Section A: Central

PATIENT STORY

A 45-year-old man began having chest pressure with exertion that was relieved with rest. He did not have diabetes, high blood pressure, or high cholesterol and had never had a myocardial infarction. His examination and resting ECG were normal. On the basis of the testing modalities available, he was scheduled for exercise stress testing. After a positive test, he underwent coronary angiography that demonstrated a significant stenosis in the left coronary artery (Figure 48-1). He underwent a stenting procedure and was placed on aspirin and cholesterol-lowering medication.

INTRODUCTION

In the United States, a person dies of coronary heart disease every 39 seconds. Coronary heart disease is a manifestation of atherosclerotic disease and has many modifiable risk factors. Patients with and without coronary heart disease should be advised to stop smoking, maintain normal blood pressure and cholesterol levels, exercise, achieve or maintain a normal weight, and control diabetes mellitus if present.

EPIDEMIOLOGY

• Coronary heart disease (CHD) is the leading cause of death in the United States, responsible for approximately 600,000 deaths in 2014.¹ The mortality rate has steadily declined for the past 30 years.

• Each year, 790,000 myocardial infarctions occur (first and recurrent) with a 14% mortality rate.¹

• Approximately 92.1 million U.S. adults have cardiovascular disease.¹

• In 2012, the prevalence of CHD among U.S. adults older than 18 years of age was higher in men than in women (12.1% vs. 9.7%) and higher in people with a less-than-high-school-diploma education (13.6% vs. 10.4% for college graduates).²

• In 2014, prevalence of heart disease was similar among white (10.9%), black (10.8%), and Hispanic (7.8%) persons.²

ETIOLOGY AND PATHOPHYSIOLOGY

• CHD is one of several manifestations of atherosclerotic disease, which begins with endothelium dysfunction.³

• Endothelium, when normal, balances vasoconstrictors and vasodilators, impedes platelet aggregation, and controls fibrin production.

• Dysfunctional endothelium encourages macrophage adhesion, plaque growth, and vasoconstriction by recruiting inflammatory cells into the vessel walls, the initiating step of atherosclerosis.

• The vessel wall lesions develop a cap of smooth muscle cells and collagen to become fibroadenomas.

• The vessels with these lesions undergo enlargement, allowing progression of the plaque without compromising the lumen.

• Two-thirds of acute coronary events are from plaque disruption and thrombus formation, instead of progressive narrowing of the coronary artery lumen.²

• Plaques most likely to rupture (high-risk plaques) have a large core of lipids, many macrophages, decreased vascular smooth muscle cells, and a thin fibrous cap.

• After plaque rupture, the exposed lipid core triggers a superimposed thrombus that occludes the vessel.

• Increased thrombosis is triggered by known cardiac risk factors including elevated low-density lipoprotein (LDL) cholesterol, cigarette smoking, and hyperglycemia.

• The other one-third of acute coronary events occurs at the site of very stenotic lesions (Figure 48-2).³

RISK FACTORS

• Family history of premature paternal or sibling myocardial infarction increases risk of heart disease by 50%.¹

• Tobacco use and secondhand smoke exposure increase the risk of CHD and smoking cessation decreases the risk.¹

• High total cholesterol, high LDL, and/or low high-density lipoprotein (HDL) are independent risk factors.

• Physical inactivity has a relative risk of CHD of 1.5 to 2.4.¹

• Overweight or obesity increases risk of heart disease by 20% (men and women) and 46% (men)/64% (women), respectively.¹

• Diabetes mellitus increases risk of heart disease (hazard ratio 2.5).¹

• Eighty percent of deaths from CVD can be prevented by healthier lifestyles including tobacco cessation, physical activity, control of blood pressure, and maintaining a healthy weight.¹

DIAGNOSIS

CLINICAL FEATURES

• Typical angina is chest pain or pressure, brought on by exertion or stress, and relieved with rest or nitroglycerin.

• Atypical angina has two of the three features of typical angina; however, women with coronary artery disease report more neck, throat, or jaw pain.⁴

• Noncardiac chest pain has zero to one of the three features of typical angina.

LABORATORY TESTING

• Risk factor assessment—Lipid profile and fasting blood glucose.

• Acute coronary syndrome—Cardiac-specific troponin is preferred; should be measured at presentation and again 3–6 hours after onset of symptoms.

• When troponin cutoff is 0.1 g/L, sensitivity is 93%, specificity is 91%, positive likelihood ratio (LR+) is 10.33, and negative likelihood ratio (LR–) is 0.08.

COMMON NONINVASIVE TESTING

• Exercise treadmill testing—Sensitivity 52% and specificity 71%, LR+ 1.79, LR+ 0.68⁵.

• Stress echocardiogram—Sensitivity 85% and specificity 77%, LR+ 3.70, LR– 0.19.

• Stress thallium—Sensitivity 87% and specificity 64%, LR+ 2.42, LR– 0.20.

Newer methods being tested include CT and MRI⁶:

• CT for coronary calcium has minimal benefit but only in those with intermediate cardiovascular risk (10%–20% 10-year CV risk)^6,7

• Coronary CT angiography is not recommended for assessment of asymptomatic patients.^6,7

• MRI is not recommended for assessment of asymptomatic patients.^6,7

DIFFERENTIAL DIAGNOSIS

Chest pain can be caused by several conditions including:

• Cardiac—Pericarditis—slower onset of pain, pain aggravated by movement or inspiration, characteristic ECG changes. Aortic dissection—acute onset with tearing type chest or upper back pain, shortness of breath, widening on mediastinum on chest X-ray

• Respiratory—Pneumothorax—acute onset with shortness of breath and characteristic radiographic findings; pneumonia—often accompanied by fever, cough, shortness of breath/hypoxia, and/or radiographic findings; pulmonary embolism—acute onset of shortness of breath, positive ventilation-perfusion scan, or spiral CT.

• GI—Gastroesophageal reflux—related to eating, responds to H₂ blockers or proton pump inhibitor (PPI).

• Musculoskeletal—Costochondritis—chest muscles tender to palpation.

