1. Ischemic Heart Disease
Ana H. Corona, FNP-Student
University of Phoenix
May 2002

2. Myocardial Ischemia
Results when there is an imbalance between myocardial oxygen supply and demand
Most occurs because of atherosclerotic plaque with in one or more coronary arteries
Limits normal rise in coronary blood flow in response to increase in myocardial oxygen demand

3. Oxygen Carrying Capacity
The oxygen carrying capacity relates to the content of hemoglobin and systemic oxygenation
When atherosclerotic disease is present, the artery lumen is narrowed and vasoconstriction is impaired
Coronary blood flow cannot increase in the face of increased demands and ischemia may result

4. Angina
When ischemia results it is frequently accompanied by chest discomfort: Angina Pectoris
In the majority of patients with angina, development of myocardial ischemia results from a combination of fixed and vasospastic stenosis

5. Chronic Stable Angina
May develop sudden increase in frequency and duration of ischemic episodes occurring at lower workloads than previously or even at rest
Known as unstable angina: up to 70% patients sustain MI over the ensuing 3 months

6. Angina: cont
Patients with mild obstruction coronary lesions can also experience unstable angina
>90% of Acute MI result from an acute thrombus obstructing a coronary artery with resultant prolonged ischemia and tissue necrosis

7. Treatment of Angina
Treatment of Chronic Angina is directed at minimizing myocardial oxygen demand and increasing coronary flow
Where as in the acute syndromes of unstable angina or MI primary therapy is also directed against platelet aggregation and thrombosis

8. Epidemiology
Modifiable Factors: hyperlipidemia- ^ LDL (<130 normal) or low HDL (>60 normal), Hypertension, cigarette smoking and diabetes, obesity, BMI of >30
Non-Modifiable Factors: advanced age, male sex, family medical history: male <55 y/o, female <65 y/o
Other: sedentary lifestyle and stressful emotional stress

9. Homocysteine
Concentration of amino acid homocysteine is related to incidence of coronary, cerebral, and peripheral vascular disease
The risk of MI is 3x > in patients with high levels of homocysteine compared with those with the lowest levels
Supplement of diet with foliate and other B vitamins lower levels of homocysteine but not known where therapy improves coronary risk

10. Fibrinogen
Elevated level of plasma fibrinogen is independent risk factor for CAD in males and females
Elevated levels of coagulation factor VII is risk factor X50 fold if with smoking or HTN
Careful HX taking: to evaluate s/s include: quality, location, radiation, precipitating factors, frequency

11. Quality
Tightness, squeezing, heaviness, pressure, burning, indigestion or aching sensation
It is rarely “PAIN”
Never: sharp, stabbing, prickly, spasmodic, or pleuritic
Lasts a few seconds < 10 minutes
Relieved by NTG s/l
Levine Sign: clench fist to sternum

12. Signs & Symptoms accompany Angina
Dyspnea, nausea, diaphoresis resolve quickly after cessation of angina
Angina is a diffuse sensation rather than discrete

13. Ischemic Heart Disease
Imbalance between Myocardial oxygen supply and demand = Myocardial hypoxia and accumulation of waste metabolites due to atherosclerotic disease of coronary arteries

14. Stable Angina
Stable Angina: chronic pattern of transient angina pectoris precipitated by physical activity or emotional upset, relieved by rest with in few minutes
Temporary depression of ST segment with no permanent myocardial damage

15. Angina Pectoris
Angina Pectoris: uncomfortable sensation in the chest or neighboring anatomic structures produced by myocardial ischemia

16. Variant Angina Typical anginal discomfort usually at rest
Develops due to coronary artery spasm rather than increase myocardial oxygen demand
Transient shifts of ST segment – ST elevation

17. Unstable Angina
Increased frequency and duration of Angina episodes, produced by less exertion or at rest = high frequency of myocardial infarction if not treated

18. Silent Ischemia Asymptomatic episodes of myocardial ischemia
Detected by electrocardiogram and laboratory studies

19. Myocardial Infarction
Region of myocardial necrosis due to prolonged cessation of blood supply
Results from acute thrombus at side of coronary atherosclerotic stenosis
May be first clinical manifestation of ischemic heart disease or history of Angina Pectoris

20. Precipitants
Exertion: walking, climbing stairs, vigorous work using arms, sexual activity
Vasoconstriction: extremities, increased systemic vascular resistance, increased in myocardial wall tension and oxygen requirements
Myocardial Ischemia displays a circadian rhythm threshold for Angina it is lower in morning hours.

