MD Medicine University Examination - Comprehensive Notes
Topics 9-17 | Cardiology
Q.9 - HFpEF (Heart Failure with Preserved Ejection Fraction) (6 marks - Short Note)
Definition
HFpEF = Heart failure with LVEF ≥ 50%, impaired diastolic filling, elevated LV filling pressures, and symptoms/signs of HF. Previously called "diastolic heart failure."
Key Features (Mnemonic: HOAFS)
| Feature | Detail |
|---|
| Hemodynamic | Elevated LVEDP/PCWP at rest or with exertion; normal LVEF |
| Obesity/Comorbidities | HTN, DM, obesity, CKD, AF, sleep apnea |
| Age/Sex | Older women predominantly |
| Fibrosis | LV hypertrophy, concentric remodeling, myocardial fibrosis |
| Symptoms | Dyspnea on exertion, fatigue, fluid retention |
Pathophysiology
HTN / DM / Obesity / Aging
↓
Systemic inflammation + oxidative stress
↓
Coronary microvascular endothelial dysfunction
↓
Cardiomyocyte hypertrophy + interstitial fibrosis
↓
Impaired LV relaxation (↑tau) + ↑LV stiffness
↓
↑LVEDP → ↑LA pressure → Pulmonary congestion
↓
HFpEF syndrome
Diagnosis (H2FPEF Score / ESC Criteria)
- Echocardiography: LVEF ≥50%, diastolic dysfunction (Grade II-III), E/e' ratio >14
- BNP/NT-proBNP: Elevated (though lower than HFrEF)
- Exercise testing: PCWP rises with minimal exertion
Treatment
| Category | Drug/Intervention |
|---|
| Proven benefit | SGLT2 inhibitors (empagliflozin, dapagliflozin) - ↓HF hospitalization |
| Diuretics | For congestion relief (symptomatic) |
| Comorbidity control | Aggressive HTN/DM/AF/obesity management |
| Exercise training | Improves functional capacity |
| Ineffective | ACEi, ARB, beta-blockers (no mortality benefit proven) |
| Avoid | PDE5 inhibitors (multiple RCTs negative) |
Key: EMPEROR-Preserved and DELIVER trials (2021-2022) established SGLT2i as first therapy with proven benefit in HFpEF.
Q.10 - Infective Endocarditis: Etiology, Diagnosis & Treatment (20 marks - Long Answer)
Definition
Microbial infection of the endocardial surface (valves or mural endocardium) characterized by vegetations composed of fibrin, platelets, and microorganisms.
Epidemiology
- Incidence: 3-10/100,000 person-years
- Mortality: ~25% at 6 months despite therapy
- Changing epidemiology: older patients, healthcare-associated IE, IVDA-related
ETIOLOGY
Predisposing Cardiac Lesions
| Risk | Examples |
|---|
| High | Prosthetic valve, prior IE, unrepaired cyanotic CHD |
| Moderate | Rheumatic HD, bicuspid aortic valve, MVP with regurgitation |
| Low/Negligible | ASD (secundum), repaired CHD, coronary artery disease |
Causative Organisms
┌────────────────────────────────────────────────────────┐
│ ORGANISMS IN IE │
│ │
│ Native Valve IE │
│ ├── Streptococcus viridans (30-40%) ← Oral/dental │
│ ├── Staph. aureus (25-30%) ← Skin, IVDA │
│ ├── Enterococcus (5-10%) ← GI/GU procedures │
│ ├── Strep. bovis (S. gallolyticus) ← Colon Ca assoc. │
│ └── HACEK organisms ← Slow-growing gram-neg │
│ │
│ Prosthetic Valve IE │
│ ├── Early (<60 days): CoNS, Staph. aureus, Gram-neg │
│ └── Late (>60 days): Like native valve │
│ │
│ IVDA-associated │
│ └── Staph. aureus >> tricuspid valve │
└────────────────────────────────────────────────────────┘
Pathogenesis
Bacteremia (dental/GI/GU/skin procedure or IVDA)
↓
Bacteria adhere to damaged endothelium (non-bacterial thrombotic endocarditis)
↓
Colonization → Vegetation formation (fibrin + platelets + organisms)
↓
Destruction of valve leaflets + embolic phenomena
DIAGNOSIS - Modified Duke Criteria
Major Criteria
