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Coronary Heart/Artery Coronary Heart/Artery DiseaseDisease

J.B. Handler, M.D.J.B. Handler, M.D.Physician Assistant ProgramPhysician Assistant ProgramUniversity of New EnglandUniversity of New England

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Abbreviations Abbreviations CHD- coronary heart diseaseCHD- coronary heart disease LDL- low density lipoproteinLDL- low density lipoprotein HDL- high density lipoproteinHDL- high density lipoprotein HTN- hypertensionHTN- hypertension CAD- coronary artery diseaseCAD- coronary artery disease PVR- peripheral vascular resistancePVR- peripheral vascular resistance HCM- hypertrophic cardiomyopathyHCM- hypertrophic cardiomyopathy EF- ejection fractionEF- ejection fraction PCI- percutaneous coronary PCI- percutaneous coronary

interventionintervention CHO- carbohydrateCHO- carbohydrate SVR: systemic vascular resistance SVR: systemic vascular resistance

(same as PVR)(same as PVR) HF- heart failureHF- heart failure

CO- cardiac outputCO- cardiac output CK- creatine kinase (also CPK)CK- creatine kinase (also CPK) AIVR- accelerated idioventricular AIVR- accelerated idioventricular

rhythmrhythm VT- ventricular tachycardiaVT- ventricular tachycardia ACEI- angiotensin converting ACEI- angiotensin converting

enzyme inhibitorenzyme inhibitor T-PA- tissue plasminogen activatorT-PA- tissue plasminogen activator UF- unfractionated (heparin)UF- unfractionated (heparin) STEMI- ST segment elevation MI STEMI- ST segment elevation MI

vs NonSTEMIvs NonSTEMI PAD- peripheral arterial diseasePAD- peripheral arterial disease PTCA- percutaneous transluminal PTCA- percutaneous transluminal

coronary angioplastycoronary angioplasty

Coronary AnatomyCoronary Anatomy

AllRefer Health

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Atherosclerosis Atherosclerosis Leading cause of cardiovascular disability and Leading cause of cardiovascular disability and

death in the U.S. More than 12 million persons death in the U.S. More than 12 million persons have CHD and sequelae; have CHD and sequelae; 500,000 deaths/yr500,000 deaths/yr

Gradual process involving the 3 major coronary Gradual process involving the 3 major coronary arteries and their branches: arteries and their branches: focal involvementfocal involvement..

Gradual reduction of arterial lumen resulting in Gradual reduction of arterial lumen resulting in ischemia due to reduced Oischemia due to reduced O22/blood supply./blood supply.

Abrupt arterial occlusion/thrombosis initiates MI. Abrupt arterial occlusion/thrombosis initiates MI.

Coronary AtherosclerosisCoronary Atherosclerosis

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Risk Factors for AtherosclerosisRisk Factors for Atherosclerosis

Lipids: Total Cholesterol, Lipids: Total Cholesterol, LDLLDL, , HDLHDL, , triglycerides triglycerides

HypertensionHypertension Cigarette smokingCigarette smoking Diabetes MellitusDiabetes Mellitus + Family history for CAD- 1+ Family history for CAD- 1stst degree degree

relative- younger the onset, higher the riskrelative- younger the onset, higher the riske.g. male <55; female <65.e.g. male <55; female <65.

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Risk Factors for AtherosclerosisRisk Factors for Atherosclerosis

Male genderMale gender Age (menAge (men 45; women 45; women 55)55) HypoestrogenemiaHypoestrogenemia Physical inactivityPhysical inactivity Central obesityCentral obesity Elevated plasma homocysteine levelsElevated plasma homocysteine levels

– Amino acid derived from digestion of meat and dairy Amino acid derived from digestion of meat and dairy proteinsproteins

Elevation of CRP, an inflammatory markerElevation of CRP, an inflammatory marker

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C-reactive Protein and C-reactive Protein and InflammationInflammation

A marker of chronic inflammationA marker of chronic inflammation Independent risk factor for CHD if elevated, Independent risk factor for CHD if elevated,

even in patients with normal LDL-C.even in patients with normal LDL-C. Inflammation is likely a component of the Inflammation is likely a component of the

atherosclerotic processatherosclerotic process Chronic inflammation may be involved in the Chronic inflammation may be involved in the

development of placque rupture and unstable development of placque rupture and unstable coronary lesions.coronary lesions.

<1 mcg/ml, 1-3 mcg/ml, >3 mcg/ml<1 mcg/ml, 1-3 mcg/ml, >3 mcg/mlLow risk Intermediate risk High risk

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Pathogenesis of Atherosclerosis: Pathogenesis of Atherosclerosis: Endothelial DysfunctionEndothelial Dysfunction

Chemical causes: LDL, homocysteine, glucose.Chemical causes: LDL, homocysteine, glucose. Hemodynamic- disturbed flow patterns, Hemodynamic- disturbed flow patterns,

hypertensionhypertension.. Biological- ??viral, endotoxin, immune Biological- ??viral, endotoxin, immune

complexes.complexes. Nitric Oxide (NO) made by endothelial cells is Nitric Oxide (NO) made by endothelial cells is

protectiveprotective: vasodilator with anti-atherosclerotic : vasodilator with anti-atherosclerotic properties- decreased or absent production in properties- decreased or absent production in presence of smoking, HTN and diabetes.presence of smoking, HTN and diabetes.

