Myocardial Infarction (MI)




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Cardiac Enzymes
- Mnemonic:Â "My Time To Call"
- Earliest Markers (Even before Myoglobin):
- HFABPÂ (Heart Fatty Acid Binding Protein).
- IMAÂ (Ischemia Modified Albumin).
Enzyme / Marker | Start (Rise) | Peak | Fall | Other Notes |
Myoglobin | ~2 hours | Very early | Falls early | ⢠Non-specific ⢠(also in skeletal injury) ⢠Not used for MI diagnosis |
Troponin T/I | 2â4 hours | ~24â48 hours | Falls by 10 days | ⢠Preferred for MI diagnosis ⢠Most used in ER Reinfarction marker: âł 20% rise from previous dayâs value = reinfarction |
CKMB | 2â4 hours | ~24 hours | Falls by 48â72 hrs | ⢠CKMB â 4 alphabets ⢠â falls before day 4 |
AST (SGOT) | ~12 hours | ~24â36 hours | Falls by 5 days | ⢠Call A â AST |
LDH 1 | 1 day | ~2â3 days | Falls by 10 days | ⢠LDH1 > LDH2 in MI ⢠(Flipping effect) ⢠Normal: LDH2>1 ⢠Heart has highest LDH1 |
Note:
- NT Pro-BNP (Precursor of brain natriuretic peptide):
- Marker of cardiac failure.

Cardiac Scans
Preferred Scan | Purpose | Key Findings |
Thallium scan | Ischemia / Perfusion | ⢠Ischemic areas â no Thallium uptake Stress and Rest test: âł ischemia induced â no uptake ⢠At rest â uptake present ⢠ie, Reversible defect â ischemia |
Tc99 Pyrophosphate scan | Infarct detection | ⢠Infarct shows hotspot ⢠Mnemonic: Hot â Fire â Pyrr |
MUGA scan ⳠMultiple Gated Acquisition | LV function | ⢠Evaluates LV function (Ejection fraction) |
Cardiac MRI | LV function test | ⢠Most accurate ⢠Gold standard for LV function |
PET scan | Cardiac viability | ⢠Differentiates hibernating myocardium vs scar/infarct ⢠Compares metabolism & perfusion |
Autopsy Findings in Myocardial Infarction








- Findings depend on duration of ischemia.
Time Frame | Findings |
Within 30 mins | - Reversible injury (avg 30 mins) - Seen only on electron microscope - Mitochondrial swelling, hydropic change - glycogen loss. |
30 mins â 4 hours | - First light microscopic change - Waviness, vacuolization of cardiac fibers Electron microscope: Amorphous densities in mitochondria from 30 mins onwards |
TPTC Stain Triphenyl tetrazolium | - Used in autopsy - Useful within 4 hours - Stains Lactate Dehydrogenase 1 - Normal: Brick red - MI: Pale - Old scars: Pearly white |
Reperfusion Injury | - Seen after restoring blood flow - Contraction Band Necrosis seen microscopically |
> 4 hours | - First Gross: Occasional mottling (color change) - Microscopy: Coagulative necrosis |
4-12 hours | Occasional dark mottling (D/t necrosis) |
12-24 hours | Dark mottling Coagulation necrosis, hyper-eosinophilia, early neutrophilic infiltrate |
1â3 days | Mottling with yellow-tan infarct centre neutrophilic infiltrate |
3 -7 days | Macrophages |
> Day 7 | Granulation tissue formation starts - Sign of repair - Rich in blood vessels |
> Day 14 | Scar formation - Stain: Mason Trichrome â ⢠Collagen (scar): blue â ⢠Muscle: red ⢠Collagen deposition (Fibrosis + remodelling) |
>2 months | Dense collagenous scar |


Complications
- Anterior transmural myocardial infarction â aneurysm
- It occurs as a result of the loss of contractile function +
- thinning of the infarcted myocardial wall.
Carditis (Inflammation of the Heart)






