1. ISCHAEMIC HEART DISEASE 3
H.A. MWAKYOMA, MD

2. Aims and Objectives Ischaemic heart disease Chest pain
Definition, manifestations, epidemiology, aetiology, pathophysiology, risk factors and prevention, relevance to dentistry
Chest pain
Differential diagnosis
Acute myocardial infarction
Assessment, treatment, complications
Cardiopulmonary resuscitation

3. Ischaemic heart disease Definition
An imbalance between the supply of oxygen and the myocardial demand resulting in myocardial ischaemia.
Angina pectoris
symptom not a disease
chest discomfort associated with abnormal myocardial function in the absence of myocardial necrosis

4. Ischaemic heart disease Definition--- cont--
Supply
Atheroma, thrombosis, spasm, embolus
Demand
Anaemia, hypertension, high cardiac output (thyrotoxicosis, myocardial hypertrophy)

7. 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

8. Ischemic Heart Disease
What is Ischemic Heart Disease (IHD)?
Ischemic heart disease results when blood flow to the myocardium is insufficient to meet the demands of the heart. IHD results in:
Angina pectoris (cardiac chest pain)
High risk for ACS
High risk for developing congestive heart failure (CHF)

9. IHD Ischemic Heart Disease: Basic Physiology
IHD results when coronary oxygen supply does not meet the oxygen demand of the myocardium, so decreased supply or increased demand may be responsible.

10. IHD: Oxygen Supply Ischemic Heart Disease: Oxygen Supply
Myocardial O2 supply is determined by two factors:
O2 carrying capacity of the blood 2) Coronary blood flow

11. IHD: Oxygen Supply Ischemic Heart Disease: O2 Carrying Capacity
The carrying capacity of the blood is determined by the hemoglobin content and the ability of the lungs to effectively oxygenate the hemoglobin.
Anemic people (those with low hemoglobin levels) are more likely to experience symptoms related to IHD.
Athletes frequently inject Epogen (erythropoietin), a drug that increased hemoglobin production, in order to enhance performance.

12. IHD: Oxygen Supply Ischemic Heart Disease: Coronary Flow
The coronary blood flow is dependant on many factors including:
Coronary perfusion pressures (related to diastolic BP)
Coronary vascular resistance
External compression of the coronary arteries
Intrinsic regulation of vasodilation/vasoconstriction
Local metabolites and endothelial factors
Nervous system innervation of the coronaries

13. IHD: Oxygen Demand Ischemic Heart Disease: Oxygen Demand
Oxygen demand is determined by three factors:
Myocardial wall stress (afterload + preload)
Heart rate (chronotropy)
Contractility (inotropy)

14. IHD: Oxygen Demand Ischemic Heart Disease: Wall Stress
The higher the stress on the walls of the heart, the higher the myocardial oxygen demand. This is explained by the “Law of LaPlace”:
Wall stress = pressure X radius_
2 X wall thickness
Note: Since the LV is the largest part of the heart, the LV wall stress, LV pressure, LV radius, and LV wall thickness is used in the above equation.

15. IHD: Oxygen Demand Ischemic Heart Disease: LV Pressure
The LV pressure is determined by the “afterload” (a.k.a. systemic vascular resistance or SVR).
Conditions that increase afterload include systemic hypertension and aortic valve stenosis.
Afterload is decreased with antihypertensive therapy and as a long-term response to exercise.
LV Wall stress =LV pressure X LV radius_
2 X LV wall thickness

16. IHD: Oxygen Demand Ischemic Heart Disease: LV Thickness
The LV thickness is the heart’s natural response to increased preload and afterload as a compensatory mechanism to try to maintain a normal LV wall stress and thus myocardial oxygen demand.
As the LV wall thickness increases, wall stress per gram of myocardium decreases by a factor of 2.
LV Wall stress = LV pressure X LV radius_
2 X LV wall

17. IHD: Oxygen Demand Ischemic Heart Disease: Heart Rate (HR)
The HR also determines myocardial oxygen demand.
Larger amounts of oxygen is required when the heart rate is high, thus tachycardia can lead to increased oxygen demand and ischemia if the HR is high enough and if it is sustained for long periods of time.
Conversely, slowing the heart rate decreases the myocardial oxygen demand. This is the reason behind using -blockers when myocardial ischemia is present

18. IHD: Oxygen Demand Ischemic Heart Disease: Contractility
The strength of contraction of the myocardium, termed contractility or inotropy, also determines oxygen demand.
Things that increase contractility include SNS stimulation (from epinephrine induced 1 receptor agonism) or inotropic medications (such as dobutamine).
Thinks that decrease contractility include -receptor blockers, again contributing to their role in decreasing myocardial oxygen demand.