MANAGEMENT

NONPHARMACOLOGIC

• Advise patients with coronary artery disease to stop smoking.⁸ SORⒶ

• Recommend 30 minutes of physical activity 5 to 7 days per week.^1,8 SORⒷ

• Advise patients in weight management with a goal body mass index (BMI) of 18.5 to 24.9.⁸ SORⒷ

MEDICATIONS

Managing risk factors:

• Lower LDL cholesterol with statin therapy (hydroxymethylglutaryl coenzyme A [HMG-CoA] reductase inhibitors) to decrease all-cause mortality (relative risk [RR] 0.90), cardiovascular mortality (RR 0.80), fatal and nonfatal myocardial infarction (MI) (RR 0.82 and 0.74).⁸ SORⒶ

• Lower blood pressure to 140/90 or 130/80 mm Hg (with diabetes or chronic renal disease); treat patients who are post-MI with a β-blocker, thiazide diuretic, or aldosterone antagonist.^8,9 SORⒶ

• Prescribe aspirin (75–162 mg) for all patients with coronary artery disease.⁸ SORⒶ

• Prescribe a P2Y12 receptor antagonist such as clopidogrel in combination with aspirin after acute coronary syndrome (ACS) or stent placement.⁸ SORⒶ

• Prescribe a β-antagonist—Several trials demonstrate mortality decreases of 25% to 40% with various β-blockers used in the acute MI or post-MI period.⁸

Treat symptoms:

• Nitroglycerin sublingual or spray for immediate relief of angina.^10,11 SORⒷ

• Long-acting nitrates or calcium antagonists if β-blockers are contraindicated, do not control symptoms, or have unacceptable side effects.^10,11 SORⒷ

REFERRAL OR HOSPITALIZATION

• Refer patients with positive noninvasive testing to be evaluated for cardiac catheterization.

• Consult with cardiologists and cardiothoracic surgeons to determine optimal management.

• Patients with greater than 50% stenosis of left main, proximal stenosis of three major arteries, or significant stenosis of the proximal left anterior descending and one other major artery are treated with coronary bypass surgery.¹² SORⒶ

• Percutaneous coronary intervention (PCI) typically involves balloon dilation plus stent placement. Drug-eluting stents decrease the risk of restenosis.¹²

PREVENTION

Prevention of CHD is accomplished by risk factor control. In a study of older men that examined the risk factors of smoking, high LDL, high blood pressure, and no aspirin use, the number needed to treat (NNT) to prevent one cardiovascular outcome were: 22, 8, 6, and 5 when 1, 2, 3, and 4 risk factors were controlled, respectively.¹⁰

FOLLOW-UP

Follow-up frequency is based on the extent of illness and symptoms and may include primary care and subspecialty care. Patients should have ongoing evaluation of risk factors and symptoms every 4 to 12 months. Patients who have new or changing ischemic symptoms should undergo stress testing to evaluate for their risk of further cardiac events.¹⁰ SORⒸ

PATIENT EDUCATION

Advise patients in the importance of lifestyle modification and medications in the long-term management of CHD.

REFERENCES

PATIENT STORY

A 40 year-old man presents to his family doctor after getting his blood pressure checked at a local health fair. His blood pressure was measured as 180/100 mm Hg. He has no symptoms or complaints. His blood pressure today was 178/98 mm Hg. Based on these two readings, he is diagnosed with stage 2 hypertension. He has a significant family history of essential hypertension. His examination is normal other than an enlarged and laterally displaced point of maximal impulse on cardiac examination. His body mass index is normal. His physician orders a urinalysis, complete blood count (CBC), fasting lipid profile, and a chemistry panel that includes serum glucose, potassium, creatinine, and calcium. An ECG shows left ventricular hypertrophy (Figure 49-1). He is counseled regarding lifestyle changes, started on two medications, and asked to follow-up within a couple of weeks.

INTRODUCTION

Hypertension (HTN) is a major risk factor for both myocardial infarction and stroke. Primary HTN constitutes 90% of HTN cases. Initial treatment includes lifestyle modifications and medications. Most patients require at least two medications to achieve control. Patients who cannot be controlled on three medications should undergo a work-up for secondary causes.

EPIDEMIOLOGY

• 29% of U.S. adults older than age 18 years have HTN.¹

• Blood pressure is controlled in approximately 50% of adults with HTN.¹

• Blood pressure control is lowest among those without health insurance (29%), Mexican Americans (37%), and younger adults ages 18 to 39 years (31%).^1,2

• In the United States, HTN contributes to 1 of every 7 deaths and to half of the cardiovascular disease-related deaths.²

• Cost of HTN to the U.S. healthcare system is estimated to be $93.5 billion per year.²

ETIOLOGY AND PATHOPHYSIOLOGY

• Primary HTN (>90% of patients)—A specific cause is unknown, but environmental factors (salt intake, excess alcohol intake, obesity) and genetics both play a role.

• Secondary HTN (5% to 10% of patients)—Causes include medications, kidney disease, renal artery stenosis (Figure 47-2), thyroid disease, hyperaldosteronism, and sleep apnea. Rare causes include coarctation of the aorta, Cushing syndrome and pheochromocytoma.

RISK FACTORS

• Family history.

• Genetic predisposition.

• Obesity.

• High sodium chloride intake.

• Medications, including oral contraceptives, NSAIDs, decongestants, and some antidepressants.

• Substances, including caffeine, licorice, amphetamines, cocaine, tobacco.

DIAGNOSIS

Average of two or more seated blood pressure readings on two or more office visits. Diagnosis can be made based on systolic (SBP) or diastolic (DBP) blood pressures.³

• Prehypertension—SBP 120 to 139 mm Hg or DBP 80 to 89 mm Hg.

• Stage 1 HTN—SBP 140 to 159 mm Hg or DBP 90 to 99 mm Hg.

• Stage 2 HTN—SBP equal to or greater than 160 mm Hg or DBP equal to or greater than 100 mm Hg.

• In 2017, the ACC/AHA released new hypertension diagnostic criteria.⁴ The new criteria lowers the threshold for the diagnosis of hypertension to systolic BP 130 or diastolic BP 80. Some national organizations including the AAFP⁵ have decided not to endorse these new guidelines but instead continue to endorse the most recent guideline from the JNC 8.⁶

CLINICAL FEATURES

• Often asymptomatic.

• When blood pressure is high, patients may have headaches or vision changes. Even higher pressures may lead to confusion, chest pain/myocardial ischemia, pulmonary edema, stroke or hematuria.

• Hypertensive retinopathy may be present (Figure 49-3 and Chapter 23, Hypertensive Retinopathy).

• An S4 can be an early finding on physical examination.

• Long standing HTN may lead to left ventricular hypertrophy which may be identified as an enlarged laterally displaced point of maximal impulse, abnormal ECG (Figure 47-1), or abnormal chest radiograph.