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Pericarditis
- Serofibrinous Pericarditis:
- Associated with: Rheumatic Heart Disease (RHD).
- Description:
- Abundant fluid (watery) +
- fibrous threads between parietal and visceral pericardium.
- Known as: "Bread and Butter Pericarditis".
Myocarditis
- Causes:
- Viral: Coxsackie virus, Herpes virus.
- Parasitic: Trichinella spiralis (well-known cause).
Endocarditis
- General feature: Vegetations (verrucae) common to all types.
- Four Types:
Feature | Rheumatic Heart Disease (RHD) | Infective Endocarditis (IE) | Non-Bacterial Thrombotic Endocarditis (NBTE) / Marantic Endocarditis | Libman-Sacks Endocarditis (LSE) |
Cause | GABHS (Streptococcus pyogenes) | Streptococcus viridans, Staphylococcus aureus, Coagulase-negative Staphylococcus (prosthetic valves) | Not bacterial. AML M3, Lung/ Pancreatic cancers. | SLE |
Vegetations | Small and warty. Along lines of closure. Mnemonic: Rheumatic â Ruler â drawn with a ruler | Large and bulky. Often extend beyond lines of closure. Can break off and embolize. | Very fragile blood clots (thrombi). | Found everywhere (upper/lower valve surface). More common on lower surface ("LS for lower surface"). |
Most Common Valve | Mitral valve. | Generally:Â Mitral valve. IV Drug Abusers:Â Right-sided valves. | ă
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Least Common Valve | Pulmonary valves. | ă
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Embolization | ă
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Acute Presentation | Mitral Regurgitation. MacCallum Patch: irregular area, posterior wall LA (due to blood turbulence). | - | - | - |
Chronic Presentation | Mitral Stenosis. Deformity: "Fish Mouth" or "Button Hole Deformity". | - | - | - |
Microscopic | Ashoff Bodies (most characteristic): Fibrinoid necrosis + Anitschkow cells (macrophages: "caterpillar" or "owl-like" nucleus). Seen in all three layers, max in myocardium | - | - | - |
Cutaneous Signs | - | Osler's Nodes: Painful ("Ouch" for Osler's). Janeway Lesions: Painless (palms/soles). | - | - |
Diagnosis | Jones criteria. | Modified Duke's Criteria. | ă
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- Immunological phenomenon
- Oslers ( Oh... painful đ hand, Made into Pulp)
- Painful, red nodules on pulp of fingers and toes.
- Immune Complex mediated.
- rOths spot
- Seen in fundus with pale center (Fibrin plug).
- Caused by retinal endothelial vasculitis
- GlomerulOnephritis syndorme


Roth spot seen in
- Infective endocarditis
- Acute leukemia

Cardiomyopathy

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Dilated Cardiomyopathy (DCM)



- Dilation: All four chambers of the heart.
- Causes:
- Most Common: Idiopathic.
- Known Cause :Â
- Alcoholism
- Doxorubicin
- Trastuzumab
- Peripartum myopathy
- Most Common Genetic Cause:Â
- Titan gene mutation (largest protein).
- Hemochromatosis â DCM > RCM
- Microscopic Finding:Â
- Ninja star appearance of cardiac fiber nucleus
- linked to alcoholism/Titan mutation
- Myocyte vacuolization
- Mnemonic:
- DCM â DC/Marvel â Drunk Titan (Titin) Ninja (Ninja star) â Got Fat (dilated) Excess alcohol drinking â He was tight (Trastuzumab), has a dog called ruby (Doxorubicin)

Takotsubo Cardiomyopathy / Broken Heart Syndrome:


- Dilation: Only left ventricle (resembles octopus pot - "Takotsubo").
- Cause: Extreme emotional stress â increased catecholamines.
- "Broken Heart Syndrome": refers to pathogenesis (emotional stress).
- Mnemonic: Takotsubo â Takashis castle â Got heart broke when it ended
Hypertrophic Cardiomyopathy (HCM)




- Mnemonic: Myren (Myosin) Dominant (AD) Hitler (Helter skelter) â Ordered to kill Awesome (HOCM) Athlete (called SAM â Systolic Ant Motion of MV) â while eating banana (Banana shaped heart) â in Camp (Mevampton)
- Mutation:Â Myosin Heavy Chain (MHC)Â mutation.
- New drug Rx â Mevacampton
- Inheritance:Â Autosomal Dominant.
- Hypertrophy: More in
- left ventricleÂ
- interventricular septum.
- Clinical Presentation: Often sudden death in a young athlete.
- Gross Appearance:Â
- Banana-shaped heart with a slit-like chamber.
- Microscopic Finding:
- Cardiac muscle fibers in random directions
- Myocyte disarray â ("Helter Skelter appearance").
Arrhythmogenic Right Ventricular Cardiomyopathy (ARVCM)