19. IHD: Syndromes Ischemic Heart Disease: Syndromes
Ischemia heart disease results from one of four possible ischemic syndromes:
Chronic stable angina (always from atherosclerosis)
Acute coronary syndromes (usually from atherosclerosis)
Variant or Pritzmetal’s Angina (not from atherosclerosis)
Silent ischemia (usually from atherosclerosis)

20. IHD: Syndromes

21. Ischemic Heart Disease
Classification = mainly 4 types
Myocardial infarction (MI)
Sudden cardiac death
Angina pectoris
Chronic IHD with heart failure

22. IHD: Stable Angina Ischemic Heart Disease: Stable Angina
Stable angina refers to myocardial ischemia that occurs with exertion and is relieved with rest.
This occurs universally from atherosclerosis and results from significant flow-limiting stenosis of the coronary arteries that causes ischemia only when oxygen demand is increased, such as during exertion.

23. IHD: Stable Angina Ischemic Heart Disease: Symptoms
Symptoms include typical cardiac chest pain lasting less than 10 minutes which is often described as:
“pressure-like” or “tightness” or “heaviness” or “indigestion” in the chest
Located substernally radiating to the left arm, neck, jaw, or shoulder (see next slide).
Levine sign: When a patient makes a fist on their chest to describe their chest pain.

24. IHD: Stable Angina

25. IHD: Stable Angina Ischemic Heart Disease: Symptoms
While many people are familiar with the classic description of cardiac chest pain, many atypical presentations of cardiac pain may occur.
These include:
Sharp or burning pain instead of pressure-like.
Radiation to the shoulders, right chest/arm, or back.
Describing the feeling as a “discomfort”, not pain.

28. IHD: Stable Angina Ischemic Heart Disease: SNS Effects
The sympathetic nervous system (SNS) is activated during ischemia due to pain, emotion, and sometimes due to the baroreceptor response (if hypotension is present).
Signs of SNS activation include:
Cold sweat (diaphoresis) ) Palpitations
3) Cold and clammy skin due to vasoconstriction
4) A feeling of impending doom

29. IHD: Stable Angina Ischemic Heart Disease: PNS Effects
The parasympathetic nervous system (PNS) is activated in order to attempt to compensate for the increased SNS activity.
Signs of PNS activation include:
Nausea and vomiting
Weakness
Note: Since -blockers can hinder SNS symptoms, PNS symptoms may predominate in people on -blockers.

30. IHD: Stable Angina Ischemic Heart Disease: Atypical Symptoms
Many “atypical” presentations of angina occur and are much more common in women. They include:
Dizziness or lightheadedness alone
Weakness alone
Fever alone
Nausea and vomiting alone
Syncope or “passing out”

31. IHD: Stable Angina Ischemic Heart Disease: Diagnosis
The diagnosis of IHD is based on 3 steps:
Suspicion of disease based on CAD risk factors and symptoms.
Screening via EKG and/or cardiac stress testing.
Confirmation of CAD via coronary angiography in people with positive stress tests.
Note: Step 2 may be skipped in people who are considered “high risk” for CAD.

32. IHD: Stable Angina Ischemic Heart Disease: Diagnosis - EKG
EKG findings during myocardial ischemia include ST segment depression and T wave inversion (not ST elevation, which is seen in acute myocardial infarction).
In stable angina, these findings should not be seen at rest. In unstable angina, these findings may be seen at rest.
Normal Horizontal ST Downsloaping ST T Wave ST
Depression Depression Inversion Elevation

33. IHD: Stable Angina Ischemic Heart Disease: Screening
Cardiac stress testing is the preferred method of screening for CAD.
Each stress test has a diagnostic modality and a means of inducing stress to the heart. Based on findings during cardiac stress testing, a coronary angiogram may or may not be recommended.

34. IHD: Stable Angina Ischemic Heart Disease: Screening
The three most common diagnostic modalities during stress testing are:
Continuous EKG monitoring
Echocardiography
Nuclear imaging

35. IHD: ACS Ischemic Heart Disease: ACS
Acute coronary syndrome (ACS) occurs when severe myocardial ischemia occurs for prolonged periods of time.
The pain is similar to that of stable angina, however it typically lasts for more than 10 minutes and is not relieved with rest.
ACS includes three distinct types (see next lecture):
Unstable Angina (UA) 2) Non-ST elevation MI (NSTEMI)
3) ST elevation MI (STEMI)

36. IHD: Variant Angina Ischemic Heart Disease: Variant Angina
Variant or “Pritzmetal’s” angina is a relatively rare syndrome that occurs due to severe vasoconstriction of the coronary arteries leading to myocardial ischemia due to decreased coronary flow.
The etiology is unclear, but may relate to dysfunctional endothelial cells present in early atherosclerosis.
Variant angina is more common in females, occurs most often in early morning hours (upon awakening), and results in ST elevation on EKG (not ST depression).