• Abdominal bruits may be present with renal artery stenosis.

LABORATORY TESTING

• Before initiating therapy for presumed primary HTN perform the following tests: urinalysis, CBC, fasting lipid profile, and chemistry panel, including fasting blood glucose, potassium, creatinine, and calcium.

• Consider testing for thyroid disorders with a thyroid-stimulating hormone (TSH) if signs or symptoms of hyperthyroidism are present.

• For patients with abnormal screening tests, signs indicating a secondary cause, or inadequate control on three medications:

  • Serum aldosterone and plasma renin activity in patients with hypokalemia.

  • 24-hour urine protein and creatinine for suspected renal disease.

  • A 24-hour urine free cortisol or a dexamethasone suppression test for suspected Cushing syndrome.

  • Plasma and urine catecholamines or metanephrines for suspected pheochromocytoma.

  • Parathyroid hormone level for suspected hyperparathyroidism.

• ECG on all patients with HTN.

• Chest radiograph is not necessary for patients diagnosed with primary HTN; however, if obtained, cardiomegaly may be present. If coarctation of the aorta is expected, rib notching may be present.

• Echocardiogram may demonstrate left ventricular hypertrophy.

• Renal artery stenosis can be seen on magnetic resonance angiography or by angiography (Figure 49-2).

• Renal ultrasound may demonstrate small or absent kidney.

DIFFERENTIAL DIAGNOSIS

• Falsely elevated blood pressure readings can be a result of improper cuff size (too small with a large arm diameter) or method (patient not seated, arm in incorrect position, etc.).

• Acute elevations in blood pressure may be caused by substances (e.g., tobacco, caffeine, cocaine).

• White coat HTN is defined as blood pressure that is consistently over 140/90 mm Hg in the presence of a healthcare provider with an ambulatory monitoring average of less than 135/85 mm Hg.

MANAGEMENT

NONPHARMACOLOGIC

• Weight reduction if overweight or obese.

• DASH (dietary approaches to stop hypertension) diet, rich in fruits and vegetables, aimed at reducing sodium intake and eating a variety of foods rich in nutrients that help lower blood pressure, such as potassium, calcium, and magnesium.

• Low-fat diet.

• Low dietary sodium chloride.

• Regular aerobic exercise.

• Moderate alcohol intake: no more than two drinks per day for men and one per day for women.

• Smoking cessation for cardiovascular risk reduction (see Chapter 248, Smoking and Tobacco Addiction).

MEDICATIONS

• Start a thiazide-type diuretic in most patients. An angiotensin converting enzyme inhibitor (ACEI) may be the initial choice in white males.^3,6

• Patients with Stage 2 HTN should be started on two medications upon diagnosis.

• Consider starting two medications when blood pressure is 20/10 mm Hg higher than goal. Goal is 140/90 mm Hg or 130/80 mm Hg in patients with diabetes or chronic kidney disease.

• Add an ACEI, angiotensin receptor blocker (ARB), β-blocker (BB), or calcium channel blocker (CCB) if control is not achieved with initial agent.

• Specific medications have compelling indications in these situations:

  • Heart failure—Diuretic, BB, ACEI, ARB, aldosterone antagonist (AA).

  • Post myocardial infarction—BB, ACEI, AA.

  • Diabetes—Diuretic, BB, ACEI, ARB, CCB.

  • Chronic kidney disease—ACEI, ARB.

  • Recurrent stroke prevention—Diuretic, ACEI.

REFERRAL OR HOSPITALIZATION

• Refer patients in whom adequate blood pressure control is not obtained.

• Women with HTN who are planning a pregnancy or who become pregnant should be referred to a provider with experience managing chronic HTN during pregnancy.

PREVENTION

Healthy lifestyle for all persons, including weight reduction (if overweight or obese), use of DASH diet, initiation and maintenance of adequate physical activity, and moderate alcohol intake.

PROGNOSIS

• Risk of cardiovascular disease increases as blood pressure increases.

• Between 115/75 and 185/115 mm Hg, every increase of 20 mm Hg systolic BP or 10 mm Hg diastolic BP doubles the risk of cardiovascular disease for adults ages 40 to 70 years.⁷

FOLLOW-UP

• Schedule visits monthly until blood pressure goal is obtained.

• Consider more frequent visits for patients with stage 2 HTN or significant comorbid conditions.

• Patients with controlled HTN should be seen every 3 to 6 months.

PATIENT EDUCATION

• HTN is a chronic disease requiring lifelong lifestyle modifications and one or more daily medications for most patients.

• Adequate control of HTN reduces the risk for heart attack and stroke.

REFERENCES

PATIENT STORY

A 60-year-old man presents to the emergency department with exertional shortness of breath increasing in severity over the past several days, along with paroxysmal nocturnal dyspnea and orthopnea. He does not have a history of heart failure or previous myocardial infarction. On examination, it was found that he had a third heart sound and an elevated jugular venous pressure. His chest radiograph showed cardiomegaly (Figure 50-1) and his B-type natriuretic peptide (BNP) was elevated at 600 pg/mL. He was diagnosed with heart failure, evaluated for underlying causes including coronary artery disease, and treated initially with an angiotensin-converting enzyme inhibitor (ACEI) and a loop diuretic. Later, he will be started on a β-blocker and an aldosterone receptor antagonist.

INTRODUCTION

Heart failure (HF) is common and increases with age. HF is a clinical syndrome that has multiple etiologies, all of which lead to a decrease in heart pumping capacity. There are two main types of heart failure: heart failure with reduced ejection fraction (HFrEF), also referred to as systolic HF, and heart failure with preserved ejection fraction (HFpEF) or diastolic HF.¹ ACEIs and β-blockers with or without aldosterone antagonists and angiotensin II blockers are the main pharmacologic therapies.

SYNONYMS

Congestive heart failure (CHF), systolic or diastolic dysfunction.

EPIDEMIOLOGY

• The prevalence of HF in the community increases with age: 0.7% (45 to 54 years); 1.3% (55 to 64 years); 1.5% (65 to 74 years); and 8.4% (75 years or older).²

• In the United States, the prevalence of HF is more than 5.8 million and the annual incidence is approximately 550,000.³

• There are race-related differences in the risk of HF, with the prevalence among black men and women about twice that of whites.⁴

• More than 40% of patients in the community with HF have an ejection fraction greater than 50%.⁵

• At age 40 years, the lifetime risk for HF is 21.0% (95% confidence interval [CI] 18.7% to 23.2%) for men and 20.3% (95% CI 18.2% to 22.5%) for women.⁵

• Survival rate is 50% at 5 years after diagnosis.¹

ETIOLOGY AND PATHOPHYSIOLOGY

• The most common cause of heart failure is ischemia, but heart pumping capacity can decline from several causes (i.e., myocardial infarction or ischemia, hypertension, valvular dysfunction, cardiomyopathy, or infections such as endocarditis or myocarditis).