- Involvement:Â Right ventricle.
- Mutation: Desmosomes (specifically, Plakoglobin gene defect).
- Gross/Microscopic:
- Right ventricle wall very thin
- appears yellow due to fatty infiltration.
- ECG
- Epsilon wave

- Associated Syndrome:Â Naxos Syndrome.
- Components: ARVCM + woolly hair + palmoplantar keratoderma.
- Mnemonic: Rv (ARV) il oru Fat (fat deposition) Nexalate (NAxos) ne kandu â He had plaques (plakoglobin) on hair (woolly hair) and hands (keratosis) â He was Desp (Desmosomes)
Restrictive Cardiomyopathy (RCM)
- Dysfunction: Diastolic dysfunction (heart cannot relax).
- Most Common Cause:Â
- Amyloidosis (amyloid protein in heart).
- Other causes:
- Hemochromatosis (DCM > RCM)
- Sarcoidosis
- Fibrosis
- Loefflers Sx
Hemochromatosis
- Dilated cardiomyopathy > RCM OR BOTH
Cardiac Hypertrophy
- Boxcar nuclei
- Secondary to hypertension or stenosis
- eg mitral stenosis
- NOT HOCM
Bacillus anthracis
- Boxcar appearance aka bamboo stick appearance
- Gram staining
Lymphocytic myocarditis

- Fever, fatigue, and left ventricular dysfunction
- Endomyocardial biopsy
- Lymphocytic infiltration
Miscellaneous Cardiac Topics


Candy (Gundy) and Nutmeg


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Nutmeg Liver | Right | Liver | Congested hepatic veins with centrilobular hemorrhagic necrosis of hepatocytes (dark color) Periphery â fatty changes (light color) |
Gamma Gandi Bodies | Right | Spleen | Venous congestion |
Heart Failure Cells/ Hemosiderin Laden macrophage | Left | lungs | Macrophages that have engulfed hemosiderin (iron-containing pigment). |
BRUGADA SYNDROME



