G-0967 Coronary Arte

Coronary Artery Disease, Coronary Artery Disease, Angina, Myocardial Angina, Myocardial

Infarction, and Congestive Infarction, and Congestive Heart FailureHeart Failure

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Review Date 3/09 G-0967

A Review of the Basics

•Smoking•High intake of alcohol•Obesity•Sedentary lifestyle•Diabetes•Hypercholestrolemia•Hyperlipidemia

Risk Factors For Coronary Artery Disease, Angina, Myocardial Infarction, and Congestive Heart Failure

•More than 45 years old for males and 55 years old for females (risk increases after menopause)

•Family history—genetics •Hypertension•Stress/personality type

Risk Factors (cont’d) For Coronary Artery Disease, Angina, Myocardial Infarction, and Congestive Heart Failure

•High low-density lipoprotein (LDL) cholesterol

•Low high-density lipoprotein (HDL) cholesterol

•Left ventricular hypertrophy

Risk Factors (cont’d) For Coronary Artery Disease, Angina, Myocardial Infarction, and Congestive Heart Failure

•Anyone with cardiac conditions– Coronary artery disease (CAD)– Myocardial infarction (MI)– Postcoronary bypass

•Hypertension•Left ventricular hypertrophy•Diabetes•Chronic obstructive pulmonary disease

Risk Factors For Congestive Heart Failure

•Pulmonary hypertension•Anemia•Hypothyroidism•Hyperthyroidism•Overweight or obesity•Alcoholism

Risk Factors (cont’d) For Congestive Heart Failure

•Blood flow to the vessels surrounding the heart is blocked

•The major underlying cause of CAD is atherosclerosis

Coronary Artery Disease: An Overview

•Elevated cholesterol and triglyceride levels

•Hypertension•Infection that initiates the inflammatory response

Plaque Development

Many factors speed up plaque development:

•Elevated iron levels—carry free radicals that damage lining

•Elevated homocysteine level•Cigarette smoking•Diabetes•Obesity•Oxidized LDL cholesterol

Plaque Development (cont’d)

Many factors speed up plaque development:

•Buildup of smooth muscle cells, macrophages, and lymphocytes

•Smooth muscle cells form a matrix of connective tissue

•Lipid and cholesterol accumulates in the matrix

The Atherosclerotic Process

•Lipid deposits and other materials (including cellular waste, fibrin, and calcium) build up and form a plaque

•After injury, platelets adhere to the arterial wall and release growth factors, which promote lesion development

The Atherosclerotic Process (cont’d)

•Fatty streaks form, often in people younger than 30 years of age

•People are asymptomatic during this first stage of CAD

•Plasma LDL enters the injured endothelial wall and forms a plaque that sometimes is prone to rupture

Development of Coronary Artery Disease

Steps to development of CAD:

•Acute, complicated lesions with rupture and either nonocclusive or occlusive thrombus form– Occlusive often results in MI and

sudden death•Hemorrhage into plaque produces thrombi; thrombus formation within arterial lumen initiated

Development of Coronary Artery Disease (cont’d)


•Progressive narrowing of lumen•Insufficient blood flow to myocardium (ischemia) results

•Chest pain or angina pectoris occurs

Development of Coronary Artery Disease (cont’d)


•Chest pain•Hypertension•Increased pulse•Increased respiration•Dyspnea on exertion•Pallor of skin•Lightheadedness with exertion

Signs and Symptoms of Coronary Artery Disease

•Diminished peripheral pulses•Intermittent claudication—cramping of the lower extremities

Signs and Symptoms of Coronary Artery Disease (cont’d)

•Antihyperlipidemic agents•Medications that lower triglycerides

•Antiplatelets (aspirin)•Antihypertensives•Antianginals (nitroglycerin)•Antimicrobials

Treatment of Coronary Artery Disease

•Chest pain caused by myocardial ischemia from reduced blood flow and/or reduced oxygen supply to myocardium

•Angina is a warning sign that a heart attack (MI) may occur

Angina Pectoris: An Overview

•Aerobic metabolism switches to anaerobic metabolism:– Lactic acid buildup– Release of histamine, bradykinins,

and enzymes, which stimulate nerve fibers in myocardium, sending pain impulses to the central nervous system

Angina Pectoris: An Overview (cont’d)

•Other causes of decreased oxygen supply to myocardium:– Congestive heart failure– Congenital heart defects– Pulmonary hypertension– Left ventricular hypertrophy– Cardiomyopathy– Severe hypertension– Narrowing of aortic valve