• Cardiac dysfunction activates the adrenergic and renin-angiotensin-aldosterone systems.

• These systems provide short-term compensation, but chronic activation leads to myocardial remodeling and eventually worsening of cardiac function.

• Norepinephrine, angiotensin II, aldosterone, and tissue necrosis factor each contributes to disease progression.

• Angiotensin II directly causes cell death through necrosis and apoptosis, as well as cardiac hypertrophy.

CLASSIFICATIONS

• Two types of classifications: Stages of HF and New York Heart Association functional classifications¹:

DIAGNOSIS

Many history, examination, radiographic, ECG, and laboratory features are helpful in making the diagnosis of HF for patients presenting with dyspnea in the emergency department.⁶

CLINICAL FEATURES

• History and physical

  • History of HF (LR + [likelihood ratio] = 5.8), myocardial infarction (LR+ = 3.1).⁶

  • Symptoms of paroxysmal nocturnal dyspnea (LR+ = 2.6), orthopnea (LR+ = 2.2), edema (LR+ = 2.1).⁶

  • Examination finding of third heart sound (LR+ = 11), hepatojugular reflex (LR+ = 6.4), jugular venous distention (LR+ = 5.1), rales or crackles (LR+ = 2.8), lower extremity edema (LR+ = 2.3).⁶

LABORATORY AND ANCILLARY TESTING

• Laboratory value of BNP ≥250 (LR+ = 4.6); BNP <100 decreases likelihood of HF.⁶

• BNP cutoff points may be different in patients with renal insufficiency, obesity, or advanced age.

• ECG finding of atrial fibrillation (LR+ = 3.8), T-wave changes (LR+ = 3.0), any abnormality (LR+ = 2.2). A normal ECG lowers likelihood (LR– = 0.640).⁶

IMAGING

• Radiographic finding of pulmonary venous congestion (Figure 50-2) (LR+ = 12.0), interstitial edema (LR+ = 12.0), alveolar edema (LR+ = 6.0), cardiomegaly (Figures 50-1, 50-2, 50-3) (LR+ = 3.3).⁶

DIFFERENTIAL DIAGNOSIS

Gradually increasing shortness of breath can also be caused by:

• Chronic obstructive pulmonary disease may have dyspnea with exertion but does not have orthopnea; chest radiograph shows a normal-size heart, hyperinflated lungs, and flattened diaphragm; pulmonary function tests may be abnormal.

• Deconditioning has a normal chest radiograph.

• Metabolic acidosis from any cause can be differentiated with an arterial blood gas.

• Anxiety has episodic shortness of breath, not associated with exertion, and a normal chest radiograph.

• Neuromuscular weakness may have abnormal pulmonary function tests and a normal chest radiograph.

• Pneumonia may have fever and an infiltrate on chest radiograph.

MANAGEMENT

NONPHARMACOLOGIC

• Telemonitoring of patients with known HF for arrhythmias reduced all-cause mortality (relative risk [RR] 0.66). Telemonitoring and structure telephone support reduced HF related hospitalization (RR 0.79 and 0.77, respectively).⁷

• Exercise rehabilitation increases quality of life and decreases hospital admissions in patients with left ventricular systolic dysfunction.⁸

• Modest salt restriction is reasonable for most patients with HF but there is insufficient evidence to determine if this has an effect on mortality in patients with HF.^1,9

MEDICATIONS

Individually, ACE-Is, β-blockers, and aldosterone antagonists (AAs) lower mortality and should be considered for all patients without contraindications. Detailed treatment recommendations can be found in the 2013 ACCF/AHA Guidelines for the Management of Heart Failure.¹

• Prescribe an ACE-I. SORⒶ ACE-Is lower overall mortality rates by 23% and decrease hospitalization. Use in all patients with HFrEF unless there is a contraindication.^1,10

• Prescribe a β-blocker. SORⒶ Use one of the three beta blockers (bisoprolol, carvedilol, and sustained release metoprolol) that have been shown to reduce mortality. β-Blockers (BBs) reduce mortality by 32%.¹¹ Begin at a small dose and double the dose every 2 to 4 weeks until the target dose is reached or the patient cannot tolerate the increased dose. One study demonstrating a decrease in mortality had a large percentage of patients in the control and intervention groups already on an ACEI, indicating that the two together may decrease mortality more than an ACEI alone.^1,10 SORⒷ

• Prescribe an AA for patients with HFrEF and an EF <35%. Use when the creatinine is less than 2.5 mg/dL (men) and 2.0 mg/dL in women; monitor renal function and potassium.¹⁰ SORⒶ AAs lowered mortality by 30% and should be used in patients who are already taking ACE-I and BB.¹ SORⒷ

• Consider an angiotensin II receptor blocker (ARB) for patients who cannot tolerate an ACEI. Combining the use of an ACEI with an ARB is not recommended.¹ SORⒸ

• Combination of hydralazine and isosorbide dinitrate in addition to ACE-I, BB, and AA reduces mortality in African American patients with NYHA class III or IV.¹ SORⒶ

• Loop diuretics (e.g., furosemide or bumetanide) should be used in patients with evidence of fluid retention. Combine with ACEI, β-blocker, AA as above.¹ Associated with worse outcomes, including higher mortality when used alone.¹¹

• Calcium channel blockers are not recommended in HF.¹ SORⒶ

• Digoxin reduces hospitalizations and improves clinical symptoms, but does not lower mortality. Consider adding digoxin when patients have symptoms despite adequate therapy with ACEI, β-blockers, and AA.^1,11 SORⒷ

REFERRAL OR HOSPITALIZATION

• Refer for evaluation for cardiac resynchronization therapy in patients with left ventricular ejection fraction (LVEF) less than 35% and QRS greater than 150 milliseconds.¹ A recent meta-analysis demonstrated that cardiac resynchronization therapy decreased all-cause mortality and hospitalizations for HF in patients with New York Heart Association (NYHA) class II. Number needed to treat (NNT) = 12 to prevent 1 hospitalization.¹²

• Refer for evaluation for implantable cardiac defibrillator (ICD) placement in patients with NYHA class II-IV and LVEF less than 35%. SORⒸ ICDs have been shown to reduce mortality up to 30% and may offer greater risk reduction than antiarrhythmic medical therapy for some patients.¹

PROGNOSIS

Absolute mortality is high in patients with HF.

