Coronary%20Heart/Artery%20Disease - PowerPoint PPT Presentation

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Coronary Heart/Artery Disease J.B. Handler, M.D. Physician Assistant Program University of New England * – PowerPoint PPT presentation

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Title: Coronary%20Heart/Artery%20Disease

Coronary Heart/Artery Disease
  • J.B. Handler, M.D.
  • Physician Assistant Program
  • University of New England

  • CHD- coronary heart disease
  • LDL- low density lipoprotein
  • HDL- high density lipoprotein
  • HTN- hypertension
  • CAD- coronary artery disease
  • PVR- peripheral vascular resistance
  • HCM- hypertrophic cardiomyopathy
  • EF- ejection fraction
  • PCI- percutaneous coronary intervention
  • CHO- carbohydrate
  • SVR systemic vascular resistance (same as PVR)
  • HF- heart failure
  • CO- cardiac output
  • CK- creatine kinase (also CPK)
  • AIVR- accelerated idioventricular rhythm
  • VT- ventricular tachycardia
  • ACEI- angiotensin converting enzyme inhibitor
  • T-PA- tissue plasminogen activator
  • UF- unfractionated (heparin)
  • STEMI- ST segment elevation MI vs NonSTEMI
  • PAD- peripheral arterial disease
  • PTCA- percutaneous transluminal coronary

Coronary Anatomy
AllRefer Health
  • Leading cause of cardiovascular disability and
    death in the U.S. More than 12 million persons
    have CHD and sequelae ?500,000 deaths/yr
  • Gradual process involving the 3 major coronary
    arteries and their branches focal involvement.
  • Gradual reduction of arterial lumen resulting in
    ischemia due to reduced O2/blood supply.
  • Abrupt arterial occlusion/thrombosis initiates

Coronary Atherosclerosis
Risk Factors for Atherosclerosis
  • Lipids Total Cholesterol, LDL, HDL,
  • Hypertension
  • Cigarette smoking
  • Diabetes Mellitus
  • Family history for CAD- 1st degree relative-
    younger the onset, higher the riske.g. male lt55
    female lt65.

Risk Factors for Atherosclerosis
  • Male gender
  • Age (men? 45 women ?55)
  • Hypoestrogenemia
  • Physical inactivity
  • Central obesity
  • Elevated plasma homocysteine levels
  • Amino acid derived from digestion of meat and
    dairy proteins
  • Elevation of CRP, an inflammatory marker

C-reactive Protein and Inflammation
  • A marker of chronic inflammation
  • Independent risk factor for CHD if elevated, even
    in patients with normal LDL-C.
  • Inflammation is likely a component of the
    atherosclerotic process
  • Chronic inflammation may be involved in the
    development of placque rupture and unstable
    coronary lesions.
  • lt1 mcg/ml, 1-3 mcg/ml, gt3 mcg/ml

Intermediate risk
Low risk
High risk
Pathogenesis of Atherosclerosis Endothelial
  • Chemical causes LDL, homocysteine, glucose.
  • Hemodynamic- disturbed flow patterns,
  • Biological- ??viral, endotoxin, immune complexes.
  • Nitric Oxide (NO) made by endothelial cells is
    protective vasodilator with anti-atherosclerotic
    properties- decreased or absent production in
    presence of smoking, HTN and diabetes.

Prevention of Atherosclerosis
  • Primary prevention Risk factor modification -
    smoking cessation, antihypertensive Rx, treatment
    of dyslipidemia, estrogen replacement
    (pre-menopause), glucose regulation/DM, regular
    exercise, aspirin prophylaxis in high risk
  • Secondary prevention Delay or abort disease
    progression in patients with documented CHD more
    aggressive risk factor modification.

Aspirin and Primary Prevention
  • Emerging data using Aspirin and primary
    prevention of 1st MI (men), stroke (women) and
    vascular death. Physicians Health Study data.
  • At risk Men age 45-79 or women age 55-79 with 2
    or more of the following risk factors Smoking,
    HTN, hypercholesterolemia, FH.
  • Diabetes ASA for all adult diabetics with ? 1
    other CV risk factor.
  • Recommendation 75 ASA daily (optimal dose
  • Must balance gain from ASA against increased risk
    of bleeding.

