Coronary artery bypass questions Flashcards
What is risk and important predictors of morbidity and mortality following CABG
Stroke (3.1%)
Deep Sternal wound infection (2.5%)
Renal Failure (7.7%)
post op AF (28%)
Post op mortality (1.2%
Long-term survival influenced by
age, DM, number of vessels of coronary artery disease, gender, LV functionLong term patency of bypass grafts
Conduit patency time
LIMA 95% 10 years
Free LIMA 90% 10 years
RIMA 90% 10 years
Radial artery 80% 9 years
GEA 63% 10 years
inferior epigastric 80% 1 year
long saphenous 80% 9 years
short saphenous 60% 3 years
Cephalic vein 45% 5 year
Cyroprhomograft vein 15% 1 year
What is evidence for radial artery for conduit
The RAPCO trial is a randomized controlled trial that assigned 621 patients to either RA, SV, or free right ITA for the largest coronary target other than the left anterior descending coronary artery.
Patency rates reported at 8 years (83.6% RA and 76.5% SV) are lower than the latest reported patency rates of RAPCO patients (90% for RA; and 82% SV on a 5-year average follow-up
mortality was 8.03% in the radial artery group versus 12.5% in the saphenous vein group
What is RAPS evidence to use radial for CABG
5 year outcomes after within-pt randomizationof bypass grafts to the circumflex arteries using saphenous vein graft (SVG) for one and radial for the the other
Functional occlusion was more common after SVG than RA (19.7% vs 12%), and complete occlusion was also more common after SVG than RA (18.6% vs 8.9%)
What are contraindications to use of the radial artery
Insufficient ulnar artery flow, Allens test > 6 seconds, or > 50% on stenosis on u/s
Raynauds’s disease
Emergency surgery
need for high dose inotropes highly likely
Musician or surgeon
Use of a radial artery graft is reasonable when?
Class II B evidence
may be reasonable when grafting left-sided coronary artery with severe stenosis (>70%) and right sided lesions (> 90%) that perfuse LV myocardium.
What are charaterisics of radial
Fenestrated internal elastic lamina
Thicker media with thick myocyte content
Stronger contraction in response to norepinephrine resulting in spasm
Responds to vasodilators such as calcium channel blockers, papavarine, nitrates and milrinone.
28% will have atherosclerosis at time of harvest compared with 6% IMA
Who should get complete arterial revascularisation
All class IIb indications
Age < 60
few or no comorbidities
Arterial graft to RCA only when a critical lesion of > 90%
Radial graft to left sided lesion > 70% and right sided lesion > 90% that perfuse LV myocardium
What are the principles of drug-eluting stents
incorporate a drug (sirolimus or paclitazel) released slowly over months, which impairs the cellular proliferation and fibromuscular hyperplasi healing response to stent deployment and ballon barotraum.
Complications of stent deployment include
1) immediate complications (occlusion, stent thrombosis, embloism, dissection, side-branch occlusion and wire fracture
2) emergency CABG (0.3%), mortality (0.5%) , MI (0.8%), local vascular problems (2%)
3) In-stent stenosis, secondary to neointimal hyperplasit, which is reduced in DES as compared to bare metal stents
4) Late stent thormbosis, more common with DES as the polymer has inhibited endothelisation of the stent, hence when dual therapy is stopped, there is an increased risk of throbosis
What are the differences between LIMA and Radial artery
LITA muscular media has 6-12 elastic lamellae
Initma and subintima lie on a prominent internal elastic lamina, with few and small fenestrations (contrast to other small arteries with larger fenestrations that may permit entry of smooth muscle cells to initiaite plaque, may limit the development of atherosclerosis).