21. Physical Examination
Arcus senilis, xanthomas, funduscopic exam: AV nicking, exudates
Signs and symptoms: hyperthyroidism with increased myocardial oxygen demand, hypertension, palpitations
Auscultate carotid and peripheral arteries and abdomen: aortic aneurysm
Cardiac: S4 common in CAD, increased heart rate, increased blood pressure

22. Ischemia
Myocardial ischemia may result in papillary muscle regurgitation
Ischemic induced left ventricular wall motion abnormalities may be detected as an abnormal precordial bulge on chest palpation
A transient S3 gallop and pulmonary rales = ischemic induced left ventricular dysfunction

23. Diagnostic Tests
Blood tests include serum lipids, fasting blood sugar, Hematocrit, thyroid (anemias and hyperthyroidism can exacerbate myocardial ischemia
Resting Electrocardiogram: CAD patients have normal baseline ECGs
pathologic Q waves = previous infarction
minor ST and T waves abnormalities not specific for CAD

24. Electrocardiogram
Electrocardiogram: is useful in diagnosis during cc: chest pain
When ischemia results in transient horizontal or downsloping ST segments or T wave inversions which normalize after pain resolution
ST elevation suggest severe transmural ischemia or coronary artery spasm which is less often

25. Exercise Stress Test Used to confirm diagnosis of angina
Terminate if hypotension, high grade ventricular disrrhythmias, 3 mm ST segment depression develop
(+): reproduction of chest pain, ST depression
Severe: chest pain, ST changes in 1st 3 minutes, >3 mm ST depression, persistent > 5 minutes after exercise stopped
Low systolic BP, multifocal ventricular ectopy or V- tach, ST changes, poor duration of exercise (<2 minutes) due to cardiopulmonary limitations

26. Other Diagnostic Tests
Radionuclide studies
Myocardial perfusion scintigraphy
Exercise radionuclide ventriculography
Echocardiography
Ambulatory ECG monitoring
Coronary arteriography

27. Management Goals to reduce Anginal Symptoms
Prevent complications – myocardial infarction, and to prolong life
No smoking, lower weight, control hypertension and diabetes
Patients with CAD – LDL cholesterol should achieve lower levels (<100)
HMG-COA reductase inhibitors are effective

28. Pharmacologic Therapy
Therapy is aimed in restoring balance between myocardial oxygen supply and demand
Useful Agents: nitrates, beta-blockers and calcium channel blockers

29. Nitrates Reduce myocardial oxygen demand Relax vascular smooth muscle
Reduces venous return to heart
Arteriolar dilators decrease resistance against- which left ventricle contracts and reduces wall tension and oxygen demand

30. Nitrates: cont
Dilate coronary arteries with augmentation of coronary blood flow
Side effects: generalized warmth, transient throbbing headache, or lightheadedness, hypotension
ER if no relief after X2 nitro's: unstable angina or MI

31. Problems with Nitrates
Drug tolerance
Continued administration of drug will decrease effectiveness
Prevented by allowing 8 – 10 hours nitrate free interval each day.
Elderly/inactive patients: long acting nitrates for chronic antianginal therapy is recommended
Physical active patients: additional drugs are required

32. Beta Blockers Prevent effort induced angina
Decrease mortality after myocardial infarction
Reduce Myocardial oxygen demand by slowing heart rate, force of ventricular contraction and decrease blood pressure

33. Beta -1
Block myocardial receptors with less effect on bronchial and vascular smooth muscle- patients with asthma, intermittent claudication

34. Beta-Agonist blockers
With partial B-agonist activity:
Intrinsic sympathomimetic activity (ISA) have mild direct stimulation of the beta receptor while blocking receptor against circulating catecholamines
Agents with ISA are less desirable in patients with angina because higher heart rates during their use may exacerbate angina
not reduce mortality after AMI

35. Beta-blockers Duration of beta-blockers depends on lipid solubility
Accounts for different dosage schedules

36. Esmolol Short acting administered intravenously
Can be used to test tolerability of beta-blockage
Used for tachydysrhythmias and unstable angina
Primary prevention trials: beta blockers decrease incidence of first MIs with hypertensive patients

37. Contraindications
Symptomatic CHF, history of bronchospasm, bradycardia or AV block, peripheral vascular disease with s/s of claudication

38. Side Effects
Bronchospasm (RAD), CHF, depression, sexual dysfunction, AV block, exacerbation of claudication, potential masking of hypoglycemia in IDDM patients

39. Abrupt Cessation Tachycardia, angina or MI
Inhibit vasodilatory beta 2 receptors
Should be avoided in patients with predominant coronary artery vasospasm

40. Beta-Blockers: Long Term effects
Serum lipids: decrease of HDL cholesterol and increased triglycerides
Effects do not occur with beta-blockers with B-agonist activity or alpha-blocking properties

