Ischemic Heart Disease
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CAD accounts for what percent of deaths in industrialized countries?
T or F, most older adults have no degree of CAD?
Are the coronary arteries located on the surface or inside of the heart? What do they supply?
- The surface (epicardium)
- They supply most of the heart muscle
Does the blood inside the heart chambers contribute to a significant portion of cardiac perfusion?
No, it only supplies 0.1 mm of the endocardial surface
What does the RCA supply?
RA, most of RV, diaphragmatic surface of the LV, posterior 1/3 of AV septum, SA node in 60% of pts, AV node in 80% of pts
What does the LCA supply?
LA, most of LV (anterior and left lateral parts), part of RV, most of interventricular septum, SA node in 40% of pts, AV node in 20% pts
What veins drain into the coronary sinus? What part of the heart do they drain?
- -great, middle, small, and oblique coronary veins
- -drain from LV into RA
What is the significance of the anterior cardiac veins? What part of the heart do they drain?
-Anterior cardiac veins drain RV into RA, drains directly into RA, does not go thru coronary sinus
What are the thebesian veins?
They are located in the walls of all 4 heart chambers and drain directly into all heart chambers
What is resting coronary blood flow?
- -70 ml/min/100 g of cardiac muscle
- -225 ml/min
- -4-5% of CO
Describe the phasic changes in coronary capillary perfusion during the cardiac cycle.
- Systole- decreased capillary blood flow as they get compressed by contracting heart muscle during systole
- Diastole- increased blood flow thru the capillaries
- -This is opposite to what occurs in the rest of the body
Is there a difference between the phasic changes of coronary perfusion between the LV and RV?
- -Yes, the phasic changes are more pronounced in the LV as it has more mass than the RV.
- -The RV experiences phasic changes but not to the same extent as the LV
How much can a normal heart increase its blood flow during strenuous exercise?
- 3-4 x normal
- 4-7 x CO normal in a young person
How much can a normal heart increase its work output under strenuous conditions?
up to 9x
If the heart can increase it's work output by up to 9x normal, but increase blood flow by only 3-4x normal, how does it compensate for the difference?
By increasing its efficiency of energy use
What's responsible for the increased cardiac workload under strenuous conditions?
The CO increases and the heart must pump against a higher than normal arterial pressure.
What do the smaller intramuscular arteries do?
Penetrate the cardiac muscle and along with the coronary arteries supply the muscle
Subendocardial arterial plexus
- -A plexus of subendocardial arteries
- -Located under the endocardium
How are the subendocardial arteries affected by systole? How do they try to compensate?
- -They receive decreased flow during systole due to compression from the contracting muscle
- -Attempt to compensate via extra vessels of the subendocardial plexus
- -However the difference in blood flow btw epicardial arteries and subendocardial arteries plays a role in certain types of ischemia
How do local tissue requirements affect coronary blood flow?
- -Increased tissue requirements will cause increased blood flow (vasodilation)
- -So increased strength of contraction will cause increased blood flow
How much O2 is usually extracted as blood flows thru the heart?
With increase O2 demand increased O2 extraction is not possible, so what occurs to meet the heart's nutritional requirements?
-Coronary blood flow increases almost exactly in proportion the O2 and nutrient requirements
What is the general means in which increased O2 consumption causes increased cardiac blood flow (via vasodilation)?
- -Poorly understood mechanism
- -Likely causes VD substances to be released
With decreased O2 concentration (due to increased consumption) what VD substance plays a major role and how is it formed?
- -With a low O2 concentration, ATP degrades to AMP, then to adenosine, acts as a VD
- -After it causes VD it is reabsorbed and reused
What other VD substances play a role in coronary dilation?
What factors control coronary blood flow? Which has the greatest effect?
- -local arteriolar VD (O2 demand and vasodilator substances), this has the greatest effect
- -Nervous control (ANS)
What are the indirect effects of SNS stimulation on coronary blood flow ?
- -NE and epi release
- -causes increased HR, contractility
- -increases metabolism of heart itself which sets off local blood flow control mechanisms to cause coronary VD
Are the direct or indirect effects of the ANS on coronary blood flow more significant?
The indirect effects
What are the indirect effects of PNS stimulation on coronary blood flow ?
- -Vagal stim (via Ach) causes decreased HR and metabolism
- -This leads to decreased O2 consumption and VC
What are the direct effects of SNS stimulation on coronary blood flow ?
- -There is extensive SNS innervation to the coronaries
- -Can cause VC or VD depending on receptor (alpha or beta)
- -Usually causes VC
Where are the alpha receptors located primarily and what effect do they usually have?
Where are the beta receptors located primarily and what effect do they usually have?
What are the direct effects of PNS stimulation on coronary blood flow ?
