Ischemic Heart Disease

1/3

0.1 mm

by small anterior cardiac veins (drain directly into RA rather than through coronary sinus)

thebesian. These are in walls of all 4 heart chambers, and drain directly into the chambers.

• great
• middle
• small 
• oblique

• RA
• Most of RV
• Diaphragmatic surface of LV
• Posterior 1/3 of AV septum
• SA node (60% of pts)
• AV node (80% of pts)

• LA
• Most of LV
• Part of RV
• Most of interventricular septum
• SA node (40% of pts)
• AV node (20% of pts)

• 70 ml/min/100g of heart muscle
• Translates to 225 ml/min
• Which is about 4-5% of cardiac output

4-7x.

9x

3-4

• Coronary flow doesn’t always keep up w/demand, heart increased efficiency of energy utilization in order to compensate for that.
• So if work output by exercise is 9x normal, we only increase blood flow 3-4x normal, where efficiency piece works to narrow that gap.

coronary capillary flow will fall to a low during systole, capillaries get compressed by contracting cardiac muscle. Then as cardiac muscle relaxes during diastole, blood flow increases through these capillaries. Opposite of what happens everywhere else) so this is talking about LV (similar phasic changes occur in RV) but muscle mass in RV isn’t as great, the inverse phasic change also isn’t as great as in the LV.

Innermost layer of cells similar to endothelium of blood vessels

Muscle of the heart

• Outer surface of the heart
• A layer of mesothelial cells

• -Epicardial coronary arteries lie on outer surface of the heart. These supply most of the heart
• muscle.
• -There are the smaller intramuscular arteries that penetrate the muscle itself.
• -Immediately underneath the endocardium there is a plexus of subendocardial arteries. During systole blood flow decreases through this subendocardial plexus (because of compression d/t contracting muscle  itself)
• -There are extra vessels in subendocardial plexus that will help to compensate but the differential in blood flow between the epicardial arteries and subendocardial plexus will paly a role in certain types of coronary ischemia

• Nutritional requirements
• Oxygen demand
• Vasodilators

• Adenosine
• Adenosine phosphate
• Potassium ions
• Hydrogen ions
• Carbon dioxide
• Prostaglandins
• Nitric oxide

TRUE

70%

Almost already at max utilization of oxygen already delivered, in case where there is an increase oxygen demand we need increase in coronary flow, because we can’t increase extraction more than it already is.

• ATP in the cell will degrade to adenosine monophosphate, further gets broken down into adenosine and gets released into interstitial fluid of cardiac muscle. 
• When adenosine gets released, it’s a vasodilator so consequently coronaries will dilated and increase coronary blood flow.
• All of the Adenosine gets reabsorbed and recycled and used again

• Comes from 2° changes in coronary circulation caused by either ↑ or ↓ activity of the heart
• Sympathetic: Norepi/Epi release, ↑ HR, ↑ contractility, so ↑ metabolism causes coronary vessel dilation

Parasympathetic: Ach release, ↓HR & ↓ contracility so ↓ metabolism causes coronary vessel constriction

• Parasympathetic stimulation
• --Limited vagal innervation to coronary arteries
• --Coronary vasodilation from acetylcholine

• Sympathetic stimulation
• --Extensive SNS innervation to coronaries
• --Constriction or dilation depends on receptors (Coronary arteries do both have alpha and beta receptors. Distributed in a few ways. In general the epicardial vessels have more alpha receptors. Whereas the  muscle itself has more beta receptor)

FALSE. Causes vasoconstriction

Vasoconstriction

Whenever the direct effect of ANS stimulation will alter coronary blood flow in the wrong direction the metabolic effects will override it into the right direction within a few seconds.

have more of a disproportional severe vasoconstriction

Most (70%) energy comes from breakdown of fatty acids instead of CHO

• energy comes from anaerobic glycolysis pathways.
• So the end product is lactic acid. Believed the build up of lactic acid is at least partly responsible for the pain we call angina

• ATP formed in mitochondria (formed by oxidative
• phosphorylation) from metabolism of food.
• Problem is ischemia! (only glycolysis can occur w/out oxygen)

So ATP can’t be generated. ATP is broken down to ADP and AMP and Adenosine. Because cardiac muscle are slightly permeable to adenosine, it will go into the circulation (via interstitial tissue) helpful in terms of vasodilation in an ischemic episode.