Prevention and Lipids
  • Increased LDL increases risk of CAD, stroke and
  • Aggressive treatment can prevent coronary events
    and stroke in patients without clinically
    manifest disease (see lecture on dyslipidemias).
  • Secondary prevention aggressive LDL lowering
    decreases progression and subsequent events in
    patients with documented atherosclerosis.
  • Disease regression unlikely, reported

Coronary Artery/Heart Disease
Myocardial Ischemia
  • Coronary stenosis once significant, results in
    imbalance between blood supply and demand. This
    limits the normal increase in perfusion when
    there is increased demand (activity, exercise).
  • Contributory factors ? myocardial O2 demand
  • Significant LVH, aortic stenosis)
  • Tachyarrhythmias (rapid Afib or flutter, others).

Effects of Active Ischemia
  • Symptoms usually present (below) but not always.
  • Cardiac Mechanical, electrical and valvular
    dysfunction (mitral regurgitation).
  • Reversible vs permanent dependent on how long
    ischemia is present prolonged ischemia?
  • Usually accompanied by characteristic ECG

Silent vs. Symptomatic Disease
  • Long asymptomatic stage before symptoms.
  • Symptoms of reversible ischemia (angina pectoris)
    occur as a result of
  • Increased myocardial O2 demand in the presence of
    fixed stenosis (?supply)
  • Reversible decrease of O2 supply vasospasm?
    significant narrowing (with or without
  • Prolonged ?O2 supply often results in unstable
    angina or infarction.
  • Placque rupture and thrombosis likely present

Coronary Atherosclerosis
Sudden Cardiac Death
  • Death within 1 hour after onset of symptoms
    usually within minutes. Malignant arrhythmia
    commonly present.
  • Common presenting manifestation of CHD.
  • Frequent end point in patients with CHD, prior MI
    and impaired LV function.
  • 15-20 of patients with AMI will die before
    reaching the hospital.

Acute Myocardial Infarction
Women are Different
  • Women with CHD often misdiagnosed presentation
    often atypical
  • Atypical symptoms Unusual pain presentations
  • Pain radiating to right arm arm pain alone
  • False negative stress tests common
  • Single vessel disease more common
  • Elderly or diabetic women may complain of
    general malaise, loss of appetite, vague
    abdominal discomfort if risk factors?get ECG!
  • Need higher index of suspicion in women with risk

Stable Angina Pectoris
  • Chest discomfort- heaviness, tightness, pressure,
    squeezing, burning, aching or choking may not be
    described as pain.
  • Levine sign substernal or to left of sternum.
  • Crescendo-decrescendo pattern, 1-5 min.
  • Radiation left shoulder and upper arm, back,
    neck, jaw and teeth.

Precipitating Factors
  • Exertion, exercise, emotional duress, cold
    weather, sexual activity, cigarette smoke, large
  • Patterns Often reproducible with activity
    patterns may vary depending on time of day,
    coronary tone threshold lower in a.m. and after
    emotional duress.
  • Sx resolve with cessation of activity, relaxation
    and following sub-lingual (rapid acting) NTG.

Clinical Presentation
  • Characteristic history
  • Presence of risk factors
  • PE often normal in between episodes may include
  • Xanthelasma, xanthomas- hyperlipidemia.
  • Funduscopic abnormalities A-V nicking,
    hypertensive, diabetic changes.
  • Cardiac- S4 gallop (during angina), bruits
    (atherosclerosis), murmurs, changes in BP.

  • Often normal in between anginal episodes. May
    show prior infarcts, ST-T changes.
  • During episode may show characteristic ischemic
    changes ST segment depression and/or T wave
    changes changes normalize within minutes
    following an anginal episode.

Stress Electrocardiography
  • Most useful non-invasive procedure for evaluating
    the patient with angina.
  • Standardized protocols utilizing exercise or
    medications are used to increase cardiac workload
    (or coronary blood flow)- see lecture on cardiac
  • Resting and stress ECGs are compared looking for
    characteristic changes of ischemia.

