Ischemic Heart Disease, CAD, Angina

Intima

Intima

What part of the vessel is intimate with the blood, a single layer of epithelial cells, and the metabolically active layer?

Media

What part of the vessel is the thickest layer and made up of the smooth muscle cells and extracellular matrix

Adventitia

What part of the vessel includes the nerves, lymphatics and provides nourishment to the arterial wall?

endothelial dysfunction, lipoprotein entry and modification, leukocyte recruitment, foam cell formation, smooth muscle migration

What are the key components of plaque formation?

endothelial dysfunction

What key component of plaque formation is the primary event in atherogenesis, tends to occur at arterial branch points, and exposure to a toxic chemical environment (smoking, elevated lipid levels, DM)

oxidation, glycation

What happens during the lipoprotein entry and modification stage?

expression of leukocyte adhesion molecules, chemoattractant signals, presence of mostly monocytes and Ts

What happens during the leukocyte recruitment phase of plaque formation?

differentiation into phagocytes, imbibe lipoprotein

What happens during the foam cell formation phase?

proliferation of smooth muscle in the intima (recruited by foam cells)

What happens during the smooth muscle migration phase of plaque formation?

interplaque hemorrhage, plaque instability and erosion

At what point in the history and progression of plaques is there potential for unstable angina and other issues?

fatty streak, fibrous cap, vasa vasorum, fibrous plaque, advanced lesion, interplaque hemorrhage, plaque instability and erosion

Give me the progression story of a plaque?

Fatty streak

What part of the development and progression of plaques do you see endothelial dysfunction, lipoprotein entry/modification, and foam cell formation?

Fibrous cap (plaque progression)

What part of the development and progression of plaques do you see smooth muscle cell migration and matrix synthesis and degradation?

Vasa vasorum

What part of the development and progression of plaques do you see - a chaotic blood supply?

fibrous plaque

What part of the development and progression of plaques do you see - connective tissue and smooth muscle?

advanced lesions

What part of the development and progression of plaques do you see necrotic lipid rich core and calcified regions?

interplaque hemorrhage

What part of the development and progression of plaques do you see neovascularization and increased neovessel permeability?

plaque instability and erosion

What part of the development and progression of plaques do you see increased ischemic events?

acute restriction of blood flow, alteration in vessel wall (calcification, rupture, hemorrhage, embolization, weakening)

What are some complications of plaques

dyslipidemia, tobacco use, HTN, DM, lack of physical activity/obesity, stress, alcohol

What are the AHA modifiable cardiac risk factors?

age, male, genetics

What are the AHA non-modifiable cardiac risk factors?

oxygen content (mostly constant), rate of coronary blood flow

Myocardial oxygen supply is dependent on

diastole

When is the heart perfused?

Ventricular wall stress, heart rate, contractility

What are the 3 determinants of myocardial oxygen demand?

atherosclerosis, endothelial dysfunction, spasm, tachycardia, anemia, hypoxia, vascular/congenital anomalies, aortic stenosis

What are some examples of things that cause supply issues?

tachycardia, hyperthyroidism, myocardial hypertrophy, aortic stenosi

What are some things that can cause demand issues?

reduction in contraction and relaxation, elevation in diastolic pressure, pulmonary congestion/dyspnea, precipitation of dangerous arrythmias

Consequences of ischemia

stable angina, unstable angina, vasospastic angina, silent ischemia

What are the different types of ischemic syndromes?

Stable angina

What type of ischemic syndromes is characterized by fixed obstructive atheromatous plaque and symptoms are triggered by physical exertion//emotional stress?

Unstable

What type of ischemic syndromes is characterized by a sudden increase in tempo/duration with lesser degrees of exertion and increased symptom severity?

LV function (CO/EF), exercise capacity, severity of symptoms

What can predict the mortality of stable angina?

vasospastic angina

What type of ischemic syndromes is characterized by a focal coronary spasm which decreases the supply and occurs at rest - responds to short acting nitrates?

ST elevation on EKG during episode with no stenosis

How do you diagnose vasospastic angina

nifedipine, diatiazem, verapamil, SL nitro, stop smoking

How do you manage vasospastic angina?

Silent ischemia

What type of ischemic syndromes is characterized by a lack of pain and maybe able to be diagnosed via exercise treadmill testing

HTN, DM

What are 2 important risk factors in silent ischemia?

Angina pectoris

What is the most common manifestation of ischemic heart disease and is often described by a “strangling in the chest?”

retrosternal, levine sign, brief duration, relieved by rest/nitrates, described as a squeezing/tightness, radiates to shoulder/neck/jaw/inner arm/epigastrium

Clinical features of stable angina

Pain is pleuritic/sharp/choking, involves the chest wall, positional, tender to palpation, random onset, lasts seconds/min/hours/days, variable response to nitro

What are signs that the chest pain is atypical, noncardiac?

physical exertion, anger, emotional excitement, large meal, cold weather, peripheral vasoconstriction

What might bring on an episode of angina?

increased heart rate, elevated blood pressure, mitral regurgitation, abnormal bulging, S4 gallop

What might you see in a patient during an anginal episode?

normal exam, bruits, diminished pulses

What might you see in a angina pectoris patient during an period of no chest pain?

resting EKG, CXR, hemoglobin, fasting glucose, fasting lipid profile, exercise tolerance test (nuclear and echo), coronary angiography (if high probability of CHD),

Diagnostic studies for angina pectoris

extent of impaired LV contractile function, poor exercise capacity, severity of disease, magnitude of clinical symptoms

What do we need to consideration before we treat angina?

decrease frequency, prevent MI, prolong survival

What are the goals when treating ischemic heart disease?

controlling risk factors, exercise, annual flu vaccine

Management of angina

drug that affect mortality/morbidity, drugs that affect symptoms only

Treatment for stable angina can be grouped into

ASA, beta blockers, ACEI, statins

What drugs affect mortality and morbidity

nitrates, CCBs

Which drugs are for symptoms only

rest, nitrates, alleviation precipitating/aggravating factor

Management of an acute angina episode

primary preventions, lifestyle changes, risk factor reduction, regular exercise, HTN treatment, tobacco cessation, lipid lowering, weight reduction, glycemic control

Management of recurrent angina episodes

Metropolol (prior MI), nifedipine, amlodipine, felodipine, nitrates (symptomatic), lipid lowering agents (everybody), ASA or clopidogrel (ASA allergies), lisinopril (does not improve angina)

1st line meds for angina

PCI, CABG

Revascularization options

inadequate response to meds, unacceptable ADRs, high risk CAD (EF under 50%)

What are the indications for revascularization in the patient with chronic stable angina?

CABG

What type of revascularization is preferred when large amounts of myocardium are at risk?

3 vessels, DM, LAD involvement, large myocardial areas at risk

When should CABG be consider

saphenous vein, left internal mammary artery

What vessels can be used as grafts for CABG?

extent of LV dysfunction, extent of atherosclerosis, risk of plaque rupture, general health and other comorbities

Prognosis of CAD depends on