• Patients with preserved ejection fraction (>50%) have a mortality rate of 121 per 1000 patient years. Patients with reduced ejection fraction (<40%) have a mortality rate of 141 per 1000 patient years.¹³

• Five-year mortality rate after hospitalization for HF is 42.3%.¹

FOLLOW-UP

Close follow-up in many forms, including telemedicine and structured telephone visits, can reduce hospitalizations and mortality.⁷

PATIENT EDUCATION

Fluid and sodium restriction are still recommended by the ACCF/AHA guidelines, but a recent Cochrane review found no evidence of mortality improvements.⁹

REFERENCES

PATIENT STORY

A 30-year-old woman presented to her family physician with increasing shortness of breath over the past 2 weeks. Two weeks ago she developed a flulike illness and felt like she never recovered. She denied chest pain or edema, did not take any medications, and had not had any recent trauma or surgery. She had a normal examination. Her chest radiograph showed a classic globular heart as demonstrated in Figure 51-1. She had nonspecific ST changes on her ECG. An echocardiogram confirmed pericardial effusion (Figure 51-2). The underlying etiology was not elucidated, but she recovered spontaneously over the next several months.

INTRODUCTION

Pericardial effusion is an abnormal amount of fluid that may accumulate in the pericardial space. The pericardial space normally contains 15–50 mL of fluid, which serves as lubrication between the visceral and parietal layers of the pericardium. The speed at which a pericardial effusion develops has a great impact on a patient's symptoms. Pericardial effusions are commonly found in the general population, and the incidence increases with age. They can be caused by cardiac disease or surgery, connective tissue disorders, neoplasms, infections, renal disease, hypothyroidism, or medications; however, a cause is identified only 50% of the time. The definitive diagnosis is made by echocardiography.

EPIDEMIOLOGY

• Six-and-a-half percent of adults (<1% ages 20 to 30 years; 15% older than 80 years of age) had echocardiogram findings consistent with pericardial effusion in a population-based study of 5652 adults and adult family members of participants in the Framingham Heart Study.¹

• Few large studies have characterized the population prevalence of pericardial effusion; however, the available data consistently show that pericardial effusion is more prevalent than is clinically evident.

• Seventy-seven percent of patients after cardiac surgery for valves or bypass have pericardial effusions, which rarely (<1%) require treatment (Figure 51-3).²

• Forty percent of healthy pregnant women have small, asymptomatic pericardial effusions in the third trimester.³

ETIOLOGY AND PATHOPHYSIOLOGY

Pericardial effusion, acute or chronic, occurs when there is increased production or decreased drainage of pericardial fluid allowing accumulation in the pericardial space. The underlying etiology is clinically apparent approximately 25% of the time and can be determined with testing in another 25% of cases, leaving 50% of cases idiopathic.⁴ Most idiopathic cases have small effusions. Moderate to large pericardial effusions have an identifiable cause in 90%.⁵

The normal pericardium can stretch to accommodate a small amount of fluid without a significant change in intrapericardial pressure, although once this pericardial reserve volume is surpassed, the pressure-volume curve becomes steep. Rapid accumulation of pericardial fluid may cause elevated intrapericardial pressures with as little as 80 mL of fluid, while slowly progressing effusions can grow to 2 L without symptoms.

RISK FACTORS

Underlying causes include:

• Congestive heart failure from other cardiac diseases, such as rheumatic heart disease, cor pulmonale, or cardiomyopathy.⁶

• After cardiac surgery or myocardial infarction.²

• Connective tissue disorders (scleroderma, lupus erythematosus, rheumatoid arthritis).^6,7

• Neoplasms: benign (atrial myxoma); primary malignant (mesothelioma); secondary malignant (i.e., lung or breast cancer).⁶

• Chronic renal disease (uremia or hemodialysis) or other causes of hypoalbuminemia.⁸

• Infections: acute (enterovirus, adenovirus, influenza virus, Streptococcus pneumonia, Coxiella burnetii—responsible for Q fever) or chronic (tuberculosis, fungus, parasites).⁴

• Medications (procainamide, hydralazine) or after radiation.⁶

• Severe hypothyroidism with myxedema.⁶

DIAGNOSIS

Clinical features, chest radiograph, and electrocardiogram suggest pericardial effusion, which is confirmed by echocardiogram. The underlying etiology is identifiable in approximately 50% of cases.⁷

CLINICAL FEATURES

Signs and symptoms occur when the volume of fluid is large enough to affect hemodynamics. Rapid accumulation of pericardial fluid may cause elevated intrapericardial pressures with as little as 80 mL of fluid. Chronic pericardial effusion allows stretching over time and may require up to 2 L to cause significant symptoms⁶:

• Hypotension, increased jugular venous pressure, and soft heart sounds form the classic Beck's triad of acute cardiac tamponade, but all three are present only in approximately 30% of cases.⁶

• Common symptoms include anorexia (90%), dyspnea (78%), cough (47%), and chest pain (27%).⁶

• Common physical examination findings include pulsus paradoxus (77% with acute tamponade, 30% with chronic effusions), sinus tachycardia (50%), jugular venous distention (45%), hepatomegaly, and peripheral edema (35%).⁶

LABORATORY AND ANCILLARY TESTING

• Electrocardiogram is abnormal in 90%. Findings include low QRS voltage and nonspecific ST-T changes (59% to 63%) and electrical alternans (0% to 10%).⁶

• When the diagnosis remains unclear, pericardial fluid can be sent for cell count and differential, protein, lactate dehydrogenase, glucose, Gram stain, bacterial cultures, fungal cultures, mycobacterial acid-fast stain and culture, and tumor cytology.

• Measure rheumatoid factor, antinuclear antibody, and complement levels when collagen vascular disease is suspected.⁶ Check HIV status in at-risk patients.

When there is no obvious cause, ordering this set of specific tests determined the underlying etiology more often than seen in historic controls (27.3% vs. 3.9%; p <0.001).⁹

• Aerobic and anaerobic blood cultures.

• Throat swab cultures for influenza, adenovirus, and enterovirus.