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Prevention of AtherosclerosisPrevention of Atherosclerosis

Primary preventionPrimary prevention: Risk factor modification - : Risk factor modification - smoking cessation, antihypertensive Rx, treatment smoking cessation, antihypertensive Rx, treatment of dyslipidemia, estrogen replacement (pre-of dyslipidemia, estrogen replacement (pre-menopause), glucose regulation/DM, regular menopause), glucose regulation/DM, regular exercise, aspirin prophylaxis in exercise, aspirin prophylaxis in high riskhigh risk groups. groups.

Secondary preventionSecondary prevention: Delay or abort disease : Delay or abort disease progression in patients with documented CHD; progression in patients with documented CHD; more aggressive risk factor modificationmore aggressive risk factor modification..

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Aspirin and Primary PreventionAspirin and Primary Prevention Emerging data using Aspirin and primary prevention of Emerging data using Aspirin and primary prevention of

1st MI (men), stroke (women) and vascular death. 1st MI (men), stroke (women) and vascular death. Physician’s Health Study data.Physician’s Health Study data.

At risk: Men age 45-79 or women age 55-79 with 2 or At risk: Men age 45-79 or women age 55-79 with 2 or more of the following risk factors: Smoking, HTN, more of the following risk factors: Smoking, HTN, hypercholesterolemia, +FH.hypercholesterolemia, +FH.– Diabetes: ASA for all adult diabetics with Diabetes: ASA for all adult diabetics with 1 other CV risk 1 other CV risk

factor. factor. Recommendation: 75 ASA daily (optimal dose unclear).Recommendation: 75 ASA daily (optimal dose unclear). Must Must balance gain from ASA against increased risk of balance gain from ASA against increased risk of

bleeding.bleeding.

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Prevention and LipidsPrevention and Lipids

Increased LDL increases risk of CAD, stroke and Increased LDL increases risk of CAD, stroke and PAD.PAD.

Aggressive treatment can prevent coronary events Aggressive treatment can prevent coronary events and stroke in patients without clinically manifest and stroke in patients without clinically manifest disease (see lecture on dyslipidemias).disease (see lecture on dyslipidemias).

Secondary prevention – aggressive LDL lowering Secondary prevention – aggressive LDL lowering decreases progression and subsequent events in decreases progression and subsequent events in patients with documented atherosclerosis.patients with documented atherosclerosis.– Disease regression unlikely, reported occasionally.Disease regression unlikely, reported occasionally.

Coronary Artery/Heart DiseaseCoronary Artery/Heart Disease

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Myocardial IschemiaMyocardial Ischemia Coronary stenosis once significant, results in Coronary stenosis once significant, results in

imbalance between blood supply and demand. imbalance between blood supply and demand. This limits the normal increase in perfusion when This limits the normal increase in perfusion when there is increased demand (activity, exercise).there is increased demand (activity, exercise).

Contributory factors: Contributory factors: myocardial O myocardial O22 demand demand – Significant LVH, aortic stenosis) Significant LVH, aortic stenosis) – Tachyarrhythmias (rapid Afib or flutter, others).Tachyarrhythmias (rapid Afib or flutter, others).

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Effects of Active Effects of Active IschemiaIschemia

SymptomsSymptoms usually present (below) but not usually present (below) but not always.always.

Cardiac: Mechanical, electrical and valvular Cardiac: Mechanical, electrical and valvular dysfunction (mitral regurgitation).dysfunction (mitral regurgitation).– Reversible vs permanentReversible vs permanent: dependent on how : dependent on how

long ischemia is present; long ischemia is present; prolonged prolonged ischemiaischemia infarction. infarction.

Usually accompanied by characteristic ECG Usually accompanied by characteristic ECG findings.findings.

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Silent vs. Symptomatic DiseaseSilent vs. Symptomatic Disease Long asymptomatic stage before symptoms.Long asymptomatic stage before symptoms. Symptoms of reversible ischemia (angina pectoris) Symptoms of reversible ischemia (angina pectoris)

occur as a result of:occur as a result of:– Increased myocardial OIncreased myocardial O22 demand demand in the in the presence of presence of

fixed stenosis (fixed stenosis (supply)supply)– Reversible decrease of OReversible decrease of O22 supply supply: vasospasm: vasospasm

significant narrowing (with or without atherosclerosis) significant narrowing (with or without atherosclerosis) Prolonged Prolonged OO22 supply supply often results in unstable often results in unstable

angina or infarction.angina or infarction.– Placque rupture and Placque rupture and thrombosis likely presentthrombosis likely present

Coronary AtherosclerosisCoronary Atherosclerosis

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Sudden Cardiac DeathSudden Cardiac Death Death within 1 hour after onset of Death within 1 hour after onset of

symptoms; symptoms; usually within minutesusually within minutes. . Malignant arrhythmia commonly present.Malignant arrhythmia commonly present.– Common presenting manifestation of CHD.Common presenting manifestation of CHD.– Frequent end point in patients with CHD, prior Frequent end point in patients with CHD, prior

MI and impaired LV function.MI and impaired LV function. 15-20% of patients with *AMI will die 15-20% of patients with *AMI will die

before reaching the hospital.before reaching the hospital.

*Acute Myocardial Infarction

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Women are DifferentWomen are Different Women with CHD often misdiagnosed; presentation Women with CHD often misdiagnosed; presentation

often atypical:often atypical:– Atypical symptoms: Unusual pain presentationsAtypical symptoms: Unusual pain presentations– Pain radiating to right arm; arm pain alone Pain radiating to right arm; arm pain alone

False negative stress tests commonFalse negative stress tests common– Single vessel disease more commonSingle vessel disease more common

Elderly or diabetic women: may complain of Elderly or diabetic women: may complain of general malaise, loss of appetite, vague abdominal general malaise, loss of appetite, vague abdominal discomfort: if + risk factorsdiscomfort: if + risk factorsget ECG!get ECG!