• Diffusion of adenosine from cells will cause a problem w/those cells (released from myocytes of cardiac muscle) after about 30min of ischemia, half of the adenosine is lost from the cardiac muscle cells.
• It takes a while to generate more adenosine so after 30min of ischemia it may be too late to prevent permanent injury and death of cardiac muscle cells

Myocardial hypoxia & accumulation of waste metabolites

• Uncomfortable sensation in chest from ischemia.
• Most common manifestation of heart disease, imbalance supply of oxygen supply/demand.

• Chronic pattern of transient angina with exertion, relieved by rest
• Caused by fixed obstructive plaque in one or more coronary arteries

• Angina at rest due to coronary artery spasm (aka: Prinzmetal angina)
• Reduction of blood flow d/t just spasm.
• Not understood how it happens.
• SNS activity together w/some endothelial dysfunction (inner layer of coronary arteries). 
• Thought that people will variant angina may have early atherosclerosis but rather seeing any plaque just have endothelial dysfunction. This can occur at rest (d/t a decrease supply rather than increased demand)

• Pattern of increased frequency and duration of ischemia
• Result from a rupture of an unstable atherosclerotic plaque. Subsequent platelet aggregation and thrombosis. 
• Acceleration of angina symptoms, sudden increase in tempo and duration of chest pain.
• Episodes occur w/less physical or emotion exertion. Even occurring at rest. Might be a precursor to an acute MI.
• Together unstable angina and acute MI are known Acute Coronary Syndromes

Region of myocardial necrosis

• angina pectoris to uncomfortable sensation pt. describe in the chest.
• ”strangling of the chest”

underlying pathophysiology process as well as timing and severity of the insult.

• Asymptomatic ischemic episodes
• Occur in pt. that have diabetes, alteration w/NS. Can occur w/pt. that on other occasions experience normal anginal pain.
• One study showed silent ischemia showed in 40% of pt w/stable symptomatic angina.
• Can occur in up to 10% of asymptomatic middle
• aged men. More common in diabetic, elderly and women.

• Refers to pt. w/typical anginal symptoms but no evidence of significant atherosclerotic stenosis on angiography.
• May show (on stress test) ischemia.
• Think it may be somehow and inadequate vasodilator reserve perhaps the resistance vessels are too small to be seen on angiography.  
• This pt. may have better prognosis than those w/avert pathology (makes sense)

• oxygen content and the rate of coronary blood flow
• oxygen content is pretty constant but regulation of coronary blood flow is main factor that comes in in terms of matching O2 requirements.

Hgb x 1.39ml x O2Saturation and the PO2 is the other part the part dissolved in plasma. (0.003 xPO2)

anemia or pulmonary disease

most of perfusion occurs during diastole instead of systole. Perfusion pressure in coronaries is approximated by aortic diastolic pressure. So then it follows that anything that decrease aortic diastolic pressure (like hypotension or AR will decrease coronary artery perfusion and decrease myocardial oxygen supply

• 1) external compression: surrounding myocardium compress coronaries arteries during cardiac cycle. When myocardium contracts, the subendocardial area, is area
• immediately adjacent of high intraventricular pressure and so consequently its subjected to greater force than the other layers of the heart muscle. Again this is why this area is particularly vulnerable to ischemic damage. 

2) intrinsic regulation: local metabolites, endothelial factors, & neural innervation.

*Autoregulation of coronary vascular resistance is the MOST important factor in providing an adequate oxygen supply because can’t increase extraction to any significant amount on demand, so if increase in oxygen demand, must come from blood flow

• wall stress
• HR
• contractility
• Also small amount of oxygen needed for basal requirements: 1)metabolism of the cell going on at all times  (like any other cell) & 2) electrical activity (depolarization) which also requires oxygen. So those two are basal requirements.

LaPlace’s law:  So w/the wall stress is related to is the intraventicular pressure, the radius of the ventricle, and the thickness of the ventricular wall.

• T = P x R
•       2 x h 

P is the systolic pressure and h is the thickness of the wall

• systolic pressure in the ventricle and so anything that will increase the pressure in LV (HTN or AS) by LaPllace's equation will increase wall stress or tension. So if it increases wall stress,  it is increasing myocardial oxygen
• consumption

Ventricular wall stress is the tangential force that acts on the myocardial fibers, tending to pull them part. That wall stress requires energy. The energy being utilized to oppose the force.

anything that increases LV filling (MR, AR) will similarly increase wall stress and oxygen consumption

INVERSELY proportional. The force gets spread out over a greater muscle mass. So a hypertrophied heart has a lower wall stress and oxygen consumption than a thinner heart muscle. So initially, LV hypertophy serves as a compensatory function, by decreasing oxygen consumption and decrease oxygen demand.

