implantation and Management: How I Teach It

Heartmate 3: Implantation Technique

LVAD: Numbers, indications

ECMO

Baldetti - LV offloading improves outcomes with VA-ECMO (OR 0,54), Preload reduction (LV vent, Impella) is the better strategy (OR 0,34) than afterload reduction (IABP)

Misc

Long Term Assist Guidelines - Non-reversible, NYHA IIIB-IV, EF <25% + sequele,

Arrhytmia surgery

Guidelines - Allt IIa/B indications, success decreases with left atrial diameter

Pathophys review - Rationale for placement of lesions

Maze Technique - Video

Hybrid ablation - CONVERGE trial - RCT, N: 153, Patients with any atrial fibrillation/any LA size, Hybrid Convergent Ablation (subxiphoid epicardial + catheter endocardial ablation) vs Catheter Ablation

Primary Endpoint: freedom from AF at 12 months: 68%/50%

Concomitant Atrial Fibrillation -

  • 2 pathophysiologic causes make surgery possible: The trigger foci that usually exist in the pulmonary veins, and the fact that fibrillation is maintained by macro re-entry circuits readily amenable to ablation

  • Indications: Symptomatic vs prognostic

    • Prognostic must be affected by the return of normal atrial function after surgery, which is decreased in patients with very large atria and persisting atrial fibrillation

  • Evidence:

    • Results at least double the effect of antiarrhythmic therapy, around 60% vs 24% with concomitant medical therapy

  • Lack of evidence:

    • Decreased mortality/stroke with antiarrhythmic therapy?

    • Return of normal atrial function after surgery? (Should at least be confirmed by ultrasound before stopping anticoagulants)

Left atrial appendage closure

LAAOS III: RCT, N: 4800, atrial fib patients, Left atrial appendage closure vs control. Follow up 3,8 years. Stroke/Systemic embolism HR 0,67, mortality NS

Gutierrez et al - Meta-analysis 280 585 patients, preoperative atrial fibrillation, surgical closure of LAA

Significantly reduced early stroke (RR 0,67) & late stroke (RR 0,71)

Patients with high burden of disease (>70% in atrial fibrillation) have the most utility

Long term mortality decreased with LAAc (RR 0,72)

AtriClip technique - Video

Complex & misc techniques

- PFO

PFO vs ASD - Failure of closure vs failure of tissue formation (ASD usually bigger)

PFO closure results - Retrospective analys - Intraop PFO, enginn munur a stroke eða mortality, ef lagað -> aukið stroke risk x2,5 - 2,8% vs 1,2%)

AAN Guidelines - PFO is found in 1/4 of the general population. In patients <60 yrs with prior embolic infarct and no other mechanism of stroke -> PFO closure recommended due to absolute stroke recurrence risk reduction of 3,4% at 5 yrs.

- Technical

Commando/UFO procedure + Cleveland

Video

The Ross Procedure

Modified Ross procedure - Standard með Dacron graft til styrkingar utan um

The Ozaki Procedure

Aortic valve repair: State of the art (Technique)

Surgical Aspects in Carcinoid Heart Disease

Aortic root replacement and reconstruction in destructive endocarditis

Femoral Cannulation

Axillary Cannulation, 2

Samurai cannulation - Þegar óljóst með falska/sanna lumen til cannyleringar

- Video

Transapical Cannulation

Wire skills for surgeons (video)

Clampless cardioplegia (Total body)

HOCM

Septal Myectomy

Long term survival better with surgical approach 5 yr (HR 1,31), 10 yr (HR 1,68)

The Cabrol Procedure - For achieving tensionless suture lines during coronary reimplantation

Cabrol patch for persistent bleeding from aortotomy

Dissection of the interatrial groove (Sondergaards)

Application of AtriClip (Video)

Pericardiectomy

Surgery for post-infarction free wall rupture

65,7% in-hospital survival, among survivors 5-& 10 year survival rates were 81% & 75%

Post-infarction VSD

Post op in-hospital/30d mortality 43%.
18,4% mortality if operated on after a week vs 54,1% if operated on within the week
87% mortality rate if in cardiac shock
For survivors, 1, 5 & 10 year mortality was: 91%, 75% & 31%

Post infarct VSD operation

- Video

Technique - Repair of posterior VSD

Dor Procedure for left ventricular aneurysm

Surgical techniques

Surgical technique

Video

- Zebras

Carney complex (Not Carney Syndrome): Multiple benign tumors most often affecting the heart, skin, and endocrine system. Endocrine abnormalities, skin pigment abnormalities, and cardiac myxomas.