- Brutal (Brugada) scene (SCN5A)
- guy like me (pseudo RBB) â drinking soda (Na channelopathy)
- sudden seizure and death ()
- Loss-of-function SCN5A
- Pseudo-RBBB
- AD
- Etiology:
- Channelopathy: Na channel.
- S2 elevation: No channel.
- Risk:
- Can lead to sudden cardiac death.
- Clinical Features (C/F:):
- Syncope.
- Seizure mimic.
- ECG findings:
- V1, V2: Coved S2 elevation.
- V1 - Vâ: STE + incomplete RBBB.
- Treatment (Rx:):
- Intra cardiac Defibrillator.
Revise Epilepsy
Epilepsy | Characteristic EEG |
GTCS | DOC ⢠Phenytoin, Valproate |
Absence / Petit mal | ⢠Spike & wave (dome) pattern ⢠3 Hz spikes DOC ⢠Ethosuximide, Valproate ⢠Absent? â Ethuvo ? (Ethosuximide) |
Infantile spasms | ⢠Hypsarrhythmia Age ⢠< 1 years DOC ⢠without tuberous sclerosis: ACTH, Prednisolone ⢠with tuberous sclerosis: Vigabatrin |
Juvenile myoclonic Epilepsy (Janz) | ⢠4â6 Hz polyspikes & slow wave discharge ⢠JME â JANZ S â 4-5 letters â 4 - 6 Hz polyspikes, slow Age ⢠10 - 19 years DOC ⢠Valproate |
Lennox Gastaut syndrome | ⢠Slow (<3 Hz) spike wave complex ⢠LGS â < 3Hz spike complex DOC ⢠Valproate, Lamotrigine |
Hepatic encephalopathy | ⢠Triphasic wave {- wave â +ve wave â - wave} |
1. SSPE â 8 years age 2. HIE 3 3. Comatose â (drug/severe hypothermia) | ⢠Burst suppression |
Prion disease (Kuru) | ⢠Periodic sharp wave complexes Age ⢠35 years |
HSV encephalitis | ⢠Periodic lateralized epileptiform discharge ⢠Affects temporal lobes ⢠DOC: IV Acylovir ⢠HSV â His Wife â Like temples (Period late) |
SSLC / SCENE Genes
SCN/SLC | Disease | Features |
SLC6A19 | Hartnupâs Disease (Chr 5) 6 days Hearty trip | ⢠Defect of tryptophan transporter ⢠Cutaneous photosensitivity (m/c symptom) ⢠Obermeyer test â indoxyl in urine Accumulation of tryptophan in intestine â bacterial decomposition â indoxyl compounds â Indoles absorbed â excreted in urine as indoxyl sulfateâ bluish discoloration of diaper |
SLC2A1 | GLUT 1 defect SSLC â 2 times â bcz brain hypoglycemia | â CSF glucose â seizures âł Rx: Pure ketogenic diet |
SCN1A | Dravet syndrome âł defective Nav1.1 Na channel âł â GABA | Seizures âł DOC: Valproate |
SCN5A (Loss of function) | Brugada syndrome âł defective Cardiac Na channel 1 Dragon drank 5 Bru | Brutal (Brugada) scene (SCN5A) guy like me (pseudo RBB) â drinking soda (Na channelopathy) â sudden seizure and death () Broad P wave â Long PQ seg â raised J point â coved ST â T inversion |
SCNN1B/G genes | Liddle Syndrome ⳠDefect: ENaC channel | ⢠AD inheritance ⢠Hypertension + Pseudoaldosteronism ⢠Hypokalemic metabolic alkalosis |
Anti GM1 Antibody | Guillain Barre Syndrome (AIDP) | ⢠Albumino-cytological dissociation ⢠Earliest sign: Distal areflexia. ⢠Bladder and bowel spared. ⢠Bilateral ascending symmetrical flaccid paralysis. ⢠Brighton Criteria for GBS |
Anti GQ1 Antibody. | Miller Fisher Fish vangan Que nikkanam | Triad ⢠Ophthalmoplegia (3rd nerve palsy). ⢠Areflexia. ⢠Ataxia. |
anti P/Q antibody | Lambert Eaton Syndrome Eat 3, 4 Amino acid (3,4 aminopyridine) â gain strength â ââ response | ⢠Pre-junctional ââ release of Ach at NMJ ⢠Oat cell cancer lung â Paraneoplastic ⢠Repetitive nerve stimulation test: âł Incremental response Treatment: ⢠DOC: 3,4 aminopyridine ⢠Pyridostigmine |
Cardiac Tumors

Most Common Cardiac Malignancy
- Metastasis (mets)Â (cancer spread from other body parts to heart).
Primary Cardiac Tumors (Within the Heart)
Category | Benign Tumor | Malignant Tumor |
In Adults | Myxoma | Angiosarcoma |
In Children | Rhabdomyoma | Rhabdomyosarcoma |
Details of Specific Primary Tumors
Feature | Myxoma | Rhabdomyoma |
Age Group | Adults | Children |
Location | Most commonly Left Atria | Most commonly Left Ventricle |
Gross Appearance | Gelatinous mass | ă
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Cells | Lepidic cells | Spider cells (look like spider webs) |
Cellular Content | ă
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Associated with | Carney complex, GNAS mutations (Mccune Albright), LAMB mutation | Tuberous Sclerosis (TSC) |
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GNAS | ⢠Mccune Albright ⢠Cardiac Myxoma |
GNAS 1 | ⢠Pseudohypoparathyroid/ Albright Hereditary Osteodystrophy |
GNAQ | ⢠Sturge Weber (Sporadic) |
Mnemonic:
- Rhabdomyoma â Rat (Rhabdomyoma) and Spider (spider cells) in a Pasta (PAS positive) tube (Tuberous sclerosis)
- Myxoma â Mixed in Los Angles (Left atrium) â Leopard (Lepidic) Kaarnnu (Carney) Nashipich (gNAS)

