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PATHOPHYSIOLOGY OF CARDIOVASCULAR DISEASE (CVD)
leading cause of death in the U.S. for men and women
42% of all deaths (1 out every 2.4 deaths)
an average of one death every 33 seconds
CARDIOVASCULAR DISEASE
claims as many lives as the other top 8 causes of death combined
1/6th are under age 65 From 1984 -1994 CVD deaths declined
22% (although the actual number of deaths dropped only 3%)
CARDIOVASCULAR DISEASE
includes: coronary artery disease stroke hypertension congenital heart disease valvular heart disease rheumatic heart disease arrhythmias
CARDIOVASCULAR DISEASE
Coronary Artery Disease (CAD) or Coronary Heart disease (CHD) single leading cause of death in the U.S.
(20% of all deaths) May result in:
angina pectoris myocardial infarction sudden cardiac death congestive heart failure
KEY TERMS: Pg 412 Resource Manual
Myocardial Infarction
1.5 million myocardial infarctions (MI’s) per year 500,000 fatal 250,000 die within an hour of onset
(sudden MI)
Myocardial Infarction
13.5 million alive today with history of MI 5% of MI in people under 40 years old 45% under 65 years old In 48% of men and 63% of women who
died suddenly of MI, there were no previous symptoms
Coronary Heart Disease
atherosclerosis progressive build-up of plaque on the
inside of the artery wall large arteries
arteriosclerosis “hardening” of the arteries thickening of arterial wall loss of elastic tissue
Coronary Heart Disease
Causes of Atherosclerosis Risk factors - increase the probability
of developing the disease Primary or major risk factors (pg 415): hypertension dyslipidemia cigarette smoking physical inactivity obesity
Coronary Heart Disease
Secondary risk factors diabetes personality type / stress family history of CHD age gender race
Coronary Heart Disease
Risk factors Key Terms – pg 96 Resource Manual Other classification scheme – Box 5-1 pg 97 Lipid classification:
Box 5-2 pg 98-100 Blood pressure pg 103 Obesity pg 104 Emerging risk factors Framingham Risk Assessment
Coronary Arteries
Normal coronary arteries left main left anterior descending (LAD) circumflex right coronary artery posterior descending artery (PDA)
Process of Atherosclerosis
Atherosclerosis - lesions of the large and medium-sized arteries with deposits in the intima of yellowish plaques containing cholesterol, lipoid material , and lipophages
3 stages of development Intimal thickening- reversible Fatty streaks - reversible Fibrous plaques - irreversible (at least
for the most part)
Process of Atherosclerosis
Endothelium or endothelial layer (figure 29-1 pg 412):
lines inside of arterial walls in direct contact with blood controls passage of substances from
blood into arterial wall Anti-thrombotic = inhibit blood clots
Process of Atherosclerosis
Endothelial Cells: Produce several vasoactive substances
Prostacyclin - vasodilator; antithrombotic
Endothelial derived relaxing factor (EDRF) or nitric oxide - inactivates platelets; inhibits smooth muscle cell migration and proliferation
Process of Atherosclerosis
Endothelial Cells under normal conditions - protect against
the development of atherosclerosis when damaged - play a major role in its
development Box 29-1 pg 413 - causes of endothelial
injury
Process of Atherosclerosis
layers of the artery intima media adventitia - contain collagen, elastin, and
fibroblasts; contain the vasa vasorum= small blood vessels
Process of Atherosclerosis
Smooth muscle cells located primarily in the medial layer contractile synthetic
sensitive to growth promoting factors(prolifitive) and migrating factors
Process of Atherosclerosis
Platelets tiny cells in the blood stream that repair
“holes” in the arterial wall (intima) “platelet plug” prevents blood loss prothrombotic - clot forming
Monocytes and Macrophages cells of the immune system activated at sites of arterial injury
Process of Atherosclerosis
Fibroblasts type of connective tissue in response to growth factors, migrate
from the media to intima and synthesize fibrous tissue (along with smooth muscles)
Foam Cells cells formed from other cells such as
macrophages which release cholesterol into the extracellular space giving rise to fatty streaks
Process of Coronary Artery Disease
Injury hypothesis of CAD endothelial disruption is the first step in a
series of events risk factors may be involved in causing the
initial injury Box 29-1 pg 413 Resource Manual - list of
factors that may result in endothelial injury
“Inflammatory response”: Box 29-2 pg 413
Process of Coronary Artery Disease
Following endothelial injury, a number of pathologic events occur which often lead to narrowing of the arterial lumen diameter
Endothelial disruption can lead to: mitogenic effects - growth of tissues
/cells chemotactic effects - migration of cells
Injury hypothesis of CAD figure 29.2 Resource Manual
Process of Coronary Artery Disease
Relationship of cardiovascular disease risk factors to the “Injury hypothesis” tobacco use - Box 29-3 pg 415 diabetes - Box 29-4 pg 415 hypertension dyslipidemia
Process of Atherosclerosis
progression of atherosclerosis is non-linear some lesions are stable over many years some progress rapidly within months
Rupture of Fissuring of plaques from turbulent flow or chemical factors may lead to mural thrombi (platelet
aggregation) of varying sizes at these sites Thrombi may be incorporated into the
plaque during this process
Process of Atherosclerosis
Coronary atherosclerosis can occur diffusely (long length of artery) with occasional discrete, localized areas of more pronounced narrowing of the vessel lumen that may produce obstruction of blood flow.