Need higher index of suspicion in women with risk Need higher index of suspicion in women with risk factors.factors.

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Stable Angina PectorisStable Angina Pectoris

Chest discomfortChest discomfort- heaviness, tightness, - heaviness, tightness, pressure, squeezing, burning, aching or pressure, squeezing, burning, aching or choking; choking; may not be described as “pain”may not be described as “pain”..

Levine sign; substernal or to left of Levine sign; substernal or to left of sternum.sternum.

Crescendo-decrescendo pattern, 1-5 min.Crescendo-decrescendo pattern, 1-5 min. Radiation: left shoulder and upper arm, Radiation: left shoulder and upper arm,

back, neck, jaw and teeth.back, neck, jaw and teeth.

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Precipitating FactorsPrecipitating Factors Exertion, exercise, emotional duress, cold Exertion, exercise, emotional duress, cold

weather, sexual activity, cigarette smoke, large weather, sexual activity, cigarette smoke, large meals.meals.

Patterns: Often reproducible with activity; patterns Patterns: Often reproducible with activity; patterns may vary depending on time of day, coronary may vary depending on time of day, coronary tone; threshold lower in a.m. and after emotional tone; threshold lower in a.m. and after emotional duress.duress.

Sx resolve with cessation of activity, relaxation Sx resolve with cessation of activity, relaxation and following sub-lingual (rapid acting) NTG.and following sub-lingual (rapid acting) NTG.

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Clinical Presentation Clinical Presentation Characteristic historyCharacteristic history Presence of risk factorsPresence of risk factors PE often normal in between episodes; may PE often normal in between episodes; may

include: include: – Xanthelasma, xanthomas- hyperlipidemia.Xanthelasma, xanthomas- hyperlipidemia.– Funduscopic abnormalities: A-V nicking, Funduscopic abnormalities: A-V nicking,

hypertensive, diabetic changes.hypertensive, diabetic changes. Cardiac- SCardiac- S44 gallop (during angina), bruits gallop (during angina), bruits

(atherosclerosis), murmurs, changes in BP.(atherosclerosis), murmurs, changes in BP.

XanthelasmaXanthelasma

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ElectrocardiogramElectrocardiogram

Often normal in between anginal episodes. Often normal in between anginal episodes. May show prior infarcts, ST-T changes.May show prior infarcts, ST-T changes.

During episode may show characteristic During episode may show characteristic ischemic changes: ischemic changes: ST segment depressionST segment depression and/or T wave changes; changes normalize and/or T wave changes; changes normalize within minutes following an anginal within minutes following an anginal episode.episode.

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Stress ElectrocardiographyStress Electrocardiography Most useful Most useful non-invasivenon-invasive procedure for procedure for

evaluating the patient with angina.evaluating the patient with angina. Standardized protocols utilizing exercise or Standardized protocols utilizing exercise or

medications are used to increase cardiac medications are used to increase cardiac workload (or coronary blood flow)- see workload (or coronary blood flow)- see lecture on cardiac testing.lecture on cardiac testing.

Resting and stress ECG’s are compared Resting and stress ECG’s are compared looking for characteristic changes of looking for characteristic changes of ischemia.ischemia.

Stress ElectrocardiographyStress Electrocardiography

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IschemiaIschemia

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Stress TestingStress Testing

Sensitivity/Specificity: Influenced by Sensitivity/Specificity: Influenced by number of involved vessels, duration of number of involved vessels, duration of exercise, and presence of resting ECG exercise, and presence of resting ECG abnormalities.abnormalities.

Sensitivity/Specificity can be improved by Sensitivity/Specificity can be improved by adding imaging techniquesadding imaging techniques: Myocardial : Myocardial perfusion scintigraphy or echocardiography- perfusion scintigraphy or echocardiography- see lecture on cardiac testing.see lecture on cardiac testing.

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Coronary ArteriographyCoronary Arteriography The “gold standard” for assessing severity The “gold standard” for assessing severity

of CAD. Defines vessels involved, degree of CAD. Defines vessels involved, degree of stenosis and LV function.of stenosis and LV function.

Angiography is used in conjunction with Angiography is used in conjunction with patient’s symptoms and extent of ischemia patient’s symptoms and extent of ischemia (via stress testing) to determine severity and (via stress testing) to determine severity and significance of disease, and is often the significance of disease, and is often the final piece of information necessary to final piece of information necessary to determine therapeutic options.determine therapeutic options.

Angiogram: Coronary StenosisAngiogram: Coronary Stenosis

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Angiogram of Stenosis in GraftAngiogram of Stenosis in Graft

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Medical Treatment of Angina Medical Treatment of Angina

Treat or eliminate aggravating factors.Treat or eliminate aggravating factors. Acute attacks: Sub-lingual NTGAcute attacks: Sub-lingual NTG - -

venodilatorvenodilator>arterial dilator. >arterial dilator. Reduces LV volume Reduces LV volume (preload) decreasing O(preload) decreasing O22 consumption consumption; may ; may improve collateral flow; also aborts coronary improve collateral flow; also aborts coronary vasospasm. Usual dose is 0.3-0.6 mg, and repeated vasospasm. Usual dose is 0.3-0.6 mg, and repeated at 3 to 5 minute intervals.at 3 to 5 minute intervals.

Prophylactic sub-lingual NTG: taken 5 minutes Prophylactic sub-lingual NTG: taken 5 minutes before activities likely to precipitate angina.before activities likely to precipitate angina.