reduced smooth muscle mass (thin medial layer, limited vasoreactivity)
No vasa vasorum
Vasodilates readily (NO, Milrinone), limited vasoconstriction
Radial artery accompanied by 2 venous comitantes difference location media thicker than other arterial conduits and devoid of elastic fibers can be calcified or atherosclerotic easy to handle vs LITA highly vasoreactive (prone to spasm)
Contraindications to SVG harvest and use as a bypass conduit
varicose degeneration
superficial phlebitis
deep vein occlusion (where SVG is an important collateral)
List the contraindications to LITA
Prior damage due to chest wall irradiation or trauma
LITA important collateral for lower limb perfusion in patients with severe peripheral vascular disease (stenosis or occlusion of aorta) e.g., Leriiche’s syndrome
subclavian artery stenosis or occlusion
stensosis of subclavian
Av fistual
List the advantages and disadvantages of ITA skeletonization
Advantages:
preserves sternal blood supply
decreased incidence of deep sternal wound infection (especially high risk patients, e.g., DM)
greater length
facilitates sequential or Y graft anastamosis
improved ability to define spasm
preserves intercostal nerves (decreased incidence of neuralgic pain
Disadvantages:
unknown long-term patency
increased risk of injury
longer harvest times
What is evidence that BIMA is better then a LITA alone
There appears to be a 10% survival benefit at 10 year an 18% survival benefit at 15 years for BIMA
List contraindications to BITA
Chronic steroid use Morbid obesity Severe COPD (FEV1 < 1 L) Advanced age Emergency operation **Poorly controlled Diabetes mellitus Subclavian stenosis Calcification of mammary AV fistula in same arm
What are contraindications of off-pump CABG
Absolute hemodynamic instability (secondary to myocardial ischemia or acute MI) electrical instability (arrhythmias) Relative intramyocardial coronary arteries extreme cardiomegaly small diffusely disease coronary arteries calcified coronary arteries
Mechanisms of SVG failure
Early SVG occlusion
thrombosis
technical factors (anastamotic stenosis, kinking)
poor distal runoff or competitive flow from native CA
Intermediate (1 month to 1 year)
intimal hyperplasia (fibroplasia)
factors include: platelet aggregation, growth factor secretion, reduced NO and prostacyclin production
Late occlusion (>1 year)
atherosclerosis
Rate of closure from year 1-6 is 2%/year loss
Rate of closure afterwards 4-5%/year
What are ways to differentiate between post MI VSD and post MI papillary rupture
- Systolic murmur with septal rupture is more prominent at the left sternal border, wheras the murmur resulting from a ruptured papillary muscle is best heard at apex
- The murmur associated with septal perforation is loud and associated with a thrill, whereas the murmur with acute MR is sifter and has no thrill
- Septal rupture is more likely associated with anterior infactions and conduction abnormalities, whereas papillary is more likely with inferior infarctions and no conduction abnormalities.
What are two tests that should be performed to assess post MI VSD or papillary muscle rupture
Right heart cath.–Septal rupture you see a step up between the right atrium and the pulmonary artery in oxygen saturation. Step up for greater then 9% confirms the presence of a shunt. Qp:Qs range from 1.4 to 8:1 and roughly correlates with the size of the shunt.
In MR there are classic giant V waves in the pulmonary artery wedge tracing pressure.
Transthoracic echo, especially with color flow doppler. Detect size of defect, location, right and left heart function, excluded coexisting mitral regurgitation
page 605 cohen.
What is natural history of post MI CSD
25% die in first 24% 50% die in 1 week 65% die in 2 weeks 80% die in 4 weeks 7% alive in one year
What are classification of post MI vsd
Apical
Anterior
posterior/inferior
what are 2 basic repair strategies for post MI VSD
infartctectomy infarct exclusion (this is best used for posterior)
What are rates, complications, and risk factors for GI complications post cardiac surgery
In a 5 year series it was reported @ 0.48%. GI bleeding (82%), Intestinal ischemia (8.5%), perforated duodenal ulcer (2.8%),
12 parameters were identified as risk: age > 65, low left ventricular function, preoperative elevated scerum cr, on pump, prolonged CPB and aortic cross clamp, congenital heart disease, aortic surgery, use of IABP, blood transfusion, HCO3
Surgical intervention needed in about 20% and in that group mortality was 85%. The highest mortality is in intestinal ischemia with a mortality of 42.8%.
What is the evidence of dual antiplatelet agents post on or off bypass
New studies appear to be suggesting that venous graft patency is improved with plavix plus asa. It appears to affect the resistance of antiplatelets (asa resistance has been as high as 32%).
When is evidence for complete arterial revascularization?