41. Calcium Channel Blockers
Anti-anginal agents prevent angina
Helpful: episodes of coronary vasospasm
Decreases myocardial oxygen requirements and increase myocardial oxygen supply
Potent arterial vasodilators: decrease systemic vascular resistance, blood pressure, left ventricular wall stress with decrease myocardial oxygen consumption

42. Nifedipine and other dihydropyridine calcium channel blockers
Fall in blood pressure, trigger increase heart rate
Undesirable effect associated with increased frequency of myocardial infarction and mortality

43. Calcium Channel Blockers
Secondary agents in management of stable angina
Are prescribed only after beta blockers and nitrate therapy has been considered
Potential to adversely decrease left ventricular contractility
Used cautiously in patients with left ventricular dysfunction

44. amlodipine and felodipine
Are newer CCB
Decrease (-) inotropic effects
Amlodipine is tolerated in patients with advanced heart failure without causing increase mortality when added with ace inhibitor, diuretic, and digoxin

45. LDL
Undergoes oxidation in proximity of arterial wall = prone to atherosclerotic process
Vitamin E 200 – 400 IU daily may lower coronary death rates

46. Drug Selection
Chronic Stable Angina: beta blocker and long acting nitrate or calcium channel blocker (not verapamil: bradycardia) or both.
If contraindication to BB a CCB is recommended (bronchospasm, IDDM, or claudication) any of CCB approved for angina are appropriate.

47. Drugs
Verapamil and Cardizem is preferred because of effect on slowing heart rate
Patients with resting bradycardia or AV block, a dihydropyridine calcium blocker is better choice
Patients with CHF: nitrates preferred amlodipine should be added if additional therapy is needed

48. Drugs
Primary coronary vasospasm: no treatment with beta blockers, it could increase coronary constriction
Nitrates and CCB are preferred
Concomitant hypertension: BB or CCB are useful in treatment
Ischemic Heart Disease & Atrial Fibrillation: treatment with BB, verapamil or Cardizem can slow ventricular rate

49. Combination Therapy
If patients do not respond to initial antianginal therapy – a drug dosage increase is recommended unless side effects occur.
Combination therapy: successful use of lower dosages of each agent while minimizing individual drug side effects

50. Combination Therapy Include:
Nitrate and beta blocker
Nitrate and verapamil or cardizem for similar reasons
Long acting dihydropyridine calcium channel blocker and beta blocker
A dihydropyridine and nitrate is often not tolerated without concomitant beta blockade because of marked vasodilatation with resultant head ache and increased heart rate

51. Combinations
Beta blockers should be combined only very cautiously with verapamil or cardizem because of potential of excessive bradycardia or CHF in patients with left ventricular dysfunction

52. Other methods
Patients with 1 – 2 vessel disease with normal left ventricular function are referred for catheter based procedures
Patients with 2 and 3 vessel disease with widespread ischemia, left ventricular dysfunction or DM and those with lesions are not amendable to catherization based procedures and are referred for CABG

53. Unstable Angina
Ischemic episodes occur more frequently more intense, last longer.
Precipitated by less activity or even at rest
May progress to acute MI due to presence of complicated coronary lesions with ulceration, hemorrhage or thrombosis at side of atherosclerotic plaque
Lesions may heal: s/s return to more stable pattern

54. Unstable Angina: cont It is a medical emergency
During episodes of angina, transient ST segment shifts or T wave flattening or inversion is likely
Signs of LV dysfunction (pulmonary rales, S3, Mitral regurgitation) may accompany ischemic episodes.

55. Unstable Angina: cont
Therapy: reduce myocardial oxygen demand with increase coronary flow
Antiplatelet and anticoagulant agents
Aspirin and IV heparin: reduces incidence of myocardial infarction and cardiac death in unstable angina
Oral Antiplatelet drug: ticlopidine: used for ASA intolerance individuals

56. Enoxaparin
Enoxaparin: low molecular weight heparin: effective in preventing ischemic events and death at 30 days and 1 year after administration than standardized IV heparin

57. Silent Ischemia Silent or painless ischemia
Presence of ST shifts with absence of symptoms
Increased risk of myocardial infarction and cardiac death common in diabetic patients
Beta blockers or calcium channel blockers and aspirin, cardiac catheterization, if left main or 3 vessels disease with left ventricular dysfunction is demonstrated

58. Acute Myocardial Infarction
Is dreaded outcome in patients with ischemic heart disease
1.5 million people sustain an MI in USA each year
Mortality rate of 25%
60% of MI related deaths occur before medical facilities are reached