- Positive blood cultures (≥2 separate cultures with typical IE organisms, OR persistent bacteremia)
- Evidence of endocardial involvement:
- Echo: oscillating vegetation, abscess, new dehiscence of prosthetic valve
- New valvular regurgitation
Minor Criteria
- Predisposing heart condition or IVDA
- Fever ≥38°C
- Vascular phenomena (emboli, Janeway lesions, mycotic aneurysm, conjunctival hemorrhage)
- Immunologic phenomena (Osler nodes, Roth spots, RF positive, GN)
- Microbiological evidence (positive culture not meeting major criteria)
Classification
| Classification | Criteria |
|---|
| Definite IE | 2 major; OR 1 major + 3 minor; OR 5 minor |
| Possible IE | 1 major + 1 minor; OR 3 minor |
| Rejected | Firm alternate diagnosis; resolution with <4 days antibiotics |
Clinical Features
MANIFESTATIONS OF IE
├── Constitutional: Fever, chills, malaise, weight loss
├── Cardiac: New murmur, changing murmur, heart failure, abscess
├── Embolic: Stroke, splenic/renal infarcts, PE (right-sided)
├── Vascular phenomena:
│ ├── Janeway lesions - painless hemorrhagic macules (palms/soles)
│ ├── Petechiae
│ ├── Splinter hemorrhages
│ └── Mycotic aneurysms
└── Immunologic phenomena:
├── Osler nodes - PAINFUL nodules (pulp of fingers) - immune complex
├── Roth spots - oval hemorrhages with pale center (retina)
└── Glomerulonephritis
Investigations
| Test | Findings |
|---|
| Blood cultures | 3 sets from different sites before antibiotics |
| Echo (TTE) | First line: sensitivity ~50-60% for vegetations |
| Echo (TOE) | Gold standard: sensitivity ~90-95%; mandatory for prosthetic valve, equivocal TTE, suspected abscess |
| CBC | Leukocytosis, normocytic anemia |
| ESR/CRP | Elevated |
| Urinalysis | Hematuria, proteinuria (GN) |
| CT/PET-CT | For embolic complications, abscesses |
TREATMENT
General Principles
- Start antibiotics after 3 blood cultures (within 1-2 hours if hemodynamically unstable)
- Prolonged parenteral therapy (4-6 weeks for native valve; 6 weeks for prosthetic)
- Multidisciplinary team: ID + Cardiology + Cardiothoracic surgery
Antibiotic Regimens
Streptococcus viridans (penicillin-sensitive: MIC <0.125 mg/L)
- Penicillin G 12-18 MU/day IV x 4 weeks; OR
- Ceftriaxone 2g IV OD x 4 weeks; ± Gentamicin for 2 weeks (short-course)
Staphylococcus aureus (MSSA - Native Valve)
- Nafcillin/Oxacillin 2g IV q4h x 6 weeks
MRSA
- Vancomycin 15-20 mg/kg IV q8-12h x 6 weeks; OR
- Daptomycin 8-10 mg/kg IV OD
Enterococcus
- Ampicillin + Gentamicin x 4-6 weeks (combination essential)
Surgical Indications
INDICATIONS FOR SURGERY IN IE
├── URGENT (same admission):
│ ├── Heart failure due to valve dysfunction
│ ├── Perivalvular extension (abscess, fistula)
│ ├── Uncontrolled infection (enlarging vegetation, persistent bacteremia)
│ └── Fungal or highly resistant organisms
└── PROPHYLACTIC (before discharge):
└── Vegetation >10mm with high embolic risk
Prophylaxis
- Indicated for high-risk patients undergoing dental procedures
- Drug: Amoxicillin 2g PO 30-60 min before procedure
- Clindamycin 600mg if penicillin-allergic
- NOT recommended for GI/GU procedures routinely
Q.11 - Pulmonary Hypertension: Definition, Classification, Diagnosis & Management of PAH (20 marks)
Definition
Pulmonary hypertension = Mean Pulmonary Arterial Pressure (mPAP) ≥ 20 mmHg at rest on right heart catheterization (updated 2022 ESC/ERS guidelines; previously >25 mmHg).
Pulmonary Arterial Hypertension (PAH) = mPAP ≥20 mmHg + PAWP ≤15 mmHg + PVR ≥2 Wood Units (pre-capillary PH).
