Ischemic heart disease &

Angina pectoris

By
Onyedika
MD5
#671
Content
Definition
Epidemiology
Pathogenesis (Acute plaque change, Inflammation,
thrombus, vasoconstriction)
Angina pectoris
Myocardial infarction
Chronic IHD
SCD


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
Determinants of myocardial
oxygen demand
The major determinants of myocardial oxygen
demand are heart rate, myocardial contractility,
and myocardial wall tension.

An adequate supply of oxygen to the myocardium
requires a satisfactory level of oxygen-carrying
capacity of the blood and an adequate level of
coronary blood flow.


Epidemiology
Leading cause of death in US and industrialized
nations

Incidence rises progressively with increasing age.

M>F. Women are protected against MI during
their reproductive years


Pathogenesis
Acute plaque change

Inflammation

Thrombus

Vasoconstriction

Acute plaque changes
In most patients, unstable angina, infarction, and
many cases of SCD occur because of abrupt
plaque change followed by thrombosis, hence the
term acute coronary syndrome.

Vulnerable plaques
Plaques containing large a areas of foam cells and
extracellular lipid

Thin fibrous cap, contain few smooth muscle cells


Role of Inflammation
Endothelial cells release CAMs, selectins

T-cells release TNF, IL-6, IFN-gamma to
stimulate and activate endothelial cells and
macrophages

CRP predicts the risk of damage in coronary heart
disease

Role of Thrombus
Total or partial vascular occlusion by a newly
formed thrombus on a disrupted
atherosclerotic plaque lead to unstable
angina or sudden death.

Organizing thrombi produce potent activators
of smooth muscle proliferation, which can
contribute to the growth of atherosclerotic
lesions.

Role of Vasoconstriction
Vasoconstriction directly compromises lumen
diameter and potentiate plaque disruption.


Classification s of IHD

Myocardial infarction (MI)

Sudden cardiac death

Angina pectoris

Chronic IHD with heart failure
Angina Pectoris

Stable = 75% vessel block, transient ( <15
minutes), aggravated by exertion, relived by rest
& Nitroglycerin (VD)

Prinzmetal = coronary spasm, episodic, Typical
EKG change ST elevation, Relived by VD but
not rest

Unstable = 90% vessel block or Acute plaque
change ( superimposed thrombus), prolonged (
>15 min.), not relived by rest, VD, Pre-infarction
Angina
Microvascular Angina
(syndrome x)
It may be due to spasm in the tiny blood
vessels of the heart, arms, and legs.

It is not characterized by arterial blockages,
so harder to diagnose but its prognosis is
excellent.
Angina - Chest Pain
Site - Jaw to navel, retrosternal, left submammary
Radiation - Left chest, left arm, jaw, mandible,
teeth, palate, back
Quality/severity - Tightness, heaviness,
compressionclenched fists
Precipitating - physical exertion, cold windy
weather, emotion
Relieving factors -Rest, sublingual nitrates, aspirin
Autonomic symptoms - Sweating, pallor,
peripheral vasoconstriction.

Chest Pain
Differential diagnosis
Cardiac pathology
Pericarditis, aortic dissection
Pulmonary pathology
Pulmonary embolus, pneumothorax, pneumonia
Gastrointestinal pathology
Peptic ulcer disease, reflux, pancreatitis, caf
coronary
Musculoskeletal pathology
Trauma, Tietzes Syndrome
Myocardial Infarction
It is necrosis of heart muscle resulting from ischemia.
Chest pain

EKG ST-segment elevation (minutes to hours)

Q-wave and T-wave inversion (hours to days)

Lab. Evaluation: CK-MB gold standard,
Troponin- specific

CRP predicts risk of AMI in angina patients

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 is by exclusion
Dr. Krishna Tadepalli, MD, www.mletips.com
19
Sudden cardiac death

It is unexpected death in one hour due to cardiac
causes with or without clinical symptoms

Cause Atherosclerosis ( 90%), others (10%)
Romano- Ward syndrome (KCNE genes)
Long Q-T syndrome ( K+, Na+ channel
defects)

Mechanism- Most likely due to arrhythmias ( VF)

21
Management
Pharmaceuticals:
Beta Blockers
Ca
++
Blockers
Nitrates - Vasculature vasodilation
Anti-Hypercholesterolemia
HMG CoA Reductase Inhibitors
Antiplatelet Medication
Clopidogrel (Plavix)
Aspirin

22
Surgical Treatment
Stenting

Angioplasty (balloon)

Coronary Artery Bypass Graft



23

Acute coronary syndrome
Syndrome Stenoses
Plaque
Disruption
Plaque-Associated
Thrombus
Stable angina >75% No No
Unstable
angina
Variable Frequent Non-occlusive
Transmural
MI
Variable Frequent Occlusive
Subendocard
ial MI
Variable Variable Widely variable
Sudden
death
severe Frequent Often small
Summary
References
Kumar, V., & Robbins, S. L. 1. (2007). Robbins basic
pathology (8th ed.). Philadelphia, PA: Saunders/Elsevier.
P.Kumar and M.Clark: Kumar & Clarks Clinical Medicine
Lindenfeld J, et al. HFSA 2010 Comprehensive Heart Faailure
Guidline.
Dr Chris Gale Clinical Research Fellow Medical Research Council -
University of Leeds
Dr.KrishnaTadepalli,MD. www.mletips.com