•Other causes of decreased oxygen supply to myocardium (cont’d):– Leakage of the aortic valve– Ventricle wall thickening– Atheroma leading to arterial

narrowing•Silent ischemia—decreased oxygen supply with no pain


•Anemia•Exercise•Thyrotoxicosis•Substance abuse, particularly cocaine

•Hyperthyroidism•Emotional stress

Causes of Increased Oxygen Demand of Myocardium

•Stable:– Caused by specific amount of

activity– Predictable– Relieved with rest and nitrates

•Unstable:– Pain occurs with increasing

frequency, severity, and duration over time

– Unpredictable– May occur at rest– High risk for MI

Four Types of Angina

•Prinzmetal’s (variant):– No identified cause– May occur at same time of day– May intensify or worsen over time– Usual cause is coronary artery

spasm•Angina decubitus:

– Occurs when a person is lying down with no cause

– Occurs because gravity redistributes body fluids

Four Types of Angina (cont’d)

•Form of angina caused by neither spasm or blockage of the large coronary arteries

•Temporary narrowing of the small coronary arteries possibly responsible

•Reasons for temporary narrowing are unknown, but possibly because of chemical imbalance in the heart or abnormal functioning of the small arteries

Syndrome X

•Pressure or heaviness in chest beneath breastbone—women are likely to have unusual types of chest discomfort

•Pain may occur down shoulder or inside of arms, or in the throat, jaw, or teeth

•Stomach pain, especially after eating

•Sweating

Signs and Symptoms of Angina

•Light-headedness•Hypotension•Pulse changes•Indigestion

Signs and Symptoms of Angina (cont’d)

•Antianginals (nitroglycerin)•Antiplatelets (aspirin)•ACE inhibitors•Beta-blockers•Calcium channel-blockers•Thrombolytic therapy (if thrombi are cause)

Treatment of Angina

•Stool softeners•Oxygen administration•Percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass graft (CABG) to prevent MI

Treatment of Angina (cont’d)

•Death of cells in the myocardium, usually related to prolonged or severe ischemia

•Necrosis, tissue damage, and sometimes death result

Myocardial Infarction: An Overview

•Cause of MI include:– Sudden onset of ventricular fibrillation– Embolus (most common cause)– Thrombosis– Artherosclerotic occlusion– Prolonged vasospasm

Myocardial Infarction: An Overview (cont’d)

•Cellular injury occurs from lack of oxygen; if prolonged, will lead to cell death

•Scar replaces muscle, but can not contract or conduct impulses; location of damage is determined by which artery is blocked

•Damage begins at subendocardial level; will progress to the epicadium with 1-6 hours

Progression of Myocardial Infarction

•Damaged cells lead to decreased contractility– Less blood ejected by left ventricle

with each beat– Decreased blood pressure– Decreased tissue perfusion

Progression of Myocardial Infarction (cont’d)

•Pain—typical is middle of chest, radiating to jaws, arms (usually the left), abdomen, and/or shoulders, and lasting about 20 minutes– Possible to have no pain or atypical

pain (particularly in females) – Sudden onset of pain, not associated

with activity

Signs and Symptoms of Myocardial Infarction

•Tachycardia•Excessive perspiration•Painful breathing and/or difficulty breathing

•Anxiety/panic•Nausea/vomiting•Fever•Stomach pain, often confused with indigestion

Signs and Symptoms of Myocardial Infarction (cont’d)

•Creatinine phosphokinase (CPK):– Not elevated in blood serum, unless

injury has occurred– CPK II is present in heart tissue and is

elevated if MI has occurred

Cardiac Enzymes

•Lactic dehydrogenase (LDH):– LDH I is present in cardiac muscle, and

LDH II is present in the reticuloendothelial system

– Usually LDH I is greater than LDH II, but following a MI, LDH II is greater than LDH I

•Troponin:– Involved in muscle contraction and

released when cells are damaged

Cardiac Enzymes (cont’d)

•If more than 50% of heart tissue is damaged, severe disability or death will result

•Pericarditis may develop up to 2 months later:– Fever– Pericardial effusion– Pleurisy– Pleural effusion– Joint pain

Complications of Myocardial Infarction

•Rupture of heart muscle•Ventricular aneurysm•Blood clots•Hypotension

Complications of Myocardial Infarction (cont’d)

•Antianginals (nitroglycerin)•Analgesics•Stool softener•Electrolyte replacement•Calcium channel-blockers•Beta-blockers•Antihypertensives•Anticoagulants

Treatment Following Myocardial Infarction

•Antiarrhythmics•Thrombolytics•Oxygen•Mild antianxiety agents

Treatment Following Myocardial Infarction (cont’d)

•Inability of the heart to pump sufficiently to meet metabolic needs, leading to decreased tissue perfusion as a result of decreased cardiac output

•Acute or chronic

Congestive Heart Failure: An Overview

•MI•Hypertension•Myocarditis•Pulmonary embolism•CAD•Kidney failure•Cardiomyopathies

Causes of Congestive Heart Failure

•Valve disorders•Inflammatory conditions•Water intoxication•Side effects of medicine, such as corticosteroids

Causes of Congestive Heart Failure (cont’d)