• The amount of ATP consumed every minute will also increase and that will increase oxygen requirements.
• Opposite is also true, give a BB will decrease O2 requirements & decrease ATP utilization

• measure of force of contraction.
• Increased w/endogenous or exogenous catecholamines (Epi) will increase oxygen utilization.
• BB will have opposite effect.

60mmHg

fall in perfusion pressure, distal to the stenotic lesion, this along w/a dysfunctional endothelial (don’t have our vasodilators working properly to bring adequate blood flow) so now we have an imbalance between oxygen supply and oxygen demand.

both reduction in blood flow (from those plaques) and endothelial dysfunctions. Abnormalities in vascular tone because the endothelial cells aren’t working properly and we don’t have the vasodilators

• Fluid mechanics: Poiseuille's and Ohm's laws
• Anatomy

• proximal epidcardial segements: are subject to overt atherosclerosis, those result in stenotic plaques. Those are the ones that will get occluded because of plaque. 
• distance resistance vessels: essentially act as reserve, because they can vasodilate and increase their diameter w/exertion.

the degree of stenosis that atherosclerotic plaque in the epicardial vessel as well as the amount of compensatory vasodilation that can occur in the arterioles (in the distal vessels).

60%; 70% (at this point, an increase in demand, increase in HR (some exertion), the coronary reserve really isn't enough and demand exceeds supply and myocardial ischemia results)

90%

• Inappropriate vasoconstriction
• Loss of normal antithrombotic properties.

• Its postulated in normal people the relaxation effect of NO will outweigh any SNS stimulation (alpha constriction) so unbalanced vasodilation results.
• The problem is in patients that have dysfunction endothelial cells, atherosclerosis, there will be impaired release of endothelial vasodilators (NO) that leaves unopposed vasoconstriction from SNS stimulation (alpha stimulation) vasoconstriction and that leads to decrease coronary blood flow and ischemia.

There also seems to be a problem w/adenosine release, our fallback  during ischemia is  not so helpful

• HTN
• cigarette smokers
• hyperlipidemia
• diabetes

*Appears to be impaired endothelial vasodilation, don’t’ normally vasodilate because of these preexisting conditions

• before 
• So that really suggests the disruption in the endothelial cell, vasodilator process occurs very early in the development of CAD.

• The factors that get released from the endothelial cells (NO & prostacycline) have the ability to exert an antithrombotic effect.
• They interfere w/platelet aggregation.
• So because the cells aren’t working properly this effect is essentially lost.
• Platelets are allowed to aggregate they secrete both procoagulants and vasoconstrictors that further contribute to thrombosis.

• Blood letting (hypotension)
• Septic shock (dec. oxygen supply)
• Low O2 content (anemia or pulmonary disease)
• HTN & ↑ HR (increased demand)

Atherosclerosis

• Genetic predisposition
• Obesity
• Sedentary lifestyle
• Hypertension

particularly in western society where it is the most common cause of death. Guyton says ~35% of US people die from this cause.

• acute coronary occlusion, Vfib, or both.
• Both of which can occur very suddenly or a more gradual process.
• Progressive deterioration of the hearts ability to pump.

• Get Enothelial dysfunction and w/that...
• Cholesterol deposits beneath endothelium
• Deposits invaded by fibrous tissue & calcified
• Atherosclerotic plaques protrude into vessel lumens impeding blood flow
• *happens in all vessels, not just coronaries

• Atherosclerotic plaque
• Coronary arterial spasm

thrombus or embolus that occludes the artery. Usually occurs where plaque breaks through the  endothelium and comes in contact w/blood flow. Plaque is there, it’s an uneven surface so platelets will adhere to it. Fibrin gets deposited and blood cells get trapped and that forms blood clot that will ultimately occlude vessel. Becomes embolus if plaque breaks off and flows to one of the distal branches

• Direct irritation of vascular smooth muscle
• D/t plaque iteself or Local nerve reflexes (hyperactive SNS)→ contraction of smooth muscle
• *if there is enough of a vasospasm flow decreases and thrombosis can also result.

Normally large coronary arteries don’t communicate w/each other but many anastomoses among the smaller arteries, when acute occlusion usually the smaller anastomoses will start to dilate within seconds.