CLASSIFICATION (Dana Point/Nice Classification - 5 Groups)
┌────────────────────────────────────────────────────────────┐
│ WHO CLASSIFICATION OF PULMONARY HYPERTENSION │
│ │
│ GROUP 1 - Pulmonary ARTERIAL Hypertension (PAH) │
│ ├── Idiopathic PAH (IPAH) │
│ ├── Heritable PAH (BMPR2, ALK1, SMAD9, CAV1, KCNK3) │
│ ├── Drug/toxin-induced (anorexigens, methamphetamine) │
│ └── Associated PAH: CTD, HIV, portal HTN, CHD, │
│ Schistosomiasis │
│ │
│ GROUP 2 - PH due to LEFT HEART DISEASE (most common) │
│ ├── HFpEF, HFrEF │
│ └── Valvular HD, congenital/acquired obstruction │
│ │
│ GROUP 3 - PH due to LUNG DISEASE/HYPOXIA │
│ ├── COPD, ILD, sleep-disordered breathing │
│ └── Developmental lung disorders │
│ │
│ GROUP 4 - Chronic THROMBOEMBOLIC PH (CTEPH) │
│ └── Potentially curable by pulmonary endarterectomy │
│ │
│ GROUP 5 - PH with UNCLEAR/MULTIFACTORIAL mechanisms │
│ └── Sarcoidosis, metabolic disorders, hematologic │
└────────────────────────────────────────────────────────────┘
Pathophysiology of PAH
Genetic predisposition (BMPR2 mutation in 70% heritable PAH)
+
Environmental triggers (drugs, infection, inflammation)
↓
Endothelial dysfunction
├── ↓ Prostacyclin (PGI2) - vasodilator, antiproliferative
├── ↓ NO production
└── ↑ Endothelin-1 - vasoconstrictor, mitogenic
↓
Pulmonary vasoconstriction
+ Smooth muscle hypertrophy/hyperplasia
+ In-situ thrombosis
+ Plexiform lesions (pathognomonic)
↓
Progressive ↑PVR → RV pressure overload
↓
RV hypertrophy → RV dilation → RV failure → Death
WHO Functional Classification (FC)
| Class | Description |
|---|
| FC I | No limitation; ordinary activity causes no symptoms |
| FC II | Slight limitation; comfortable at rest; ordinary activity causes dyspnea/fatigue |
| FC III | Marked limitation; comfortable at rest; less than ordinary activity causes symptoms |
| FC IV | Inability to carry out any activity; symptoms at rest; signs of right heart failure |
DIAGNOSIS
Clinical Features
- Dyspnea on exertion (most common), fatigue, syncope, chest pain
- Signs: Loud P2, RV heave, TR murmur, JVP elevation, pulsatile liver, peripheral edema, ascites
Diagnostic Algorithm
SUSPECTED PH
↓
Echocardiography (screening)
│ ├── Low probability: sPAP <36, no other signs
│ ├── Intermediate: sPAP 36-50 or signs present
│ └── High probability: sPAP >50 or multiple signs
↓
Further investigations:
├── ECG: RV strain, RBBB, right axis deviation
├── CXR: Enlarged main PA, pruning of peripheral vessels, cardiomegaly
├── PFTs + ABG: Rule out Group 3
├── V/Q scan: Rule out CTEPH (Group 4)
├── CT thorax: ILD, emphysema
├── Serology: ANA, anti-Scl70 (CTD-PAH), HIV, LFTs
└── 6-Minute Walk Test (6MWT): functional assessment
↓
RIGHT HEART CATHETERIZATION (Gold Standard - MANDATORY before starting PAH therapy)
├── mPAP ≥20 mmHg
├── PAWP ≤15 mmHg (pre-capillary)
├── PVR ≥2 Wood Units
└── Vasoreactivity testing (inhaled NO) - for IPAH only
└── Positive: ↓mPAP ≥10 mmHg to <40 mmHg → CCB responder
Investigations Summary
| Investigation | Finding/Purpose |
|---|
| Echo | Screening; TAPSE <18mm (RV dysfunction) |
| RHC | Diagnostic gold standard; hemodynamic profile |
| CT-PA | Pulmonary emboli, parenchymal disease |
| V/Q scan | CTEPH (more sensitive than CT-PA for chronic thrombi) |
