G-0967 Coronary Heart Disease, Myocardial

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Coronary Heart Disease,

Myocardial Infarction, and Heart Failure

A Review of the Basics

Review Date 12/13

G-0967

Defining Heart Disease

Heart disease is a broad term used to describe a range of diseases that affect your heart, such as:

• Coronary heart disease (CHD)

• Atherosclerosis

• Myocardial infarction (MI)

• Heart failure (formerly called congestive heart failure)

Risk Factors for CHD and MI

• Smoking

• High intake of alcohol

• Obesity

• Sedentary lifestyle

• Diabetes

• Hypertension

Risk Factors for CHD and MI (cont’d)

• More than 34 years of age for males and

55 years of age for females (risk increases after menopause)

• Family history—genetics

• Hypertension

• Stress

• Chronic kidney disease

Risk Factors for CHD and MI (cont’d)

• High low-density lipoprotein (LDL) cholesterol

• Low high-density lipoprotein (HDL) cholesterol

• Left ventricular hypertrophy

Risk Factors for Heart Failure

• Obesity

• Hypertension

• Overweight or obesity

• Ischemic heart disease

• Changes in cardiovascular structure, such as diseases to the heart valves or muscle

Coronary Heart

Disease: An Overview

• Blood flow to the vessels surrounding the heart is blocked

• The major underlying cause of CHD is atherosclerosis or a buildup of plaque in the arteries

Plaque Development

• Many factors speed up plaque development:

̶ Elevated cholesterol and triglyceride levels

̶ Hypertension

̶ Infection that initiates the inflammatory response

̶ Elevated iron levels—carry free radicals that damage lining

̶ Elevated homocysteine level

̶ Cigarette smoking

̶ Diabetes

̶ Obesity

̶ Oxidized (LDL) levels

The Atherosclerotic

Process

• 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 (cont’d)

• 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

Coronary Heart Disease

Development

• Steps to development of CHD:

̶ Fatty streaks form, often in people younger than

30 years of age

̶ People are asymptomatic during this first stage of CHD

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

̶ Acute, complicated lesions with rupture and either nonocclusive or occlusive thrombus form (occlusive form often results in MI and sudden death)

̶ Hemorrhage into plaque produces thrombi—thrombus formation with arterial lumen initiated

Coronary Heart Disease

Development (cont’d)

• Steps to development of CHD (cont’d):

̶ Progressive narrowing of lumen

̶ Insufficient blood flow to myocardium (ischemia) results

̶ Chest pain or angina pectoris occurs

Signs and Symptoms of

Coronary Heart Disease

• Chest pain

• Hypertension

• Increased pulse

• Increased respiration

• Dyspnea on exertion

• Pallor of skin

• Light-headedness with exertion

• Diminished peripheral pulses

• Intermittent claudication—cramping of the lower extremities

Treatment of Coronary

Heart Disease

• Antihyperlipidemic agents

• Medications that lower triglycerides

• Antiplatelets (aspirin)

• Antihypertensives

• Antianginals (nitroglycerin)

• Antimicrobials

Angina Pectoris:

An Overview

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

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

Angina Pectoris:

An Overview (cont’d)

• Aerobic metabolism switches to anaerobic metabolism:

̶ Lactic acid buildup

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

Angina Pectoris:

An Overview (cont’d)

• Other causes of decreased oxygen supply to the myocardium:

̶ Congestive heart failure

̶ Congenital heart defects

̶ Pulmonary hypertension

̶ Left ventricular hypertrophy

̶ Cardiomyopathy

̶ Severe hypertension

̶ Narrowing of the aortic valve

Angina Pectoris:

An Overview (cont’d)

• Other causes of decreased oxygen supply to the myocardium (cont’d):

̶ Leakage of the aortic valve

̶ Ventricle wall thickening

̶ Atheroma leading to arterial narrowing

• Silent ischemia—decreased oxygen supply with no pain

Causes of Increased

Oxygen Demand

• Causes of increased oxygen demand on the myocardium:

̶ Anemia

̶ Exercise

̶ Thyrotoxicosis

̶ Substance abuse, particularly cocaine

̶ Hyperthyroidism

̶ Emotional stress

Four Types of Angina

• 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

(cont’d)

• Prinzmetal’s (variant):

̶ Has no identified cause

̶ May occur at same time of day

̶ May intensify or worsen over time

̶ Is usually caused by coronary artery spasm

• Angina decubitus:

̶ Occurs when a person is lying down with no cause

̶ Occurs because gravity redistributes body fluids

Signs and Symptoms of Angina

• 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 (cont’d)

• Light-headedness

• Hypotension

• Pulse changes

• Indigestion

Treatment of Angina

• Antianginals (nitroglycerin)

• Antiplatelets (aspirin)

• ACE inhibitors

• Beta-blockers

• Calcium channel blockers

• Thrombolytic therapy (if thrombi are the cause)

• Oxygen administration

• Percutaneous transluminal coronary angioplasty or coronary artery bypass graft to prevent MI

Myocardial Infarction:

An Overview

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

• Necrosis, tissue damage, and sometimes death results

• Cause of MI include:

̶ Sudden onset of ventricular fibrillation

̶ Embolus (most common cause)