- Most Common Cardiac Valve Tumor:
- Papillary Fibroelastoma (PFE).
- Appearance: Many papillary projections â "sea anemone-like appearance".
ACUTE RHEUMATIC FEVER
- Roomatic fever
- Vijayan â Jai Vigyan
- Marginal ds (Erythema marginatum)
- Carry and Oomb in Middle of room â Carey coomb murmur
- Give mouth like a fish in her button hole (Fish mouth/Button hole stenosis)
- Show ass everywhere (Aschoff bodies â All layers â max in myocardium), Apply some butter (bread and butter â fibrinous pericarditis)
- Do Per Rectal (Prolonged PR)
- Buy benz (Benzathine Penicillin) & Get 12 lakh every 3 weeks () (for adults)
Etiology and Pathogenesis
- Etiology:
- Post streptococcal disorder
- Group A β hemolytic streptococci (Strains: 1, 3, 5, 6, 18)
- Age: School-going children (5-15 years).
- Incidence:Â m = F.
Pathogenesis:
- Pharyngitis
- 10 days to few weeks
- Type II hypersensitivity reaction (antibody mediated).
- Streptococcal M-protein cross reacts withÂ
- glycoprotein in heart and joints
- molecular mimicry
Affected Valves
- Most common valve affected:Â
- mitral valve.
- Least common valve affected:Â
- Pulmonary valve.
- Mitral valve (F > m) > Aortic valve (m > F).
Presentations
- Acute RHD:Â
- mitral regurgitation.
- Chronic RHD:Â
- mitral stenosis.
LAE/Mitral stenosis:


- Straightening of left heart border (Image 1).
- Splaying of carinal angle.
- Double density sign/ double right heart border sign (Image 2).
- Walking man sign:
- lateral chest x-ray (Image 3).
- Left atrium cause elevation of left bronchus

- Third Mogul sign (Image 4):
- Prominent third Mogul
- because of left atrium.
- Dysphagia
- Left atrium â Esophageal compression (Image 5)
- Trans esophageal echocardiography (TEE) is done.
Chamber Enlargement Signs
- RVH: Apex up.
- LVH: Apex down and out.

Revised Jones Criteria
Major Criteria (J.O.N.E.S)
- Joint Arthritis:Â
- Monoarthritis / Polyarthritis / Polyarthralgia
- Migratory polyarthritis:
- Involving large joints.
- Non-erosive.
- Excellent response to aspirin.
- Complete recovery (No residual joint damage)
- DONT include MONOARTHRALGIA
- Pancarditis:
- Clinical
- Subclinical (ECHO Findings+)
- Subcutaneous nodules.
- Painless.
- Erythema marginatum.
- Most common & earliest manifestation.
- Raised rash, sparing the face.
- Transient
- Sydenham's chorea.
- DOC: Haloperidol
Essential Criteria
- â ASO titre.
- Throat swab positive for streptococci:
- Risk of false positive/negative â not preferred.
- History of preceding sore throat (< 50%).
Diagnosis

- All cases require Essential criteria.
- First Episode:
- 2 major criteria OR
- 1 major + 2 minor criteria
- Recurrence:
- 2 major criteria OR
- 1 major + 2 minor criteria OR
- 3 minor criteria
- Mnemonic: Jones â JO â start from 2 major criteria
Pancarditis
- Early finding (within 2 weeks).
- Most serious:Â
- Permanent damage of valves can occur.
- Most common feature of ARFÂ
Pericardium:

Fibrinous pericarditis


- Pericarditis: chest pain + frictional rub.
- Deposition of fibrinous exudate between the layers of pericardium.
- Appearance:Â Bread and butter appearance.
Myocardium:Â

- Aschoff bodies.
- Pathognomonic of RHD.
- Seen in all layers.
- Maximum in myocardium.
- Components:
- Anitschkow
- AKA caterpillar cells.
- Macrophages with slender wavy ribbon-like nuclei.
- Fibrinoid necrosis.
- Inflammatory cells.
Types of valvulitis:
Mitral valvulitis:
- Carey coombs murmur (delayed diastolic murmur).
- CC murmur â DD murmur
Mitral regurgitation:
- In acute RHDÂ
- Soft Sâ
- Pan systolic murmur.
- Hemodynamic overload â LVF (morbidity/mortality in ARF).
Mitral Stenosis
- In chronic RHDÂ
- fibrosis & calcifications of MV.
- Loud Sâ
- Fish mouth/Button hole stenosisÂ
Subendocardial Jets / McCallum Plaques
- Thickening of left atrial wall due to mitral regurgitation.
Mitral Valve Thickening / Commissural Fusion
- Shortening & thickening of chorda tendinae.