Stress Electrocardiography
Stress Testing
  • Sensitivity/Specificity Influenced by number of
    involved vessels, duration of exercise, and
    presence of resting ECG abnormalities.
  • Sensitivity/Specificity can be improved by adding
    imaging techniques Myocardial perfusion
    scintigraphy or echocardiography- see lecture on
    cardiac testing.

Coronary Arteriography
  • The gold standard for assessing severity of
    CAD. Defines vessels involved, degree of
    stenosis and LV function.
  • Angiography is used in conjunction with patients
    symptoms and extent of ischemia (via stress
    testing) to determine severity and significance
    of disease, and is often the final piece of
    information necessary to determine therapeutic

Angiogram Coronary Stenosis
Angiogram of Stenosis in Graft
Medical Treatment of Angina
  • Treat or eliminate aggravating factors.
  • Acute attacks Sub-lingual NTG -
    venodilatorgtarterial dilator. Reduces LV volume
    (preload) decreasing O2 consumption may improve
    collateral flow also aborts coronary vasospasm.
    Usual dose is 0.3-0.6 mg, and repeated at 3 to 5
    minute intervals.
  • Prophylactic sub-lingual NTG taken 5 minutes
    before activities likely to precipitate angina.

Beta Receptor Blockers
  • Prevent angina by decreasing myocardial O2
    consumption (MVO2) decrease HR, contractility
    and BP. Improve exercise tolerance and reduce
  • Other benefits of ß-blockers
  • Reduce mortality post MI
  • Reduce mortality in patients with heart failure

Beta Receptor Blockers
  • Can induce bronchospasm in patients with asthma
    or COPD Role for ß-1 selective agents.
  • Numerous ß-blockers available. Choice may be
    influenced by selectivity and other features.
    Widely used in Rx of HTN, arrhythmias, HF,
    essential tremor and prevention of migraine
  • Propranolol, Atenolol, Metoprolol, Carvedilol, et

Long Acting Nitrates
  • Long acting nitrates- Oral, topical
    formsIsosorbide dinitrate or mononitrate
    (oral)NTG ointment or patches (topical).
  • Used to prevent angina- ?MVO2 improve exercise
  • Tolerance - need for nitrate free intervals.
  • Side effects headaches, hypotension.
  • Must DC Viagra when using nitrates!

Calcium Channel Blockers
  • Decrease myocardial O2 requirements by dilating
    peripheral arteries/arterioles, reducing BP, LV
    wall stress, and afterload also reduce coronary
    tone and spasm- induce vasodilation.
  • Result is ?MVO2 (myocardial O2 consumption)
  • Improve exercise tolerance/prevent angina
  • Some Ca blockers also have negative inotropic and
    chronotropic effects? ?MVO2
  • Do not reduce mortality post MI (compared to

Dihydropyridine Ca Blockers
  • Dilate arterioles, ?PVR? afterload ? MVO2 Minimal
    negative inotropic and chronotropic effects.
  • Best used in addition to ?-blockers in the
    treatment of angina.
  • Long acting preparations reduce likelihood of
  • Numerous available Nifedipine, amlodipine, and

Diltiazem and Verapamil
  • Useful as an adjunct to nitrates in the treatment
    of angina (vs ?-blocker).
  • Dilate arterioles ?HR and contractility ?
  • Diltiazem can be used cautiously with ?-blocking
    agents in treatment of angina- avoid Verapamil.
  • Both are also useful in hypertension and for
    certain cardiac arrhythmias.
  • Avoid in patients with heart failure.

Ranolazine (Interest Only)
  • New (2006) for treatment of chronic angina in
    patients without adequate response to standard
    meds (above) modest improvement in Sx.
  • Unique MOA ?s late Na current, ?ing intracelular
    calcium. Also decreases fatty acid
    metabolism,?ing CHO metabolism which takes less
  • No significant effect on HR or BP.
  • Side effects Dizziness, HA, constipation and
  • ECG Increases Q-T interval caution.