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Beta Receptor BlockersBeta Receptor Blockers

PreventPrevent angina by decreasing myocardial angina by decreasing myocardial OO22 consumption (MVO consumption (MVO22); ); decrease HR, decrease HR, contractility and BPcontractility and BP. . Improve exercise Improve exercise tolerancetolerance and reduce symptoms. and reduce symptoms.

Other benefits of Other benefits of ßß-blockers:-blockers:– Reduce mortality post MIReduce mortality post MI– Reduce mortality in patients with heart failure Reduce mortality in patients with heart failure

(HF)(HF)

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Beta Receptor BlockersBeta Receptor Blockers

Can induce bronchospasm in patients with asthma Can induce bronchospasm in patients with asthma or COPD: Role for or COPD: Role for ß-1 selectiveß-1 selective agents. agents.

Numerous Numerous ßß-blockers available. Choice may be -blockers available. Choice may be influenced by selectivity and other features. influenced by selectivity and other features. Widely used in Rx of HTN, arrhythmias, HF, Widely used in Rx of HTN, arrhythmias, HF, essential tremor and prevention of migraine essential tremor and prevention of migraine headaches.headaches.

Propranolol, Propranolol, Atenolol, Metoprolol, Atenolol, Metoprolol, Carvedilol, et Carvedilol, et al.al.

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Long Acting NitratesLong Acting Nitrates

Long acting nitrates- Oral, topical forms:Long acting nitrates- Oral, topical forms:Isosorbide dinitrate or mononitrate (oral)Isosorbide dinitrate or mononitrate (oral)NTG ointment or patches (topical).NTG ointment or patches (topical).

Used to Used to preventprevent angina- angina- MVOMVO22;; improve improve exercise tolerance.exercise tolerance.

Tolerance - need for nitrate free intervals.Tolerance - need for nitrate free intervals. Side effects: headaches, hypotension.Side effects: headaches, hypotension. Must DC Viagra when using nitrates!Must DC Viagra when using nitrates!

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Calcium Channel BlockersCalcium Channel Blockers Decrease myocardial ODecrease myocardial O22 requirements by requirements by dilating dilating

peripheral arteries/arteriolesperipheral arteries/arterioles, reducing BP, LV , reducing BP, LV wall stress, and wall stress, and afterloadafterload; also reduce coronary ; also reduce coronary tone and spasm- induce vasodilation.tone and spasm- induce vasodilation.– Result is Result is MVOMVO2 2 (myocardial O(myocardial O22 consumption) consumption)– Improve exercise tolerance/prevent anginaImprove exercise tolerance/prevent angina

Some Ca blockers also have negative inotropic Some Ca blockers also have negative inotropic and chronotropic effectsand chronotropic effects MVOMVO22

Do not reduce mortality post MI (compared to Do not reduce mortality post MI (compared to ß-ß-blockersblockers..

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Dihydropyridine Ca Blockers Dihydropyridine Ca Blockers Dilate arterioles, Dilate arterioles, PVRPVR afterload afterload

MVOMVO22 Minimal negative inotropic and Minimal negative inotropic and chronotropic effects.chronotropic effects.

Best used Best used in addition to in addition to -blockers-blockers in the in the treatment of angina.treatment of angina.

Long acting preparationsLong acting preparations reduce reduce likelihood of hypotension.likelihood of hypotension.

Numerous available: Nifedipine, Numerous available: Nifedipine, amlodipine, and others.amlodipine, and others.

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Diltiazem and VerapamilDiltiazem and Verapamil

Useful as an adjunct to nitrates in the treatment of Useful as an adjunct to nitrates in the treatment of angina (vs angina (vs -blocker).-blocker).

Dilate arterioles Dilate arterioles ++ HR and contractility HR and contractility MVOMVO2.2.

Diltiazem can be used cautiously with Diltiazem can be used cautiously with -blocking -blocking agents in treatment of angina- avoid Verapamil.agents in treatment of angina- avoid Verapamil.

Both are also useful in hypertension and for Both are also useful in hypertension and for certain cardiac arrhythmias.certain cardiac arrhythmias.

Avoid in patients with heart failure.Avoid in patients with heart failure.

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Ranolazine (Interest Only)Ranolazine (Interest Only)

New (2006) for treatment of chronic angina in New (2006) for treatment of chronic angina in patients without adequate response to standard meds patients without adequate response to standard meds (above); modest improvement in Sx.(above); modest improvement in Sx.

Unique MOA: Unique MOA: s late Na current, s late Na current, ing intracelular ing intracelular calcium. Also decreases fatty acid metabolism,calcium. Also decreases fatty acid metabolism,ing ing CHO metabolism which takes less energy/OCHO metabolism which takes less energy/O22..

No significant effect on HR or BP. No significant effect on HR or BP. Side effects: Dizziness, HA, constipation and nausea.Side effects: Dizziness, HA, constipation and nausea. ECG: Increases Q-T interval; caution. ECG: Increases Q-T interval; caution.

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Anti-Platelet AgentsAnti-Platelet Agents

Low dose aspirin (81-325 mgs.) has been shown Low dose aspirin (81-325 mgs.) has been shown to reduce coronary events post myocardial to reduce coronary events post myocardial infarction. Indications: infarction. Indications: all pts with CHDall pts with CHD.. ’’s incidence of subsequent MI, cardiac death.s incidence of subsequent MI, cardiac death.

Clopidogrel: inhibits ADP-induced platelet Clopidogrel: inhibits ADP-induced platelet aggregation; option if ASA is contraindicated.aggregation; option if ASA is contraindicated.

