Ischemic Heart Disease I and II

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					                              Ischemic Heart Disease I and II

                                   Laura Wexler, M.D.

Ischemia –lack of oxygen due to inadequate tissue perfusion

Infarction –tissue necrosis due to sustained loss of perfusion

The most common cause of ischemic heart disease is atherosclerosis of the coronary

1.     Risk factors for coronary artery disease (CAD)
           a. Male > 45
           b. Female > 55
           c. Family history of premature CAD
           d. Cigarette smoking
           e. Hypertension
           f. Lipid abnormalities
           g. Diabetes
           h. Menopause (esp. Premature)
           i. Obesity/physical inactivity

2.      Other risk factors for CAD
          a. Hyperhomocysteinemia
          b. Hyperfibrinoginemia
          c. Elevated C-reactive protein
          d. Elevated Lp (a) levels

3.      Etiologies of ischemic heart disease other than atherosclerosis
           a. Thrombosis
           b. Thromboembolism
           c. Vasospasm
           d. Amyloid
           e. Fibromuscular hyperplasia
           f. Vasculitis
           g. Congenital coronary anomalies (e.g., coronary artery originates from
              pulmonary artery)

4.      Clinical presentation of ischemic heart disease
           a. Angina or “anginal equivalent”
           b. Acute myocardial infarction
           c. Ischemic cardiomyopathy
           d. Sudden cardiac death
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5.        William Heberden’s original description of “angina pectoris” (1802):
“But there is a disorder of the breast marked with strong and peculiar symptoms,
considerable for the kind of danger belonging to it, and not extremely rare, which
deserves to be mentioned more at length. The seat of it, and sense of strangling, and
anxiety with which it is attended, may make it not improperly be called angina pectoris.
They who are afflicted with it, are seized while they are walking, (more especially if it be
up hill, and soon after eating) with a painful and most disagreeable sensation in the
breast, which seems as if it would extinguish life, if it were to increase or to continue; but
the moment they stand still, all this uneasiness vanishes”.

          Key features: “Strangling” sensation in the chest.
                        “Fear of impending doom”
                         Exertion induced
                         Relieved by rest

6. Grading of angina pectoris by the Canadian Cardiovascular Society classification
           a. Class I - Ordinary physical activity does not cause angina, such as
               walking, climbing stairs. Angina occurs with strenuous, rapid, or
               prolonged exertion at work or recreation.
           b. Class II – Slight limitation of activity. Angina occurs on walking or
               climbing stairs rapidly, walking uphill, walking or stair climbing after
               meals, or in cold, or in wind, or under emotional stress, or only the few
               hours after awakening. Walking more than two blocks on the level and
               climbing more than one flight of ordinary stairs at a normal pace and in
               normal condition.
           c. Class III – Marked limitations of ordinary physical activity. Angina
               occurs on walking one to two blocks on the level and climbing one flight
               of stairs in normal conditions and at a normal pace.
           d. Class IV - Inability to carry on any physical activity without discomfort-
               anginal symptoms may be present at rest.

7. Effects of ischemia
           a. Mechanical – Failure of normal contraction (hypokinesis, akinesis,
               dyskinesis); impaired relaxation.
           b. Biochemical – Shift from FA oxidation to glycolysis and lactate
               production; decreased pH, ATP, CK; impaired membrane function – K+
           c. Electrical – repolarization changes (ST segment and T wave);
               vulnerability to ventricular arrhythmias (VT/VF)
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      8. Effects of ischemia – symptoms
             a. Angina pectoris
             b. Dyspnea : transient systolic and or diastolic LV dysfunction leads to
                 elevated LV diastolic pressures which causes abrupt elevation in
                 pulmonary venous pressure and pulmonary capillary pressure, which
                 results in sensation of dyspnea.
             c. Associated symptoms related to sympathetic NS stimulation (anxiety,
             d. Gastrointestinal symptoms related to parasympathetic NS stimulation
                 (vagal)…nausea, vomiting
             e. There may be no symptoms: “Silent ischemia”

9.      Physical findings that may be associated with myocardial ischemia:
            a. Dyskinetic apical impulse
            b. Pulmonary rales
            c. S3 (systolic dysfunction), S4 (diastolic dysfunction).
            d. Mitral regurgitation murmur if there is ischemia of the papillary muscle.
            e. Evidence of sympathetic stimulation: rapid HR, diaphoresis, elevated BP.