| 6MWT | Prognosis and therapy monitoring |
| BNP/NT-proBNP | Severity marker; RV stress |
| Cardiac MRI | RV structure and function |
MANAGEMENT
General Measures
- Avoid pregnancy (high mortality - WHO Class IV contraindication)
- Avoid excessive physical exertion; supervised exercise training
- Supplemental O2 (maintain SpO2 >90%)
- Anticoagulation: Warfarin for IPAH (controversial; not for CTD-PAH)
- Diuretics for RV failure
- Digoxin for RV failure with AF
PAH-Specific Therapy (3 Pathways)
┌────────────────────────────────────────────────────────────┐
│ PAH SPECIFIC DRUG PATHWAYS │
│ │
│ 1. PROSTACYCLIN PATHWAY (↑cAMP) │
│ ├── IV: Epoprostenol (Flolan) - Gold standard; FC IV │
│ ├── SC: Treprostinil │
│ ├── Inhaled: Iloprost, Treprostinil │
│ └── Oral: Selexipag (IP receptor agonist) │
│ │
│ 2. ENDOTHELIN PATHWAY (block ET-1) │
│ ├── Bosentan (dual ERA - ETA+ETB) │
│ ├── Ambrisentan (selective ETA) │
│ └── Macitentan (dual ERA, better outcomes) │
│ │
│ 3. NO-cGMP PATHWAY │
│ ├── PDE5 inhibitors: Sildenafil, Tadalafil │
│ └── sGC stimulators: Riociguat │
│ (do NOT combine riociguat + PDE5i) │
└────────────────────────────────────────────────────────────┘
Risk Stratification and Treatment Algorithm
Initial Assessment
↓
LOW RISK (FC I-II, good 6MWT, normal RV)
→ Oral combination: ERA + PDE5i (e.g., Ambrisentan + Tadalafil)
INTERMEDIATE RISK (FC II-III)
→ Dual oral combination; reassess at 3-6 months
→ If inadequate: triple therapy (add prostanoid)
HIGH RISK (FC IV, low 6MWT, pericardial effusion, RV failure)
→ IV Epoprostenol (gold standard) + oral combination
→ List for lung/heart-lung transplantation
Calcium Channel Blockers
- Only for vasoreactive responders on RHC testing
- Drugs: Nifedipine (high dose), Diltiazem, Amlodipine
- NOT for non-responders (can worsen outcome)
Interventional / Surgical
- Balloon Atrial Septostomy (BAS): Palliative; creates R-to-L shunt; reduces RV preload
- Pulmonary Endarterectomy: Potentially curative for Group 4 (CTEPH)
- Balloon Pulmonary Angioplasty: Inoperable CTEPH
- Lung/Heart-Lung Transplantation: Refractory PAH; last resort
Q.12 - Narrow QRS Tachycardia & Its Management (6 marks - Short Note)
Definition
Narrow QRS tachycardia = HR >100 bpm with QRS duration <120 ms, implying supraventricular origin (conduction via normal His-Purkinje system).
Classification
NARROW QRS TACHYCARDIA
├── REGULAR
│ ├── Sinus tachycardia
│ ├── AVNRT (AV Nodal Reentrant Tachycardia) - MOST COMMON SVT
│ ├── AVRT (AV Reciprocating Tachycardia) - WPW
│ ├── Atrial tachycardia (focal)
│ ├── Atrial flutter with regular block (2:1, 3:1)
│ └── Junctional tachycardia
└── IRREGULAR
├── Atrial fibrillation (most common irregular)
├── Atrial flutter with variable block
└── MAT (Multifocal atrial tachycardia)
ECG Features of Common SVTs
| Arrhythmia | Rate | P waves | RP interval |
|---|
| AVNRT (typical) | 150-250 | Buried in QRS or pseudo-r' in V1 | Short RP (<70ms) |
| AVRT (orthodromic) | 150-250 | Inverted P after QRS | Short RP |
| Atrial tachycardia | 100-250 | P before QRS (abnormal axis) | Long RP |
| Atrial flutter | 250-350 (atrial) | Saw-tooth (negative II,III,aVF) | Regular 2:1 |
Management Algorithm
NARROW QRS TACHYCARDIA
↓
HEMODYNAMICALLY UNSTABLE?