Class IIb evidence:
Maybe reasonable in patients less then 60 years of age with minimal comorbidities
for elective surgery when should Plavix and Ticragrelor be stopped?
When should Eptifibatide or tirofiban be stopped?
When should abciximab be stopped?
Elective
5 days for clopidogrel and ticrelor and 7 days for prasugrel
Urgent at least 24 hours
Short-acting Glycoprotein IIb/IIA inhibotors (eptifibatide or tirogiban should be stopped for 2-4 hours) and abciximab for at least 12 hours).
What are indications for ACE inhibitors post CABG
Class I
any patient with ejection fraction less then 40%, Hypertension, diabetes, chronic kidney disorder,
Class IIa is everyone (inlcluding those with a normal LV function)
When do you consider doing combined CABG and carotid
Class IIa
In the CABG patient with a previous TIA or stroke and a significant (50% to 99%) carotid artery stenosis it is reasonable to consider cartoid revascularization in conjuction with CABG.
In such an individual, the sequence and timing (simultaneous o staged) of carotid intervention and CABG should be determined by the patient’s relative magnitude of cerebral and myocardial dysfunction
Class IIb
If no history of TIA or stroke carotid revascularization may be considered in the presence of bilateral severe (>70% to 99%) stenosis or a unilateral severe carotid stenosis with a contralateral occlusion
What are complications and outcomes from coronary endarectomy
Complication:
Occlusion of the vessel or other branches
Dissection
Emboli
Myocardial Infarction
Leak (bleeding at the anastomosis)
Patency rate: at 1 year: 73-86% for right coronary, 62-86% for LAD and 75% for CX
Periop MI: RCA 7%, LAD 2%, Cx 11%; overall 6%
In hospital mortality: overall 6%
Coronary endarterectomy. What is the chance of peri-operative MI and what is the mortality risk?
Indications:
Severe diffuse coronary disease
Distal target unsuitable for bypass
Vessel completely occluded
Technique:
1-closed technique: only a small incision: good for the right coronary
2-opened technique: a lengthy incision mid portion of the artery: good for LAD
What is the mechanism of injury during reperfusion
Edema
Increased intracellular Calcium
Reduced capacity to secrete NO
C3a leads to neutrophil chemotaxis
Accelerated release of oxygen free radicals due to abundance of oxygen during reperfusion
Increased MAC present in the injured area resulting in incoming neurtrophil adhesion and activation
Coronary endarterectomy: what is the chance of peri-operative MI and what is the mortality
Peroperative mortality is 5% if used in selected circumstance
graft patency in ednarterectomized arteries
72% at 30 months
When was first CABG
Kolessov 1967 LIMA to LAD 6 pts
What are indications for Emergent CABG
1) Acute MI in who PCI has failed or cannot be performed
2) coronary anatomy is suitable for CABG
3) Persistent ischemia of a significant area of myocardium that is refractory to nonsurgical theraoy
4) Pts undergoing post infarction mechanical complication of MI
5) Pt its in cardiogenic shock suitable for CABG irrespective of time
6) Pts with life-threatening Ventricular arrhythmias (ischemic in origin) in the presence of left main stenosis greater than 50% and/or 3VD
List Class IIa indications for CABG in emergent situations
1) Pts with 3VD with recurrent angina or MI within the first 48 hours of STEMI presentation as alternative to a more delayed strategy
2) Early CABG is reasonable for selected pts greater then 75 years of age with STEMI or LBBB who are suitable for revascularization irrespective of the time interval from MI to onset of shock
What is benefit of revascularization after 24 to 36 hours after infarction?
