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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 function


Long 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

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
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

hemodynamic instability (secondary to myocardial ischemia or acute MI)
electrical instability (arrhythmias)
intramyocardial coronary arteries
extreme cardiomegaly
small diffusely disease coronary arteries
calcified coronary arteries


Mechanisms of SVG failure

Early SVG occlusion
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)
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

1. 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
2. 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
3. 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



what are 2 basic repair strategies for post MI VSD

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?

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

Occlusion of the vessel or other branches
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?

Severe diffuse coronary disease
Distal target unsuitable for bypass
Vessel completely occluded
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

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

CAD/MI (95%)
Chagas’s disease
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)
ventricular arrhythmia
thromboembolic complications (50% of patients will have a thrombus, ?% will embolize)
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
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%.

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