1/2; 8-24

helps to increase blood flow through collaterals doubling the size  by the second or third day.

within about a month

w/progression of atherosclerotic disease the collaterals themselves become atherosclerotic and the ability to compensate is overwhelmed by impaired perfusion and ultimate result is pump failure.

TRUE! With ischemia and the switch from aerobic to anaerobic metabolism, and a decrease in ATP production, both systole and diastole are compromised

If there is increase in LV diastolic pressure ultimately that will back up into LA and pulmonary capillaries and results in pulmonary congestion

• 1.Pulmonary congestion → Dyspnea
• 2.Lactate, etc accumulation → Angina
• 3.Ion channel abnormalities → Arrhythmias
• 4.Stunned myocardium
• 5.Hibernating myocardium

• accumulation of byproducts (serotonin, lactic acid, etc. 
• That will  activate peripheral pain receptors C7-T4 & will cause pain we call angina.

Ion channel transport abnormalities

• The result after ischemic injury is a spectrum of complete recovery and irreversible.
• In the middle, there can be a time of prolonged period of contractile dysfunction w/out necrosis and ultimately normal function can recover
• Tissue experiences severe episode of transient ischemia but necrosis doesn’t result. Period of systolic dysfunction even after blood flow returns to normal, but eventually that contractile function recovers. Magnitude of stunning, depends on degree of ischemia (often the result of ischemia that just falls short of that that would cause necrosis)

both the severity and duration of both the imbalance between oxygen supply & demand

• Tissue demonstrates chronic contractile dysfunction d/t persistent decrease in blood supply usually from multivessel CAD.
• Some intervention has to happen for blood to return to normal, and provided flow can be restored via angioplasty/surgery and irreversible damage hasn’t occurred then recovery can happen

• a)Quality
• b)Location
• c)Accompanying symptoms
• d)Precipitants
• e)Frequency
• f)Risk factors
• g)Differential diagnosis

• pressure, discomfort, tightness, burning, heaviness, (described as pain) it isn’t sharp or stabbing, doesn’t vary w/inspriation or moving of chest wall.
• Lasts for a few minutes but rarely longer than 5-10min. Always lasts more than a few seconds (distinguishes it from musculoskeletal pains)

Levine's sign

• Diffuse rather than localized to single point. Mostly retrosternal. Or the L precordium.
• But can occur really anywhere, chest, back, arms, neck, lower face, upper abdomen.
• Often radiates to shoulder and inner aspect of arm, particularly on the L side.

• Autonomic NS stimulation s/s: ↑ HR, diaphoresis, Nausea.
• Can be both transient alteration in both LV
• contraction and relaxation.
• Dyspnic because of increase ventricular diastolic pressure & pulmonary congestion
• Particularly elderly may c/o weakness & fatigue. Some of these in absence of typical chest pain are referred to as anginal equivalents.

• Physical exertion (anything to throw oxygen balance off)
• Not so obvious, large meal cold weather (vasoconstriction which causes additional myocardial wall stress)
• If there is a precipitating factor, usually angina resolves in minutes if activity d/c’d.
• Typically resolved even faster w/sublingual nitro, 3-5min. If pain relieved w/that, pretty diagnostic that it really is angina

• Hard to quantify, pt. that have chronic angina typically learn what precipitates it and avoid those activities.
• Good to ask what their ADLs are (Metabolic equivalents). They often compensate.

HTN, hyperlipidemia, smoking, diabetes, family hx

• •Retrosternal pressure, radiating to neck, etc.
• •Few minutes duration (usually < 10)
• •With exertion, relieved by rest or NTG
• •EKG: transient ST depression or elevation or flattened or inverted T waves

• Sharp pleuritic pain varying with position
• Friction rub on auscultation
• Lasts for hours to days
• EKG: diffuse ST elevation and PR depression

Pleuritic changes w/respiratory movements and changes w/the cycle of breathing.

Pleuritic chest pain could also occur in acute pneumothorax

• •Retrosternal burning
• •Precipitated by certain foods, worsened by supine position, no change with exertion
• •Relieved by antacids

• •Epigastric ache or burning
• •Occurs after meals, no change with exertion
• •Relieved by antacids, not by NTG

• •Retrosternal pain with dysphagia
• •Precipitated by meals, no change with exertion
• •May be relieved with NTG

• •Constant, deep pain in RUQ; can last hours
• •Caused by fatty foods, no change with exertion
• •Not relieved by antacids or NTG

• •Sternal pain worsened by chest movement
• •Costochondral junctions tender to palpation
• •Relieved by NSAIDS, not NTG

• •Constant ache or shooting pains, may be in a dermatomal distribution
• •Worsening by neck motion.

