Dr S.Sadeghian

Ischemic Heart Disease

IHD

Imbalance between myocardial oxygen supply and demand.

The most common cause: atherosclerosis 50% stenosis: limitation of blood flow on exercise 80%: limitation of blood flow at rest

Causes of Myocardial Ischemia

Coronary atherothrombosis Gradual, progressive Sudden, ± occlusive

Other causes of coronary flow Active spasm Lack of vasodilatation

Cold Anemia Carbon monoxide High altitude Cigarette smoking

HR Exercise, stress Smoking

LV stress LVH, HTN Aortic stenosis, HCM

Cold Food Hyperthyroidism

Reduced Oxygen Supply

IncreasedOxygen Demand

Pathophysiology of CAD: Atherosclerosis FoamCells

FattyStreak

IntermediateLesion Atheroma

FibrousPlaque

ComplicatedLesion/

Rupture

From FirstDecade

From ThirdDecade

From FourthDecade

Endothelial Dysfunction

Cardiovascular Risks

Cardiovascular Risks

LipidsHTN

DiabetesBehavioral

HemostaticThrombotic

Inflammatory Genetic

Atherosclerosis is a Diffuse Process

10%: Manifested Claim ECG Other lab data

90%: Hidden Physician judgment Careful history taking

Myocardial Ischemia

Angina & ACS

ArrhythmiaBreathlessness

Sudden Death

Most myocardial ischemia is painless (“silent”) …

TransientLV

Dysfunction

ProgressiveLV

Dysfunction

Clinical Manifestations Of IHD

AnginaClassification

ExertionalVariantAnginal equivalent syndromePrinzmetal’s anginaSyndrome-XSilent ischemia

Clinical Classification of CP (Chronic Stable Angina) Probability

Definite (typical) angina: Substernal discomfort, with a characteristic quality and

duration and radiation Provoked by exertion or emotional stress Relieved by rest or nitroglycerin in less than 10 minutes.

Atypical angina meets 2 of the of characteristics Noncardiac CP meets 1 of the typical angina

characteristics. “Definitely not” angina: ? CP is unrelated to activity,

appears to be clearly non-cardiac origin and is not relieved by nitroglycerin.

Grading of Angina of Effort by the Canadian Cardiovascular Society

Comment Definition Canadian Class

Angina only with extraordinary exertion at work or recreation

Ordinary physical activity does not cause angina

I

Angina with walking more that two blocks on a level surface or climbing more that one flight of stairs at a normal pace

Slight limitation of ordinary activity

II

Walking 1-2 blocks on a level surface or climbing 1 flight of stairs at a normal pace

Marked limitation of ordinary physical activity

III

Angina at rest or with minimal activity or stress

Inability to carry out any activity without discomfort

IV

Types of Stressors

Exercise Treadmill Bicycle, upright or supine

Pharmacologic Vasodilators

DipyridamolAdenosine

Positive inotropes/chronotropesDobutamine

Types of Documents

Imaging Scintigraphy Echo CT angio Angiography

Exercise

Anti-ischemic and preventive drugs for IHD

The treatment of angina is aimed at decreasing oxygen demand and/or increasing oxygen supply.

Antiischemic and anti-anginal drugs (most commonly, a combination of these agents is used for management.

A = Anti-platelet (aspirin) and anti-thrombotic therapy and antianginal therapy (nitrates) and ACE inhibitors

B = Beta-blocker and BP

C = Cigarette smoking and Cholesterol lowering agents and Calcium antagonists

D = Diet and Diabetes

E = Education and Exercise

Effects of Treatment of Chronic Stable Angina

Treatment Angina Control Improved Prognosis/ Prevention Of MI

Nitrates Yes No

BB Yes Yes

CCBs Dihydropyridines:

Short actingLong acting

Nondihydropyridines: Diltiazem, Verapamil

PoorYes

Yes

No (prognosis ↓)?

?No

Aspirin No Yes

Statins ?yes Yes

ACEIs ?yes Yes

PTCA Yes ?

CABG Yes Yes

Acute Coronary Syndrome

ACSs

ACS

UA NSTEMI STEMI

What is ACS?

All have sudden ischemia due to sudden occlusion of one or more of the coronary arteries, resulting in decreased oxygen supply to the heart muscle.

