Download ISCHAEMIC HEART DISEASE 3

ISCHAEMIC HEART
DISEASE 3
H.A. MWAKYOMA, MD
Aims and Objectives
• Ischaemic heart disease
– Definition, manifestations, epidemiology,
aetiology, pathophysiology, risk factors and
prevention, relevance to dentistry
• Chest pain
– Differential diagnosis
• Acute myocardial infarction
– Assessment, treatment, complications
• Cardiopulmonary resuscitation
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
Ischaemic heart disease
Definition--- cont-• Supply
– Atheroma, thrombosis, spasm, embolus
• Demand
– Anaemia, hypertension, high cardiac output
(thyrotoxicosis, myocardial hypertrophy)
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
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)
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.
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
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.
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
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)
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.
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
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
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
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.
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)
IHD: Syndromes
Ischemic Heart Disease
Classification = mainly 4 types
– Myocardial infarction (MI)
– Sudden cardiac death
– Angina pectoris
– Chronic IHD with heart failure
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.
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.
IHD: Stable Angina
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.
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)
2) Palpitations
• 3) Cold and clammy skin due to vasoconstriction
• 4) A feeling of impending doom
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.
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”
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.
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
Depression
Downsloaping ST
Depression
T Wave
Inversion
ST
Elevation
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.
IHD: Stable Angina
• Ischemic Heart Disease: Screening
• The three most common diagnostic
modalities during stress testing are:
• Continuous EKG monitoring
• Echocardiography
• Nuclear imaging
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)
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).
IHD: Variant Angina
Ischemic Heart Disease: Variant Angina
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.
Ischaemic heart disease
Manifestations
•
•
•
•
•
•
•
Sudden death
Myocardial infarction
Acute coronary syndrome
Stable angina pectoris
Heart failure
Arrhythmia
Asymptomatic
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
Ischaemic heart disease
Aetiology
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)
Ischaemic heart disease
Pathophysiology
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
Ischaemic heart disease
Pathophysiology
An atherosclerotic lesion
Schematic illustration
Endothelium
Macrophage foam cell
Smooth muscle cell
Thrombus formation
Lymphocytes
Media
(smooth muscle cells)
Ischaemic heart disease
Acute coronary syndromes
•
Atherosclerosis
Fatal /
non-fatal AMI
Unstable
angina
Coronary
Artery
spasm
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
Ischaemic heart disease
Risk factors and prevention
Ischaemic heart disease
Risk factors and prevention
•
•
•
•
•
•
Family History
Smoking
Hypertension
Diabetes Mellitus
Hypercholesterolaemia
Lack of exercise
• PRIMARY PREVENTION
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!
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
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
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
MI
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
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)
MI
Ischemic Heart Disease
• MI
• 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
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
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
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
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!)
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”
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
Heart - Pathology
Syndrome
Stenoses
Plaque
Disruption
Plaque-Associated Thrombus
Stable angina
>75%
No
No
Unstable angina
Variable
Frequent
Non-occlusive
Transmural MI
Variable
Frequent
Occlusive
Subendocardial
MI
Variable
Variable
Widely variable
Sudden death
severe
Frequent
Often small
MI- chest pain
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 = subendocardial myocyte vacuolization
Ischemic Heart Disease
TTC
MI- MICROSCOPY
One-day-old
infarct
coagulative necrosis
1 -2 weeks
Granulation tissue
Up to 3 days duration
Neutrophilic infiltrate
>3 weeks
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
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
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