• Dyskinetic apical pulse: ↓systolic function
• Rales: pulmonary congestion d/t ↓ systolic function and ↓ diastolic compliance
• S4: ↓ diastolic compliance
• Mitral regurgitation: Papillary muscle dysfunction
• Diaphoresis, ↑HR, & ↑BP:  ↑sympathetic tone

Typically w/myocardial ischemia we would see ST segment and T wave changes.

Acute ischemia usually results in transient either horizontal or down sloping ST segments and T wave is either flattened or inverted

subendocardial ischemia and transmural ischemia

• ischemia going through myocardial wall, not just endocardium.
• This can also be seen in situations of severevasospasm of variant angina
• ST segment elevations

• pt. w/acute MI the ST deviations that are seen in stable angina, quickly normalize w/resolution of symptoms.
• ½ of all pt. that have stable angina in between of ischemia or anginal symptoms their EKGs are completely normal
• In other pts there will be that, non specific ST changes. Not really normal but not diagnostically abnormal either.

pt had a prior MI

• walk on treadmill or ride bike to progressively higher workloads, and monitored for periods of ischemia on EKG or SOB.
• Test will continue until pt. develops angina or s/s of ischemia on EKG or until a target HR is achieved (85% of max HR)
• Or stop if pt. becomes too fatigued to continue.
• Test is considered positive if it elicits the patients usually pain.
• If there are EKG changes consistent w/ischemia (which means a greater than 1mm horizontal or down sloping ST depression)

Max HR is 220-age.

a greater than 1mm horizontal or down sloping ST depression

• Sensitivity: if test says pt. has disease they really have the disease. How likely the stress test will pick up positive ischemia
• Specificity: probably the negative test really means they don’t have the disease (flip side)

• Sensitivity of approx. 65-70%
• Specificity of 75-80% for detecting anatomically significant CAD.

• 1. if ischemic changes develop during the 1st 3
• min of exercise or persists for 5min after exercise is stopped.

2. 1mm down sloping ST segment or if magnitude is greater than 2mm 

3.if BP falls, represents systolic dysfunction.

4. high grade ventricular arrhythmia.

5. if pt. can’t exercise for 2min because of severe cardiopulmonary limitations

24-48 hr

Some sort of radio nucleotide, either technesium 99 or thallium 201, gets injected during peak exercise and then they do some imaging. This material will accumulate in proportion to the degree of viable myocardium, areas of ischemia will show up as cold spots.

• But they want to differentiate between reversible and irreversible ischemia.
• Take images before or several hours after test, if cold spot filled in it’s reversible if persists likely an area of irreversible infarct

used when standard stress test not helpful if pt. has baseline ST segment abnormalities (LV hypertrophy or LV BBB)

• Sensitivity: 80-90% 
• Specificity: 80% 

(Better than standard stress testing)

• useful if pt. has some baseline ST T wave abnormalities or standard stress test and results are somewhat equivocal.
• Do an ECHO and then put pt. on bike (or treadmill), then immediately after do the ECHO again. So what we’re looking for here if pt. has some sort of ventricular contractile dysfunction (hypokinesis  or akinesis) w/exertion

• Sensitivity 80%
• Specificity 90%.
• Possible that someone who is obese may not image well.

for people can’t exercise d/t some other limitation. Hip/knee arthritis, peripheral vascular disease and claudication, etc.

• Few drugs: dobutamine, will ↑myocardial oxygen
• demand, then there are two vasodilators persantine (dipyridomole) and adenosine. Because the ischemic tissues are already maximally dilated, a drug like adenosine or prosantine that will vasodilate and increase flow to healthy tissue and essentially create that steal phenomenon like we saw w/Isoflurane.

So together w/the drugs that will be coupled w/ some sort of nuclear imaging to try and reveal regions of impaired perfusion

Inject contrast dye and look radio graphically.

• Benefits: most direct means of identifying
• coronary stenosis. Usually reserved for pt. who don’t response to drug therapy or present as unstable and revascularization is likely next step. 

Cons: really only shows anatomic info not functional info. Not predictive of whether plaque is likely to rupture or not.