Thrombosis with sub-total (UA, NSTMI) or total coronary artery occlusion (STEMI)

Can not be differentiated in the first hours All have the same initiating events:

Plaque rupture Thrombus formation Vasoconstriction

Pathophysiology of Acute Coronary Syndromes

Unstable Plaque

Pathophysiology of Acute Coronary Syndrome

UA ST depression, T Wave inversion or normal No enzyme release

NSTEMI ST depression, T Wave inversion or normal Usually no Q waves at presentation CPK, LDH + Troponin release

STEMI ST elevation + Q waves at discharge CPK, LDH + Troponin release

Epicardial Coronary Artery

Lateral Wall of LV

Positive Electrode

Septum

Left Ventricular

Cavity

Interior Wall of LV

The Three I1. Ischemia

Thrombus

Ischemia

The Three I2. Injury

Infarcted Area Electrically Silent

Thrombus

Depolarization

Ischemia

The Three I3. Infarction

UA Syndromes

New onset angina (1 month)Crescendo angina

Increased frequency, severity, or duration (prolonged episodes (>10-15min))

Decrease in exertion required to provokeAcute coronary syndrome (ACS)

Ischemic chest pain >20 minutesOnset at rest or awakening from sleepFailure to abate with >2-3 S.L. NTGPost infarction anginaPrinzmetal’s (variant) angina

Unstable Angina

Up to 70% patients sustain MI over the ensuing 3 months

>90% of AMI result from an acute thrombus obstructing a coronary artery with resultant prolonged ischemia and tissue necrosis

SYMPTOMS SUGGESTIVE OF ACS

Noncardiac Diagnosis Chronic Stable Angina

Possible ACSDefinite ACS

Treatment as indicated by

alternative diagnosis

ACC/AHA Chronic Stable Angina

Guidelines

No ST-Elevation ST-Elevation

Nondiagnostic ECG Normal initial serum cardiac biomarkers

ST and/or T wave changes

Ongoing pain

Positive cardiac biomarkers

Hemodynamic abnormalities

Evaluate for reperfusion therapy

ACC/AHA STEMI Guidelines

Observe

≥ 12 h from symptom onset

No recurrent pain; negative follow-up studies

Recurrent ischemic pain or positive follow-up studies

Diagnosis of ACS confirmed

Stress study to provoke ischemia

Consider evaluation of LV function if ischemia is present (tests may be performed either

prior to discharge or as outpatient)

Negative

Potential diagnoses: nonischemic discomfort; low-risk ACS

Arrangements for outpatient follow-up

Positive

Diagnosis of ACS confirmed or highly likely

Admit to hospital

Manage via acute ischemia pathway

Algorithm for evaluation and management of patients suspected of having ACS. Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 2.

Risk Scores

TIMI GRACE

History

AgeHypertensionDMSmoking↑ CholesterolFamily historyHistory of CAD

Age

Presentation

Severe anginaAspirin within 7 daysElevated markersST-segment deviation

HR SBPElevated creatinineHeart failureCardiac arrestElevated markersST-segment deviation

Antman EM, et al. JAMA 2000;284:835–42. Eagle KA, et al. JAMA 2004;291:2727–33. GRACE = Global Registry of Acute Coronary Events; TIMI = Thrombolysis in Myocardial Infarction.

Likelihood That S&S Represent an ACS Secondary to CAD

LOW LIKELIHOOD

INTERMEDIATE LIKELIHOOD

HIGH LIKELIHOOD FEATURE

Absence Of High- Or Intermediate Likelihood Features But May Have:

Absence Of High-likelihood Features And Presence Of Any Of The Following:

Any Of The Following

Probable ischemic symptoms in absence of any of the intermediate-likelihood characteristics

Recent cocaine use

Chest or left arm pain or discomfort as chief symptom

Age >70 yearsMale sexDiabetes mellitus

Chest or left arm pain or discomfort as chief symptom reproducing prior documented angina

Known history of CAD, including MI

History

Chest discomfort reproduced by palpation

Extracardiac vascular disease

Transient MR murmur, hypotension, diaphoresis, pulmonary edema, or rales

Examination

T wave flattening or inversion less than 1 mm in leads with dominant R waves

Normal ECG

Fixed Q wavesST depression 0.5 to 1 mm

or T wave inversion greater than 1 mm

New, or presumably new, transient ST-segment deviation (≥1 mm) or T wave inversion in multiple precordial leads

ECG

Normal Normal Elevated cardiac TnI, TnT, or CK-MB

Cardiac markers

ACC/AHA System for Risk Stratification of Patients with UA

LOW RISK (30 DAYS DEATH/MI RISK:

<3%)

INTERMEDIATE RISK (30 DAYS DEATH/MI

RISK: 3-8%)

HIGH RISK (30 DAYS DEATH/MI RISK: 8-15%)

FEATURE

No High- Or Intermediate-risk Feature But May Have One Of The Following Features:

No High-risk Feature But Must Have One Of The Following:

At Least One Of The Following:

Prior MI, peripheral or cerebrovascular disease, or CABG; prior aspirin use

Accelerating tempo of ischemic symptoms in preceding 48 hr

History

New-onset or progressive CCS class III or IV angina the past 2 wk without prolonged rest pain but with moderate or high likelihood of CAD

Prolonged rest angina, now resolved, with moderate or high likelihood of CAD

Rest angina <20 min or relieved with rest or sublingual NTG

Prolonged ongoing (>20 min) rest pain Character of pain

Age >70 Pulmonary edema, most likely caused by ischemia

New or worsening MR murmurS3 or worsening ralesHypotension, bradycardia,

tachycardiaAge >75

Clinical findings

Normal or unchanged ECG during an episode of chest discomfort

T wave inversion >0.2 mVPathologic Q waves

Angina at rest with transient ST-segment changes >0.05 mV

BBB, new or presumed newSustained VT

ECG

normal Slightly elevated elevated Cardiac markers

Selection of Initial Treatment Strategy: Initial Invasive Versus Conservative Strategy

Invasive Recurrent angina/ischemia at rest with low-level activities despite intensive medical therapy

Elevated cardiac biomarkers (TnT or TnI)

New/presumably new ST-segment depression

Signs/symptoms of heart failure or new/worsening mitral regurgitation

High-risk findings from noninvasive testing

Hemodynamic instability

Sustained ventricular tachycardia

PCI within 6 months

Prior CABG

High risk score (e.g., TIMI, GRACE)

Reduced left ventricular function (LVEF < 40%)

Conservative

Low risk score (e.g., TIMI, GRACE)

Patient/physician presence in the absence of high-risk features

Angina: Prognosis

LV function Number of coronary arteries with

significant stenosis Extent of jeoporized myocardium

Unstable Angina / NTMI Pharmacologic Therapy

ASA and Heparin beneficial for ACSs (UA, NSTEMI, STEMI)

Decrease MVO2 with nitrates, BBs, CCBs, and ACE inhibitors

consider platelet glycoprotein IIb / IIIa inhibitor and / or LMWH

Preparation for Discharge After UA/NSTEMI

Antiplatelet Rx ASA 75 - 162 mg/day Clopidogrel 75 mg/day

Beta blocker ACEI/ARB

Especially if DM, HF, EF <40%, HTN Statin

LDL <100 mg/dL (ideally <70 mg/dL) Secondary prevention measures (control of RF)

Pharmacological Therapy for Musculoskeletal Symptoms With Known CVD or Risk Factors for IHD

Acetaminophen, ASA, tramadol, narcotic analgesics (short term)

Nonacetylated salicylates

Non COX-2 selective NSAIDs

NSAIDs with some COX-2 selectivity

COX-2 selective NSAIDs

Select pts at low risk of thrombotic events

Prescribe lowest dose required to control symptoms

Add ASA 81 mg and PPI to pts at ↑ risk of thrombotic events*

Regular monitoring for sustained hypertension (or worsening of prior BP control), edema, worsening renal function, or GI bleeding

If these occur, consider reduction of the dose or discontinuation of the offending drug, a different drug, or alternative therapeutic modalities, as dictated by clinical circumstances*Addition of ASA may not be sufficient protection against thrombotic events.

Reproduced with permission from Antman EM, et al. Circulation 2007;115:1634–42. PPI = proton-pump inhibitor.

New

Myocardial Infarction

Definition of MI

Death of part of the heart muscle due to its sudden loss of blood supply.

Often causes chest pain and electrical instability of the heart muscle tissue.

EtiologyFormation of a blood clot on a

cholesterol plaqueOccasionally: rupture of the surface of

the cholesterol plaque

AMI Clinical Features

Typical: intense, oppressive chest pressure radiating to left arm

Atypical – 25% of all AMIs Pleuritic or sharp/stabbing CP Palpable CP (10-33% AMI) Arm pain only Indigestion SOB only (40% in elderly) “Dizziness” (5% AMI) Nausea Syncope

Diagnosis of AMI: ECG

Defines location, extent, and prognosis of infarction

ST elevation diagnostic of coronary occlusionQ-waves do NOT signify completed infarctionST depression or T inversion: unlikely total

coronary occlusionST elevation in V4R for RV infarctionObserve up to 24 hrs for non-diagnostic ECGDifferentiate from early repolarization

Acute Myocardial Infarction

Wavefront phenomenon of ischemic evolution - endocardium to epicardium

If limited area of infarction homeostasis achieved

If large area of infarction (>20% LV) congestive heart failure

If larger area of infarction (>40% LV) hemodynamic collapse

AMI - Wavefront Phenomenon

Anterolateral Wall MI

Inferior Wall MI

Inferior + RV MI

Posterior Wall MI

Lateral Wall MI

Timing of Release of Various Biomarkers After Acute Myocardial Infarction

Shapiro BP, Jaffe AS. Cardiac biomarkers. In: Murphy JG, Lloyd MA, editors. Mayo Clinic Cardiology: Concise Textbook. 3rd ed. Rochester, MN: Mayo Clinic Scientific Press and New York: Informa Healthcare USA, 2007:773–80. Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 5.