Management of Coronary Artery Aneurysms:

Correlated with increased mortality and MACE

MACE Events decrease with anticoagulation

Indications for surgical intervention: Left main, multiple aneurysms, >20 mm, >4x reference vessel, SVG aneurysm (post CABG)

Surgical treatment: Open suture ligation and bypass,

 Lung Surgery

Misc

- Postop air leak

Pathophysiology of air leak - Air leak >5 days: Lobectomy 8,6%, segmentectomy 6,7%, wedge 3,5%

- Air leak after segmentectomy - Propensity score matched historical cohort (N=42)

Patients with persistent air leakage after segmentectomy treated with chemical pleurodesis have worse post operative pulmonary function than those treated conservatively

FVC at 12 months -20,8% vs 6,8%, FEV1 at 12 months 19,6% vs 9,7%

Cancer surgery

- Patient Selection

Lung Cancer Staging

- Prognosis

Thor årsrapport 2018 - Lung cancer surgery

Mortality: Total 30D: 0,9%, Pulmectomy:2,3%, Bilobectomy: 1,1%, Lobectomy: 0,5%, Segment: 0,4%, Wedge: 0%

Complications: Reop: 4,4%, Air leak: 9,1%

5-Year survival: 65%, IA: 79%, IB: 70%, IIA: 55%, IIB: 50%, IIIA: 40%,

Metastatectomy: 5 year survival 52%

Metastatectomy:

PulmICC - (RCT 93 pat, 1-6 metastases) - Op/NoOp - median survival 3,5-3,8 yr, HR 0,93 (NS)

Dutch Lung Cancer Registry 2020 - (Historic cohort 2012-2017, 2090 pat) Primary, Colorectal 52%, Urogen 14,2%. 80% Single metastasis. 30d mortality 0,7%

Pneumothorax

- Patient Selection

Trauma PTX - Conservative meðferð gengur vel með <35 mm spalt, mælt á CT (96% sjúklinga klára conservative treatment)

Spontaneous PTX - RCT á unilateral miðlung til stórum PTX (>32% samfall) sýndi non-inferiority með conservative treatment við 8 vikur
(Conservative: Ekkert dren, 4 klst obs og ný rtg eftir það ekki aukinn PTX né mikil einkenni, 15% treatment failure)

- Prognosis

Pleurodesis with Talc powder vs slurry - Enginn munur, 22-24% failure rate at 90 days

Empyema

20-40% of hospitalized pneumonias develop parapneumonic effusion, 5-10% of those develop empyema 1 2

ABX therapy is recommended for at least 2 weeks from time of drainage

Stages:

Stage I: Exudative (Parapneumonic effusion)

Stage II: Fibrinopurulent (Pus, positive bacterial cultures, fibrous pockets)

Stage III: Organizing (Pleural peel forms, hemithoracal contraction and rib space narrowing)

Thoracocentesis for drainage is not recommended, pleural drain placement is

Image guided small bore catheters are recommended for loculated effusions in patients who are not surgical candidates

Chest tube placement should be followed by a CT to confirm adequacy of drainage, undrained fluid should prompt more aggressive management

Drain flushing is considered routine, due to high likelihood of drain obstruction

Fibrinolytic therapy with Alteplase and a DNase can decrease the need for surgical intervention

Surgery

2 goals: Evacuation and Expansion

Video

VATS should be the first-line approach in patients with acute empyema without an organized pleural peel (stage II) who can tolerate single lung ventilation

Extensive resection is to be avoided, because bronchial stumps in infected fields are prone to fistulization

Tissue flaps (muscle or omentum) can be used to fill space when total expansion is not achieved

Thoracoplasty with rib resection may be conisidered for difficult cases, open thoracic window +- VAC treatment is another option

Post pulmectomy empyema

Prompt intervention is recommended to rule in or out the diagnosis

An aggressive surgical approach is recommended

 Thoracic Surgery

Congenital deformities

Pectus Excavatum

Nuss bars and MRI

Thymus resection

- Patient selection and prognosis

Myasthenia gravis:

Cochrane Analysis, nonthymomatous, 2013: No RCT articles to review

126 Pt RCT, nonthymomatous, 2016. Lower Quantitative Myasthenia Gravis score over 3-yr (6,15/8,99), Lower Prednisolone dose (32 mg/54 mg), Lower need for other immunosuppression (17%/48%), Decreased hospitalization (52%/23%), -life threatening events (12%/2%)

- Technique

VATS thymectomy

 Thoracic Transplantation

Scandiatransplant figures: Sahlgrenska 2019, 40 lungs (30 DL, 10 SL), 33 hearts

Acute transplant complications

Immunology

Rejection is usually considered to be antibody mediated, throught HLA mismatch (Clinical guide to heart transplantation)

- Donor Specific Antibodies

Pre-transplant (due to pregnancy, blood transfusion, previous transplant) 3-11% or de novo (10-30% of recipients after transplant, worse prognosis)

Risk factor for antibody mediated rejection and mortality

Mean fluorescence intensity (MFI) - Measure of DSA levels. ≥5000 is recognised as a risk factor

- Human Leukocyte Antigens (HLA)

Cell surface proteins that present intracellular peptides to leukocytes (eg viral)

Crucial in differentiating self from non-self

More than 14.000 alleles have been identified, not everybody has the same types of HLA molecules

Mismatch is common, some are serious, some are inconsequential

Class I: HLA-A, HLA-B, HLA-C (Primarily intracellular antigens, present on every nucleated cell)

Class II: HLA-DR, HLA-DQ, HLA-DP (Primarily extracellular antigens, present on lymphocytes and antigen presenting cells)

Antibody production can be stimulated by sensitizing events such as pregnancy, transfusion and previous transplant.

Antibody isotypes show varying capability of activating the complement pathway: IgG3>IgG1>IgG2>IgG4

Non HLA antibodies have also been implicated in rejection

Diagnostics

- Microlymphocytotoxic assay

Developed in 1964, the first standard test for determining antibody types present, A way of testing recipient serum against a panel of HLA-typed lymphocytes.

- Complement-dependent cytotoxicity (CDC) assays - to evaluate the ability of recipient serum to lyse a pool of T or B cells. Can not differentiate between IgG and IgM, nor HLA classes. Only shows HLA-antibodies that activate the complement system.

- Luminex Assay, next gen HLA test, developed in the early 2000s. Luminex beads with a single HLA antigen on different coloured beads. Can differentiate between HLA classes and quantify strength of response (antibody binding), represented by MFI (Mean Fluorescence Intensity). Does not differentiate between complement activating antibodies and those that do not activate the complement system.
The C1q variation introduces the first step of the complement cascade and can differentiate between complement activating antibodies and non-activating.

Virtual Crossmatching:

Solid phase assays identify and measure strength of antibody binding to different HLA antigens, mapping the HLA antibody profile of the recipient and then comparing to the donor HLA profile (HLA typing). The primary benefit as opposed to crossmatching, is that there is no need for recipient blood to be present at the donor hospital.

Calculated PRA (Panel Reactive Antibodies)

The cPRA value represents a percentage of a given population that the recipients anti-HLA antibodies will react with. Only antibodies above a certain threshold (eg >5000 MFI) are included in the calculations.

Patients with cPRA above 50% can be considered for sensitization therapy

Transplantability score:

1oo-cPRA and then take into account ABO type of recipient as well as ABO prevalence in population

Outputs percentage likelihood of a match between recipient and a single donor. Multiply by annual donor number (500 for scandiatransplant) for mean number of acceptable donors per year.

- Immunosuppression:

Induction therapy with Thymoglobulin and corticosteroids is started before implantation plus a calcineural inhibitor for lung transplants.

Thymoglobuline: Polyclonal antibodies against a variety of lymphocytes. Given as an induction dose to deplete lymphocyte number

Standard maintenance therapy is with triple therapy, with a calcineurin inhibitor, anti proliferative and corticosteroids

Calcineurin inhibitors (Ciclosporin/Tacrolimus): Inhibit the key signalling phosphatase calcineurin. MOA is suppression of T-cell activation via inhibition of calcineurin.

Ciclosporin (Sandimmun): Can cause renal failure, other nephrotoxic medicines should be avoided, NSAIDS are contraindicated. Grapefruit juice can increase serum concentration by inhibition of CYP3A4. Colchicine should also be avoided due to an increase in Colchicine concentration.

Tacrolimus (Advagraf/Adport): Long half-life means dosage should not be adjusted daily, instead waiting 3-5 days. Less nephrotoxic than Ciclosporin. NSAIDS are contraindicated. Voriconazole/Itraconazole therapy mandates a decreased dosage.