- -Direct causes release of Ach which causes VD
- -However, there is minimal direct vagal stim to the heart
T or F, the direct effects of ANS control on coronary blood flow are from direct innervation of the ANS fibers themselves
Where does most of the energy for cardiac muscle come from?
What type of metabolism occurs when the heart is ischemic? What's its significance?
- -End product is lactic acid
- -LA build up is partly responsible for the pain of angina
What happens to adenosine after 30 mins of ischemia?
- -It goes into the systemic circulation (cardiac muscle cell membrane is slightly permeable to it)
- -After 30 mins half of the adenosine is lost from the cardiac muscle cells and it takes a while to generate more (this is bad as adenosine causes VD)
- -So after 30 mins it may be too late to prevent injury and death of the cardiac cells
- -This is likely the etiology of MI
What happens to fatty acids after they are metabolized?
Used to form ATP in the mitochondria
- -uncomfortable chest sensation from ischemia
- -coined in 1772 by a british MD
- -chronic pattern of transient angina with exertion, relieved by rest
- -caused by a fixed obstruction of plaque in 1 ore more coronary arteries
- -inappropriate VC
variant angina (prinzmetal)
- -angina at rest due to coronary artery spasm
- -no overt plaque
- -spasm causes decreased blood flow
- -due to decreased O2 supply vs increased demand
What is thought to cause the spasms associated with variant angina?
- -Not completely understood
- -possibly due to early artherosclerosis
- -possibly due to endothelial dysfunction
- -asymptomatic ischemic episodes
- -can occur in people who normally experience anginal pain
- -common in pts with DM, elderly, and women
- -pts with anginal symptoms that have no arterosclerosis on angiography
- -ischemia may show up on stress test
- -due to inadequate vasodilator reserve
- -rx vessels may be too small to be seen on angiography
- -better prognosis than pts with overt pathology
- -pattern of increased frequency and duration of ischemia
- -episodes occur with bless physical or emotional exertion, or at rest
- -MI precursor
- -plaque can rupture
- -unopposed VC
- -acute coronary syndrome
- -unstable angina and MI
- -due to rupture of unstable plaque leading to subsequent plt aggregation and thrombosis
what factors influence myocardial supply (delivered O2)?
- -O2 content
- -Coronary blood flow
what factors affect O2 content?
(hgb x 1.39 x O2 sat) + (0.003 x PO2)
Is O2 content constant?
Yes in the absence of anemia and pulmonary disease
what factors affect coronary blood flow? Do they affect it directly or inversely?
- -coronary perfusion pressure
- -coronary vascular rx
- flow = pressure / rx
Since most of coronary artery perfusion occurs during diastole what approximates their perfusion pressure?
aortic diastolic pressure
Are the epicardial coronary arteries patent throughout the cardiac cycle?
- -The subendocardial vessels are compressed during systole
How will AR or hypotension (which decrease aortic diastolic pressure affect coronary O2 supply?
It will decrease coronary O2 supply as flow will be decreased (most of perfusion occurs during diastole)
Why is the subendocardial layer more prone to ischemic damage?
- -It is adjacent to high intraventricular pressure and is subject to a greater force
- -Also they have greater difficulty obtaining adequate flow as they get compressed during systole
What factors can affect rx of the coronary vasculature and thus affect O2 supply?
- -anything that compresses the coronary arteries (systole)
- -alteration of the intrinsic tone of the arteries
What's the most important factor affecting the heart's ability to have an adequate O2 supply?
autoregulation of the coronary vascular rx to provide increased blood flow when O2 demand is increased
what 3 factors affect O2 demand?
- -wall stress
How does wall stress affect O2 demand? Who's equation explains this?
- T (wall stress) = P (systolic pressure in ventricle) x intraventricular radius / 2 h (wall thickness)
What factors contribute to the pathophysiology of ischemia?
- -fixed vessel narrowing
- -endothelial cell dysfunction
How does fixed vessel narrowing contribute to the pathophysiology of ischemia?
- -fluid mechanics (Ohm's and P's Laws)
- -significance of a stenotic lesion depends on it's length (rx is directly proportional to stenosis length)
- -anatomy proximal epicardial arteries are more subject to overt artherosclerosis; smaller and distal arterioles act as a reserve and can increase diameter with exertion
At what level of stenotic narrowing can the rx vessels (arterioles) no longer compensate?
- >70% at this level the resting flow is ok, but with full dilation of rx vessels, max flow decreases and with increased demand the supply is not enough, and ischemia results
- >90% ischemia at rest
How does endothelial cell dysfunction contribute to ischemia?