• Serologic tests for Cytomegalovirus, influenza, C. burnetii, Mycoplasma pneumonia, and Toxoplasma.

• Blood tests for antinuclear antibody (ANA) and thyroid-stimulating hormone (TSH).

IMAGING

• Chest radiograph shows a globular enlarged cardiac silhouette (see Figure 51-1) (sensitivity 78%, specificity 34% with moderate or severe effusions) and pericardial fat stripe (Figure 51-3) (sensitivity 22%, specificity 92%).⁶

• Echocardiography is the preferred imaging test. Echo can be used to quantify volume of pericardial effusion (correlation to amount of fluid withdrawn 0.7).¹⁰ Echo-free, as opposed to echogenic, fluid is associated with a lower risk of constrictive pericarditis or recurrent pleural effusion.¹¹

• CT scanning, typically done for another purpose, can demonstrate the presence of a pericardial effusion, but does not quantify volume as well as echocardiography (correlation to amount of fluid withdrawn 0.4).¹⁰

DIFFERENTIAL DIAGNOSIS

• Congestive heart failure has many similar signs and symptoms (dyspnea, jugular venous distention, hepatomegaly, and edema) but may have pulmonary rales, which are unusual in pericardial effusions. A lateral radiograph in a patient with congestive heart failure (without pleural effusion) should have a normal thin pericardium (Figure 51-4).

• Pleural effusions may also present with dyspnea, but have different physical examination and radiographic findings.

• Acute pericarditis (without pericardial effusion) can present with chest pain and nonspecific ECG changes also seen with pericardial effusion. In contrast, acute pericarditis often has elevated inflammatory markers and a normal chest radiograph.¹²

MANAGEMENT

Most acute idiopathic or viral pericarditis occurrences are self-limited and respond to treatment with a nonsteroidal anti-inflammatory drug (NSAID).⁷ Colchicine or prednisone may be administered for severe inflammatory pericardial effusions or when NSAID treatment has failed. Colchicine is preferred over steroids (unless specifically indicated), as the latter is associated with an increased incidence of recurrent pericarditis.¹³

Pharmacotherapy for pericardial effusion includes use of the following agents, depending on the etiology:

• NSAIDs (e.g., indomethacin, ibuprofen, naproxen, diclofenac, ketoprofen, aspirin)

• Corticosteroids (e.g., prednisone, methylprednisolone, prednisolone)

• Anti-inflammatory agents (e.g., colchicine)

• Antibiotics (e.g., vancomycin, ceftriaxone, ciprofloxacin, isoniazid, rifampin, pyrazinamide, ethambutol)

• Antineoplastic therapy (e.g., systemic chemotherapy, radiation)

• Sclerosing agents (e.g., tetracycline, doxycycline, cisplatin, 5-fluorouracil)

• Treat any identified underlying cause.

• When the diagnosis is unclear and the patient is hemodynamically stable, NSAIDs may be beneficial, especially if inflammatory markers are elevated.

Pericardiocentesis:

• Required when there is hemodynamic compromise. Also useful when the pericardial effusion is large or suspected to be secondary to a bacterial infection or neoplastic process.

• Pericardiocentesis should be performed under local anesthesia as follows: Elevate the patient to a 45-degree angle. Insert a needle in the angle between the left costal arch and the xiphoid process, directed 15-degrees posterior, and angled toward the head or either shoulder. Complications are reduced when this procedure is guided by echocardiography. Fluid often reaccumulates. An indwelling catheter can be placed for up to 72 hours without increasing the risk of infection, until a more permanent procedure can be performed to decrease the likelihood of reaccumulation.

• Sclerosing therapy reduces the recurrence of symptoms from reaccumulation or the need for a repeat procedure for 30 days in more than 70% of patients. A caustic substance such as bleomycin or tetracycline is instilled into the pericardial space and held there for up to 4 hours.

• Other options to reduce recurrence include balloon pericardiotomy performed in a cardiac catheterization laboratory, radiation therapy, and surgery (i.e., pericardial window).

PROGNOSIS

Prognosis depends on the underlying cause.

In a study of older adults undergoing echocardiography for reasons other than a pericardial effusion, patients with an incidental small pericardial effusion had a higher 1-year mortality (26%) than did patients without an effusion (11%).¹⁴

FOLLOW-UP

Follow-up is based on the underlying cause. Pericardial effusions often disappear when the underlying illness resolves, and reappear when the underlying illness does not resolve (metastatic cancer).

PATIENT EDUCATION

• The underlying cause of a pericardial effusion is identified only 50% of the time; however, specific tests should be done to find treatable causes.

• In patients without an obvious underlying illness, infections (such as the flu, Q fever, or tuberculosis) and cancer are the two most commonly identified causes of pericardial effusions.

REFERENCES

PATIENT STORY

A 25-year-old man presented to the office because he had been feeling tired and feverish for several weeks. He admitted to injecting heroin regularly in the last 2 months. On examination, he was febrile and had a heart murmur of which he was previously unaware. His fingernails showed splinter hemorrhages (Figure 52-1). His funduscopic examination revealed Roth spots (Figures 52-2 and 52-3). An echocardiogram demonstrated vegetation on the tricuspid valve. He was hospitalized and treated empirically for bacterial endocarditis. After his blood cultures returned Staphylococcus aureus, his regimen was adjusted based on sensitivities and continued for 6 weeks.

INTRODUCTION

Bacterial endocarditis is a serious infection seen most commonly in patients with prosthetic valves; injection drug users; patients with HIV, especially those who use intravenous (IV) drugs; and patients who are immunosuppressed. Diagnosis is made using the Duke Criteria. Treatment is IV antibiotics or surgical valve replacement. Mortality, even with treatment, is 26% to 37%.

EPIDEMIOLOGY

• 3 to 7.0 cases per 100,000 patient years.¹

  • Historically more common in men; however, the incidence in women is increasing. Men 8.6 to 12.7 and women 1.4 to 6.7 cases per 100,000 person years, respectively¹

  • Average age has increased from 46.5 years (1980–1984) to 70 years (2001–2006)¹

  • Incidence in IV drug users is 3 per 1000 person years or 1% to 5% per year²

  • Incidence in HIV-positive IV drug users is 13.8 per 1000 person years²

  • Incidence of vegetations forming on intracardiac devices has increased from 13.8% (1998) to 18.9%³

• Morbidity and mortality is increasing. It is ranked the 3rd or 4th most common cause of life-threatening infection.¹

• Seen in immunosuppressed patients with central venous catheters or hemodialysis patients.