Treatment & Prophylaxis
Treatment:
- Bed rest for 2 weeks.
Penicillin:
- Benzathine Penicillin G:
- >Â 30 kg:Â
- 1.2 million/ 12 lakh IU every 3 weeks.
- < 30 kg:Â
- 6 lakh IU every 2 weeks.
- Oral Penicillin V:Â
- 250 mg BD.
- If allergic to Penicillin:
- Erythromycin 250 mg BD.
Anti-inflammatory Medications
- For 12 weeks
- Steroids:
- Preferred (especially in cardiac problems).
- Oral Prednisolone:Â (12 weeks - 3/9)
- 2 mg/kg/day (max 60 mg/day) x 3 weeksÂ
- â Taper over 9 weeks.
- Aspirin:Â (12 weeks - 10/2)
- 90-120 mg/kg/day in 4 divided doses x 10 weeksÂ
- â Taper over next 2 weeks.
Duration of Prophylaxis

Scenario | Prophylaxis Duration |
No carditis | For next 5 years or till age 18, whichever is longer. |
Carditis (without Residual Heart Disease) | For next 10 years or till age 25, whichever is longer. |
Established Residual Heart Disease/ underwent surgery | Till age 40 (Ideal: Life long). |
Infective Endocarditis - Introduction

- Definition:
- Infection of valvular endocardium and mural endocardium.
- IE occurs on a damaged valve (native or prosthetic) or an intracardiac device.
- Predisposing Factors/Damage Types:
- Congenital:Â
- Mitral valve prolapse (MVP)Â is most common.
- Rare: ASD, MS, MVP without MR.
- Rheumatic:
- Often left-sided.Â
- Mitral valve >> Aortic valve.
- Degenerative:
- Aortic stenosis (in elderly).
- IV drug abuse:
- Often right-sided
- Tricuspid valve affected.
- Common Locations:
- Left-sided IEÂ (75%):
- Mitral Valve commonly involved.
- Right-sided IEÂ (10%):
- In IV drug abusers (Tricuspid valve affected).
- Mixed: 15%.
- Other General Notes:
- MC congenital heart lesion:Â
- VSD.
- IV catheters in CKD patients can lead to IE.
- Mitral valve involvement:Â
- MVP +MR
Pathogenesis
Endothelial Injury on Damaged Valve
â
Fibrin and Platelet Thrombi
- Non-bacterial thrombotic endocarditis (NBTE)
/ Cachectic-marantic Endocarditis
â
Mucosal Injury:
- Dental procedures, Abscess.
- Traumatic mucosal erosion, incisional Biopsy.
- Tonsillectomy/Adenoidectomy.
- IJV catheter insertion in CKD patients etc.
â
Bacteremia
â
Vegetations formation
Acute vs. Subacute IE
Feature | Acute IE | Subacute IE |
Prognosis | 100% Fatal (if untreated) | Most commonly seen IE |
Presentation | Acute Febrile illness | Fever, Chills, Anorexia (over 2 weeks) |
Valvular damage | Complete valvular destruction | ă
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Underlying Cause | Sepsis | ă
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Features (primarily in Subacute IE)
- New onset murmur or worsening of murmur.
- Arterial embolization:
- Stroke, mesenteric ischemia, acute coronary syndrome.
- Clubbing and Splenomegaly.
Complications
- Heart Failure:
- New onset
- Due to valvular insufficiency.
- Embolization:
- ACS, Stroke.
- Perivalvular Abscess:
- Conduction Abnormalities orÂ
- persistent fever with a lesion near the aortic valve.
- Right-sided IE Specific Complications
- Common in IV drug abusers.
- Fever + Septic Pulmonary Emboli.
- Right heart failure, Pulmonary abscess
- Mycotic aneurysm of pulmonary artery.
Diagnosis (Duke's Criteria)
- 2 major ORÂ
- 1 major plus 3 minor ORÂ
- 5 minor criteria.
Situation | Most Common Organism | Notes |
Common Causes | Streptococci viridans, Staphylococcus Aureus, Enterococci | ă
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Prosthetic Valve IE (After 1st year) | Streptoccocus viridans | ă
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Prosthetic Valve IE (1st year post-replacement) | CoNSÂ (Staphylococcus Epidermidis) | 85% of cases |
IV Drug Abusers | Staphylococcus Aureus | 70%, affects Tricuspid valve (Right-sided IE) |
Native Valve IE | Staphylococcus Aureus | Including MRSA |
Major Criteria
1. Blood Culture:
- 3 sets from 3 sites.
- Each set 20 ml (1 aerobic / 1 anaerobic) over 30 min apart
- Out of which â 1 central sample
- Repeat cultures every 12 to 24 hours.
- Positive Culture
- Typical Organisms:
- Positive in âĽ2 site enough.
- Atypical Organisms:
- Persistently positive (even after 18-24 hours).
- Coxiella Burnetii:
- Single Sample positive ORÂ
- PCR positive.
- IFA for Bartonella for IgG and IgM
2. Involvement of heart valves
- Echocardiogram Findings:
- TEEÂ >>Â TTE.
- Vegetations.
- Abscess.
- New onset AR or MR.
- New partial dehiscence of the prosthetic valve.
- Indications for TEE:
- Prosthetic valves.
- Cardiac implantable electrical device.
- Myocardial abscess.
- Valvular perforation.
- Vegetations <3mm.
- Presence of Intracardiac Fistula.
- Cardiac CT
- FDG PET
- Direct visualisation during heart surgery
Minor Criteria