ASA or Clopridogrel ASA or Clopridogrel also recommmended in also recommmended in patients with PAD and carotid disease.patients with PAD and carotid disease. ’’s incidence of subsequent MI, cardiac death, stroke.s incidence of subsequent MI, cardiac death, stroke.

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Revascularization: Indications Revascularization: Indications Patients with Patients with unacceptable symptomsunacceptable symptoms in spite of in spite of

optimal medical Rx. optimal medical Rx. 3 Vessel CAD especially with LV dysfunction3 Vessel CAD especially with LV dysfunction Left main or left main equivalent diseaseLeft main or left main equivalent disease Following treatment of unstable angina if there is Following treatment of unstable angina if there is

evidence of early onset ischemia.evidence of early onset ischemia. Patients post MI with ongoing ischemia, or with Patients post MI with ongoing ischemia, or with

early onset ischemia via stress testing.early onset ischemia via stress testing. Acute MI (see below) Acute MI (see below)

CABG

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Catheter Based Techniques Catheter Based Techniques Angioplasty and related techniques can be Angioplasty and related techniques can be

performed with low morbidity, mortality, and performed with low morbidity, mortality, and rapid recovery.rapid recovery.

Indicated primarily for single or 2 vessel disease. Indicated primarily for single or 2 vessel disease. Comparable mortality and infarction rates Comparable mortality and infarction rates

compared to CABG over 1compared to CABG over 1stst three years, but high three years, but high rate of repeat procedures rate of repeat procedures until recentlyuntil recently..

Major drawback: Major drawback: RestenosisRestenosis requiring requiring repeat/multiple proceduresrepeat/multiple procedures improved last 5 yrs improved last 5 yrs with newer drug eluting stents (below).with newer drug eluting stents (below).

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Catheter Based TechniquesCatheter Based Techniques Catheters used to open stenosed/occluded Catheters used to open stenosed/occluded

coronary arteries or bypass grafts.coronary arteries or bypass grafts. Angioplasty (PTCA), Atherectomy, etc.Angioplasty (PTCA), Atherectomy, etc.

– Problem: 30-40% re-stenosis rate.Problem: 30-40% re-stenosis rate. Stent Placement- insertion of metal “sleeve” into Stent Placement- insertion of metal “sleeve” into

stenosis: stenosis: re-stenosis-15-20%re-stenosis-15-20% Using drug eluting (Sirolimus, Paclitaxel) stents Using drug eluting (Sirolimus, Paclitaxel) stents

’s re-stenosis- 5-8%: problems with late stent ’s re-stenosis- 5-8%: problems with late stent thrombosis thrombosis intense anti-platelet Rx.. intense anti-platelet Rx..

Coronary AngioplastyCoronary Angioplasty

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Coronary Angioplasty and StentCoronary Angioplasty and Stent

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Stent PlacementStent Placement

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Coronary Artery Bypass SurgeryCoronary Artery Bypass Surgery

Obstructed coronary arteries are bypassed Obstructed coronary arteries are bypassed using veins or using veins or arteriesarteries. Low mortality (1-. Low mortality (1-4%) if LV function preserved.4%) if LV function preserved.

Best long term results of patency and flow.Best long term results of patency and flow. Saphenous veins, radial artery and Saphenous veins, radial artery and internal internal

mammarymammary arteries are commonly used to arteries are commonly used to bypass diseased segments.bypass diseased segments.

Coronary Bypass Graft SurgeryCoronary Bypass Graft Surgery

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Coronary Artery Bypass SurgeryCoronary Artery Bypass Surgery

Operative mortality increased if age > 70, Operative mortality increased if age > 70, EF< .35.EF< .35.

Vein closure rates: 10-20% in 1st year, then 4% Vein closure rates: 10-20% in 1st year, then 4% annually; vein grafts and native vessels subject to annually; vein grafts and native vessels subject to recurrent disease.recurrent disease.

Internal mammary grafts-high patency rate over Internal mammary grafts-high patency rate over time- best option for grafts where possible.time- best option for grafts where possible.

Radial artery grafts are better than vein grafts, but Radial artery grafts are better than vein grafts, but use is limited.use is limited.

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Coronary VasospasmCoronary Vasospasm

May present in patients with normal coronaries, or May present in patients with normal coronaries, or superimposed on atherosclerotic disease.superimposed on atherosclerotic disease.

Often induced by exposure to cold, emotional Often induced by exposure to cold, emotional stress, meds (ergot), or drugs (cocaine).stress, meds (ergot), or drugs (cocaine).

Clinical presentation: Chest discomfort Clinical presentation: Chest discomfort accompanied by accompanied by ST segment elevationST segment elevation and and arrhythmias.arrhythmias.

May progress to MI (and consequences) if spasm May progress to MI (and consequences) if spasm does not resolve.does not resolve.

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Prinzmetal’s Angina Prinzmetal’s Angina Coronary ischemia as a result of vasospasm.Coronary ischemia as a result of vasospasm. Symptoms at rest, often in early A.M.Symptoms at rest, often in early A.M. WomenWomen > men. AKA “variant angina”. > men. AKA “variant angina”. Coronary arteriography often identifies Coronary arteriography often identifies

normal appearing vesselsnormal appearing vessels- vasospasm can - vasospasm can be induced pharmacologically in cardiac be induced pharmacologically in cardiac cath lab.cath lab.

Treatment very successful with nitrates and Treatment very successful with nitrates and calcium channel blockers.calcium channel blockers.

