vascular disease

ASCVD definition

atherosclerosis in any arterial bed in the body

ASCVD most common areas

cerebral

peripheral

coronary

atherosclerosis timeline

foam cells

fatty streak

intermediate lesion

atheroma

complicated lesion/rupture

fibrous plaque

growth mainly by lipid accumulation occurs during

first 3 decades

What is present in the 1st decade

foam cells and fatty streak

what is present in the third decade

intermediate lesion and atheroma

what is present from the fourth decade

complicated lesion/rupture and fibrous plaque

fibrous plaque is made up of

smooth muscle and collagen

symptoms of CAD

ischemic heart disease

acute manifestation of CAD is

acute coronary syndrome

PAD symptoms

intermittent claudication

acute manifestation of PAD

acute limb ischemia

acute manifestation of cerebrovascular

acute stroke/TIA

for every patient with ischemic stroke

there is 3 patients with coronary heart disease

for every patient with peripheral artery disease

there is 2 patients with coronary heart disease

types of peripheral arterial disease

lower extremity

renal

mesenteric

abdominal

peripheral arterial disease definition

an obstructive disease of lower or upper extremities that reduces arterial flow at rest or with exercise

intermittent claudication definition

exertional discomfort which is relieved with rest

chronic limb ischemia definition

severe compromised blood flow that may lead to amputation within 6 months

acute limb ischemia definition

a rapid or sudden decrease in limb perfusion which threatens tissue viability

patients with 1 form of vascular disease often

have other forms of vascular disease

CVD patients have what percent chance of having ASCVD in another arterial bed

40%

CAD patients have what percent chance of having ASCVD in another arterial bed

25%

PAD patients have what percent chance of having ASCVD in another arterial bed

60%

up to what fraction of PAD patients will die in 5 years

1/3

what percent of PAD pts die of CV causes

75%

diagnostic methods (3)

ankle-brachial indices

toe-brachial indices

duplex ultrasound

ABI diagnostic of PAD

< 0.90

how to measure ABI

1. measure brachial blood pressure

2. measure dorsalis pedis pressure

3. measure posterior tibial pressure

resting ABI should be used to establish lower extremity PAD diagnosis in which pt populations (2)

patients > 70 with exertional symptoms

patients > 50 plus smoking or DM

ABI should be measured in both legs in

all new PAD pts

TBI should be measured in

pts where ABI is suspected to be unreliable

PAD subsets (4)

asymptomatic

chronic symptomatic

chronic limb threatening ischemia

acute limb ischemia

asymptomatic PAD recommendations

CV risk reduction

• lipid lowering

• antihypertensive therapy

• diabetes management

smoking cessation

preventive foot care

flu and covid vaccine

single antiplatelet therapy

symptomatic PAD interventions with no recent vascularization

single antiplatelet therapy

• clopidogrel 75 mg daily

• aspirin 75 - 325 mg daily

low dose aspirin + rivaroxaban 2.5 mg bid

symptomatic PAD recommendations

CV risk reduction

• lipid lowering

• antihypertensive therapy

• diabetes management

smoking cessation

structured exercise

cilostazol

preventive foot care

wound care, pressure offloading, management of infection

flu and covid vaccine

aspirin MoA

irreversible acetylation of COX-1 and 2 inhibits synthesis of TXA2

effects of aspirin last

the life of the platelet (7 - 10 days)

dipyridamole MoA

inhibits PDE resulting in increased cAMP levels

dipyridamole is used in combo with

low dose aspirin

P2Y12 antagonist MoA

inhibits ADP mediated platelet activation by interacting with platelet P2Y12 receptor

oral P2Y12 agents

clopidogrel

ticlopidine

prasugrel

ticagrelor

IV P2Y12 agonist agent

cangrelor

clopidogrel loading dose

300 - 600 mg

clopidogrel maintenance dose

75 mg qd

clopidogrel adverse events

bleeding

thrombocytopenia

PRONTO conclusions

wide response variability to clopidogrel

mechanism of clopidogrel variability

limited absorption at 600 mg loading dose

PGP

4 CYP enzymes play a role

thrombin is a potent

platelet activator

PAR-1 activation results in (4)

conformational change of the platelet

increase TxA1

release of ADP

stimulation of platelet pro-coagulant activity

vorapaxar is CI in pts with hx of

stroke or TIA

vorapaxar approved for pts with hx of

MI or PAD

15% of strokes are

hemorrhagic

85% of strokes are

infarctions

80% of cerebral infarctions are

CVD

15% of cerebral infarctions are

cardiogenic embolism

cerebrovascular disease (3)

atherothrombotic disease

cerebral ischemia

TIAs

acute ischemic stroke presentation

acute neurologic defect

hemiparesis, hemisensory deficit, aphasia, gaze deviation, facial droop, dysphagia

incoordination, diplopia, decreased eye movements, dizziness, unreactive pupils

may experience gradual deterioration or may have a sudden presentation of severe neurologic findings

acute ischemic stroke diagnosis

CT scan

acute ischemic stroke pharmacologic treatment

thrombolytics within 4.5 hours

thrombolytic MoA

activate the fibrinolytic system by catalyzing the reaction of plasminogen to plasmin

thrombolytic agents

alteplase

tenecteplase

reteplase

urokinase

streptokinase

alteplase dosing

0.9 mg/kg IV over 60 min with 10% given as a bolus

major thrombolytic agent CIs

surgery or internal organ biopsy (7-10 days)

CVA or neurosurgery (2 months)

recent needle puncture of noncompressible vessel

active GI or GU bleed

uncontrolled HTN

pregnancy

recent trauma with internal injures

CPR with rib fracture

minor thrombolytic CIs

paracentesis

thoracentesis (repeated attempts are major CI)

septic thrombophlebitis

how often should you measure BP and give neurological assessments on a pt who has been given alteplase

every 15 minutes during infusion

every 15 minutes for 2 hours after infusion

every 30 minutes for the next 6 hours

every hour until 24 hours after infusion

discontinue alteplase infusion and obtain emergency CT scan if pt develops (5)

severe headache

acute hypertension

nausea

vomiting

worsening neurological examination

increase frequency of BP measurements and administer antihypertensive medications if

SBP > 180 OR

DBP > 105

delay placement of what in alteplase pts (3)

nasogastric tubes

indwelling bladder catheters

intra-arterial pressure catheters

what should be obtained before starting antiocoagulants or antiplatelets after alteplase

follow up CT or MRI 24 hours after infusion