Non-atherosclerotic coronary obstructions Coronary vasospasm Intracoronary thrombus
Atherosclerotic Plaques
Described as “percent occlusion” or “percent stenosis” Example 90% stenosis of the LAD
Obstructive coronary atherosclerosis is used to describe CAD that is severe enough to reduce blood flow
Severity of coronary atherosclerosis is detected using coronary angiography coronary angiogram
Atherosclerotic Plaques
Regression of CAD using non-invasive interventions Diet Exercise Medications
Treatment Options for CAD
“Revascularization” Procedures Percutaneous Transluminal
Coronary Angioplasty (PTCA) Coronary Artery Bypass Surgery
(CABS) or Coronary Artery Bypass Graft (CABG) surgery
Coronary Atherectomy and Rotablator
Laser Angioplasty
Percutaneous Transluminal Coronary Angioplasty (PTCA)
Coronary Obstructions After Cardiac Interventions
Restenosis - reocclussion of obstructive lesion
Tend not to be as lipid rich as original plaque and are highly related to thrombosis
Approximately 35% at 5 years from original CABS
Approximately 45% at 6 months for PTCA Restenosis rate reduced using coronary
stents after PTCA
Progression of Atherosclerosis
Rate of progression is highly related to number and severity of risk factors Native vessels Saphenous vein grafts Internal mammary grafts After PTCA and other interventions
Exercise and Atherosclerosis
Independently reduces risk of CAD Slows rate of progression by acting on
other risk factors Increases fibrinolytic activity May stimulate the formation of collateral
vessels when one or more obstructive lesions are present
Manifestations of Coronary Atherosclerosis: Coronary Blood Flow
heart - completely aerobic organ coronary blood flow = “myocardial oxygen
“supply” oxygen requirements of the myocardium =
myocardial oxygen “demand” at rest, myocardium extracts 85% or more
of oxygen from blood exercise: 5-6 fold increase in coronary
blood flow
Coronary Blood Flow
Normal conditions: coronary supply is closely regulated to myocardial O2 demand
auto regulation factors of myocardial oxygen demand:
heart rate stroke volume cardiac output systolic blood pressure total peripheral resistance
Coronary Blood Flow
Determined by arterial pressure and vascular resistance
intramyocardial pressure also affects coronary flow systole vs. diastole (figure 29.5 pg 417
Resource Manual) reduction of luminal diameter reduces flow
luminal area obstruction of >75% causes blood flow reduction at rest
“hemodynamically significant lesion”
Coronary Blood Flow
Atherosclerotic arteries have limited ability to vasodilate
Atherosclerotic arteries are deficient in EDRF (nitric oxide) which increase likelihood of a mural thrombus
Myocardial Ischemia
coronary blood flow does not adequately meet myocardial oxygen demand
results in progressive abnormalities in cardiac function = ischemic cascade stiffening of the left ventricle results in decreased diastolic filling
(diastolic dysfunction) impaired systolic emptying
hypokinesis, akinesis, dyskinesis
Myocardial Ischemia
Systolic impairment demonstrated by segmental wall motion abnormalities reduction in left ventricular ejection
fraction reduced stroke volume
echocardiogram “stress echo”
Myocardial Ischemia
EKG changes ST segment depression ST segment elevation T wave inversion ventricular arrhythmias
Myocardial Ischemia
reversible no permanent cardiac damage prolonged ischemia
irreversible damage may occur = necrosis of myocardial tissue (myocardial infarction)
Angina Pectoris
heart pain due to myocardial ischemia characteristics of “typical” or “classic”
pressure, tightness, squeezing, heaviness, or choking
radiates down left arm, back, and/or jaw occurs with physical activity, emotional
stress, cold weather, heavy meals last few minutes or until activity ceases
Myocardial Ischemia
angina pectoris relieved with rest nitroglycerin
stable angina atypical angina unstable angina Prinzmetal’s angina
STABLE CAD
Presence of hemodynamicaly significant lesion(s)
anatomically stable lesions that result in: predictable, reproducible ischemia
and/or angina
Myocardial Infarction
Result of severe, prolonged (>60 min) ischemia in the presence or absence of angina
irreversible heart muscle damage - necrosis MI can occur in lesions with less than 50%
stenosis rupture prone plaques explains why many persons who
experience MI do not report a history of angina before infarction
Acute MI
Thickness of walls affected: transmural infarction - Q wave subendocardial infarction - non Q wave
Location of wall anterior,posterior, lateral, anterolateral,
inferior, septal Location by ECG (Table 29.1 pg 420)
Acute Myocardial Infarction
Location of obstructive lesion determines wall(s) affected proximal vs. distal occlusion
Diagnosis of Acute MI
Symptoms ECG
figure 27.4 Resource Manual evaluation of cardiac enzymes
page 235 Resource Manual lactate dehydrogenase (LDH) Creatinine phosphokinase (CK)
CK-MB elevated in first 24 hrs
Treatment of MI
Early reperfusion streptokinase or tissue plasminogen
activator (tpa) “rescue” angioplasty emergent CABS
nitroglycerine beta blockers
Post-Myocardial Infarction
Necrosis, scarring during first 6-12 weeks Infarct dilation and remolding - thinning
of ventricular wall and enlargement of cardiac chambers
may develop congestive heart failure
Myocardial Infarction
Characteristics associated with higher risk of reinfarction and death EF<40% ischemia during low intensity exercise poor exercise capacity (<4 METS) complex ventricular arrhythmias