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Acute Coronary SyndromesAcute Coronary Syndromes Unstable Angina (UA)Unstable Angina (UA) Myocardial Infarction:Myocardial Infarction:

– MI: STEMIMI: STEMI– MI: NSTEMIMI: NSTEMI

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

Plaque RupturePlaque Rupture

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Unstable Angina (UA)Unstable Angina (UA) Angina at rest or with minimal activity, often Angina at rest or with minimal activity, often

lasting > 10 min. (without MIlasting > 10 min. (without MI negative negative cardiac markers).cardiac markers).

New onset angina (< 4 wks) with progressive New onset angina (< 4 wks) with progressive symptomssymptoms more severe pain. more severe pain.

Accelerating or creshendo angina in patient with Accelerating or creshendo angina in patient with previously stable angina.previously stable angina.

50% of patients will have abnormal ECG (St 50% of patients will have abnormal ECG (St depression and T wave inversion).depression and T wave inversion).

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Characteristics: Unstable AnginaCharacteristics: Unstable Angina Pathology: Pathology: complex coronary lesions- stenosis complex coronary lesions- stenosis

with placque rupture, hemorrhage, thrombuswith placque rupture, hemorrhage, thrombus.. Prognosis (untreated): Prognosis (untreated): High risk of developing High risk of developing

MI in following days/weeks. MI in following days/weeks. ECG evidence of ischemia- ECG evidence of ischemia- ST depression, TW ST depression, TW

inversioninversion; LV dysfunction common during ; LV dysfunction common during ischemia (echo imaging).ischemia (echo imaging).

No elevation of cardiac markers/enzymes.No elevation of cardiac markers/enzymes.– Presentation of Presentation of Non-STEMINon-STEMI infarct often infarct often

indistinguishable from unstable angina (but indistinguishable from unstable angina (but enzymes/markers are elevated with NSTEMIenzymes/markers are elevated with NSTEMI).).

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Treatment: Unstable AnginaTreatment: Unstable Angina Hospitalize, bedrest, OHospitalize, bedrest, O22, monitoring., monitoring. Full anticoagulation + anti-platelet therapy:Full anticoagulation + anti-platelet therapy:

Heparin (UF Heparin or Heparin (UF Heparin or LMW) LMW) plus plus ASAASA plusplus Clopidogrel; Clopidogrel; other anti-platelet agents (IV other anti-platelet agents (IV glycoprotein IIb/IIIa antagonists- (eptifabatide, glycoprotein IIb/IIIa antagonists- (eptifabatide, tirofiban) should be added in highest risk patients tirofiban) should be added in highest risk patients and before PCI.and before PCI.

Nitrates (topical, IV), Nitrates (topical, IV), -blockers, and Ca-blockers -blockers, and Ca-blockers commonly used to commonly used to MVOMVO22..

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Outcomes with Unstable AnginaOutcomes with Unstable Angina

20% remain unstable and require invasive 20% remain unstable and require invasive evaluation and revascularization.evaluation and revascularization.

80% improve medically. Once stable, some 80% improve medically. Once stable, some form of stress testing is performed. An form of stress testing is performed. An early + test is an indication for invasive early + test is an indication for invasive evaluation and revascularization based on evaluation and revascularization based on the anatomy.the anatomy.

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Acute Myocardial InfarctionAcute Myocardial Infarction

Definition: Prolonged ischemia resulting from Definition: Prolonged ischemia resulting from inadequate tissue perfusion leading to tissue inadequate tissue perfusion leading to tissue necrosis and myocardial cell death.necrosis and myocardial cell death.

Includes ST segment elevation MI and non-ST Includes ST segment elevation MI and non-ST segment elevation MI.segment elevation MI.

STEMI: CADSTEMI: CADPlacque rupturePlacque rupture PlateletsPlateletsClotting Clotting Occlusive Thrombus. Occlusive Thrombus.– Inflammation contributes to placque rupture/thrombosis.Inflammation contributes to placque rupture/thrombosis.

CAD with Thrombus CAD with Thrombus

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Acute Myocardial InfarctionAcute Myocardial Infarction

Statistics: > 1.1 million events/yr. in U.S. Statistics: > 1.1 million events/yr. in U.S. Death in >350,000 (half are sudden) Death in >350,000 (half are sudden) >750,000 hospitalizations/yr.>750,000 hospitalizations/yr.

Infarct location and size correlates with Infarct location and size correlates with distribution of occluded vessel, collateral distribution of occluded vessel, collateral circulation, and presence of additional circulation, and presence of additional disease.disease.

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Clinical PresentationClinical Presentation

Often in early A.M hours.Often in early A.M hours. 1/3 with premonitory history of unstable angina1/3 with premonitory history of unstable angina Chest pain Chest pain much more severemuch more severe than angina; than angina;

atypical presentations.atypical presentations. Patients are anxious, restless, diaphoretic and in Patients are anxious, restless, diaphoretic and in

distress.distress. LV dysfunction or stiffness can result in SOB.LV dysfunction or stiffness can result in SOB. Painless infarction common in diabetics.Painless infarction common in diabetics.

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Physical FindingsPhysical Findings Pulse and BP variable and change Pulse and BP variable and change

frequently; hemodynamic instability frequently; hemodynamic instability common.common.

Irregularities in pulse may represent Irregularities in pulse may represent arrhythmias.arrhythmias.

Lungs usually clear unless heart failure Lungs usually clear unless heart failure present.present.

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Physical FindingsPhysical Findings

S4 gallopS4 gallop in most; S3 unusual unless CHF. in most; S3 unusual unless CHF. Transient Transient apical mitral regurgitantapical mitral regurgitant

murmurs usually represent papillary muscle murmurs usually represent papillary muscle dysfunction.dysfunction.

