CARDIAC INFECTIONS

CARDIAC INFECTIONS

Assoc Prof Dr. Meral SÖNMEZOĞLUYeditepe University Hospital

Learning Objectives

• Recognize the risk factors, signs, and symptoms of cardiac infections

• Understand the many approaches to diagnosing endocarditis, myocarditis and pericarditis.

• Appreciate the necessity of rapid treatment.

• Anticipate possible complications.

Cardiac Infections

• Endocarditis• Myocarditis• Pericarditis

INFECTIVE ENDOCARDITIS

Definition

• Infectious Endocarditis (IE): an infection of the heart’s endocardial surface

• Classified into four groups: – Native Valve IE– Prosthetic Valve IE– Intravenous drug abuse (IVDA) IE– Nosocomial IE

Sites of lesions

• Mitral Valve: 85% (Left atrium/ventricle)– Common site for Strep viridans group

• Aortic valve: 55% (Left ventricle)– Emboli would effect systemic organs brain,

kidneys, spleen• Tricuspid valve: 20% (Right atrium/ventricle)

– Common site for IV drug users (Staph. spp)– Emboli to lung

• Pulmonary valve: 1% (Right ventricle)

Further Classification

• Acute– Affects normal heart

valves– Rapidly destructive– Metastatic foci– Commonly Staph.– If not treated, usually

fatal within 6 weeks

• Subacute– Often affects

damaged heart valves

– Indolent nature– If not treated, usually

fatal by one year

Further Classification

• Acute• Rapid progression

of symptoms – Less than 6 weeks

duration– Significant systemic

signs/symptoms• Fever• Elevated systemic

WBC/ left shift

• Subacute• Slower, more

chronic progression of symptoms– Low grade fevers– Vague clinical

signs/symptoms• weakness, anorexia,

malaise,etc.

Acute NVE

• Frequently involves normal valves and usually has an aggressive course.

• Rapidly progressive illness in persons who are healthy or debilitated

• Virulent organisms, S aureus and group B streptococci are typically the causative agents

Subacute NVE

• Typically affects only abnormal valves. • Its course, even in untreated patients, is

usually more indolent than that of the acute form and may extend over many months.

• Alpha-hemolytic streptococci or enterococci, usually in the setting of underlying structural valve disease

Early PVE

• Early PVE occurs within 60 days of valve implantation.

• Traditionally, – coagulase-negative staphylococci, – gram-negative bacilli, and – Candida species have been the common

infecting organisms.

Late PVE

• Late PVE occurs 60 days or more after valve implantation.

• Staphylococci, • alpha-hemolytic streptococci, and • enterococci are the common causative

organisms. • Recent data suggest that S aureus may now

be the most common infecting organism in both early and late PVE

Pathophysiology

1. Turbulent blood flow disrupts the endocardium making it “sticky”

2. Bacteremia delivers the organisms to the endocardial surface

3. Adherence of the organisms to the endocardial surface

4. Eventual invasion of the valvular leaflets

Pathogenesis

• Multiple independent pathophysiological processes– “Trauma” of the heart surfaces– Platelet/fibrin deposition over traumatized tissue (non-

bacterial thrombotic endocarditis)– “Bacteremia” subsequent infection of the platelet/fibrin

deposition (Bacterial endocarditis)– Bacterial multiplication (10 9,10 cfu/gram of tissue)

Epidemiology

• Incidence difficult to ascertain and varies according to location

• Much more common in males than in females

• May occur in persons of any age and increasingly common in elderly

• Mortality ranges from 20-30%

Risk Factors• Intravenous drug abuse• Artificial heart valves and pacemakers • Acquired heart defects

– Calcific aortic stenosis– Mitral valve prolapse with regurgitation

• Congenital heart defects• Intravascular catheters• Permanent central venous access lines • Prior valve surgery • Recent dental surgery • Weakened valves

Predisposing factors

• rheumatic heart disease (25-30%)• congenital heart disease (10-20%)• mitral valve disease (10-30%)• IV drug abuse (15-35%)• no predisposition (25-45%)

• Common bacteria• S. aureus• Streptococci • Enterococci

• Not so common bacteria• Fungi• Pseudomonas• HACEK

Infecting Organisms

Infecting Organisms• Overall, S aureus infection is the most

common cause of IE, including PVE, acute IE, and IVDA IE.

