Drug-Induced Cardiac Disease- Myocardial Ischemia and ACS Flashcards
Mechanisms of Drug-Induced Myocardial Ischemia and ACS
Increased myocardial oxygen demand
Decreased myocardial oxygen supply
Drug-induced ACS
Mechanism of myocardial oxygen demand
An increase in demand of the heart muscle leads to an imbalance in O2 demand and supply → muscle is devoid of O2 or doesn’t get enough
Result of myocardial oxygen demand
Increased HR and contractility
Drugs that cause increased HR and contractility
COCAINE, beta-agonists, sympathomimetics, potent vasodilators
Mechanism of decreased myocardial oxygen supply
Anything that prohibits blood from flowing through the coronary artery freely –> increases coronary resistance and vasospasms
Result of decreased myocardial oxygen supply
Increased coronary resistance
Drugs that can increase coronary resistance
COCAINE, antimigraine agents (triptans)
AVOID IN CAD Hx
Mechanism of drug-induced ACS
Mismatch in O2 supply and demand –> cardiac muscle damage
Result of drug-induced ACS
coronary artery thrombosis/vasospasm; increased CV risk
Drugs that can cause coronary artery thrombosis/vasospasm
COCAINE, NSAIDs, OCs, estrogens, antimigraine agents
Drugs that can increase CV risk
COCAINE, NSAIDs, estrogens, OCs, rosiglitazone
How does a cocaine-induced MI occur?
Vasospasm and vasoconstriction of coronary arteries
Patho behind cocaine-induced MI
Decrease amount of oxygenated blood we can bring to the cardiac muscle → stunned → necrotic → MI
Cocaine: sympathomimetic crisis
Cocaine inhibits the reuptake of NE leading to increased NE concentrations and enhanced alpha-1 mediated vasoconstriction
Cocaine-induced MI treatment: chest pain
ASA, benzos
Cocaine-induced MI treatment: persistent HTN
BZDs, IV NTG
Cocaine-induced MI treatment: other ACS treatments
possibly avoid acute beta-blocker administration, but otherwise proceed as normal
Cocaine-induced MI treatment: long-term ACS treatment
possibly avoid beta-specific beta-blockers, drug abuse counseling
Mechanism of NSAID-induced cardiotoxicity
NSAIDs block COX-II –> vasoconstriction and decreased amount of oxygenated blood that can be delivered to the heart muscle, also will increase platelet aggregation
NSAID BBW
May cause increased risk of serious CV thrombotic events, MI, and stroke, which can be fatal. This risk may increase with duration of use. Patients with CVD or risk factors for CVD may be at greater risk
Risk factors for acute MI with NSAIDs: when
risk of MI is highest early in therapy (within 7 days)
Risk factors for acute MI with NSAIDs: how much
Increases risk by ~20-50%
Risk factors for acute MI with NSAIDs: which ones
No difference between selective and nonselective
Risk factors for acute MI with NSAIDs: which doses
Higher doses, higher risk
> 1200mg/day ibuprofen
750mg/day naproxen
May need smaller doses for chronic treatment
Risk factors for acute MI with NSAIDs: duration
Duration doesn’t appear to increase risk