Extremities: cyanosis/cold indicate low CO.Extremities: cyanosis/cold indicate low CO.

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Serum MarkersSerum Markers

Enzymes and proteins released from Enzymes and proteins released from necrotic myocardial cells.necrotic myocardial cells.

CK (creatine kinase) enzyme released from CK (creatine kinase) enzyme released from damaged skeletal muscle and damaged skeletal muscle and heartheart. Total . Total CK (aka CPK) always elevated with MI. CK (aka CPK) always elevated with MI. IsoenzymesIsoenzymes distinguish between source: distinguish between source:– CK MBCK MB fraction: fraction: HeartHeart – nl <4% of total CK – nl <4% of total CK

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Serum MarkersSerum Markers

CK MB isoenzymes rise within CK MB isoenzymes rise within 4-6 hrs4-6 hrs, peak in , peak in 16-24 hrs (2-10x nl), fall to baseline in 2-3 days.16-24 hrs (2-10x nl), fall to baseline in 2-3 days.

Cardiac specific troponins:Cardiac specific troponins: cTnIcTnI (& cTnT) rises (& cTnT) rises within within 4-6 hours4-6 hours, peak in 8-12 hours and remains , peak in 8-12 hours and remains elevated for 5- 7 days. Somewhat elevated for 5- 7 days. Somewhat more more sensitive/specific for small MI. Also usensitive/specific for small MI. Also useful if seful if symptoms are several days old. Abnormal if > symptoms are several days old. Abnormal if > 0.05ng/mL; diagnostic for MI with high 0.05ng/mL; diagnostic for MI with high sensitivity/specificity if > 0.1ng/mLsensitivity/specificity if > 0.1ng/mL

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Lab and Other FindingsLab and Other Findings Leukocytosis common.Leukocytosis common. ECG: Diagnostic criterion for STEMI vs. ECG: Diagnostic criterion for STEMI vs.

NonSTEMI (see ECG lectures).NonSTEMI (see ECG lectures). CXR often normal, unless there is HF or CXR often normal, unless there is HF or

prior cardiac problems.prior cardiac problems. Echocardiography: Provides bedside Echocardiography: Provides bedside

assessment of global and regional LV assessment of global and regional LV function. Identifies Mitral regurg if present.function. Identifies Mitral regurg if present.

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ECG: Acute Anterior MIECG: Acute Anterior MI

Myocardial InfarctionMyocardial Infarction

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Management of MIManagement of MI

Pre-hospital care: management of electrical and Pre-hospital care: management of electrical and hemodynamic instability; race against time; Ohemodynamic instability; race against time; O22, , analgesia, other meds as indicated.analgesia, other meds as indicated.

Parenteral narcotics: Parenteral narcotics: MorphineMorphine sulfate sulfate Aspirin given early in EDAspirin given early in ED Nitroglycerin usually initiated IV and titrated.to Nitroglycerin usually initiated IV and titrated.to

pain and BP. pain and BP. IV followed by oral IV followed by oral -blockers- decrease MVO-blockers- decrease MVO22, ,

reduce in hospital and post discharge mortality.reduce in hospital and post discharge mortality.

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Thrombolytic Therapy: STEMIThrombolytic Therapy: STEMI Indications: Indications: ST elevationST elevation of >1 mm. in two or of >1 mm. in two or

more contiguous/adjacent leads. more contiguous/adjacent leads. Not indicated Not indicated with ST depression or TW inversion alonewith ST depression or TW inversion alone..

Goal: Reduced mortality and infarct size.Goal: Reduced mortality and infarct size. Greatest benefits with large infarcts and when given Greatest benefits with large infarcts and when given

within the first 1-3 hrs of symptoms (50% reduction within the first 1-3 hrs of symptoms (50% reduction in mortality).in mortality).

Contraindications: uncontrolled HTN, prior stroke Contraindications: uncontrolled HTN, prior stroke (within one year) or cerebral hemorrhage, known (within one year) or cerebral hemorrhage, known bleeding diathesis, recent head trauma.bleeding diathesis, recent head trauma.

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Thrombolytic Therapy: STEMIThrombolytic Therapy: STEMI Relative contraindications: recent (within 3 Relative contraindications: recent (within 3

weeks) abdominal or thoracic surgery.weeks) abdominal or thoracic surgery. Agents: Recombinant Agents: Recombinant t-PAt-PA (Alteplase), (Alteplase),

Reteplase, Tenecteplase. All given by IV Reteplase, Tenecteplase. All given by IV injection or infusioninjection or infusion similar efficacy. similar efficacy.

Risks: Bleeding and intracerebral Risks: Bleeding and intracerebral hemorrhage.hemorrhage.

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Post -Thrombolytic ManagementPost -Thrombolytic Management

Includes ASA (ongoing) and Heparin (x 24 Includes ASA (ongoing) and Heparin (x 24 hours). Clopidogrel often given as well. hours). Clopidogrel often given as well.

Rapid resolution of painRapid resolution of pain Ventricular arrhythmias (PVC’s, VT, Ventricular arrhythmias (PVC’s, VT,

AIVR)AIVR) Rapid evolution of ECG (often to Q waves)Rapid evolution of ECG (often to Q waves)

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Post -Thrombolytic ManagementPost -Thrombolytic Management

10-20% of infarct related vessels will re-10-20% of infarct related vessels will re-occlude during the hospitalization- occlude during the hospitalization- recurrent pain and ECG changes; indication recurrent pain and ECG changes; indication for catheterization and revascularization. for catheterization and revascularization.