10.      ECG evidence of myocardial ischemia:
            a. ST segment depression in those leads reflecting the ischemic area.
            b. T wave inversion        “ “       “       “      “      “      “ .

      11.       Myocardial ischemia is caused by an imbalance between myocardial oxygen
            demand and myocardial oxygen delivery. Normally, coronary artery flow can
            increase by as much as a factor of five when there is increased demand. This is
            accomplished by vasodilation (decreased resistance) of the dense network of
            intra- myocardial resistance arterioles. The capacity to augment flow is called the
            coronary vascular reserve. If there is narrowing of an epicardial coronary artery
            and decreased flow at rest, the distal arterioles will vasodilate to normalize flow at
            rest ….this will compromise the capacity to further increase flo w when demand
            increases, i.e., coronary artery reserve is limited. Ischemia will ensue if demand
            exceeds supply. Coronary reserve begins to be limited when an artery is
            narrowed by more than 50%. Myocardial perfusion at rest is compromised when
            the artery is narrowed by >80%.

      12. Myocardial oxygen demand:
           Determinants of myocardial oxygen demand (MVO2)
            a. Heart rate
            b. Contractility
            c. Wall stress ( p x radius/wall thickness).
            d. (minor) Basal metabolism, activation energy, fiber shortening.
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13. Recognizing and alleviating ischemia: look for factors that alter myocardial oxygen
supply/demand balance
                 a. Increased oxygen demand
                         i. Heart rate (fever, tachycardia, hyperthyroidism)
                        ii. Afterload (aortic stenosis, hypertension)
                       iii. Preload (cardiac dilation, high cardiac output)
                       iv. Enhanced inotropic state (stress, cocaine, sympathomimetic
                 b. Decreased oxygen supply
                         i. Anemia
                        ii. Hypoxemia
                       iii. Abnormal hemoglobin
                       iv. Carbon monoxide (smoking)
                        v. Hypotension
                       vi. Spasm (cocaine)

14.     Therapeutic armamentarium for angina pectoris
                    a. Supportive therapies
                           Risk factor reduction
                            Control of aggravating conditions (see above).
                            Stress modification
                            Supervised exercise (improves cardiac efficiency).
                    b. Specific pharmacotherapy
                            Beta blockers
                            Ca++ blockers
                            Combinations of the above.
                    c. Revascularization
                            Bypass surgery

      15. Determinants of prognosis of ischemic heart disease
            a. Left ventricular function – ejection fraction
            b. Location and severity of coronary artery stenoses
            c. Instability of ischemia – accelerating symptoms, unresponsive to medical
            d. Easily inducible ischemia on a stress test
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      16. Unstable angina, aka, acute coronary syndrome: a state of impending infarction
           usually caused by rupture of a coronary plaque. Platelet aggregation, coronary
           spasm and clot formation result in intermittent/near vessel occlusion. Risk of
           total occlusion by clot is high.
             a. Severity grading of unstable angina (Braunwald; Circulation 1989;80:410)
                 I. New onset severe angina or significant aggravation of previous angina,
                 without rest pain
                II Angina at rest within past month but not within the past 48 hours
               III Angina at rest within the past 48 hours

17.        Management of unstable angina
             a. Inhibit platelet aggregation: aspirin, GP IIbIIIa
             b. Prevent thrombosis: heparin
             c. Decrease myocardial O 2 demand: beta blockers, sedation, pain control
             d. Increase myocardial oxygen supply: nitrates, CA++ blockers
             e. Stabilize plaque: ?HMGCoA reductase inhibitors
             f. Consider urgent revascularization : PTCA/stent, CABG

18.        Prinzmetal’s angina : angina causes by severe coronary artery spasm, either
            with or without underlying atherosclerosis.
             a. Associated with transient ST segment elevation
             b. Maybe associated with other vasospastic syndromes: Raynard’s
                 phenomenon, migraine headaches

19.        Angina with normal coronary arteries
             a. Coronary artery spasm
             b. Severe hypertension
             c. Hypertrophic cardiomyopathy
             d. Aortic stenosis
             e. Pulmonary hypertension
             f. Myocardial bridging
             g. Microvascular angina (Syndrome X)

20.        Acute myocardial infarction
             a. Cardiac muscle necrosis secondary to protracted lack of coronary
             b. Usual etiology: thrombus at site of a ruptured atherosclerotic plaque.