• Can show some coronary artery calcification that correlates well w/severity of CAD.
• Not as sensitive as coronary angiography so it’s mostly helpful in excluding significant CAD in pt. w/chest pain but low suspicion.

• location and extent of stenosis
• how impaired is the LV function.
• How poor is the exercise capacity.
• Even the magnitude of anginal symptoms

• Stop whatever activity precipitated the attack Sub lingual Nitro is drug of choice, nitrates cause venodilation, ↓ venous return, ↓ preload, ↓LV volume, (all of that is then a determinant of ventricular wall stress)
• There are also coronary vasodilators, that will increase coronary blood flow. So the thing is the pt. who is ischemic and is already having compensatory vasodilation nitro won’t do anything more because already at max dilation but for pt. vasospasm mediated ischemia then nitrates can be helpful. 

• Organic nitrates: good for symptomatic relief but not chronic
• Beta blockers: ↓HR & ↓myocardial oxygen demand by both ↓ rate and contraction
• Calcium channel blockers: ↓oxygen demand (venodilation) and arterial dilation which will ↓wall stress. Also cause coronary vasodilation so they increase oxygen supply because like BB they will decrease force of contraction and HR they are helpful in decrease oxygen demand.

• Airway disaese: want selective B1 ideally
• HF: can intensify HF in pt. w/decompensated LV dysfunction. So decreased contractility is good to a point but if already an issue there it can be problematic

Interesting enough, the short acting Ca+ blockers shown in meta-analysis to increase MI And mortality, so in this application only use agents given once a day ror pt.w/chronic angina.

2nd line tx if combo of BB and nitrates haven't taken care of symptoms.

Combining BB and Ca+ blockers, combined effect on contractility which can be problem in some pt. (Combined effect w/HR as well

• Antiplatelet therapy: reduce risk of thrombosis & platelet aggregation
•  a) ASA->inhibit platelet aggregation and
• release of procoagulants and also  vasoconstrictors. Helpful in stabilizing plaque. 
•  b) Clopidogrel -> also prevents platelet activation & aggregation. So it can be used in pt. who is allergic to ASA or in combo w/ASA. Together they are more effective than ASA alone. 
• Statins: good if pt. has high cholesterol
• levels (esp. LDL) 
• ACE inhibitors: helpful to decrease risk of death, stroke, and MI.

recommendations for LDL keep it lower & lower have changed such that new guidelines say that for the pt. w/risk factors for CAD good to keep LDL less than 70. 

• Recommended if pt. s/s don’t respond to pharmacologic therapy or as a result of meds some unacceptable SE result.
• Or if pt. is found to high risk coronary artery disease and in their situation coronary revascularization has been shown to improve survival.

• includes coronary angioplasty (PTCA)
• This is where a balloon tip catheter inserted via femoral, brachial, radial artery and maneuvered to the area of stenosis in coronary artery.
• Balloon gets inflated under high pressure to dilate that area of stenosis and then the balloon gets deflated and the catheter is removed

Good: risk of MI less than 1.5% and mortality is less than 1% 

Bad: about 1/3 of pt. develop recurrent symptoms within 6 months and recurrent tx is needed. (need to keep getting it or go to next step and get a stent or CABG)

YES, stents themselves are thrombogenic (even the drug eluding ones)

• neointimal proliferation (Smooth muscle cells
• migrate and produce extracellular matrix) can be a problem
• These get coated with some sort of anti-proliferative medication and that gets released over period of  2-4 weeks to prevent endothelialization of the stent.

50%

• graft portions of pt. native vessels in order to bypass obstructed coronary arteries. 
• Two types:
• --1st uses native vein (typically the
• saphenous vein) so it gets sutured to base of Aorta. That’s the proximal and then to coronary segment downstream from the area of stenosis. --2nd uses arteriole (usually the internal mammary) that’s a superfluous branch of the subclavian artery) so that can get directly anastomosed distal to the stenotic coronary lesion.

80%; 50%

• 90% 
• So if there is a choice, the IMA is used particularly in areas of critical flow like the LAD

• Less invasive
• Shorter hospital stay & easier recuperation
• Superior to pharmacologic treatment for angina relief

• More effective for long-term relief than either PCI or pharmacologic treatment
• Most complete revascularization
• Improved survival in patients with:
•  •> 50% left main stenosis
•  •3 vessel CAD, esp. with impaired LV contractile function
•  •2 vessel disease with tight (> 75%) LAD stenosis, esp. with impaired LV function
•  •Diabetes & multivessel disease