• Approximately 35-60.5% of staphylococcal bacteremias are complicated by IE.

• More than half the cases are not associated with underlying valvular disease.

Infecting Organisms

HACEK - slow growing, fastidious organisms that may need 3 weeks to grow out of culture

Haemophilus sp.ActinobacillusCardiobacteriumEikenellaKingella

Native valve endocarditis• Viridans streptococci (30-60%)• Staphylococcus aureus (30-40%)

usually causes acute endocarditis• Gram negative bacteria

(e..g.Haemophilus) (5-10%)• Coagulase negative staphylococci

(e.g. S.epidermidis) (5%)• Streptococcus pneumoniae (1-3%)

Fungi (1-2%)

Prosthetic valve endocarditis• Coagulase negative staphylococi

(10-33%)• Streptococci (1-31%,the proportion

of cases of endocarditis due to streptococci increases progressively in the first 12 months post valve replacement)

• S. aureus (20%)• Gram negative bacteria (10%)• Fungi (1%)

Symptoms  • Chills • Fatigue • Fever • Heart murmur • Joint pain • Muscle aches and pains • Night sweats • Nail abnormalities (splinter hemorrhages under

the nails) • Paleness • Red, painless skin spots on the palms and soles

(Janeway lesions)

Symptoms 

• Red, painful nodes in the pads of the fingers and toes (Osler's nodes)

• Shortness of breath with activity • Swelling of feet, legs, abdomen • Weakness • Weight loss

Note: Endocarditis symptoms can develop slowly (subacute) or suddenly (acute).

Symptoms

• Acute– High grade fever

and chills– SOB– Arthralgias/ myalgias– Abdominal pain– Pleuritic chest pain– Back pain

• Subacute– Low grade fever– Anorexia– Weight loss– Fatigue– Arthralgias/ myalgias– Abdominal pain– Nausea/Vomiting

The onset of symptoms is usually ~2 weeks or less from the initiating bacteremia

Signs• Fever • Heart murmur• Nonspecific signs – petechiae, subungal

or “splinter” hemorrhages, clubbing, splenomegaly, neurologic changes

• More specific signs - Osler’s Nodes, Janeway lesions, and Roth Spots

Duke’s Criteria• MAJOR• Positive blood culture for appropriate organism• Evidence of endocardial involvement

• MINOR• Predisposition• Fever• Vascular phenomena• Immunological phenomena• Microbiological evidence not meeting major criteria• Echo finding not meeting major criteria• Raised inflammatory markers

• DIAGNOSIS• Two major• One major + Three minor• Five minor

Janeway Lesions

1. More specific2. Erythematous, blanching macules 3. Nonpainful4. Located on palms and soles

Janeway lesion

IE:Janeway Lesions

Splinter Hemorrhages

1. Nonspecific2. Nonblanching3. Linear reddish-brown lesions found under the nail bed4. Usually do NOT extend the entire length of the nail

IE: Splinter hemorrhages

Osler’s Nodes

1. More specific2. Painful and erythematous nodules3. Located on pulp of fingers and toes4. More common in subacute IE

American College of Rheumatologywebrheum.bham.ac.uk/.../ default/pages/3b5.htm www.meddean.luc.edu/.../

Hand10/Hand10dx.html

IE: Osler Nodes

Petechiae

Photo credit, Josh Fierer, M.D. medicine.ucsd.edu/clinicalimg/ Eye-Petechiae.html

Harden Library for the Health Scienceswww.lib.uiowa.edu/ hardin/md/cdc/3184.html

1.Nonspecific2.Often located on extremities

or mucous membranesdermatology.about.com/.../ blpetechiaephoto.htm

Roth spot

Roth’s spotsRetinal haemorrhagesAlso seen in leukaemia,Diabetes, pernicious anaemia

Exams and Tests   

• CBC -anemia• Chest x-ray • Echocardiogram• ECG • Erythrocyte sedimentation rate (ESR) • Repeated blood culture and sensitivity

Investigations• Blood tests• FBC• U&E• CRP to monitor disease activity• LFT• Blood cultures are essential, with a minimum of three

samples taken from different sites at least an hour apart (preferably more) sent for analysis, before initiation of antibiotics.