Anti proliferatives:

Cellcept-Mycophenolate mofetil is a prodrug of Mycophenolic acid (Myfortic). MPA is an inhibitor of de novo synthesis of the purine GMP (as opposed to the salvage pathway). Lymphocytes rely almost exclusively on de novo synthesis, leading to selective inhibition of DNA replication in T cells and B cells.

Azathioprine (Imurel): Mainly used as an alternative to MPA. Dosage is adjusted based on leukocyte levels (between 4-9 E9/L). Can cause leukopenia, anemia or thrombocytopenia due to bone marrow suppression, as well as liver toxicity.

MTOR inhibitors (Sirolimus\Everolimus):

Everolimus (Certican): Add-on therapy to a calcineurin inhibitor in cases of inadequate rejection therapy, to decrease calcineurin inhibitor dose due to renal impairment and beginning chronic rejection. It has also been shown to reduce coronary allograft vasculopathy.

Main side effect is failure to heal surgical wounds\sternal dehiscence. Everolimus is antiproliferative (and used as a cancer drug) as well as immunosuppressive.

MOA is inhibition of mammalian target of rapamycin. The mTOR is a kinase that serves as a core component of 2 protein complexes, mTOR1 & mTOR2, that regulate different cellular functions, such as cell growth, cell proliferation, cell motility, cell survival, proteins synthesis etc. It inhibits activation of T cells and B cells by reducing their sensitivity to interleukin-2.

Primary Graft Dysfunction

ISHLT consensus

Pathogenesis:

Brain death is associated with factors that result in imparied myocardial contractility and sensitization to reperfusion injury

Noradrenaline release results in mitochondrial and and cytosolic calcium overload

Calcium overload can lead to necrosis and contracture of contractile proteins

Exogenous catecholamine administration may contribute to desensitization of myocardial beta-signaling and to activation of pro-inflammatory mediators, including complement

Decreased serum levels of thyroid hormones, cortisol and insulin following brain death likely contribute to decreased myocardial contractility

Older hearts are less tolerant to ischemia, in part due to coronary disease, ventricular hypertrophy and decreased endogenous myocardial protective factors

Anaerobic metabolism during ischemia results in lactic acidosis, Na+/H+ pump activation and high intracellular Na levels, causing cellular swelling, the Na/Ca+ pump is activated in turn, resulting in increased intracellular Ca+

Reperfusion leads to further calcium overload and free radical damage, which in an energy depleted cell can result in mitochondrial leak and subsequent necrosis (Ciclosporine inhibits the mitochondrial leak)

Recipient factors also play a role:

High PVR, increases cardiac stress and PDG

Systemic inflammatory response in the recipient (hostile environment) can cause refractory vasoplegia and through poorly understood factors (pro inflammatory cytokines and inducible nitric oxide synthase) affect the newly transplanted heart

Organ Procurement

ISHLT consensus statement

Medical Management of Brain-dead Organ Donors (including protocols)

Brain Death and its Implications for management of the potential organ donor

SFAI - Vård av organdonatorer

Donor management:

General

  • Cardiac dyskinesia is normal, when area does not correspond to a single coronary artery

  • 90% of brain-dead donor develop progressive hypotension requiring vasopressors (Vasopressin first line choice)

    • Catecholamines worsen cardiac transplant outcomes

  • Brain death results in a rapid decline in cortisol, ADH, thyroid hormones and insulin

    • Everyone should receive steroids (mainly for attenuating the inflammatory response and decrease vasopressor need)

      • Also consider ADH (Also for diabetes insipidus prophylaxis), T3 and insulin

Cardiac

  • Increased ICP -> Cushing reflex -> Bradycardia, hypertension

  • Early catecholamine storm -> increased afterload, increased vascular tone, visceral ischemia, depletion of cardiac ATP

  • Progression to spinal cord iscemia results in loss of vascular tone, hypotension and decreased afterload

    • Other factors contributing to hypotension: DI (loss of ADH), hyperglycemic/hypothermic diuresis and following hypovolemia, inadequate fluid resuscitation, ongoing blood loss, patient rewarming and relative adrenal insufficiency

Pulmonary

  • Only 10-20% of lungs offered are eligible for transplantation

  • Sympathetic storm -> Increased afterload (Vasoconstriction) -> Increased LAP/PAP -> Neurogenic pulmonary edema (NPE)

