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CVPR: CV Unit II > Ischemic Heart Disease I > Flashcards

Ischemic Heart Disease I Flashcards

1
Q

Treatable risk factors for development of coronary atherosclerosis (with consequent reduced risk)

A
  • smoking
  • HTN
  • dyslipidemia
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2
Q

unique features of coronary circulation

A
  • myocardium operates ONLY on aerobic metabolism
  • @ rest: near maximal O2 extraction occurs @ coronary arteries –> must INCREASE FLOW in order to increase O2 delivery
  • LV is perfused during DIASTOLE only
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3
Q

major determinants of myocardial O2 supply

A
  • coronary blood flow rate: perfusion pressure, perfusion time(=1/HR), vascular resistance
  • O2 content of blood
  • O2 delivery (mmol/min) = CBF rate (ml/min) x O2 content (mmol/ml)
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4
Q

pathophysiology of stable coronary artery disease

A
  • obstructive coronary lesion –> limited coronary blood flow –> myocardial ischemia
  • myocardial ischemia = imbalance btwn coronary O2 delivery and myocardial O2 demand
  • ischemia occurs more frequently when cardiac work/O2 demand increase
  • major sx: angina pectoris (chest pain)
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5
Q

pathophysiology of unstable coronary artery disease

A
  • inflammation of arterial wall
  • weak cap –> plaque rupture/fissure
  • rupture –> thrombosis + complete/partial vessel occlusion
  • vessel occlusion –> myocardial injury and/or necrosis –> cardiac dysfxn, arrythmias, death
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6
Q

Major categories of treatment of stable coronary artery disease

A
  • increase oxygen delivery to myocardium

- decrease oxygen demand of myocardium

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7
Q

Progressive process of atherosclerosis

A
  1. endothelial injury –> lipid deposition + WBC recruit
  2. WBCs + smooth muscle –> fibrous plaque
  3. progressive lipid accumulation at core of plaque –> occlusive atherosclerotic plaque and sx: angina, claudication
  4. plaque disruption –> acute vascular events
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8
Q

Major acute vascular events resulting from artherosclerotic plaque disruption

A
  • unstable angina
  • MI
  • stroke
  • critical leg ischemia
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9
Q

Treatable risk factors for development of coronary atherosclerosis (with unclear/possible reduced risk)

A
  • diabetes
  • obesity
  • sedentary lifestyle
  • inflammation
  • psychological stress
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10
Q

Untreatable risk factors for development of coronary atherosclerosis

A
  • male gender
  • age
  • genetic factors
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11
Q

Smoking impact on CAD risk

A
  • 50% increase in risk; cessation can normalize risk
  • mechanisms:
  • clot formation
  • aryl hydrocarbons
  • CO decreases myocardial O2 delivery
  • decreases HDL
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12
Q

HTN impact on CAD risk

A
  • graded risk based on BP; tx reduces risk
  • mechanisms:
  • direct endothelial cell injury
  • pathologic cell signaling
  • circulating hormones increase
  • LVH
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13
Q

Diabetes/insulin resistance impact on CAD risk

A
  • both dx diabetes and insulin resistance have similar increased CV risk
  • mechanisms:
  • inflammation
  • oxidative stress
  • dyslipidemia
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14
Q

Dyslipidemia definiton and impact on CAD risk

A
  • dyslipidemia = high LDL (low-density lipoprotein) cholesterol + low HDL (high-density lipoprotein) cholester + high triglycerides
  • each aspect = independent risk factors
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15
Q

LDL impact on CAD risk

A
  • LDL oxidized –> pro-inflammatory and atherogenic
  • mechanisms:
  • injury to vascular endothelium
  • deposited in arterial wall –> macrophages take up –> progressive increase in plaque volume
  • activated inflammatory cells
  • activates platelets –> pro-thrombotic
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16
Q

HDL impact on CAD risk

A
  • low HDLs are bad b/c HDL = anti-atherosclerotic
  • mechanism:
  • inhibits oxidation of LDLs
  • inhibits tissue factor (clot formation)
  • inhibits endothelial adhesion mlx
  • stimulates NO production
  • enhances reverse cholesterol transports
17
Q

Inflammation impact on CAD risk

A
  • inflammation contributes to progression of atherosclerosis
  • lipid-laden macrophages = pro-inflammatory
  • extravascular inflammation –> increase risk of CV events
  • inflammatory markers (e.g. IL-6, CRP)–> info about future CAD risk
18
Q

major determinants of myocardial O2 demand

A
  • heart rate
  • wall tension: determined by BP and chamber dimensions (Law of LaPlace)
  • inotropic state
19
Q

Characteristics of autoregulation of blood flow to myocardium (and impact of CAD)

A
  • autoregulation allows vessels to adapt to changes in perfusion pressure/protect from moderate pressure changes
  • occurs @ level of arterioles
  • w/CAD: autoregulation may become exhausted when pressure drops across an epicardial coronary stenosis
20
Q

Impact of tachycardia on coronary flow

A
  • tachycardia can compromise coronary flow b/c LV is perfused predominately during diastole
  • intramural coronary vessels are compressed during systole
  • increased HR –> shortened cardiac cycle via shortening of diastole
21
Q

Treatments that help increase oxygen delivery to myocardium

A
  • prevent coronary hypotension
  • rate-slowing drugs (beta-blockers)
  • decrease coronary resistance via vasodilators, coronary angioplasty or bypass surgery
  • treat anemia or hypoxemia
22
Q

Treatments that help reduce myocardial oxygen demand

A
  • antihypertensive drugs
  • rate-slowing drugs (beta-blockers, calcium channel blockers)
  • limit LV size via limiting preload (diuretics, nitrates)
  • negative inotropes
23
Q

unstable angina vs. acute MI

A
  • unstable angina=near-complete occlusion, negative biomarkers, “threatened” heart attack
  • acute MI=usually complete occlusion, severe and constant chest pain @ rest, positive biomarkers –> cardiac dysfxn and failure
24
Q

Common biomarkers of vascular inflammation/myocardial injury

A
  • inflamed vessel: CRP, other inflammatory markers

- injury: troponin, creatine kinase

CVPR: CV Unit II (17 decks)

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