The boarder zone maybe under perfused in the early days after an infarction with a dilated and pressure overloaded ventricle resulting in loss of more muscle in the boarder zone. Maneuvers with IV NTG, IABP, and LVAD may help
What is evidence for short term mortality benefit of LITA-LAD (Perioperative) vs SVG to LAD
Circulation (2001), at 26 000 patients and showed those with LITA had a peri-operative mortality of 2.2% vs 4.9% in those that had SVG.
when subdivided this mortality benefit was seen in pts > 70 years of age, poor EF, left main, Emergency surgery, 3VD
Overall a 60% reduction in risk
What are reasons for why LITA-LAD has short term benefit
Correct size match (1.7mm vs 4mm)-prevents early occlusion/RBC sludging
Less resistance to injury/trauma during harvest
Fewer fibroblast growth factors
Higher nitric oxide and prostacyclin production
relaxation to thrombin
Low vasconstrictor sensitivity and high vasodilator sensitivity
Higher flow reserve and shear resistance
What are contraindications to CABG
No demonstrable ischemia on noninvasive testing
No or only small area of viable myocardium
Poor, non-graftable targets
Insignificant coronary stenosis (< 50% diameter reduction)
Poor LV w/o evidence of intermittent ischemia and significant revascularizable viable myocardium
No conduits
Comorbidities that increase risk to that above medical management
Relative contraindications would include porcelain aorta
Comorbid condition (malignancy, AIDS) that severely limits survival
What are risk factors for Diastolic dysfunction
- HTN (LV hypertrophy)
- unstable angina: stunning post-op
- old age, female, diabetes
- CAD: more difficult myocardial protection
What is Definition of Diastolic Dysfunction
Limitation of the ventricle to fill to an adequate end-diastolic volume w/o an abnormally ↑ in end-diastolic pressure. Disturbance in ventricular relaxation, distensibility or filling – regardless of whether the EF is normal or depressed and whether the pt is symptomatic or asymptomatic.
What is treatment for Diastolic dysfunction
↓ HR: β-blockers, calcium channel blockers
Prevent/regress ventricular hypertrophy: ACEI, ARBs, aldosterone antagonists
Prevent/treat myocardial ischemia: long acting nitrate, revascularization
maintain AV synchrony
Diuretics (loop, thiazide, spironolactone)
What are indications for PCI of vein Grafts
- Symptomatic patients with normal LV function.
- Early (< 5years) SVG stenosis.
- Single stenotic vein graft
- Progression of native disease suitable for PTCA.
- focal SVG disease not to LAD.
- Patent LIMA to LAD with stenosis of other SVGs
What are indications for redo surgery for vein grafts
late (≥ 5yrs) stenosis multiple stenotic vein grafts diffusely atherosclerotic vein grafts stenotic LAD vein graft no patent LAD abnormal LV fx
What are important predictors for outcomes in redo CABG
- Sternal reentry.
- Stenotic or patent SVGs: atheroemboli
- Patent arterial grafts.
- Aortic atherosclerosis.
- locating grafts and native coronaries.
- lack of conduits.
- diffuse native coronary disease
- early SVG thrombosis
- incomplete revasc
- air embolism
- hypoperfusion d/t replacing SVGs w/ arterial grafts
- inadequate myocardial protection
Define Low Cardiac output syndrome
need for IABP or inotropic support for more than 30 minutes in the ICU post cardiac surgery to maintain S BP > 90mmHg and CI > 2.2L/min/m2.
The incidence of LOS is 5–9% after CABG, and it carried a mortality of 17%.
The causes of LOS include:
- Poor LV function preop
- Poor myocardial protection
- Perioperative MI
List predictors of LCOS
- Preop LVEF< 20%
- Emerg OR
- ♀
- DM
- > 70 yo
- LM disease
- Recent MI
- 3VD
What is definition of LV aneursym
85-90% anterolateral, 5-10% posterior
strict: distinct area of abnormal LV diastolic contour w/ systolic dyskinesia or paradoxical bulging
looser: any large area of LV akinesia or dyskinesia that reduces LVEF
Intra-op: an area that collapses upon LV decompression
What is natural history and etiology of LV aneurysms
Etiology: CAD/MI (95%) trauma Chagas’s disease sarcoidosis Natural Hx: 10yr survival for asymptomatic pts 90% 10yr survival for symptomatic pts 46% risk of thromboembolism low (0.35%/yr) and long-term α-coag not recommended however, in the 50% of pts w/ mural thrombus visible by echo, 19% dvp T-E over 2yr f/u therefore α-coag if there is a thrombus seen on echo
What are indications for OR for LV aneursym
documented expansion or large size (Indexed ESV > 80, Indexed EDV > 120)
symptoms:
angina
CHF
ventricular arrhythmia
thromboembolic complications (50% of patients will have a thrombus, ?% will embolize)
rupture
pseudoaneurysm
congenital aneurysm – d/t the presumed risk of rupture
concomitant surgery
What are relative contraindications for LV aneursym resection
excessive anesthesia risk
impaired function of residual myocardium outside aneurysm
resting CI < 2.0L/min/m2
signif MR
evidence of nontransmural infarct (hibernating myocardium)
lack of a thin-walled aneurysm w/ distinct margins
Significantly depressed Right ventricular dysfunction
What are techniques for repair of LV aneurysm
Linear closure
plication
Circular patch
Endoventrcular patch
What is mechanism and action of spinal cord stimulation for reducing angina
Mechanism: stimulation of the dorsal aspect of the T1-T2 spinal cord
- Suppresses pain assoc w/ myocardial ischemia by modulation of activity of intrinsic cardiac neurons
- Improved myocardial perfusion ± alterations in the oxygen supply/demand ratio
Improved myocardial lactate metabolism
Redistribution of coronary blood flow from ischemic to non-ischemic area (?! Could be the opposite)
Decrease Myocardial oxygen consumption
Decrease sympathetic flow.