21.        Other etiologies of acute myocardial infarction
             a. Coronary embolus
             b. Coronary spasm
             c. Coronary anomaly
             d. Primary in situ thrombosis
             e. Vasculitis
             f. Hypotension
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22.        Determinants of extent of damage
             a. Territory supplied by the occluded vessel
             b. Duration of occlusion
             c. Existence of collaterals
             d. Oxygen demand at time of occlusion
             e. Superimposed vasospasm

23.        Presenting symptoms of acute myocardial infarction
              a. Pain
                       i. Typical – crushing substernal chest pain
                      ii. Atypical – jaw, neck, shoulder, back pain, indigestion, fatigue
                     iii. Painless – “silent”
              b. Dyspnea – systolic and/or diastolic dysfunction
              c. Dizziness- hypotension, arrhythmia
              d. Nausea, vomiting
              e. Elderly patients: failure to thrive
              f. Anxiety, restlessness, “sense of impending doom”
24.        Possible presenting signs in acute myocardial infarction
              a. Appearance – pallor, diaphoretic, anxious
              b. Vital signs – normal or abnormal BP and P
                       i. Hypertension and tachycardia: SNS
                      ii. Hypotension and tachycardia
                              1. Cardiogenic shock
                              2. Myocardial rupture
                              3. Tachyarrhythmia
                     iii. Hypotension and bradycardia
                              1. Vagal stimulation
                              2. Bradyarrhythmia
              c. Lungs – rales – CHF
              d. Heart
                       i. Displaced LV impulse
                      ii. S3
                     iii. S4
                     iv. Murmur of mitral regurgitation (papillary muscle damage).
                      v. Murmur of ventricular septal rupture
                     vi. Pericardial rub

25.        Diagnosis of acute MI:
             a. ECG: ST elevation Twave inversionloss of initial QRS forces
                 (pathologic Q wave) (see illustration on- line).
             b. Cardiac specific enzymes: CKMB, Troponin
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26.        Natural history of acute myocardial infarction
             a. Death
                       i. Arrhythmia: VT/VF
                      ii. Asystole
                    iii. Myocardial rupture with pericardial tamponade
                     iv. Cardiogenic shock
             b. Chronic heart failure
                       i. LV dysfunction and progressive dilation – “remodeling”
                      ii. Papillary muscle dysfunction: MR
                    iii. RV dysfunction (RV infarct)
             c. Stabilization – with or without compensated LV dysfunction
             d. Post-infarction angina/ischemia (spontaneous or induced)
             e. Recurrent MI
             f. Post-infarction ventricular tachycardia

27.        Treatment of acute myocardial infarction: acute phase
              a. Prevent/resuscitate from sudden death: monitor, admit to CCU
              b. Re-establish coronary flow
                     i. Thrombolytic therapy
                    ii. Primary infarct angioplasty/stent….may be more effective but
                         depends on how fast you can get patient to the cath lab.

28.        Major contraindications to the use of thrombolytic therapy
             a. Any previous history of hemorrhagic stroke
             b. History of stroke, dementia, or central nervous system damage within one
             c. Head trauma or brain surgery within six months
             d. Known intracranial neoplasm
             e. Suspected aortic dissection
             f. Internal bleeding within six weeks
             g. Active bleeding or known bleeding disorder
             h. Major surgery, trauma, or bleeding within 6 weeks
             i. Traumatic cardiopulmonary resuscitation within three weeks