- -inappropriate VC
- imbalance btw SNS mediated VC and impaired VD, VC results
- -loss of normal anti-thrombotic properties
- VD substances released from endothelial cells also have anti-thrombotic properties
Who's at risk for endothelial cell dysfunction?
- -CAD, HTN, cigarette smoker, HL, DM
- -impaired released of VD substances
T or F, endothelial dysfunction often occurs before the development of visible atherosclerosis ?
What are antecedents to artherosclerosis ?
- -genetic predispo
- -sedentary lifestyle
- -all lead to endothelial cell dysfunction
most common cause of reduced coronary blood flow
What are the consequences of atherosclerosis?
- -cholesterol deposits beneath the endothelium (in all areas of the body)
- -deposits are invaded by fibrous tissue and calcified
- -atherosclerotic plaques protrude into vessel lumen and impede blood flow
How does an acute coronary occlusion develop? Does it develop in someone with normal coronaries?
- 1) atherosclerotic plaque
- 2) coronary arterial spasm
-occurs in someone with atherosclerosis, not in someone with normal coronaries
T or F, a hyperactive SNS can cause coronary arterial spasm leading to acute coronary occlusion
-what is it?
-can it compensate?
- -the large arteries don't communicate with each other but there are anastamoses among the smaller arteries
- -with an acute occlusion, the smaller anastamoses with dilate in seconds
- -the blood flow is only 1/2 of what's needed
How does it take for collateral circulation to have normal blood flow?
- -flow increases after 8-24 hours
- -doubles by day 2-3
- -after 1 month blood flow approximates normal
Is it better if atherosclerosis develops gradually? Can it affect the collaterals?
- Yes as it is less likely an acute episode will develop as the collaterals have time to develop.
- But with progression of arteriosclerosis, the collaterals themselves can become atherosclerotic and pump failure results
consequences of ischemia
- -pulmonary congestion causing dyspnea
- -lactate accumulation causing angina
- -ion channel abnormalities causing arrhythmias
- -stunned or hibernating myocardium
What is the ultimate fate of a cardiac ischemic attack?
- -It depends on the severity and duration of imbalance btw O2 supply and demand
- -Can range from complete recovery to irrev. necrosis and death
- -prolonged period of contractile dysfunction WITHOUT necrosis
- -normal function ultimately resumes
- -severe episode of transient ischemia -magnitude of stunning (impaired contractile process) if often due to ischemia just short of causing necrosis
- -needs an intervention!!!!
- -tissue has chronic contractile dysfunction
- -usually due to persistent decreased blood supply, often from multi-vessel CAD
- -if flow is restored and irreversible damage has not occurred the heart can recover
quality of chronic stable angina
pressure, tightness, discomfort, burning, heaviness, pain
NOT- sharp, no variance with movement or inspiration
location of chronic stable angina
diffuse, often retrosternal, left precordium, can radiate to arm or shoulder
pt's place their fist over their chest, indicative of angina
accompanying symptoms of chronic stable angina
- -tachycardia, diaphoresis, nausea, dyspnea
- -due to ANS stimulation
precipitants of chronic stable angina
- -physical exertion, large meal, cold weather (VC causing add'l wall stress)
- -usually resolves with cessation of activity
what does it mean if SL NTG relieves the CP?
this is indicative of angina
risk factors for chronic stable angina
HTN, HL, tobacco, family hx
timing of chronic stable angina
- -lasts for a few mins, rarely longer than 5-10 mins
- -lasts for longer than a few secs
differential diagnosis GI issues vs. angina
GI issues are usually precipitated by food and are unrelated to exertion
differential diagnosis musculoskeletal issues vs. angina
- -localized pain, pt can point to the pain
- -superficial pain
- -worsened with movement
what signs might be seen on PE during an acute MI, what would cause them?
- -dyskinetic apical impulse (due to systolic dysfunction)
- -rales (systolic and diastolic dysfunction leading to pulm. congestions)
- -S4 (decreased diastolic compliance)
- -MR (papillary muscle dysfunction)
- -diaphoresis, tachycardia, HTN (increased SNS tone)
acute MI vs stable angina ST changes
- acute MI- ST changes do not resolve with resolution of symptoms
- stable angina- ST changes resolve with resolution of symptoms
Diagnostic studies: EKG
- -acute MI: ST segment changes, flat or inverted T wave
- -will only see changes if pt is ischemic at the time of EKG
EKG of transmural ischemia vs. subendocardial ischemia
- transmural- ST elevation
- subendo- ST depression (either horizontal or downsloping)
Diagnostic studies: standard stress test
- -pt walks on treadmill or rides bike until they experience angina, achieve target HR (85% of max), fatigue, develop signs of ischemia on EKG
- -positive test= pt's usual pain is elicited or ischemic changes are seen (>1mm ST segment depression)
the test says the pt has the disease and they actually do
probability that a negative test means that the pt does not have the disease
sensitivity and specificity of std stress test
What constitutes a markedly positive stress test? What does this mean?