37. IHD: Variant Angina
Ischemic Heart Disease: Variant Angina

38. IHD: Silent Ischemia Ischemic Heart Disease: Silent Ischemia
Myocardial ischemia can occur in the absence of any symptoms!
This is common in diabetics who have peripheral neuropathy making it difficult to feel cardiac chest pain.
Elderly people may also frequently be asymptomatic during ACS.

39. Ischaemic heart disease Manifestations
Sudden death
Myocardial infarction
Acute coronary syndrome
Stable angina pectoris
Heart failure
Arrhythmia
Asymptomatic

40. Ischaemic heart disease Epidemiology
Commonest cause of death in the Western world. (up to 35% of total mortality)
Over 20% males under 60 years have IHD
Health in one study showed;
3% of adults suffer from angina
1% have had a myocardial infarction in the
past 12 months

41. Ischaemic heart disease Aetiology

42. Ischaemic heart disease Aetiology—cont--
Fixed
Age, Male, +ve family history
Modifiable – strong association
Dyslipidaemia, smoking, diabetes mellitus, obesity, hypertension
Modifiable - weak association
Lack of exercise, high alcohol consumption, type A personality, OCP, soft water
(Atherosclerosis)

43. Ischaemic heart disease Pathophysiology

44. Ischaemic heart disease Pathophysiology
Response to injury hypothesis
ATHEROSCLEROSIS
Accumulation of cholesterol within the vessel wall intima. Smooth muscle cell proliferation
SCLEROSIS
Expansion of fibrous tissue
INFLAMMATION
Chronic inflammatory cells migrate into wall, release cytokines
GROWTH FACTORS/INFLAMMATORY MEDIATORS

45. Ischaemic heart disease Pathophysiology

46. Ischaemic heart disease Acute coronary syndromes
Atherosclerosis
Fatal /
non-fatal AMI
Coronary
Artery spasm
Unstable
angina

47. Ischaemic heart disease Acute coronary syndromes
Fatal AMI
Small, fat rich plaques. Plaque RUPTURE. Thrombus in lipid core and on plaques surface. Vessel lumen OCCLUDED.
Non-fatal AMI
Plaque EROSION rather than rupture. OCCLUSIVE thrombus.
Unstable angina
Usually mod-severe stenosis. Multiple vessels. Collaterals often formed. Thrombus formation and vasoconstriction. Myocardial infarction may ensue

48. Ischaemic heart disease Risk factors and prevention

49. Ischaemic heart disease Risk factors and prevention
Family History
Smoking
Hypertension
Diabetes Mellitus
Hypercholesterolaemia
Lack of exercise
PRIMARY PREVENTION

50. Ischaemic heart disease Relevance to dentistry
IHD is common
Subjects with IHD have more severe dental caries and periodontal disease – association or causation?
Angina is a cause of pain in the mandible, teeth or other oral tissues
Stress provokes ACS!

51. Chest Pain Myocardial ischaemia
Site
Jaw to navel, retrosternal, left submammary
Radiation
Left chest, left arm, jaw….mandible, teeth, palate
Quality/severity
tightness, heaviness, compression…clenched fists

52. Chest Pain Myocardial ischaemia
Precipitating/relieving factors
physical exertion, cold windy weather, emotion
rest, sublingual nitrates
Autonomic symptoms
sweating, pallor, peripheral vasoconstriction, nausea and vomiting

53. Chest Pain Differential diagnosis
Cardiac pathology
Pericarditis, aortic dissection
Pulmonary pathology
Pulmonary embolus, pneumothorax, pneumonia
Gastrointestinal pathology
Peptic ulcer disease, reflux, pancreatitis, ‘café coronary’
Musculoskeletal pathology
Trauma, Tietze’s Syndrome

54. Ischemic Heart Disease
MI= Also called Heart attack
Incidence = disease of old
elderly (45% in 65 yrs. old)
young ( 10% in 40yrs. Old),
Sex = Male > Female
Ethnic = same in African & American
Risk factors
Major modifiable- DM, HTN, Smoking, Hypercholesterolemia
HRT for Postmenopausal females – will not protect the heart

55. Acute Myocardial Infarction
250,000 deaths per year.
150,000 presentations to hospital.
30% of deaths occur in the first 2 hours.
(Cardiac muscle death occurs after 45 mins of ischaemia)

56. Ischemic Heart Disease
Pathogenesis
Coronary vessel occlusion
Atherosclerosis with thrombus = MC cause ( 90% cases)
Others = vasospasm (10%)
Most important mechanism = dynamic changes in the plaque (rather than plaque size),
Plaque disruption PLTS aggregation thrombus and VC (happens in minutes)
Irreversible changes = after 30 minutes of ischemia
ATP < 10% of normal
Mechanism of cell death = necrosis ( Coagulative

