STABLE ANGINA
STROKE & TIA | |
|Signs |Symptoms |
|no specific signs but ↑ |speech difficulties (temporary loss, or trouble |
|BP/glucose levels are |understanding speech) |
|“indirect” signs |sudden blindness in one eye |
| |diplopia |
|Note: neurologic |headache (sudden/severe) |
|manifestations differ |seizure |
|depending on: |unsteadiness or sudden falls |
|1) stroke type, |sudden weakness, numbness and/or tingling of the face,|
|2) location of insult |arms or leg (may be transient) |
|(area of brain affected),|hemiplegia (facial/body paralysis of one side of body,|
|3) extent of ischemia, |opposite side of lesion) |
|infarct or hemorrhage |abrupt personality changes (confusion, disorientation)|
| |difficulty swallowing |
| |*these sx often occur early in the morning or at rest |
|Left-Brain Injury: |Right-Brain Injury |
|affects speech, right hand, |affects left hand, music, artistic |
|reasoning, # skills, written |abilities, creativity, insight, spatial |
|language |tasks, perception |
Definitions
Stroke ( syndrome caused by the disruption of blood flow to the brain resulting in sudden onset of a focal neurological deficit that persists for at least 24 hours
TIA ( episode of focal ischemic neurologic deficit lasting < 24 hrs (usually 5-10 minutes); may have the same sx of a stroke; reversible, temporary, no permanent damage; due to a 2º clot
Diagnosis
• CT Scan ( confirms ischemic stroke
• dx of TIA is difficult b/c it is over before pt can be examined
• usu. based on patient recollection of event
Pathophysiology
|Ischemic Stroke (85%) |Hemorrhagic Stroke (15%) |
|lasts 5-10 mins |lasts >1 hr |
|largely caused by either: |escape of blood from a ruptured |
|a) atherosclerosis or thrombosis of |cerebral vessel to surrounding brain |
|cerebral vessels (carotid arteries) ( |tissue ( mass formation ( brain tissue |
|can occur while sleeping or after |is compressed/displaced ( impaired |
|rising |brain function |
|b) cerebral embolism b/c clot, plaque |BLEED |
|or platelet aggregate blocks an artery | |
|( occurs while pt is awake | |
|CLOT | |
Cerebro Vascular Disease (80%)
Infarction (85%)
Cardiogenic Embolism (15%)
Stroke
Brain tissue & Subarachnoid hemorrhage (15%)
• intracranial atherosclerosis (20%)
• carotid plaque with arteriogenic emboli (60%)
• cardiogenic emboli (20%) of which AF (10%)
Similar Signs & Sx
|Drug-Related |Disease-Related |
|oral contraceptives |tumor/trauma to the brain |
|illicit drug use (cocaine, heroin, |Multiple Sclerosis |
|amphetamines, LSD, PCP, etc.) |seizure disorder |
|ASA |electrolyte abnormalities |
|antihypertensives |diabetes (neuropathies) |
Risk Factors
|Non-Modifiable |Modifiable |
|age (risk doubles > 55 yrs) |HTN (a factor in 70% of strokes)* |
|♂ |diabetes |
|family hx |heart disease (↑ risk 2x) |
|Blacks/Asians/ Hispanics |AF |
|Sickle cell disease (clumps RBC, |dyslipidemia |
|restricts blood flow) |mitral stenosis |
|prior stroke/ TIA* |left atrial enlargement |
| |structural abnormalities |
| |MI |
| |migraine (due to VC) ??? |
| |fibrinogen/( elevated hematocrit |
| |lifestyle factors |
| |alcohol |
| |diet |
| |smoking (↑ risk 2-3x) |
| |obesity |
| |physical inactivity |
| |acute triggers – emotional stress |
| |illicit drug use |
Risk Classification – Framingham Profile (( RF (stroke)
• systolic BP
• serum cholesterol
• glucose intolerance
• cigarette smoking
• LVH
Need to Treat?