Anti-Platelet Agents
  • Low dose aspirin (81-325 mgs.) has been shown to
    reduce coronary events post myocardial
    infarction. Indications all pts with CHD.
  • ?s incidence of subsequent MI, cardiac death.
  • Clopidogrel inhibits ADP-induced platelet
    aggregation option if ASA is contraindicated.
  • ASA or Clopridogrel also recommmended in patients
    with PAD and carotid disease.
  • ?s incidence of subsequent MI, cardiac death,

Revascularization Indications
  • Patients with unacceptable symptoms in spite of
    optimal medical Rx.
  • 3 Vessel CAD especially with LV dysfunction
  • Left main or left main equivalent disease
  • Following treatment of unstable angina if there
    is evidence of early onset ischemia.
  • Patients post MI with ongoing ischemia, or with
    early onset ischemia via stress testing.
  • Acute MI (see below)

Catheter Based Techniques
  • Angioplasty and related techniques can be
    performed with low morbidity, mortality, and
    rapid recovery.
  • Indicated primarily for single or 2 vessel
  • Comparable mortality and infarction rates
    compared to CABG over 1st three years, but high
    rate of repeat procedures until recently.
  • Major drawback Restenosis requiring
    repeat/multiple procedures? improved last 5 yrs
    with newer drug eluting stents (below).

Catheter Based Techniques
  • Catheters used to open stenosed/occluded coronary
    arteries or bypass grafts.
  • Angioplasty (PTCA), Atherectomy, etc.
  • Problem 30-40 re-stenosis rate.
  • Stent Placement- insertion of metal sleeve into
    stenosis ?re-stenosis-15-20
  • Using drug eluting (Sirolimus, Paclitaxel) stents
    ??s re-stenosis- 5-8 problems with late stent
    thrombosis ? intense anti-platelet Rx..

Coronary Angioplasty
Coronary Angioplasty and Stent
Stent Placement
Coronary Artery Bypass Surgery
  • Obstructed coronary arteries are bypassed using
    veins or arteries. Low mortality (1-4) if LV
    function preserved.
  • Best long term results of patency and flow.
  • Saphenous veins, radial artery and internal
    mammary arteries are commonly used to bypass
    diseased segments.

Coronary Bypass Graft Surgery
Coronary Artery Bypass Surgery
  • Operative mortality increased if age gt 70, EFlt
  • Vein closure rates 10-20 in 1st year, then 4
    annually vein grafts and native vessels subject
    to recurrent disease.
  • Internal mammary grafts-high patency rate over
    time- best option for grafts where possible.
  • Radial artery grafts are better than vein grafts,
    but use is limited.

Coronary Vasospasm
  • May present in patients with normal coronaries,
    or superimposed on atherosclerotic disease.
  • Often induced by exposure to cold, emotional
    stress, meds (ergot), or drugs (cocaine).
  • Clinical presentation Chest discomfort
    accompanied by ST segment elevation and
  • May progress to MI (and consequences) if spasm
    does not resolve.

Prinzmetals Angina
  • Coronary ischemia as a result of vasospasm.
  • Symptoms at rest, often in early A.M.
  • Women gt men. AKA variant angina.
  • Coronary arteriography often identifies normal
    appearing vessels- vasospasm can be induced
    pharmacologically in cardiac cath lab.
  • Treatment very successful with nitrates and
    calcium channel blockers.

Acute Coronary Syndromes
  • Unstable Angina (UA)
  • Myocardial Infarction
  • There is considerable overlap between UA and
    NSTEMI. The pathology is nearly identical. The
    major difference with NSTEMI there are abnormal
    cardiac markers (CK MB or troponins) that
    indicate cell necrosis. With UA, no cell
    necrosis has occurred (yet).

Plaque Rupture
Unstable Angina (UA)
  • Angina at rest or with minimal activity, often
    lasting gt 10 min. (without MI? negative cardiac
  • New onset angina (lt 4 wks) with progressive
    symptoms? more severe pain.
  • Accelerating or creshendo angina in patient with
    previously stable angina.
  • 50 of patients will have abnormal ECG (St
    depression and T wave inversion).

Characteristics Unstable Angina
  • Pathology complex coronary lesions- stenosis
    with placque rupture, hemorrhage, thrombus.
  • Prognosis (untreated) High risk of developing MI
    in following days/weeks.
  • ECG evidence of ischemia- ST depression, TW
    inversion LV dysfunction common during ischemia
    (echo imaging).
  • No elevation of cardiac markers/enzymes.
  • Presentation of Non-STEMI infarct often
    indistinguishable from unstable angina (but
    enzymes/markers are elevated with NSTEMI).