  • Fifty percent healthcare-associated, 43% community-acquired, and 7.5% nosocomial⁴

  • Mortality ranges from 16% to 37%⁵

• Patients with endocarditis who require surgery is increasing, now about 50%¹

• Prosthetic valve endocarditis makes up 10% to 15% of endocarditis cases.⁶

  • Incidence of 0.1% to 2.3% person year⁶

  • Can occur early (2 months after surgery) or late

ETIOLOGY AND PATHOPHYSIOLOGY

• Endothelium is injured by mechanical or inflammatory processes.

• Microbes adhere to compromised endothelium during transient bacteremia.

• Common organisms include S. aureus (IV drug users, nosocomial infections, prosthetic valve patients), Streptococcus gallolyticus (previously known as S. bovis, seen in elderly patients), enterococci (nosocomial infections), and Staphylococcus epidermidis (early infection in prosthetic valve patients).

• Blood contacts subendothelial factors, which promotes coagulation.

• Pathogens bind and activate monocyte, cytokine, and tissue factor production, enlarging the vegetations on the heart valves.

• The vegetations enlarge and damage the heart valves (Figure 52-4). This process can lead to death if not treated adequately in time.

• Septic emboli can occur, most commonly to the brain, spleen, or kidney.⁶

RISK FACTORS

• Prosthetic heart valve.

• Injection drug use.

• HIV infection.

• Immunodeficiency.

DIAGNOSIS

1. Modified Duke Criteria¹

   1. The Modified Duke criteria use a combination of history, physical examination, laboratory, and echocardiogram findings, and have a sensitivity of approximately 80% across several studies.

   2. Definition of Infective Endocarditis

      1. Definite Endocarditis

         1. Pathological Criteria

            1. Microorganisms demonstrated by culture/histological review of vegetation specimen

            2. Abscess formation

         2. 2 Major Criteria; 1 Major criterion and 3 minor criteria; OR 5 minor criteria

      2. Possible Endocarditis

         1. 1 Major criterion and 1 minor criterion; OR 3 minor criteria

      3. No Endocarditis

         1. Definite alternative diagnosis explaining signs and symptoms

         2. Resolution of endocarditis with <4 days of antibiotic therapy

         3. No pathological or histological evidence of infection in patients treated with <4 days of antibiotics

         4. Does not meet criteria for definite or possible endocarditis

   3. Major Criteria

      1. Positive blood cultures

         1. Three sets of blood cultures from different venipunctures sites with the first and last culture being no different than one hour apart

         2. Minimum of two blood cultures showing infection required to designate "Positive Blood cultures"

         3. A single culture positive for Coxiella burnetii or anti–phase 1 IgG antibody titer ≥1:800 is sufficient to designate as "positive"

         4. Organisms

            1. Staphylococcus aureus—most common in United States

            2. Streptococci viridans

            3. Streptococcus gallolyticus (bovis)

            4. HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

            5. Community-acquired enterococci

         5. Microorganisms present on recurrent blood cultures drawn at least 12 hours apart.

      2. Endocardial involvement as evidenced by:

         1. Echocardiogram evidence of vegetation, abscess, or new partial dehiscence of a prosthetic valve.

         2. New valvular regurgitation.

      3. Echocardiogram findings consistent with infected vegetation (NOTE: This was previously a minor criterion). Echocardiogram should be performed on any patient with suspected endocarditis.

   4. Minor Criteria

      1. Predisposition (e.g., heart condition such as a congenital or acquired valvular defect, injection drug use, prior history of endocarditis).

      2. Temperature >38°C (100.4°F).

      3. Clinical signs: arterial emboli, septic pulmonary infarcts, mycotic aneurysms, intracranial hemorrhages, Janeway lesions (Figures 52-5 and 52-6).

      4. Glomerulonephritis, Osler nodes, Roth spots, or positive rheumatoid factor (see Figures 52-2, 52-3, and 52-6).

      5. Positive blood culture not meeting major criteria.

CLINICAL FEATURES

• Fever—Seen in 85% to 99% of patients, typically low-grade, approximately 39°C (102.2°F).

• New or changing heart murmur—Seen in 20% to 80% of patients.

• Septic emboli—Seen in up to 60%, largely dependent on the size (>10 mm) and mobility of the vegetation.

• Intracranial hemorrhages—Seen in 30% to 40% of patients, bleeding from septic emboli or cerebral mycotic aneurysms.

• Mycotic aneurysms—Aneurysms resulting from infectious process in the arterial wall, most commonly in the thoracic aorta, also found in the cerebral arteries.

• Janeway lesions—Very rare, flat, painless, red to bluish-red spots on the palms and soles (Figures 52-5 and 52-6).

• Splinter hemorrhages—Red, linear streaks in the nail beds of the fingers or toes (Figure 52-1).

• Glomerulonephritis—Immune mediated; can result in hematuria and renal insufficiency, occurs in approximately 15% of patients with endocarditis.

• Osler nodes—Tender, subcutaneous nodules in the pulp of the digits (Figure 52-6).

• Roth spots—Retinal hemorrhages from microemboli, seen in approximately 5% of endocarditis (Figures 52-2 and 52-3).

• Positive rheumatoid factor—Seen in up to 50% of patients.

TYPICAL DISTRIBUTION

• Native endocarditis: Mitral valve is most common location (prior rheumatic fever or mitral valve prolapse), followed by aortic (prior rheumatic fever, calcific aortic stenosis of bicuspid valve).

• Prosthetic valve endocarditis: Site of any prosthetic valve.

• In IV drug users: Tricuspid valve, followed by aortic.²

LABORATORY AND ANCILLARY TESTING

In addition to blood cultures, consider a complete blood count for anemia and leukocytosis, erythrocyte sedimentation rate (ESR) (elevated in approximately 90%), and urinalysis for proteinuria or microscopic hematuria (seen in approximately 50%).

• Positive blood culture—First two sets of cultures are positive in 90%.⁶

IMAGING

• Abnormal echocardiogram in 85%.⁷

• If transthoracic echocardiogram is normal and endocarditis is still suspected, order a transesophageal echocardiogram (TEE).⁶ SORⒸ

  • TEE should be ordered in all patients with history of prosthetic valves, when there is concern of abscess formation, and when poor cardiac windows are expected (obese, history of chronic obstructive pulmonary disease [COPD], previous thoracic surgery)¹

  • If initial TEE is negative for endocarditis but there is a high suspicion, repeat TEE in 3–5 days to look for changes¹

  • Repeat TEE if there are clinical signs of complication of the disease

  • Transthoracic echocardiogram may be done after completion of antibiotic therapy to establish a new baseline¹

  • Vegetation >10 mm have a higher risk of embolization

• Cardiac MRI and CT scans are currently being studied as imaging modalities to diagnose endocarditis, but no clear guidelines and recommendations have yet been established.

