Drug-Induced Cardiac Disease- Myocardial Ischemia and ACS

Question 1

Mechanisms of Drug-Induced Myocardial Ischemia and ACS

Answer 1

Increased myocardial oxygen demand
Decreased myocardial oxygen supply
Drug-induced ACS

Question 2

Mechanism of myocardial oxygen demand

Answer 2

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

Question 3

Result of myocardial oxygen demand

Answer 3

Increased HR and contractility

Question 4

Drugs that cause increased HR and contractility

Answer 4

COCAINE, beta-agonists, sympathomimetics, potent vasodilators

Question 5

Mechanism of decreased myocardial oxygen supply

Answer 5

Anything that prohibits blood from flowing through the coronary artery freely –> increases coronary resistance and vasospasms

Question 6

Result of decreased myocardial oxygen supply

Answer 6

Increased coronary resistance

Question 7

Drugs that can increase coronary resistance

Answer 7

COCAINE, antimigraine agents (triptans)

AVOID IN CAD Hx

Question 8

Mechanism of drug-induced ACS

Answer 8

Mismatch in O2 supply and demand –> cardiac muscle damage

Question 9

Result of drug-induced ACS

Answer 9

coronary artery thrombosis/vasospasm; increased CV risk

Question 10

Drugs that can cause coronary artery thrombosis/vasospasm

Answer 10

COCAINE, NSAIDs, OCs, estrogens, antimigraine agents

Question 11

Drugs that can increase CV risk

Answer 11

COCAINE, NSAIDs, estrogens, OCs, rosiglitazone

Question 12

How does a cocaine-induced MI occur?

Answer 12

Vasospasm and vasoconstriction of coronary arteries

Question 13

Patho behind cocaine-induced MI

Answer 13

Decrease amount of oxygenated blood we can bring to the cardiac muscle → stunned → necrotic → MI

Question 14

Cocaine: sympathomimetic crisis

Answer 14

Cocaine inhibits the reuptake of NE leading to increased NE concentrations and enhanced alpha-1 mediated vasoconstriction

Question 15

Cocaine-induced MI treatment: chest pain

Answer 15

ASA, benzos

Question 16

Cocaine-induced MI treatment: persistent HTN

Answer 16

BZDs, IV NTG

Question 17

Cocaine-induced MI treatment: other ACS treatments

Answer 17

possibly avoid acute beta-blocker administration, but otherwise proceed as normal

Question 18

Cocaine-induced MI treatment: long-term ACS treatment

Answer 18

possibly avoid beta-specific beta-blockers, drug abuse counseling

Question 19

Mechanism of NSAID-induced cardiotoxicity

Answer 19

NSAIDs block COX-II –> vasoconstriction and decreased amount of oxygenated blood that can be delivered to the heart muscle, also will increase platelet aggregation

Question 20

NSAID BBW

Answer 20

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

Question 21

Risk factors for acute MI with NSAIDs: when

Answer 21

risk of MI is highest early in therapy (within 7 days)

Question 22

Risk factors for acute MI with NSAIDs: how much

Answer 22

Increases risk by ~20-50%

Question 23

Risk factors for acute MI with NSAIDs: which ones

Answer 23

No difference between selective and nonselective

Question 24

Risk factors for acute MI with NSAIDs: which doses

Answer 24

Higher doses, higher risk

> 1200mg/day ibuprofen
750mg/day naproxen

May need smaller doses for chronic treatment

Question 25

Risk factors for acute MI with NSAIDs: duration

Answer 25

Duration doesn’t appear to increase risk