Treatment Unstable Angina
  • Hospitalize, bedrest, O2, monitoring.
  • Full anticoagulation anti-platelet therapy
    Heparin (UF Heparin or LMW) plus ASA plus
    Clopidogrel other anti-platelet agents (IV
    glycoprotein IIb/IIIa antagonists- (eptifabatide,
    tirofiban) should be added in highest risk
    patients and before PCI.
  • Nitrates (topical, IV), ?-blockers, and
    Ca-blockers commonly used to ?MVO2.

Outcomes with Unstable Angina
  • 20 remain unstable and require invasive
    evaluation and revascularization.
  • 80 improve medically. Once stable, some form of
    stress testing is performed. An early test is
    an indication for invasive evaluation and
    revascularization based on the anatomy.

Acute Myocardial Infarction
  • Definition Prolonged ischemia resulting from
    inadequate tissue perfusion leading to tissue
    necrosis and myocardial cell death.
  • Includes ST segment elevation MI and non-ST
    segment elevation MI.
  • STEMI CAD?Placque rupture? Platelets?Clotting ?
    Occlusive Thrombus.
  • Inflammation contributes to placque

CAD with Thrombus
Acute Myocardial Infarction
  • Statistics gt 1.1 million events/yr. in U.S.
    Death in gt350,000 (half are sudden) gt750,000
  • Infarct location and size correlates with
    distribution of occluded vessel, collateral
    circulation, and presence of additional disease.

Clinical Presentation
  • Often in early A.M hours.
  • 1/3 with premonitory history of unstable angina
  • Chest pain much more severe than angina atypical
  • Patients are anxious, restless, diaphoretic and
    in distress.
  • LV dysfunction or stiffness can result in SOB.
  • Painless infarction common in diabetics.

Physical Findings
  • Pulse and BP variable and change frequently
    hemodynamic instability common.
  • Irregularities in pulse may represent
  • Lungs usually clear unless heart failure present.

Physical Findings
  • S4 gallop in most S3 unusual unless CHF.
  • Transient apical mitral regurgitant murmurs
    usually represent papillary muscle dysfunction.
  • Extremities cyanosis/cold indicate low CO.

Serum Markers
  • Enzymes and proteins released from necrotic
    myocardial cells.
  • CK (creatine kinase) enzyme released from damaged
    skeletal muscle and heart. Total CK (aka CPK)
    always elevated with MI. Isoenzymes distinguish
    between source
  • CK MB fraction Heart nl lt4 of total CK

Serum Markers
  • CK MB isoenzymes rise within 4-6 hrs, peak in
    16-24 hrs (2-10x nl), fall to baseline in 2-3
  • Cardiac specific troponins cTnI ( cTnT) rises
    within 4-6 hours, peak in 8-12 hours and remains
    elevated for 5- 7 days. Somewhat more
    sensitive/specific for small MI. Also useful if
    symptoms are several days old. Abnormal if gt
    0.05ng/mL diagnostic for MI with high
    sensitivity/specificity if gt 0.1ng/mL

Lab and Other Findings
  • Leukocytosis common.
  • ECG Diagnostic criterion for STEMI vs. NonSTEMI
    (see ECG lectures).
  • CXR often normal, unless there is HF or prior
    cardiac problems.
  • Echocardiography Provides bedside assessment of
    global and regional LV function. Identifies
    Mitral regurg if present.

ECG Acute Anterior MI
Myocardial Infarction
Management of MI
  • Pre-hospital care management of electrical and
    hemodynamic instability race against time O2,
    analgesia, other meds as indicated.
  • Parenteral narcotics Morphine sulfate
  • Aspirin given early in ED
  • Nitroglycerin usually initiated IV and pain and BP.
  • IV followed by oral ?-blockers- decrease MVO2,
    reduce in hospital and post discharge mortality.