- Predisposing Heart disease.
- Fever ⼠38°C.
- Vascular phenomena:
- Major emboli
- Splenomegaly
- Clubbing
- Micro-embolization
- Petechiae:
- Most common.
- Found on palpebral conjunctiva, buccal & palatal mucosa, extremities.
- Splinter/Subungual Haemorrhages:
- Dark red, linear or flame-shaped streaks.
- Located in proximal nail bed.
- Janeway lesion
- Non-tender, small, erythematous macular or nodular lesions
- soles or palms.

- Blood culture not meeting major criteria.
- Immunological complications
- Immunological phenomenon
- Oslers ( Oh... painful đ hand, Made into Pulp)
- Painful, red nodules on pulp of fingers and toes.
- Immune Complex mediated.
- rOths spot
- Seen in fundus with pale center (Fibrin plug).
- Caused by retinal endothelial vasculitis
- GlomerulOnephritis syndorme
- Infective endocarditis
- Acute leukemia


Roth spot seen in

Other Laboratory Tests
- Anemia.
- WBC count increased in acute IE.
- Thrombocytopenia is rare.
- ESR elevated in all patients.
- Rheumatoid factor ââ in 50% (Immunological).
- MPGN
Treatment
Antibiotic Regimens
Organism/Situation | Antibiotic Regimen | Duration |
Streptococcus viridians | Penicillin G 2-4 MU Q4h OR Ceftriaxone 2g IV OD | 4 weeks |
Enterococci (Penicillin susceptible) | Penicillin G 4-6 MU Q4h + Gentamicin 1mg/kg IV TDS | 4-6 weeks |
Enterococci (Penicillin Resistant) | Vancomycin 15mg/kg IV BD + Gentamicin 1mg/kg IV TDS | ă
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MRSA (Native valve IE) | Vancomycin 15mg/kg IV BD | 6 weeks |
MRSA (Prosthetic valve IE) | Vancomycin 15mg/kg IV BD + Gentamicin 1mg/kg IV TDS + Rifampicin 300mg orally TDS | 2 weeks (Gentamicin); 6 weeks (Vanc, Rif) |
Culture Negative IE | Vancomycin + Gentamicin | ă
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Culture Negative IE (HACEK group) | Ceftriaxone + Gentamicin | Organisms don't grow in normal culture media |
Surgery Indications
- Native Valve IE:
- Acute AR or MR with evidence of increased filling pressure.
- Fungal Endocarditis.
- Acute valve stenosis or regurgitation with Heart Failure.
- Complicated by heart block, annular or aortic abscess.
- Prosthetic Valve IE:
- Heart failure.
- Dehiscence.
- Increasing obstruction/worsening regurgitation.
Secondary Prophylaxis (To prevent further episodes/carditis):
- PROPHYLAXIS NOT NEEDED IN ASD
- Dental procedures.
- Invasive procedures:Â
- Tonsillectomy, Adenoidectomy.

Prophylaxis Regimen
- Sensitive to Penicillin:
- Amoxicillin 2g orally 30-60 min before surgery.
- Unable to take oral meds:
- Ampicillin 2g IV or IM. OR
- Ceftriaxone 1g IV or IM.
- Allergic to Penicillin:
- Oral cephalexin 2g.
- Oral clindamycin 600 mg.
- Oral azithromycin 500mg.
- Allergic to Penicillin + Unable to take oral meds:
- Clindamycin 600mg IV or IM.

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