    • Increased pulmonary capillary pressure can cause structural damage with time

  • Lung protective ventilation increases lung transplant rate

  • Assessing borderline lungs in vivo, you may uncouple the ETT and assess compliance by seeing if the lungs deflate normally. If not it is typically a sign of interstitial edema, major atelectasis, pneumonia or obstructive disease

Renal

  • Main factors of post brain death renal tubular injury are proinflammatory and procoagulant effects of brain death

Endocrine

  • Brain death can cause ant\post pituitary failure (80% for posterior (Oxytocin and Vasopressin) leading to DI)

  • The anterior gland is usually at least partially preserved, most brain dead donors show normal levels of TSH, ACTH and Human Growth Hormone

    • Decreased T3 levels are found in 60-80% of cases, severely so in 15%. The cause is typically the sick euthyroid syndrome that accompanies critical illness, rather than TSH deficiency

  • Hyperglycemia is common due to reduced insulin concentration and insulin resistance

Misc

  • SIRS is common and can be very severe

  • Anemia is common, along with coagulopathy

    • Isolated head injuries present with coagulopathy in 34% of cases

    • Necrotic brains release tissue thromboplastin and plasminogen activators, which can cause DIC

  • Hypothermia is common due to loss of hypothalamic function, reduced metabolism, heat loss or loss of shivering, as well as instillation of cold fluids

Technical points:

  • Consider extra long sternotomy incision, cephalad, to improve exposure

  • If a single lung transplantation is planned, strongly consider individual pulmonary venous gases

  • Kg for Kg, female hearts have 10% less muscle mass than male

  • Open the interatrial groove, this effectively lengthens the left atrium, increasing available cuffs for both teams

  • Standard heparin dose is 400 U/kg

Organ Procurement Donor Assessment Checklist

HCV positive donators:

  • 44 patients (36 lungs, 8 hearts) with a measurable viral load

  • 4 week antiviral treatment post-operatively, started a few hours after operation

  • Viral load in recipients became undetectable at 2 weeks and is undetectable at 6 months follow up

  • Increased risk of acute cellular rejection ( 54% vs 30 % for lungs, 43% vs 33% for hearts)

  • No adverse events from antiviral treatment

Heart-Lung Procurement - Technique Steps

Heart Procurement

- Selection

- Technique (1) (2)

Organ preservation strategy is crucial (Cardioplegia administration, donor ventricular hypertrophy is of particular interest in this regard)

Video

Technique for DCD

Video for DCD NRP Cardiac explantation

Lung Procurement

- Selection

- Technique (1) (2)

Lung explantation video

DCD Lung procurement technique

Heart-Lung Procurement

- Selection

- Technique (1)

Hearl-Lung Transplantation

Technique

Cardiac transplantation

- Patient selection

Seattle Heart Failure Model for prognosis of patients with heart failure

- Organ selection

Shah - Oversizing not protective for recipients with moderate pulmonary hypertension, undersizing (>15%) is associated with worse outcomes

Age of donor: Increased mortality based on donor age, 30-39 OR 1,3, 40-49 OR 1,7, 50-59 OR 1,8 (Hong, pre transplant risk factors, observational N:11 703)

- Technique

Bicaval vs Biatrial anastomosis - Meta analysis - N= 3208 vs 3555

Bicaval is better

Long term mortality HR 1,77 with biatrial, long term tricuspid regurgitation HR 2,14 with biatrial

Early pacemaker insertion OR 2,5 with biatrial

Technique - Cardiectomy Video

Technique - Video

Heart transplantation after LVAD

Heart transplantation after congenital heart disease

Pediatric Heart-Lung Transplantation

- Post op

Survival:

Sweden: >90% 1 yr, >80% 5 yr, >70% 10 yr

ISHLT: 86,9% 1 yr, 81,1% 3 yr

Lung transplantation

- Patient selection

Overview in läkartidningen

Median time on waiting list 54 days, on list mortality 7%

Median time on post op ward 3 weeks

Idiopathic Pulmonary Fibrosis prognosis

3-5 yr median survival at diagnosis, <2 yrs with DLco <35-40%, See also the Du Bois Prognostic Index for 1 yr survival

2019 Sweden Epidemiology

39 DLTx +16 SLTx = 56 Total lung transplantations (40 in GBG)

60 Heart Transplantations (33 in GBG)

- Organ selection

- Technique

Tips and tricks

Reconstruction of inadequate donor left atrial cuff

Bilateral sequential lung transplantation

- Post operative

Survival

ISHLT: DLTx, 1 yr 83%, 5 yr 60%, 10yr 38%, 20 yr 18%. Median survival 7,6 yr for DLTx, 4,7 yr for SLTx

Sweden: DLTx 1 yr 85%, 5 yr 75%, 10 yr 60%

Rejection:

Restrictive Allograft Syndrome (RAS): A form of Chronic Lung Allograft Dysfunction (CLAD), characterized by fibrosis instead of obstructive and small-airway pathology. Worse prognosis than other CLAD.