• Serological tests for exotic organisms are usually done for culture negative IE if splenic absceses are suspected

Investigations• Chest radiograph - this may detect septic lung infarcts

(commoner in IE secondary to drug abuse), signs of cardiac failure, and evidence of pulmonary infection

• Urine dipstick/ MSU to detect haematuria• Electrocardiogram to provide a "baseline“

prolongation of the PR interval may mean the development of an aortic root abscess)

• Abdominal ultrasound or CT Abdomen may be indicated

Possible Complications    • Arrhythmias, such as atrial fibrillation • Blood clots or an infected clot from the endocarditis that

travels to the brain, kidneys, lungs, or abdomen, causing severe damage to, and infection of, these organs

• Brain abscess • Brain or nervous system changes • Congestive heart failure • Glomerulonephritis • Jaundice• Severe heart valve damage • Stroke

Prevention 

• People with certain heart conditions often take preventive antibiotics before dental procedures or surgeries involving the respiratory, urinary, or intestinal tract.

• Those with a history of endocarditis should have continued medical follow-up.

Treatment

• If patient stable defer until adequate blood cultures done

• liaise with microbiology re appropriate antibiotics

• International guidelines exist• Review with culture results• Usually six weeks treatment, at least four on

iv

Treatment 

• Long-term antibiotic therapy is needed to get the bacteria out of the heart chambers and valves.

• usually have therapy for 6 weeks • must be specific for the organism • blood culture and the sensitivity tests

Treatment

• Parenteral antibiotics– High serum concentrations to penetrate

vegetations– Prolonged treatment to kill dormant bacteria

clustered in vegetations• Surgery

– Intracardiac complications• Surveillance blood cultures

Complications requiring surgery

• Infected prosthetic material: less than 1 year out from original heart surgery

• Refractory congestive heart failure (Leading cause of death)

• Unresponsive infection/ continued infection despite appropriate antibiotics

• Pt. experiences more than 1 major emboli

MYOCARDITIS

Myocarditis

• an inflammation of the heart muscle

• an uncommon disorder that is usually caused by viral infections such as coxsackie virus, adenovirus, and echovirus

Myocarditis

• may also occur during or after various viral, bacterial, or parasitic infections (such as polio, influenza, or rubella).

• exposure to chemicals or allergic reactions to certain medications

• associated with autoimmune diseases.

• muscle becomes inflamed and weakened

Symptoms   • History of preceding viral illness • Fever • Chest pain that may resemble a heart attack • Joint pain or swelling • Abnormal heart beats• Fatigue • Shortness of breath • Leg swelling • Inability to lie flat

*total absence of symptoms is common

Additional symptoms • Fainting, often related to arrhythmias • Low urine output • Other symptoms consistent with a viral

infection -- headache, muscle aches, diarrhea, sore throat, rashes

Exams and Tests

• Electrocardiogram (ECG) • Chest x-ray• Ultrasound of the heart (echocardiogram) -- may show

weak heart muscle, an enlarged heart, or fluid surrounding the heart.

• White blood cell count • Red blood cell count• Blood cultures for infection • Blood tests for antibodies against the heart muscle and the

body itself • Heart muscle biopsy - rarely performed

Treatment 

• Antibiotics• reduced level of activity• low-salt diet. • Steroids and other medications may be

used to reduce inflammation. • Diuretics

Treatment 

• If the heart muscle is very weak, standard medicines to treat heart failure are also used.

• Abnormal heart rhythm may require the use of additional medications, a pacemaker or even a defibrillator.

• If a blood clot is present in the heart chamber, blood thinning medicine is given as well.

Possible Complications  

• Heart failure• Pericarditis • Cardiomyopathy

Prevention 

• Prompt treatment of causative disorders may reduce the risk of myocarditis.

PERICARDITIS

Acute Pericarditis

Inflamation of the pericardium• Idiopatic• Viral• TB• Post-MI• Autoimmune disease• Uraemia• Treat cause//NSAIDs• Myocarditis rarer but can co-exist

Acute Pericarditis

Pericardium

• Visceral / serous – Direct contact with epicardium (ST elev)– single layer mesothelial cells

• Parietal / fibrous– mesothelial and fibrous layer

Pericardial AnatomyVisceral – transparent

Parietal – translucent

Transverse sinus – curved probe

Acute Pericarditis

• Pericarditis– Acute

• With or without tamponade– Pericardial window

– Chronic• Constrictive pericarditis

– Total pericardioectomy» Cardiopulmonary bypass

– Lymphadenitis• Cervical (scrofula)• Mediastinal

– Drainage

Etiology – Acute Pericarditis• Infectious

– Viral : Coxsackie, Echo, EBV, Influenza, HIV– Bacterial: TB, staph, hemophillus, pneumococcal, salmonella– Fungal/other: histo/blasto/coccidio, rickettsia