├── YES → SYNCHRONIZED DC CARDIOVERSION immediately (50-200J biphasic)
│
└── NO → Assess regularity
↓
REGULAR:
Step 1: VAGAL MANEUVERS (Valsalva, carotid sinus massage)
↓ If fails
Step 2: IV ADENOSINE 6mg rapid bolus (then 12mg if needed)
↓ If fails
Step 3: IV Verapamil 5-10mg OR Diltiazem
OR Beta-blockers (metoprolol IV)
↓ If fails
Step 4: Synchronized cardioversion
IRREGULAR (likely AF):
→ Rate control: Beta-blocker or Diltiazem
→ Anticoagulation assessment (CHA2DS2-VASc)
→ Rhythm control if indicated
Long-Term Management
- Radiofrequency catheter ablation: Definitive treatment for AVNRT, AVRT, focal AT (>90% success)
- Long-term antiarrhythmics: Beta-blockers, Flecainide, Propafenone (for recurrent SVT refusing ablation)
Note: Adenosine is the drug of choice for acute termination of AVNRT/AVRT. It works by transiently blocking AV nodal conduction.
Q.13 - ARNI (Angiotensin Receptor-Neprilysin Inhibitor) (Short Note)
Mechanism of Action
ARNI = Sacubitril/Valsartan (LCZ696) = Sacubitril (neprilysin inhibitor) + Valsartan (ARB)
DUAL MECHANISM:
┌─────────────────────────────────────────────────────────┐
│ SACUBITRIL (Prodrug → Sacubitrilat) │
│ ↓ │
│ Inhibits NEPRILYSIN │
│ ↓ │
│ ↓ Degradation of natriuretic peptides (BNP, ANP, CNP) │
│ ↓ Degradation of bradykinin │
│ ↓ │
│ ↑ Natriuresis, vasodilation, ↓ fibrosis, ↓ RAAS │
│ │
│ VALSARTAN │
│ ↓ │
│ Blocks AT1 receptor │
│ ↓ │
│ ↓ Vasoconstriction, ↓ aldosterone, ↓ remodeling │
└─────────────────────────────────────────────────────────┘
Key Clinical Trial - PARADIGM-HF
- 8442 patients, HFrEF (LVEF ≤40%), NYHA II-IV
- Sacubitril/valsartan vs. enalapril
- Results: 20% relative risk reduction in cardiovascular death or HF hospitalization
- 16% reduction in all-cause mortality
- Better quality of life, fewer HF hospitalizations
Indications
- HFrEF (LVEF ≤40%): NYHA Class II-IV, already on stable ACEi/ARB
- HFpEF: PARAGLIDE and PARAGON-HF trials - modest benefit; considered for LVEF in lower-normal range (40-60%)
Dosing
- Starting dose: Sacubitril/Valsartan 24/26 mg BD (if naive or low BP)
- Target dose: 97/103 mg BD
- Must washout ACEi for 36 hours before starting (risk of angioedema)
Side Effects & Contraindications
| Side Effect | Important Points |
|---|
| Hypotension | Most common; start at low dose |
| Angioedema | 2-3x more common than ACEi (due to bradykinin accumulation via neprilysin inhibition) |
| Hyperkalemia | Monitor K+ |
| Renal impairment | Monitor creatinine |
| Contraindicated | With ACEi (concurrent); prior history of angioedema; pregnancy |
Place in HF Guidelines (2022 ESC)
- Class I recommendation for HFrEF - preferred over ACEi to reduce mortality
- Part of the "Fantastic Four" of HFrEF therapy: ARNI/ACEi + Beta-blocker + MRA + SGLT2i
Q.14 - Constrictive Pericarditis vs Restrictive Cardiomyopathy (20 marks)
Introduction
Both conditions cause diastolic heart failure with elevated filling pressures and normal/near-normal LVEF. Distinguishing them is critical because constrictive pericarditis is potentially surgically curable (pericardiectomy).