Thrombolytic Therapy STEMI
  • Indications ST elevation of gt1 mm. in two or
    more contiguous/adjacent leads. Not indicated
    with ST depression or TW inversion alone.
  • Goal Reduced mortality and infarct size.
  • Greatest benefits with large infarcts and when
    given within the first 1-3 hrs of symptoms (50
    reduction in mortality).
  • Contraindications uncontrolled HTN, prior stroke
    (within one year) or cerebral hemorrhage, known
    bleeding diathesis, recent head trauma.

Thrombolytic Therapy STEMI
  • Relative contraindications recent (within 3
    weeks) abdominal or thoracic surgery.
  • Agents Recombinant t-PA (Alteplase), Reteplase,
    Tenecteplase. All given by IV injection or
    infusion? similar efficacy.
  • Risks Bleeding and intracerebral hemorrhage.

Post -Thrombolytic Management
  • Includes ASA (ongoing) and Heparin (x 24 hours).
    Clopidogrel often given as well.
  • Rapid resolution of pain
  • Ventricular arrhythmias (PVCs, VT, AIVR)
  • Rapid evolution of ECG (often to Q waves)

Post -Thrombolytic Management
  • 10-20 of infarct related vessels will re-occlude
    during the hospitalization- recurrent pain and
    ECG changes indication for catheterization and
  • Stable patients post reperfusion stress testing
    prior to discharge.

Acute Primary PCI
  • Available in a few centers-alternative to
    thrombolytic therapy with better results.
  • Patients taken from ED directly to cath lab for
    acute angioplasty/stenting. Goals
  • Open artery within 3 hours of onset of symptoms
    (includes transportation).
  • Open artery within 90 after presenting to
    hospital that does PCI/angioplasty/stenting.
  • Requires capability of CABG if necessary.

PCI- percutaneous coronary intervention
Acute Primary PTCA
  • More effective than thrombolytics in opening
    occluded arteries improved outcomes.
  • An alternative approach if thrombolysis
    contraindicated. Preferred in elderly patients.
  • Lower risk of hemorrhage.
  • If within 1.5 hours of hospital that does acute
    angioplasty (with rapid response rate), think
    about transfer rather than thrombolytics.

Hospital Phase Care
  • CCU care
  • B-blockers, nitrates, aspirin/clopidogrel as
  • ACE Inhibitors Improve short and long term
    survival and aid in LV remodeling post
    MI.Beneficial with large infarcts complicated by
    significant LV dysfunction, low EF or CHF.
  • Aldosterone blockers patients with large MI,
    ?EF or symptoms of heart failure.

Complications of Acute MI
  • Arrhythmias atrial and ventricular.
  • Left ventricular dysfunction CHF-primary cause
    of intra-hospital death.
  • Papillary muscle dysfunction Mitral
    Regurgitation- new murmur
  • Hypotension and shock
  • RV infarction
  • Conduction abnormalities
  • Ventricular aneurysm formation

Ventricular Aneurysm
  • Infarcts characterized by by prolonged ischemia,
    small elevations of cardiac markers and EKG
    changes showing ST depression and/or T wave
  • CAD?Placque rupture?Platelets?Clotting ?
    Thrombus. Similar Rx as Unstable Angina.
  • Considered incomplete infarcts with lower
    initial mortality but high risk of re-infarction
    and with high mortality.
  • Very aggressive management often involving
    angiography and revascularization.

Uncomplicated Infarction
  • Pre-discharge low level stress test with maximal
    stress test 6 wks. post discharge.
  • Cardiac Rehabilitation
  • Aggressive risk factor modification
  • Use of B-blocking agents and ACE Inhibitors.
  • HOPE trial ACEI in patients with LV dysfunction
    post MI mortality ?20.
  • Statins to ?LDL lt??? (see Dyslipidemias).

Post Infarction Management (IO)
  • In hospital mortality 10-15 determined by size
    of the infarct.
  • Patients at increased risk post MIRecurrent
    ischemic painNonSTEMI infarctCHFLVEF lt
    .40Stress test (low level) induced ischemiaHigh
    grade ventricular arrhythmias late in course
  • Invasive evaluation and revascularization.

Revascularization Post MI (IO)
  • Recurrent ischemia post thrombolysis.
  • Recurrent ischemia post infarct.
  • LV dysfunction with ongoing ischemia.
  • Patients with markedly positive stress tests and
    multi-vessel disease.
  • And others
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