What are indications for TMR
Indications: refractory angina on maximal medical therapy not amenable to PTCA or CABG surgery, with reversible ischemia in that territory(CCS III(advanced) and IV)
List contraindications for TMR
coronary arteries amenable to CABG or PTCA
low ejection fraction
Patients listed for transplant or transplant candidate
relative: advanced age, other advanced organ disease affecting survival
What is mechanism is outcomes of TMR
Mechanisms of TMR (1) Creating channels (Least effective) (2) Sympathetic de-enervation (3) Neoangiogenesis Short term (1) Improved angina (2) Improved quality of life (3) Less hospital admissions (4) Improved exercise tolerance Long term (1) Improves perfusion (Controversial)
When do limitations of flow occur with degree of blockage
Hemodynamic lesions occur with exertion when >75% reduction of cross-sectional area, which corresponds to 50% loss of arterial diameter.
What is time related effect of CABG in pts with acute STEMI
Need for emergent CABG has low incidence of 3 to 10% of pts
CABG performed < 6 hours the onset of hospital mortality and 10 year survival is better than if CABG is performed > 6 hours
What are outcomes of CABG performed for STEMI at different times
CABG < 6 hour 12% mortality
CABG 6 to 23 hours –23 to 50% mortality
CABG 4 to 7 days after STEMI 2.4%
What are limitation of trials comparing CABG to PCI
Most trials did not report outcomes on subset such as race/renal/obesity/PAD
Most enrolled pt were male, 1-3 vessel disease, and normal LV function–which would make them unlikely to benefit from CABG
The enrolled pts were only a small fraction of screened pts (5-10%), making the generalizability of the results poor
What was primary outcome result of SYNTAX for all comers at 3 years
composite outcome of death, stroke, MI or repeat revascularization was
20.1 for CABG vs 28% for PCI
What was repeat revascularization rate for PCI at 3 years (according to syntax)
about 20%
What is relative risk reduction for CABG over medical therapy for left main disease
66% relative risk reduction
CASS registry
Median survival 13.3 for CABG
6.6 for MED
What are outcomes of transit Doppler flow
Analysis includes the evaluation of the maximum peak flow, the minimum peak flow, the mean flow, the back flow and the pulsatility index (maximum peak flow – minimum peak flow/mean flow).
There are no strictly normal values (the flow in the graft is depending on the length of the graft, the driving pressure, the resistances to the flow and to the size of the graft itself), an acceptable value for the pulsatility index has to be 3 or below.
The presence of a huge diastolic flow guarantees an unrestricted flow into the graft
What is a positive Exercise ECG test
ST depression > 2 mm ST elevation Chest pain increased R wave voltage inverted u waves failure SBP to rise with exercise ventricular arrhythmias New MR
Short and long-term results for patients undergoing CABG
Indication outcome 30 day survival 98-99% 1-year 97% 2-year 96% 3 year 93% 5 year 90% 10 year 80% 15 year 60% 20 year 40%
5 year freedom from angina is 83% and 10 year is about 63%.