•Damage to the heart leads to decreased output and tissue perfusion

•Andrenergic nervous system, renin-angiotensin system, and cytokine system are activated to compensate for the damage

Development of Congestive Heart Failure

•Decreased cardiac output causes release of norepinepherine to increase heart rate and contractility– Causes vasoconstriction– Increases cardiac output

Development of Congestive Heart Failure (cont’d)

•Decreased cardiac output decreases renal perfusion and activation of the renin-angiotensin-aldosterone system– Causes vasoconstriction and leads to

the production of aldosterone and antidiuretic hormone (ADH)

– Aldosterone causes sodium reabsorption and water retention—blood pressure increases

– ADH inhibits water excretion and raises blood pressure


•Vasoconstriction causes increased blood return to heart:*– Causing more stretch of the heart

muscle and enlargement of the heart chambers

– Increasing cardiac output in the short term


*Frank-Starling law: The greater the stretch of cardiac muscle fibers, the greater the force of contraction.

•Ventricular hypertrophy results from excess fluid and pressure:– First leads to an increase in

contraction– With time, leads to a decrease in

contraction•Increased heart rate leads to ischemia and decreased cardiac output


•Beta-receptors in heart become less sensitive to sympathetic-nervous-system stimulation, decreasing heart rate and contractility

•Alpha-receptors on peripheral blood vessels have increased sensitivity:– Promoting vasoconstriction– Increasing cardiac workload


•Ventricular dilation leads to ventricular wall thinning, degeneration, and loss of contractility


•Systolic dysfunction: – Heart contracts with less force and

can not pump out as much blood to the rest of the body as normal

– Blood accumulates in the ventricles and veins

Types of Congestive Heart Failure

•Diastolic dysfunction: – Heart is stiff and does not relax after

contracting– Heart does not allow as much blood

to enter its chambers from the veins, and the blood accumulates in the veins

Types of Congestive Heart Failure (cont’d)

•Left sided: – More common– Fluid backs into lungs– Signs and symptoms include:


• Fatigue • Coughing• Activity intolerance

• Pulmonary crackles

• Dizziness • Tachycardia• Syncope • urine output• Dyspnea • Shortness of breath

when lying down

•Right sided: – Caused by pulmonary hypertension or

right ventricular infarction– Fluid backs into rest of body, with

abdominal organ congestion and peripheral edema

– Signs and symptoms:


• Lower extremity edema in the ambulatory

• Sacral edema in the bedridden

• Liver engorgement and right upper quadrant pain

• Anorexia and nausea• Jugular venous

distension

•Biventricular (signs and symptoms of both left and right heart failure):– Signs and symptoms:


• All symptoms of right and left heart failure

• Dyspnea at rest• Hepatomegaly and

splenomegaly abdominal

pressure• Ascites• Anorexia

• Nausea and vomiting

digestion and absorption of nutrients

• Dysrhythmias• Cardiogenic shock

or acute pulmonary edema

•35%-55% of patients with moderately severe congestive heart failure (CHF) develop cardiac cachexia

•Loss of lean body mass >10% of total weight

•Resultant loss of cardiac muscle mass

•Impaired fat absorption

Cardiac Cachexia

•Many other metabolic changes:– Decreased sodium– Increased catabolic catecholamines– Tumor necrosis factor—causes weight

loss in animals and is increased in CHF patients

Cardiac Cachexia (cont’d)

•Diuretics•Dopamine•Analgesics•Antihypertensives•ACE inhibitors•Direct vasodilators•Antidysrhythmics•Cardiac glycosides (digitalis)•Aldosterone agonists

Treatment of Coronary Heart Disease

•Antibiotics, if necessary•Iron supplementation, if necessary•Supplemental oxygen•Nitrates•Beta blockers•Anticoagulants

Treatment of Coronary Heart Disease (cont’d)

References and Recommended Readings

•Arnold M. Heart failure. In: Merck Manual of Medical Information, Second Home Edition. Whitehouse Station, NJ: Merck Research Laboratories; 2003:150-158.

•Hogan MA, Hill K. Pathophysiology: Reviews and Rationales. Upper Saddle River, NJ: Pearson Education; 2004:43-61.

•Krummel DA. Medical nutrition therapy for heart failure and transplant. In: Mahan LK, Escott-Stump S. Krause’s Food, Nutrition, and Diet Therapy. 11th ed. Philadelphia, PA: WB Saunders; 2004:919-935.

•Krummel DA. Medical nutrition therapy in cardiovascular disease. In: Mahan LK, Escott-Stump S. Krause’s Food, Nutrition, and Diet Therapy. 11th ed. Philadelphia, PA: WB Saunders; 2004:860-899.

•Warnica JW. Coronary artery disease. In: Merck Manual of Medical Information, Second Home Edition. Whitehouse Station, NJ: Merck Research Laboratories; 2003:199-215.

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G-0967 Coronary Arte