• Rheumatologic– SLE, Sarcoid, RA, Dermatomyositis, Ankylosing Spondylitis,

Scleroderma, PAN• Neoplastic

– Primary: angiosarcoma, mesothelioma– Metastatic: breast, lung, lymphoma, melanoma, leukemia

• Immunologic– Celiac sprue, Inflammatory Bowel Disease

• Drug– Hydralizine, Procainamide

• Other– MI, Dressler’s, Post Pericardiotomy, Chest Trauma, Aortic dissection– Uremic, Post Radiation– IDIOPATHIC

Acute Pericarditis – Clinical

• History– preceding viral illness, etc

• Symptoms– Chest pain

• Signs– Friction Rub

• ECG– early: PR / ST changes– late: isoelectric ST/ T inv

History

• Often preceding viral illness 1-2wk prior• Chest Pain

– Sudden, sharp,pleuritic, constant– worse supine/ L lat decub, relief sitting up– radiation: back, trapezius ridge– symptoms usually resolve by 2 weeks, ECG

abnormalities may persist for months

Auscultory – Rub(s)

• Endopericardial (classic)– “triphasic”: atrial sys, ventricular sys, early diastole– may only hear 2 phase (afib or tachycardia) or 1– loudest LSB, raised extremities/increased venous return

• Pleuropericardial– “exopericardial”, extension into adjacent structures– marked resp variation, musical quality

• Conus– dilation of pulm conus in hyperactive heart– PE, thyroid storm, acute beriberi

• Pneumohydropericardium– air/gas overlying pcard fluid– metallic tinkle (small amt) ; churning/splashing “mill-wheel sound” (lg)

ECG

• PR depression• ST elevation

– concave up, ST/T V6 >.25, no reciprocal• DDx:

– Acute MI– Early Repolarization– Myocarditis– Aneurysm– other: Brugada, BBB

ECG

Acute Pericarditis - Stages

• Stage I– first few days 2 weeks– ST elev, PR depression– up to 50% of pt with sxs/rub do NOT have/evolve stage I1

• Stage II– last days weeks– ST returns to baseline, flat T

• Stage III– after 2-3 weeks, lasts several weeks– T wave inversion

• Stage IV– lasts up to several months– gradual resolution of T wave changes

1 Spodick DH, Pericardial Disease. Braunwauld 6th

Cardiac Isoenzymes - ? helpful

• 2 year study, ER based1

– 14 pt with 2/3 findings (CP typical for PCARD, rub, and ECG changes c/w PCARD)

– 71% had elevated TropI (pk 21) with negative CAD workup

• Not reliable to differentiate MI vs PCARD

1Brandt RR, et al. Am J Card 2001, June 1

Treatment

• NSAIDS/ASA– ASA 650 q3-4hr– Ibuprofen 300-600 q 6-8 hrs x 1-4days

• Avoid Indocin, reduces CBF• Steroids

– if no response after 48hr NSAID– use concurrent NSAID

• Colchicine– .6 q12 chronic +/- NSAID– useful in recurrent pericarditis– symptom free period 3.1 +/- 3mos vs 43 +/- 35mos (p<.00001)

in largest multicenter trial to date1

– Anecdotal evidence of benefit in Acute PCARD, effusion

1Adler Y, et al. Circulation, 1998 June 2

Complications

• Pericardial Effusion/Tamponade• Constrictive Pericarditis

– can be “transient” – 10% may have transient sxs within 1st month, resolves by 3 months

• Recurrent Pericarditis (20-25%)– Rx – NSAIDS/Colchicine +/- steroids

Gross Pathology

“Bread & Butter” appearance Fibrinous stranding

Possible Complications    • Arrhythmias, such as atrial fibrillation

• Cardiac tamponade

• Constrictive pericarditis, where inflammation of the pericardial sac results in fibrosis and thickening of the pericardium with adhesions (sticky scars) between the pericardium and the heart.

• The pericardium creates a rigid "case" around the heart, which can severely limit the ability of the heart to fill with blood. Patients with constrictive pericarditis may develop heart failure, which responds poorly to treatment.