59. Etiology
MI: is due to prolonged myocardial ischemia - leads to irreversible necrosis of heart muscle
90% due to acute thrombus at site of underlying coronary atherosclerosis
Non-atherosclerotic causes: cocaine use – due to ability of cocaine to increase myocardial 02 demand, induce coronary vasospasm & promote coronary thrombosis in association with platelet activation and endothelial cell dysfunction

60. Clinical Presentation
Initial diagnosis: presenting history, PE, and ECG
Most common S/S: severe crushing chest pain
Lasts longer than Angina, more intense, nausea, diaphoresis, dyspnea and feeling of impending doom

61. Symptoms
Circadian variability: occurring most commonly in morning hours, soon after awakening
Symptoms usually begin while at rest, and only occasionally are brought on by physical exertion
Some patients have less pronounced symptoms: generalized weakness, dyspnea, and indigestion.
20% cases have no s/s: detected by ECG changes

62. MI
Common physical findings in MI relate to impaired left ventricular systolic and diastolic function, associated inflammatory responses and stimulation of the sympathetic and parasympathetic nervous system

63. Other causes of substernal chest pain
Aortic dissection or pulmonary emboli may be fatal if not quickly recognized
Inappropriate administration of thrombolytic therapy to patients with pericarditis or aortic dissection could result in severe complications or death

64. Electrocardiogram
Q wave infarction, initial hyperacute T waves and ST elevation are present in the leads overlying involved myocardium
As cell death occurs, there is loss of the R wave and progressive Q wave development
The T wave begins to invert, followed by return of the ST segment over subsequent days

65. ECG: cont T wave may remain inverted for weeks to months
The new Q wave persists permanently
Posterior wall infarctions: mirror image pattern in anterior chest leads
With initial ST segment depression
T wave inversion and development of tall R waves in leads VI and V2

66. ECG: cont
Non Q wave infarction: new ST depression and/or T wave inversions persist for 48 hours or longer in leads overlying infarcting segments
BBB: diagnostic ECG evolution may not occur and diagnosis of Mi relies on presence of serum markers and laboratory modalities

67. Serum Markers of Infarction
Certain proteins are released into circulation during an MI
Creatine kinase CK rises in plasma within 4 to 8 hours, peaks at 24 hours, returns to normal by 48 hours to 72 hours
Not specific for myocardial damage: skeletal muscle trauma and IM injection, and hypothyroidism

68. CK-MB CK-MB isoenzyme is more specific for diagnosis of AMI
Not influenced by skeletal muscle injuries
CK-MB rises and peaks slightly earlier than total CK and returns to normal within 36 – 72 hours
May be elevated in: myocarditis after surgery, hypothyroidism, repetitive cardioversion

69. Enzymes Acute MI: CK-MB is greater than 2.5% of total serum CK
Serum CK and CK-MB isoenzyme should be measured on admission, then 12 and 24 hours later in diagnostic evaluation of an acute MI

70. Troponin
Troponin I and T are sensitive and highly specific markers of acute MI
Levels begin to rise within 3 hours after onset of infarction and remain elevated for several days
Higher Troponin I levels or early (+) of Troponin T assay correlate with greater short-term mortality

71. Myoglobin
Myoglobin is released into circulation very early after myocardial injury and detected within 2 hours of infarction
Rapid renal clearance and low specificity limit it s diagnostic role

72. Lactate Dehydrogenase (LDH)
Rises within 24 to 48 hours of MI
Peaks at 3 – 5 days and returns to baseline by 7-10 days
Usefulness in patients who are admitted to hospital 2 – 3 days after onset of symptoms
Level of LDH-1 greater than LDH-2 = myocardial necrosis

73. Thrombolytic Therapy
Activates the natural fibrinolytic system to dissolve responsible thrombus
Reduces mortality and improves recovery of left ventricular function following AMI
Streptokinase SK, anisoylated plasminogen-SK activator (APSAC), tissue plasminogen activator (alteplase or t-PA), and modified plasminogen activator (reteplase or r-PA)

74. Thrombolytics
Each of these drugs results in conversion of the proenzyme plasminogen to active plasmin which dissolves fibrin clots
Bleeding is the most important risk of each of these agents and their adjunctive therapies
Successful reperfusion: relief of chest pain and early peak of CK within 12 hrs

75. Thrombolytics
Reperfusion dysrhythmias are common: accelerated idioventricular rhythm, not require intervention
Antiplatelet and anticoagulant therapy used to maintain patency of coronary vessels following thrombolysis

76. Thrombolytics
Aspirin inhibits platelet function and reduces reocclusion following thrombolysis: 160 – 325 mg/day
Intravenous heparin needed to maintain vessel patency after initial thrombolytic therapy and is administered to achieve an activated PTT of 50 to 75 seconds for 48 hours