57. Ischemic Heart Disease
MI = Clinical
Silent MI = DM, Elderly, Cardiac transplantation recipients,
Typical features = Rapid, weak pulse and sweating profusely (diaphoretic), Dyspnea, chest pain
Lab=
Diagnostic
Best markers = Troponins ( T & I), both sensitive and cardio – specific
Next best – CK-MB
Predictive
CRP- >3mg/l – highest risk

58. Myocardial Infarction
Partial or total occlusion of one or more of the coronary arteries due to an atheroma, thrombus or emboli resulting in cell death (infarction) of the heart muscle
When an MI occurs, there is usually involvement of 3 or 4 occluded coronary

59. MI, Atheroma
When there is an atheroma, as mentioned before there can be rupture resulting in thrombus formation because of the build up of platelets
When there is breakage of the thrombus there is emboli formation
An emboli can travel to the brain (cerebral infarct) can remain in the heart (myocardial infarct) or even travel to the extremities cutting off blood supply(Gangrene)
As the area beneath the is disrupted atheroma hemorrhages, there can is increased risk of abscess formation and infection

60. Complications of Myocardial Infarctions
Infarction leading to inability of the heart to function properly leading to Heart Failure
Angina/Pain
Cardiogenic shock
Ventricular aneurysm and rupture
Embolism Formation
Arrhythmias  Myocardial Infarctions can lead to Ventricular Fibrillation (shockable!)

61. Sudden Death Sudden Death :
250,000 deaths in the US per year are caused by what is referred to as “sudden” cardiac death
Sudden Cardiac Death is also known as a “Massive Heart Attack” in which the heart converts from sinus rhythm to ventricular fibrillation
In V-Fib, the heart is unable to contract fully resulting in lack of blood being pumped to the vital organs
V-Fib requires shock from defibrillator “SHOCKABLE RHYTHM”

62. MI - Types Transmural Full thickness
Superimposed thrombus in atherosclerosis
Focal damage
Sub-endocardial
Inner 1/3 to half of ventricular wall
Decreased circulating blood volume( shock, Hypotension, Lysed thrombus)
Circumferential

63. Plaque-Associated Thrombus
Heart - Pathology
Syndrome
Stenoses
Plaque Disruption
Plaque-Associated Thrombus
Stable angina
>75% No
Unstable angina
Variable
Frequent
Non-occlusive
Transmural MI
Occlusive
Subendocardial MI
Widely variable
Sudden death
severe
Often small

64. MI- chest pain

65. MI MI -Morphology light microscopy
First 12 hrs. after MI – no change
Up to 3 days = Coagulative necrosis, neutrophils
1-2 weeks = Granulation tissue
≥ 3 weeks = fine scar
≥ 2 months = dense scar
EM – membrane disruption and Mitochondrial densities
Special stain = TTC ( Triphenyl Tetrazolium chloride),
Detects and stains Mahogany brown with Lactate dehydrogenase
Unstained area = infarction
Mahogany brown = viable
White, glistening= scar
Most common and nonspecific change in ischemia = sub-endocardial myocyte vacuolization

66. Ischemic Heart Disease TTC

67. MI- MICROSCOPY Up to 3 days duration Neutrophilic infiltrate
One-day-old infarct
Up to 3 days duration
coagulative necrosis
Neutrophilic infiltrate
1 -2 weeks
>3 weeks
Granulation tissue

68. Ischemic Heart Disease
MI –Complications
In 75% of Patients with MI
Poor prognosis in = elderly, females, DM, old case of MI, Anterior wall infarct – worst, posterior –worse, Inferior wall – best
1. Arrhythmia = Ventr. Fibrillation – MC arrhythmia lead to sudden death in MI patients, before they reach hospital
2. pump failure – LVF, cariogenic shock, if >LV wall infarcts, lead to death ( 70% of hospitalized MI patients)
3.Ventricular rupture = Free or lateral LV wall – MC site, later cause false aneurysm,
4.True aneurysm = rupture is very rare
5.Pericarditis = Dressler’s syndrome ( Late MI complication)
6.Recurrence

69. Ischemic Heart Disease
Sudden cardiac death = unexpected death in one hour due to cardiac causes with or without clinical symptoms
Cause – Atherosclerosis ( 90%), others (10%)
Romano- Ward syndrome – Long Q-T syndrome
( K+, Na+ channel defects)
Mechanism- Most likely due to arrhythmias ( VF)
Patients – young athletes, with Pul. HTN, IHD
Morphology
Prominent finding – increased heart mass
Vacuolations in Sub – endocardial myocardium

70. Ischemic Heart Disease
Chronic IHD = also called ischemic cardiomyopathy
Patients = post heart transplant receipts, previous MI or CABG pts
Cause =compromised ventricular function
Morphology =vacuoles, Myocyte Hypertrophy
Diagnosis= by exclusion