Markers of MI: Troponin I

Sample Admitting Orders IV access: NS or D5W to KVO

Vital signs: Q 1/2 hr until stable, then q 4 hr and PRN. Notify if HR <60 or >110; BP <90 or >150; RR <8 or >22.

Pulse oximetry x 24 hrs Activity: CBR for 12 hrs, with bedside commode and progress as tolerated after 12 hrs Monitor: 24 hours Diet: heart-healthy diet Medications: MONA:

Morphine Oxygen nasal: 2L/min x 3 hrs Nitrates: IV NTG for 24-48 hrs if no / HR or BP Aspirin: 165-300 mg QD β-blocker: IV→po (if no contraindications): metoprolol 12.5 mg po q6 No prophylactic antiarrhythmics Heparin

IV: large anterior MI, PCI, LV thrombus, alteplase/reteplase use (for ~48 hours) SQ: for all other MI

Clopidogrel GP IIb/IIIa inhibitors (Eptifibatide) ACEi in all MI if no hypotension: captopril 6.25 mg po q8 Statin: atorvastatin 80 mg po

Indications For Reperfusion

ST elevation >0.2 in 2 adjacent chest leads

ST elevation >0.1 in 2 adjacent limb leads

Dominant R waves and ST depression in V1-V3 (posterior infarct)

New LBBB

Absolute Contraindications Patients >75 years may get less overall benefit

than younger patients but advanced age is no longer considered a major contraindication for TT

Previous hemorrhagic stroke at any time; other strokes or cerebrovascular events within one year

Known intracranial neoplasm or AVMActive internal bleeding (does not include menses)Suspected aortic dissection

Relative Contraindications and Cautions for Fibrinolytics in AMI

Severe uncontrolled HTN on presentation (BP >180/110 mm Hg) History of severe poorly controlled chronic hypertension History of prior nonhemorrhagic CVA beyond 1 yr or known intra-cerebral pathology

not covered in contraindications Current use of anticoagulants in therapeutic doses (INR 2-3); no bleeding diathesis Recent trauma (within 2-4 weeks) including head injury Recent (within 2-4 weeks) internal bleeding Active peptic ulcer Known bleeding diathesis (e.g., from significant liver dysfunction, or neoplasm) Pregnancy For SK, APSAC, anistreplase: prior exposure (especially within 5 d-2 yrs) or prior

allergic reaction Prior central venous or noncompressible vascular puncture

Prolonged cardiopulmonary resuscitation (>10 minutes) Recent surgery (<2 weeks) excluding intracranial or spinal surgery which may

require a longer interval

Risks

Bleeding is the primary complication of TT and stroke is the greatest concern (1.8%)

Stroke: 1.4%. Predictors: Patients with a previous TIA or stroke were at particularly high risk Older age SBP >140 mm Hg DBP >100 mm Hg Lower body weight

Allergic reactions can be seen in patients treated with SK

Extension / Ischemia

Complications of AMI

AMI

Arrhythmia

Heart Failure

Expansion / Aneurysm RV Infarct

Pericarditis

Mechanical Mural Thrombus

AMI Management Pharmacologic Therapy on Hospital Discharge

Aspirin indefinitely (ticlopidine or clopidogrel for aspirin allergy or intolerance)

Beta blockers for at least 2-3 years

ACE inhibitors for CHF, LVEF <40%, or large infarction (even with preserved LVEF)

Lipid lowering agents

Warfarin for mural thrombus, extensive anterior infarct, DVT, AF

Risk Stratification Post-MI Revascularization Strategy

Low RiskLow Risk High Risk*High Risk*

LV SF LV SF Nl LV SFNl LV SF

Stress Imagingor

Catheterization

Stress Imagingor

Catheterization

Nl LV SFNl LV SF LV SF LV SF

Angiography±

Revascularization

Angiography±

Revascularization

Stress ImagingStress Imaging

NormalNormalDirectCath

DirectCath

* (Re) MI or CP, VT, CHF, Prior MI, Prior Revascularization