̶ Thrombosis

̶ Atherosclerotic occlusion

̶ Prolonged vasospasm

Myocardial Infarction

Progression

• Cellular injury occurs from lack of oxygen:

̶ If prolonged, will lead to cell death

• Scar replaces muscle, but cannot contract or conduct impulses:

̶ Location of damage is determined by which artery is blocked

• Damage begins at subendocardial level:

̶ Will progress to the epicardium within 1 to 6 hours

Myocardial Infarction

Progression (cont’d)

• Damaged cells lead to decreased contractility:

̶ Less blood ejected by left ventricle with each beat

̶ Decreased blood pressure

̶ Decreased tissue perfusion

Myocardial Infarction:

Signs and Symptoms

• Pain, typically in middle of chest, radiating to jaws, arms (usually the left), abdomen, and/or shoulders, and lasting 20 minutes:

̶ Possible to have no pain or atypical pan (particularly in females)

̶ Sudden onset of pain, not associated with activity

Myocardial Infarction:

Signs and Symptoms

(cont’d)

• Tachycardia

• Excessive perspiration

• Painful breathing and/or difficulty breathing

• Anxiety/panic

• Nausea/vomiting

• Fever

• Stomach pain, often confused with indigestion

Laboratory Evaluation

• Creatinine kinase

• Trophin

• Myoglobin

Myocardial Infarction

Complications

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

Myocardial Infarction

Complications (cont’d)

• Pericarditis may develop up to 2 months later:

̶ Fever

̶ Pericardial effusion

̶ Pleurisy

̶ Pleural effusion

̶ Joint pain

̶ Rupture of heart muscle

̶ Ventricular aneurysm

̶ Blood clots

̶ Hypotension

Treatment Following

Myocardial Infarction

• Antianginals (nitroglycerin)

• Analgesics

• Electrolyte replacement

• Calcium channel blockers

• Beta-blockers

• Antihypertensives

• Anticoagulants

Treatment Following

Myocardial Infarction

(cont’d)

• Antiarrhythmics

• Thrombolytics

• Oxygen

• Mild antianxiety agents

Heart Failure:

An Overview

• 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

• Left sided or right sided

• Systolic or diastolic

Causes of Heart Failure

• Hypertension

• MI

• Cardiomyopathies

• Congenital heart disease

• Valve disorders

• Side effect of medication or alcohol

Types of Heart Failure

• Systolic dysfunction:

̶ Heart contracts with less force and cannot pump out as much blood to the rest of the body as normal

̶ Blood accumulates in the ventricles and veins

• 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 Heart Failure

(cont’d)

• Left sided:

̶ More common

̶ Fluid backs into lungs

̶ Signs and symptoms include:

• Fatigue

• Activity intolerance

• Dizziness

• Syncope

• Dyspnea

• Coughing

• Pulmonary crackles

• Tacycardia

•  urine output

• Shortness of breath when lying down

Types of Heart Failure

(cont’d)

• 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 include:

• Lower extremity edema in the ambulatory

• Sacral edema in the bedridden

• Liver engorgement and right upper quadrant pain

• Anorexia and nausea

• Jugular venous distension

Types of Heart Failure

(cont’d)

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

̶ Signs and symptoms include:

• 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

Cardiac Cachexia

• 10% to 15% of patients with heart failure develop cardiac cachexia

• Loss of 6% of nonedematous body weight over 6 months

• Concurrent loss of cardiac muscle mass as a result

Cardiac Cachexia

(cont’d)

• Many other metabolic changes:

̶ Increased catabolic catecholamines

̶ Tumor necrosis factor is increased, contributing to a lower body mass index and catabolic state

Treatment of Coronary

Heart Disease

• Diuretics

• Dopamine

• Analgesics

• Antihypertensives

• ACE inhibitors

• Direct vasodilators

• Antidysrhythmics

• Cardiac glycosides (digitalis)

• Aldosterone agonists

Treatment of Coronary

Heart Disease (cont’d)

• Antibiotics, if necessary

• Iron supplementation, if necessary

• Supplemental oxygen

• Nitrates

• Beta-blockers

• Anticoagulants

References

Academy of Nutrition and Dietetics. Nutrition Care Manual

[by subscription]. Nutrition Care Manual Web site.

® www.nutritioncaremanual.org

. Accessed December 1, 2013.

Cleveland Clinic. Acute myocardial infarction. Cleveland Clinic Center of

Continuing Education Web site. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/ cardiology/acute-myocardial-infarction/ . Accessed

December 1, 2013.

Cleveland Clinic. Heart failure. Cleveland Clinic Center for Continuing

Education Web site. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/ cardiology/heart-failure . Accessed December 1, 2013.

References (cont’d)

Raymond JL, Couch SC. Medical nutrition therapy for cardiovascular disease. In: Mahan, LK, Escott-Stump S, Raymond JL.

2012:742-781.

Krause’s Food and the Nutrition Care Process.

13th ed. St Louis, MO: Elsevier Saunders;

The Merck Manual for Health Care Professionals. Cardiovascular disorders. Merck Manuals Web site. http://www.merckmanuals.com/professional/cardiovascular_disorders.ht

ml . Accessed December 1, 2013.

What is angina? National Heart, Lung, and Blood Institute Web site. http://www.nhlbi.nih.gov/health/health-topics/topics/angina/ . Accessed

December 1, 2013.

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