RAS primer

 Physiology

Ohm’s Law: I(Flow)=V(Pressure)/R(Resistance)

Hydraulic analogy


Echocardiography

VTI (Velocity Time Integral)

Flow*time = Volume, but cardiac flow is not steady so the VTI compensates for that. The doppler line is placed on a valve, and the stroke volume is calculated from the integral of the doppler velocity and the diameter (eg LVOT)



Vascular resistance

Peripheral vascular resistance is mediated locally by metabolites, and over a distance on a neuro-hormonal level

The central dictation of peripheral vascular resistance occurs at the level of the arterioles. The arterioles dilate and constrict in response to different neuronal and hormonal signals.

In the human body there is very little change in blood pressure as it travels in the aorta and large arteries, but when the flow reaches the arterioles, there is a large drop in pressure, and the arterioles are the main regulators of SVR.

R is the resistance of blood flow [change in pressure between the starting point and end point]

There are several mechanisms by which systemic vascular resistance may be altered

Renin-Angiotensin system - Vasoconstriction

The autonomic nervous system - Alpha-1 receptors for vasoconstriction, Beta-2 receptors for vasodilation

At the endothelial level, nitrous oxide is released for vasoconstriction and endothelin for vasoconstriction

Several other molecules have uncertain effects (ANP, thromboxane, bradykinin)

Flow resistance in the pulmonary circulation is only about 10% of the total peripheral resistance in the systemic circulation

Typical pulmonary vascular resistance is 1,8 Wood units and a typical pressure drop of 10 mmHg

Low PVR maximizes the distribution of blood to the peripheral alveoli and ultimately allows for proper gas exchange

During increased CO the PVR decreases to allow increased flow, primarily by capillary recruitment (mostly from the apical zone where cap pressures are lowest) and capillary distension (the ovular vessels become more circular)

Lung collapse increases resistance in associated vessels (by increasing pressure from parenchyma)

Additionally, low resistance allows for the pulmonary system to pump the entire cardiac output at low pressures

Disease processes that cause chronic hypoxia will increase pulmonary vascular resistance through hypoxic pulmonary vasoconstriction

Typical systemic vascular resistance is 18 Wood units and a typical pressure drop of 100 mmHg

Ohm’s Law: ΔP (Pressure difference, mmHg) = Q(flow, L/min)R (resistance, mmHg*min/L (Wood Units))

The blood pressure in the pulmonary artery is much lower than the aortic pressure. The pulmonary vessels have relatively thin walls and their environment (air- filled lung tissue) is highly compliant. Increased cardiac output from the right ventricle therefore leads to expansion and thus to decreased resistance of the pulmonary vessels. This prevents excessive rises in pulmonary artery pressure during physical exertion when cardiac output rises.

On coronary blood flow control:

Adaptation of the myocardial O2 supply according to need is therefore primarily achieved by adjusting vascular resistance. The (distal) coronary vessel resistance can nor- mally be reduced to about 1/4 the resting value (coronary reserve). The coronary blood flow Q. cor (approx. 250 mL/min at rest) can therefore be increased as much as 4–5 fold. In other words, approx. 4 to 5 times more O2 can be supplied during maximum physical exertion.

Compliance

C=ΔV/ΔP (volume change/pressure change)

Veins have 30x the compliance of arteries

Afterload

When the aortic pressure load (afterload) increases, the aortic valve will not open until the pressure in the left ventricle has risen accordingly. Thus, the stroke volume (SV) in the short transitional phase (SVt) will decrease, and End Systolic Volume will rise (ESVt). Consequently, the start of the isovolumic contraction shifts to the right along the passive Pressure–Volume curve. SV will then normalize despite the increased aortic pressure (D2), resulting in a relatively large increase in ESV (ESV2).