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Coronary Heart Coronary Heart Disease, Myocardial Disease, Myocardial Infarction, Infarction, and Heart Failure and Heart Failure Provided Courtesy of Nutrition.com Review Date 12/13 G-0967 A Review of the Basics

Coronary Heart Disease, Myocardial Infarction, and Heart Failure Provided Courtesy of Nutrition.com Review Date 12/13 G-0967 A Review of the Basics

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Coronary Heart Coronary Heart Disease, Myocardial Disease, Myocardial

Infarction, Infarction, and Heart Failureand Heart Failure

Provided Courtesy of Nutrition.com

Review Date 12/13 G-0967

A Review of the Basics

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

•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

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 InfarctionComplications

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

Myocardial InfarctionComplications (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. Krause’s Food and the Nutrition Care Process. 13th ed. St Louis, MO: Elsevier Saunders; 2012:742-781.

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