COMPARISON TABLE
| Feature | Constrictive Pericarditis | Restrictive Cardiomyopathy |
|---|
| Etiology | TB (commonest globally), viral pericarditis, post-cardiac surgery, post-radiation, connective tissue disease | Amyloidosis, sarcoidosis, hemochromatosis, Löffler's eosinophilic, idiopathic, post-radiation |
| Pathophysiology | Fibrotic, calcified pericardium limits diastolic filling | Myocardial disease causes ↑stiffness; filling restriction |
| Ventricular interdependence | MARKED (hallmark) - pericardial constraint couples ventricles | Absent or mild |
| Pericardium | Thickened (>4mm by CT/MRI), may be calcified | Normal thickness |
| Myocardium | Normal | Abnormal (infiltration, fibrosis) |
| Systolic function | Usually normal | Usually normal early; impaired late (esp. amyloid) |
CLINICAL FEATURES
| Feature | Constrictive Pericarditis | Restrictive Cardiomyopathy |
|---|
| History | Prior pericarditis, TB, cardiac surgery, radiation | Systemic disease (amyloid, sarcoid) |
| JVP | ↑↑ with Kussmaul's sign (JVP rises on inspiration) | ↑ with Kussmaul's sign (also present) |
| Pericardial knock | Present (early diastolic sound) | Absent |
| 3rd heart sound | Absent | May be present |
| Regurgitation | Rare | Common (esp. amyloid - bilateral AV valve involvement) |
| Peripheral edema, ascites | Prominent | Present |
| Cachexia | Common | Less common |
| AF | Common | Common (amyloid) |
INVESTIGATIONS
ECG
| Constrictive Pericarditis | Restrictive Cardiomyopathy |
|---|
| Voltage | May be low | Low voltage (esp. amyloid) - QRS voltage inversely proportional to amyloid infiltration |
| Conduction | Non-specific | AV block, bundle branch block (amyloid, sarcoid) |
| Pattern | Non-specific | Pseudo-infarct pattern (amyloid) |
Echocardiography
┌──────────────────────────────────────────────────────────────┐
│ ECHO DIFFERENTIATION │
│ │
│ Constrictive Pericarditis: │
│ • Pericardial thickening/calcification │
│ • Septal bounce ("interdependence") │
│ • Annulus REVERSUS: Septal e' > Lateral e' (reversed │
│ normal pattern - "annulus reversus") │
│ • E/e' normal or low (<15) │
│ • Significant respiratory variation in E velocity (>25%) │
│ • IVC dilated, non-collapsing │
│ │
│ Restrictive Cardiomyopathy: │
│ • Biatrial enlargement │
│ • Myocardial granular sparkling (amyloid) │
│ • Normal annular e' velocities pattern │
│ • E/e' markedly elevated (>15) │
│ • MINIMAL respiratory variation in E velocity │
│ • Thickened walls (amyloid: "bright speckled" pattern) │
└──────────────────────────────────────────────────────────────┘
CT/MRI (Key Differentiator)
| Constrictive Pericarditis | Restrictive Cardiomyopathy |
|---|
| CT | Pericardial thickening >4mm, calcification | Normal pericardium |
| Cardiac MRI | Pericardial enhancement (gadolinium), thick pericardium | Late gadolinium enhancement of myocardium (amyloid: subendocardial/diffuse; sarcoid: mid-myocardial; hemochromatosis: T2* signal loss) |
Cardiac Catheterization (Gold Standard for Hemodynamics)
┌──────────────────────────────────────────────────────────────┐
│ HEMODYNAMIC DIFFERENTIATION │
│ │
│ BOTH: "Dip and plateau" (square root sign) in RV/LV │
│ pressure tracing; ↑RA pressure │
│ │
│ Constrictive Pericarditis: │
│ • LVEDP = RVEDP (equalization of end-diastolic pressures) │
│ • Discordance of LV/RV pressures with respiration │
│ (LV ↑ on inspiration when RV ↓) - HALLMARK │
│ • RVSP usually <50 mmHg │
│ │
│ Restrictive Cardiomyopathy: │
│ • LVEDP > RVEDP (>5 mmHg difference) │
│ • Concordance of LV/RV pressures with respiration │
│ • RVSP often >50 mmHg │
└──────────────────────────────────────────────────────────────┘
Additional Tests
| Test | Finding |
|---|
| Serum amyloid/SPEP | Amyloid (light chains) |
| Ferritin/transferrin saturation | Hemochromatosis |
| ACE levels | Sarcoidosis |
| Congo Red staining (biopsy) | Amyloid (apple-green birefringence) |
| Endomyocardial biopsy | Definitive for RCM (e.g., amyloid fibrils) |
TREATMENT
| Constrictive Pericarditis | Restrictive Cardiomyopathy |
|---|
| Definitive | Pericardiectomy (surgical decortication) - potentially curative | No cure for most (treat underlying cause) |
| Medical | Diuretics (temporary); anti-TB for tuberculosis etiology | Diuretics; treat underlying (e.g., tafamidis for ATTR amyloid) |
| Prognosis | Good post-surgery if done early | Poor, especially amyloid |
Q.15 - Atrial Fibrillation: Etiopathogenesis & Management (20 marks)
Definition
Atrial fibrillation (AF) = Supraventricular arrhythmia characterized by uncoordinated atrial activation with consequent deterioration of atrial mechanical function. ECG: Absent P waves; irregularly irregular rhythm; fibrillatory baseline.