Stable patients post reperfusion: stress Stable patients post reperfusion: stress testing prior to discharge.testing prior to discharge.

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Acute Primary *PCIAcute Primary *PCI Available in a few centers-alternative to Available in a few centers-alternative to

thrombolytic therapy with thrombolytic therapy with better results.better results. Patients taken from ED directly to cath lab Patients taken from ED directly to cath lab

for acute angioplasty/stenting. Goals: for acute angioplasty/stenting. Goals: – Open artery within 3 hours of onset of Open artery within 3 hours of onset of

symptoms (includes transportation). symptoms (includes transportation). – Open artery Open artery within 90”within 90” after presenting to after presenting to

hospital that does PCI/angioplasty/stenting. hospital that does PCI/angioplasty/stenting. Requires capability of CABG if necessary.Requires capability of CABG if necessary.

*PCI- percutaneous coronary intervention

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Acute Primary PTCAAcute Primary PTCA More effectiveMore effective than thrombolytics in opening than thrombolytics in opening

occluded arteries; improved outcomes.occluded arteries; improved outcomes. An alternative approach if thrombolysis An alternative approach if thrombolysis

contraindicated. Preferred in elderly patients.contraindicated. Preferred in elderly patients. Lower risk of hemorrhage.Lower risk of hemorrhage. If within 1.5 hours of hospital that does acute If within 1.5 hours of hospital that does acute

angioplasty (with rapid response rate), think about angioplasty (with rapid response rate), think about transfer rather than thrombolytics.transfer rather than thrombolytics.

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Hospital Phase CareHospital Phase Care CCU careCCU care B-blockersB-blockers, nitrates, aspirin/clopidogrel as , nitrates, aspirin/clopidogrel as

tolerated.tolerated. ACE Inhibitors: Improve short and long term ACE Inhibitors: Improve short and long term

survival and aid in LV remodeling post MI.survival and aid in LV remodeling post MI.Beneficial with Beneficial with large infarctslarge infarcts complicated by complicated by significant LV dysfunction, low EF or CHF.significant LV dysfunction, low EF or CHF.

Aldosterone blockers: patients with large MI, Aldosterone blockers: patients with large MI, EF EF or symptoms of heart failure.or symptoms of heart failure.

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Complications of Acute MI Complications of Acute MI

Arrhythmias: atrial and Arrhythmias: atrial and ventricular.ventricular. Left ventricular dysfunctionLeft ventricular dysfunction: CHF-primary cause : CHF-primary cause

of intra-hospital death.of intra-hospital death. Papillary muscle dysfunction: Papillary muscle dysfunction: Mitral Mitral

Regurgitation- new murmurRegurgitation- new murmur Hypotension and shockHypotension and shock RV infarctionRV infarction Conduction abnormalities Conduction abnormalities Ventricular aneurysm formationVentricular aneurysm formation

Ventricular AneurysmVentricular Aneurysm

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NonSTEMI NonSTEMI Infarcts characterized by by prolonged ischemia, Infarcts characterized by by prolonged ischemia,

small elevations of cardiac markers and EKG changes small elevations of cardiac markers and EKG changes showing showing ST depression and/or T wave inversionsST depression and/or T wave inversions..

CADCADPlacque rupturePlacque rupturePlateletsPlateletsClotting Clotting ThrombusThrombus. Similar Rx as Unstable Angina.. Similar Rx as Unstable Angina.

Considered “incomplete infarcts”Considered “incomplete infarcts” with lower initial with lower initial mortality but mortality but high risk of re-infarction and with high risk of re-infarction and with high mortality. high mortality.

Very aggressive management often involving Very aggressive management often involving angiography and revascularization.angiography and revascularization.

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Uncomplicated InfarctionUncomplicated Infarction Pre-discharge low level stress test with Pre-discharge low level stress test with

maximal stress test 6 wks. post discharge.maximal stress test 6 wks. post discharge. Cardiac RehabilitationCardiac Rehabilitation Aggressive risk factor modificationAggressive risk factor modification Use of Use of B-blockingB-blocking agents and agents and ACE ACE

Inhibitors.Inhibitors.– HOPE trial – ACEI in patients with LV HOPE trial – ACEI in patients with LV

dysfunction post MI –mortality dysfunction post MI –mortality 20%.20%. Statins to Statins to LDL <??? (see Dyslipidemias).LDL <??? (see Dyslipidemias).

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Post Infarction Management Post Infarction Management (IO)(IO)

In hospital mortality 10-15% determined by size In hospital mortality 10-15% determined by size of the infarct.of the infarct.

Patients at increased risk post MI:Patients at increased risk post MI:Recurrent ischemic painRecurrent ischemic painNonSTEMI infarctNonSTEMI infarctCHFCHFLVEF < .40LVEF < .40Stress test (low level) induced ischemiaStress test (low level) induced ischemiaHigh grade ventricular arrhythmias late in courseHigh grade ventricular arrhythmias late in course– Invasive evaluation and revascularization. Invasive evaluation and revascularization.

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Revascularization Post MI (IO)Revascularization Post MI (IO)

Recurrent ischemia post thrombolysis.Recurrent ischemia post thrombolysis. Recurrent ischemia post infarct.Recurrent ischemia post infarct. LV dysfunction with ongoing ischemia.LV dysfunction with ongoing ischemia. Patients with markedly positive stress tests Patients with markedly positive stress tests

and multi-vessel disease.and multi-vessel disease. And others………And others………