29.        Treatment of acute myocardial infarction, con’t: acute phase
              a. Decrease myocardial oxygen demand
                      i. Pain relief/anxiolytics (Morphine sulfate)
                     ii. Slow HR, control BP (beta blockers…improve survival)
              b. Increase myocardial oxygen supply
                      i. Supplemental oxygen
                     ii. Prevent platelet aggregation/coronary thrombus propagation
                         (aspirin, GP IIB IIIA inhibitors, clopidigrel/heparin)
                    iii. Prevent spasm (nitrates)
                    iv. Augment collateral flow (nitrates)
              c. Stabilize plaques, restore endothelial function
                      i. ? HMG CoA reductase inhibitors (“statins”)
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               d. Prevent ventricular remodeling (improves survival)
                      i. ACE inhibitors
               e. Prevent mural thrombus/embolization
                      i. Heparin
                     ii. Coumadin for patients at high risk of clot: anterior wall akinesis

30.        Treatment of acute myocardial infarction - intermediate phase…watch for early
              a. Monitor/treat arrhythmias
              b. Monitor/treat heart failure: systolic, diastolic, MR
              c. Monitor/treat recurrent ischemia/infarction
              d. Watch for pericarditis, Dressler’s Syndrome
              e. Monitor for myocardial rupture (free wall, VSD, MR)
              f. Monitor for stroke

31.        Determinants of prognosis after acute MI
             a. How much LV damage did the patient sustain? LV function (ejection
             b. Is patient at high risk for another MI? Is there easily inducible ischemia?
                 What is the coronary anatomy?
             c. Is the patient at risk for a fatal arrhythmia (VT/VF)?

32.        Treatment of acute myocardial infarction: Pre-discharge risk assessment
              a. Tests for LV function
                      i. Echocardiogram
                     ii. Radionuclide ventriculogram (MUGA)
                   iii. Contrast left ventriculogram (cath)
              b. Echocardiogram in acute myocardial infarction
                      i. Wall motion abnormalities
                     ii. Ejection fraction
                   iii. Thrombus
                    iv. Right ventricular myocardial infarction
                     v. Papillary muscle dysfunction – mitral regurgitation
                    vi. Free wall rupture/ventricular septal defect/papillary muscle rupture
              c. Exercise stress test
                      i. Positive – ischemic ST segment depression - > 1 mm horizontal or
                         downsloping ST depression
                     ii. Negative – Patient reaches 85% maximum predicted heart rate
                         (MPHR) without #1
                   iii. Nondiagnostic: No ischemia but patient fails to reach 85% MPHR
              d. Thallium stress test
                      i. Injection of radionuclide (radioactive thallium) that is distributed
                         in the myocardium in proportion to coronary flow. During exercise
                         or after injection of a coronary vasodilator, areas perfused by a
                         stenosed artery will be unable to augment perfusion (i.e., areas
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                             with impaired coronary reserve) and will take up less radionuclide
                             than areas, which can increase flow maximally.

33.        Treatment of acute myocardial infarction late phase (post hospital)
              a. Risk factor reduction
                      i. Smoking
                     ii. Hypertension
                    iii. Diabetes
                    iv. Dyslipidemia
                     v. Obesity/sedentary lifestyle
                    vi. Hyperhomocysteinemia
                   vii. Stress/depression
              b. Monitor for recurrent ischemia
              c. Monitor for LV remodeling/CHF

34.        ABC’s of treatment and secondary prevention of AMI
             a. Aspirin-prophylactic Rx for recurrent ischemic event; give for at least
                three months after AMI, probably indefinitely
             b. Beta blockers-prophylactic, for reduction of cardiac mortality; Rx for two
                year – indefinitely
             c. Converting enzyme inhibitors – all patients with LV dysfunction to reduce
                risk of progressive heart failure and death
             d. Diet and lipid lowering Rx-statins have been shown to reduce risk of
                subsequent MI, need for revascularization and mortality (4S, Care)
             e. Exercise and rehabilitation-essential in restoration of confidence and
                improvement in quality of life.

      35. Ways to reduce risk of heart attack (Harvard Health Letter September 1992,
           Sullivan. Obstet Gynecol 87:36S, 1996)
            a. Stop smoking - 50-70% risk reduction
            b. Regular exercise - 45% risk reduction
            c. Maintain ideal weight - 35-55% risk reduction (compared to 20% above
            d. Reduce total cholesterol by 1% - 2-3% risk reduction
            e. Reduce diastolic pressure 1 mmHg – 2-3% risk reduction