Classification
| Type | Definition |
|---|
| Paroxysmal AF | Self-terminating within 7 days (usually <48h) |
| Persistent AF | Lasting >7 days or requires cardioversion |
| Long-standing persistent | Continuous AF >12 months; rhythm control strategy chosen |
| Permanent AF | AF accepted; no further rhythm control attempts |
| First diagnosed AF | First detected episode (regardless of duration) |
ETIOPATHOGENESIS
Etiology (Mnemonic: PIRATES)
P - Pulmonary (PE, COPD, pneumonia)
I - Ischemic heart disease / Infarction
R - Rheumatic heart disease (mitral stenosis)
A - Alcohol ("Holiday heart syndrome"), Anemia
T - Thyrotoxicosis (most reversible cause)
E - Electrolyte abnormalities (hypokalemia, hypomagnesemia)
S - Sepsis, Surgery (post-cardiac), Sleep apnea, Sick sinus syndrome
+ Hypertension (most common underlying cause globally)
+ Heart failure
+ Idiopathic (lone AF - young patients, no structural disease)
Pathogenesis
TRIGGERS (ectopic foci → usually pulmonary veins)
+
SUBSTRATE (atrial remodeling)
↓
┌─────────────────────────────────────────────┐
│ PATHOGENESIS OF AF │
│ │
│ Triggers: Ectopic foci in pulmonary vein │
│ sleeves (90% of cases) │
│ ↓ │
│ Multiple wavelet hypothesis: │
│ Simultaneous propagation of multiple │
│ small re-entrant wavelets in atria │
│ ↓ │
│ Electrical remodeling: │
│ ↓ APD, ↓ Refractory period │
│ "AF begets AF" │
│ ↓ │
│ Structural remodeling: │
│ Atrial fibrosis, dilatation │
│ (substrate perpetuation) │
└─────────────────────────────────────────────┘
Consequences of AF
- Hemodynamic: Loss of atrial kick (15-20% reduction in CO); tachycardia-induced cardiomyopathy
- Thromboembolic: LA appendage thrombus → stroke (2-7x risk); AF causes 25% of strokes in elderly
- Symptoms: Palpitations, dyspnea, fatigue, presyncope
MANAGEMENT
Overview - "ABCD" Approach (ESC 2020 AF Guideline)
A - Avoid stroke (Anticoagulation - CHA2DS2-VASc)
B - Better symptom control (Rate or Rhythm control)
C - Cardiovascular risk factor management
D - Dynamic comorbidity assessment
1. ANTICOAGULATION (Stroke Prevention)
CHA2DS2-VASc Score
| Risk Factor | Score |
|---|
| Congestive heart failure | 1 |
| Hypertension | 1 |
| Age ≥75 | 2 |
| Diabetes mellitus | 1 |
| Stroke/TIA (prior) | 2 |
| Vascular disease (prior MI, PAD, aortic plaque) | 1 |
| Age 65-74 | 1 |
| Sex category (female) | 1 |
- Score 0 (men) / 1 (women): No anticoagulation
- Score 1 (men): Consider anticoagulation
- Score ≥2 (men) / ≥3 (women): Anticoagulate (OAC)
Choice of Anticoagulant
- NOACs preferred over Warfarin: Dabigatran, Rivaroxaban, Apixaban, Edoxaban
- Warfarin (INR 2-3): If valvular AF (mitral stenosis, mechanical prosthetic valve) - NOACs contraindicated
- HAS-BLED score: Assess bleeding risk (not a reason to withhold anticoagulation if score <3)
2. RATE CONTROL
Targets
- Lenient control: Resting HR <110 bpm (equally effective as strict control - RACE II trial)
- Strict control: Resting HR <80 bpm (if symptomatic with lenient control)
Drugs
| Drug | Route | Use |
|---|
| Beta-blockers (metoprolol, bisoprolol, carvedilol) | Oral/IV | First line, especially with HFrEF |
| Diltiazem/Verapamil | Oral/IV | Effective; avoid in HFrEF (negative inotropy) |
| Digoxin | Oral/IV | Add-on therapy; useful in HF, sedentary patients; less effective during exercise |