- -Ischemic changes develop during the first 3 mins of exercise or persist for 5 mins after exercise stopped, ST segment depression > 2 mm, hypotension (systolic dysfunction), high grade ventricular arrhythmia, can't exercise for 2 mins due to severe cardiopulmonary limitations
- -likely multi-vessel disease
Can beta blockers affect test results?
yes, hence they are often held for 24 - 48 hours prior
Diagnostic studies: nuclear stress test
- -used in pts where a std stress test would not be useful due to preexisting ST abnormalities due to LVH or L BBB
- -radioactive dye injected during peak exercise and imaging is done
- -dye accumulates in proportion to degree of viable tissue
- -ischemia shows up as a cold spot
how do you differentiate btw reversible and non-reversible ischemia on nuclear stress test?
- -images are done at rest either before or several hours before exercise
- -if the cold spot has filled in, you know it's reversible ischemia
- -if cold spot not filled in, it's an area of irreversible infarct
sensitivity and specificity of nuclear imaging
Diagnostic studies: exercise echo
- -used in pts where a std stress test would not be useful due to preexisting ST abnormalities or prior stress test undiagnostic
- -do echo, pt exercises, echo again
- -looking for contractile dysfunction with exertion (hypokinesis or akinesis)
- -poor imaging in an obese pt
sensitivity and specificity of exercise echo
Diagnostic studies: pharm stress test
- -for a pt who can't exercise (due to PVD or arthritis)
- -use dobutamine (increases heart's O2 demand)
- -also can use VD like persantine or adenosine
- -ischemic tissue is already max dilated
- -VD drug will increase the flow to healthy areas ("steal")
- -combined with imaging to reveal regions of impaired perfusion
Diagnostic studies: coronary angiography
- -most direct means of diagnosing stenosis
- -anatomic info only, NOT functional
- -does not predict if plaque is likely to rupture
- -gold std for dx of CAD
- -reserved for pts who are unstable, require revasc or are unresp to drugs
- -contrast dye inject and look under radiograph
Diagnostic studies: cardiac CT
- -non invasive
- -shows calcification of coronary arteries with severity of CAD
- -excludes significant CAD in a pt with CP and low suspicion
- -less sensitive than cardiac angiography
what factors affect the natural history of atherosclerosis?
- -location and extent of stenosis
- -degree of LV impairment
what's the goal in the treatment of CAD?
- -decrease the frequency of attacks
- -prevent acute attacks (MI)
- -prolong survival
- -maintain balance between O2 supply and demand
medical treatment to prevent recurrence of angina
- -nitrates - limited as a tolerance develops, no evidence they improve survival but they do help with symptom relief
- -beta blockers- decrease rate recurrent infarction and mortality post MI, 1st line CAD tx
- -calcium channel blockers - decrease O2 demand via venodilation and arterial dilation to decrease wall stress
are long or short acting calcium channel blockers used for treatment of CAD?
- long acting
- -shorting acting are associated with increased rate of MI and mortality
What can occur when combining beta blockers and calcium channel blockers?
- -Combined effect on HR and contractility
- -May be problematic for some pts
- -Could intensity HF symptoms
medical tx to prevent acute cardiac events
- -anti platelet therapy (ASA and plavix)
what do ASA and plavix to?
- -both inhibit plt aggregation
- -more effective when used together
- -good for lowering LDL
- -want LDL < 70 in pts with high risk for HD
-decrease risk death, stroke, MI
- 1) PTCA percutaneous transluminal coronary angioplasty
- 2) CAGB
In what pts would revascularization be indicated?
- -high risk CAD
- -symptoms do not respond to drugs or have bad SE from meds
risk MI and mortality from revascularization?
- -angioplasty with balloon
- -1/3 of pts restenosis
- -hence stents were developed
issues with BM stents
- -stents are thrombogenic
- -need ASA and plavix
- -neointimal proliferation, smooth muscle cells migrate and produce extra cellular matrix
- -hence drug eluding stents developed
drug eluding stent
- -drug released over 2-4 weeks
- -coated with anti-proliferative medication
- -prevents neointimal proliferation and endothelialization of the stent
- -need for revasc decreased by 1/2
CAGB- 2 techniques
- 1) native vein (usually saphenous)
- 2) arterial graft (internal mammary)
CABG, vein vs. artery graft
- Vein- patency 80% after 1 year
- -vulnerable to atherosclerosis
- -after 10 years only 50% patent
Artery- after 10 years only 90% patent, better choice especially in an area of critical flow like the LAD
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