3. What Are They?
• In ischaemic patients
exacerbation (e.g. chest pain, unstable angina, MI, multiple ventricular ectopics,
ventricular fibrillation, acute coronary insufficiency)
• In non ischaemic patients
~ palpitations, tremor, sweating, tachycardia and marked ST segment depression
4. When Do They Appear?
• ~b/w 1-21d
~ ischaemic attack for other reasons
5. Underlying Mechanisms
• 1st Hyper-responsiveness of beta adrenergic
maybe due to expression of more receptors during treatment (?) augmented
sympathetic responsiveness (~isoprenaline)
e.g. after propranolol withdrawal, a vasodilator was given to the subjects
profound tachycardia was seen, meaning increased sympathetic activity
• 2nd Some studies found increased population
50% increase in BRs density in human lymphocytes after 5 days of propranolol
160mg/d
• 3rd Increase in plasma catecholamines
few studies support this
55% increase urinary adrenaline 26% noradrenaline
another study found an overshoot of carecholamines after withdrawal
6. • 4th Thyroid hormones
few suggest that increased level of thyroid hormones after withdrawal beta Rs
responsiveness
• 5th Platelet aggregation
patients w/ angina more susceptible to platelet-ADP interaction after withdrawal
from propranolol aggregation release of coronary constrictors
• 6th Unmasking of the progressing disease process
• 7th Partial Agonist
may provide sufficient stimulation to prevent generation of more receptors
atenolol, pindolol and propranolol found to unaffected by abrupt withdrawal in
normal subjects
7. If Gradual
• reduction of the dosages until cessation after 14 days had shown no increase
in sensitivity to isoprenaline compared to abrupt withdrawal