• yes
• TIAs often precede ischemic stroke; if untreated, may develop stroke w/in 5 yrs
• greatest risk of stroke is w/in first few wks of TIA; 20% w/i 1st month; 50% w/i 1 year
• poorest prognosis with intracranial hemorrhage
Treatment Principles
elimination/management of RF is most important aspect of plan when RF occur in combo, tx should be initiated aggressively
management of HTN is essential
every pt who has had stroke/TIA need to receive anti-platelet as 2º prevention unless CI
Stroke Patients may need…
• snap caps
• larger print on labels
• compliance aids
• alternate dosage form (if having trouble swallowing)
Counseling
• educate pt - most patients unaware of stroke warning signs and are unaware that they have RFs that ( their risk for stroke; ( # of TIA = ( risk of stroke
• regular BP check-ups, low-fat diet, smoking cessation, regular exercise, moderate alcohol consumption
• communication – use Y/N questions; pt may have visual field defects and/or impaired judgment
Pharmacological Options for Ischemic Stroke
Anti-Platelet therapy = prevents platelet aggregation and vasoconstriction
1) ASA – 1st Line
Efficacy
• 1º prevention – no evidence showing ASA is useful; trials showed ( risk of hemorrhagic stroke ( benefit DOES NOT outweigh risk ( do not use ASA UNTIL pt experiences a TIA or stroke
• 2º prevention – clinical benefit seen in low doses; no significant improvement with ↑ doses; ↓ risk of stroke & death by 31%
Evidence
• SALT Trial – 75 mg/d ASA vs. placebo (for every 2 people Tx w/ ASA for 2.5 yrs, there was a clinical benefit ( good to take after TIA)
• UKTIA Trial – 1200 mg/d vs 325 mg/d ASA ( higher doses ( SE but same benefit w/ high and low dose
MOA: irreversibly inhibits platelet COX ( inhibits TXA2 (VC and platelet aggregation inducer)
Onset: minutes (if not EC); max platelet effect in a few days
Dosing:81 mg OD not covered by ODB(use 325 mg OD but take every other day (lowest effective dose is 75 mg OD); chew non-EC for faster onset
SE: GI bleed, GI upset, thrombocytopenia (rare), allergy
DI:anticoagulants (( bleed), anti-platelets (( bleed), alcohol (( bleed), NSAIDS (( risk of GI upset), corticosteroids, ACEI, diuretics, βB, MTX, uricosuric agents (probenecid, sulfinpyrazone); hypoglycemics & phenytoin (( ASA levels);
phenobarbital (( ASA levels)
CI: hypersensitivity, NSAID allergy, active PUD, hemophilia, active bleeding, not for children or those with viral infections (risk of Reye’s syndrome)
Cost:$
2) ASA + dipyridamole (Aggrenox®)
Efficacy
ESPS –1 - combo (vs placebo) significantly MORE effective in preventing stroke (fatal/nonfatal), death, and all end points combined
• ESPS –2 - ASA vs dipyridamole vs combo vs placebo; effects of combo are additive and more effective than either agent given alone, however does not ( severity of of recurrent strokes
• monotherapy w/ dipyridamole ( no use in stroke Pt
MOA: not well understood; may (1) ( [cAMP] by inhibiting adenosine uptake into platelets( inhibit platelet aggregation (2) inhibit cGMP phosphodiesterase ( inhibit platelet aggregation/ activation (3) stimulate prostacyclin synthesis (inhibits platelet aggregation)
Dosing: dipyridamole ER 200 mg + ASA 25 mg BID
Onset: ER few days to max effect
SE: GI (dyspepsia, N/D), h/a, dizziness, serious bleeding events. (risk of bleeding is similar to that of ASA alone)
DI w/ Dipyridamole: adneosine cholinesterase inhibitors
Cost: $1.50/day LU coverage by ODB (2º prevention)
3) clopidogrel (Plavix®)
Use: 2nd line for pts who are intolerant to ASA; ASA + Plavix® can be used after stent surgery
Efficacy
• CAPRIE Trial – 75 mg/d vs ASA 325 mg/d ( clopidogrel more effective than ASA b/c there was a RRR of 9.4% in ischemic stroke, MI or vascular death
• 2º Prevention – for pts who are high-risk; further studies to evaluate effect on risk of stroke
MOA: thienopyridine agent inhibits ADP-induced platelet aggregation (ADP induces fibrinogen binding to platelets)
Dosing: 75 mg OD
Onset: 1-2 hrs, lag time of 3-7 d for platelet effect (delayed compared to ASA)
SE: most common is rash & diarrhea, less GI than ASA, rare: thrombocytopenia
DI: no major DI’s, other antiplatelets (but ASA and Plavix® can be combined b/c different MOA), NSAIDs, thrombolytics, theoretically CYP 2C9 inhibitors (but not documented)
CI: bleeding, hemorrhage
Cost: $3/day – Section 8 Coverage
4) ticlopidine (Ticlid®)
Use: 3rd Line - failure to ASA tx, or intolerant/allergic to ASA
Efficacy
TASS Study – 250 mg BID vs ASA 650 mg BID ( Ticlid® had a 21% greater RRR for stroke than ASA 650 mg BID ( BETTER than ASA for stroke prevention
CATS Trial – Ticlid® vs placebo - ( RR of stroke, MI, vascular death by 30% (high risk stroke pts w/ moderate-severe stroke).
CATS looked at higher risk pts than those in ASA studies
less potent that Plavix® (prodrug)
MOA: same as Plavix
Onset: w/i 6 hrs, platelet effect at 4 days, max effect in 8-11 d
Dosing: 250 mg BID with FOOD
SE: most common is rash & diarrhea; neutropenia and thrombocytopenia (2% - more common than other drugs)
DI: dig, theophylline; more DI’s than Plavix® (although same MOA) b/c excreted renally
CI: liver impairment, gastric bleed, neutropenia, thromboctopenia
Cost: $0.70/tab
Anti-Coagulation (Warfarin)
Use: pts who remain symptomatic w/ TIA on optimal platelet tx who do not have surgical disease
Evidence: no evidence that these are better than anti-platelets in preventing TIA/stroke; trials show no diff b/t tx and control in incidence of recurrent stroke or death; use in stroke is associated with ↑ risk for hemorrhagic complications; long term anti-coagulation ( risk of stroke for pts who previously had MI
Anti-Thrombolytic
Tissue Plasminogen Activator (t-PA)
Use: 3 hrs, uncontrolled HTN, oral anti-coagulants, heparin w/in 48 hrs
Dosing: IV 0.9 mg/kg (max 90 mg) over 1 hour
Cost: expensive
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