• 3D TEE may be useful in detecting vegetations and their effect on the surrounding structures, but resolution is not high enough for routine use.¹

DIFFERENTIAL DIAGNOSIS

Fever without a clear cause may be seen with:

• Connective tissue disorders—Typically with other signs depending on the disorder, negative blood cultures, normal echocardiogram.

• Fever of unknown origin—Negative blood cultures or positive cultures with atypical organisms, normal echocardiogram in noncardiac causes.

• Intra-abdominal infections—Fever and positive blood cultures, normal echocardiogram.

• Echocardiogram findings similar to bacterial endocarditis may be seen with:

  • Noninfective vegetations—No fever and negative blood cultures

  • Cardiac tumors—Embolic complications, right or left heart failure, often located off valves in cardiac chambers, negative blood cultures

  • Cusp prolapse—No fever and negative blood cultures

  • Myxomatous changes—Extra connective tissue in the valve leaflets

  • Lambl excrescences—Stranding from wear and tear on the valve, most commonly aortic, no fever, and negative blood cultures

MANAGEMENT

• Draw blood cultures (three sets) and admit suspected cases to the hospital for IV antibiotics. SORⒸ

• Consider infectious disease consultation. SORⒸ

MEDICATIONS

• Start antibiotics empirically SORⒸ for specific regimens (Table 52-1).

  • Do not use gentamicin for right-sided Staphylococcus-related native valve endocarditis^1,8

  • Do not use gentamicin to treat methicillin-sensitive Staphylococcus aureus (MSSA) or methicillin-resistant Staphylococcus aureus (MRSA)

  • Clindamycin is not recommended for treatment of infective endocarditis due to high rate of recurrence

  • Patients with vancomycin-resistant Staphylococcus should be managed by an infectious disease consultant

• Alter antibiotics based on culture results.¹ SORⒶ

• Anticoagulation and aspirin are not indicated for infective endocarditis and are contraindicated with cerebral complications or aneurysms.

SURGICAL CONSULTATION

• Surgical excision of infected tissue has a 10% to 16% mortality rate in the immediate postop period.^9,10

• Consider surgical consultation when:

  • Congestive heart failure is severe with mitral or aortic regurgitation

  • Fever and/or bacteremia persist for 5–7 days despite adequate antibiotic therapy, abscesses or perivalvular involvement occurs, fungal organisms are identified, or heart block occurs¹

  • Embolic events recur on adequate antibiotic therapy or the risk of embolic events is high because of vegetations larger than 10 mm. SORⒸ

  • Consider postponing surgery in cases with large ischemic stroke or hemorrhagic stroke.

PREVENTION

• Prophylactic antibiotics are recommended for high-risk patients before certain procedures¹¹: SORⒷ

  • Patients with prosthetic cardiac valves

  • Patients with previous bacterial endocarditis

  • Cardiac transplant recipients with cardiac valvuloplasty

  • Patients with these congenital heart defects: unrepaired cyanotic congenital defects, heart defects repaired with prosthetic material within the last 6 months, congenital heart defects with a residual defect at or adjacent to the site of a prosthetic device

• Prophylactic antibiotics are only for patients undergoing one of the following:

  • Any dental procedure that involves manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa SORⒸ

  • Respiratory procedures involving incision or biopsy of the respiratory mucosa such as a tonsillectomy or adenoidectomy SORⒸ

  • Procedures on infected skin or musculoskeletal tissue

• Prophylactic antibiotics are not recommended for patients with mitral valve prolapse.

• Endocarditis prophylaxis is not recommended for patients undergoing gastrointestinal or genitourinary procedures. SORⒷ

• Antibiotic regimens:

  • Prescribe a one-dose regimen taken 30 minutes to 1 hour before the procedure¹¹:

  • Amoxicillin 2.0 g orally for adults, 50 mg/kg for children

  • If unable to take oral medications:

    • Adults—Ampicillin 2.0 g IM or IV or cefazolin/ceftriaxone 1 g IM or IV

    • Children—Ampicillin 50 mg/kg 30 minutes before the procedure; or cefazolin or ceftriaxone 50 mg/kg IM or IV

  • Penicillin allergic:

    • Adults—Clindamycin 600 mg PO, IM, or IV; or azithromycin or clarithromycin 500 mg orally

    • Children—Clindamycin 20 mg/kg orally, IM, or IV; or azithromycin/clarithromycin 15 mg/kg orally

  • If allergy to penicillin is not anaphylaxis, angioedema, or urticaria, may also use cephalexin 2.0 g PO for adults, 50 mg/kg PO for children; or cefazolin or ceftriaxone 1 g IM or IV for adults, 50 mg/kg for children.

PROGNOSIS

Bacterial endocarditis requires early detection and aggressive antibiotic therapy to decrease mortality.

• Thirty-day mortality is 16% to 25%.⁵

• Ninety-day mortality is 14.5%.⁵

• Greater than 6-month mortality is 20% to 37%.⁵

• Myocardial infarction (MI) occurs in about 5.5%; stroke and central nervous system (CNS) infection occur in about 13.3%.

FOLLOW-UP

• Most patients with bacterial endocarditis will require 4 to 6 weeks of IV antibiotics.

• Depending on the antibiotics, some patients will need to have medication levels monitored.

• Repeat blood cultures to ensure response to therapy.

• An echocardiogram at the end of treatment provides baseline imaging, as patients with endocarditis are at risk for recurrence.¹ SORⒸ

• Patients with history of IV drug abuse should be established in a rehab program.¹ SORⒸ

• Patients should follow up with a dental evaluation.¹ SORⒸ

• Patients should be educated on signs and symptoms of recurrence and complications that can occur from endocarditis.¹ SORⒸ

PATIENT EDUCATION

• Bacterial endocarditis is a serious disease with a significant mortality rate.

• Finish all antibiotics and keep follow-up appointments to ensure adequate treatment.

• Mortality remains elevated even 6 months after an episode.

• Recurrence is common, especially if risk factors remain (i.e., immunosuppression or IV drug use).

REFERENCES