| Amiodarone | IV/Oral | Refractory cases; also has rhythm control properties |
3. RHYTHM CONTROL
Cardioversion
AF CARDIOVERSION
├── PHARMACOLOGICAL:
│ ├── Flecainide or Propafenone (no structural HD) - "pill-in-pocket"
│ └── Amiodarone, Vernakalant (IV)
│
└── ELECTRICAL (DC Cardioversion):
├── Synchronized; 200J biphasic (monophasic 360J)
└── Anticoagulation protocol:
├── AF <48 hours: Cardiovert after heparin; anticoagulate for ≥4 weeks post-CV
└── AF >48 hours or unknown: Either
├── Anticoagulate (warfarin/NOAC) for ≥3 weeks THEN cardiovert, OR
└── TOE-guided (rule out LA thrombus) then cardiovert
Antiarrhythmic Drugs (Maintain Sinus Rhythm)
CHOOSING AAD FOR AF:
├── No structural heart disease:
│ ├── Flecainide, Propafenone (preferred)
│ ├── Sotalol
│ └── Dronedarone
├── LVH:
│ └── Amiodarone (or Dronedarone)
└── HFrEF / Coronary disease:
└── AMIODARONE ONLY (others proarrhythmic)
4. NON-PHARMACOLOGIC RHYTHM CONTROL
Catheter Ablation
- Pulmonary vein isolation (PVI): Gold standard ablation strategy
- Superior to AADs for maintaining sinus rhythm
- Indicated: Symptomatic paroxysmal or persistent AF failing ≥1 AAD
- CASTLE-AF trial: Ablation reduced mortality and HF hospitalization in AF + HFrEF
Surgical Ablation
- Cox-Maze procedure: Surgical lines of block to prevent AF circuits
- Often combined with mitral valve surgery
Management of Special Situations
| Situation | Management |
|---|
| Acute AF + WPW | IV Procainamide or cardioversion; avoid adenosine, digoxin, verapamil |
| Acute AF + hemodynamic compromise | Emergency DC cardioversion |
| Thyrotoxicosis-related AF | Treat hyperthyroidism first; beta-blockers for rate control |
| Post-operative AF | Usually resolves; rate control; anticoagulate if persists |
Q.16 - Recent Diagnostic Modifications for IHD (6 marks - Short Note)
Overview
Ischemic Heart Disease (IHD) diagnosis has evolved from ECG + enzyme-based to multimodal imaging and high-sensitivity biomarkers.
1. High-Sensitivity Cardiac Troponin (hs-cTn)
CONVENTIONAL TROPONIN HIGH-SENSITIVITY TROPONIN
- Detects myonecrosis - Detects even minimal injury
- Undetectable in first 4-6h - Detectable within 1 hour
- Serial sampling needed - 0h/1h or 0h/2h algorithms
- Lower 99th percentile URL
- Sex-specific cutoffs
- 0h/1h ROMI/ROMO Algorithm (ESC 2020):
- Rule OUT MI: hs-cTnT <5 ng/L at 0h; OR <12 ng/L with Δ<3 ng/L at 1h
- Rule IN MI: hs-cTnT >52 ng/L at 0h; OR absolute Δ>6 ng/L at 1h
- Observe zone: Repeat at 3h
2. Coronary CT Angiography (CCTA)
- NICE/ESC guidelines: First-line investigation for stable chest pain (intermediate pre-test probability)
- Advantages: Non-invasive; high negative predictive value (>99%); detects plaque burden
- Plaque characterization: Low-attenuation plaque, positive remodeling → high-risk features
- CT-FFR (Fractional Flow Reserve): Functional significance without catheterization
- SCOT-HEART and PROMISE trials: CCTA-guided strategy improved outcomes
3. Coronary Artery Calcium Score (CACS)
- Agatston score; quantifies coronary calcification
- CACS = 0: Very low event rate; rule out obstructive CAD
- CACS >400: High-risk; intensify preventive therapy
- Role: Reclassification of intermediate cardiovascular risk
4. Cardiac MRI (CMR)
- Stress perfusion CMR: High sensitivity/specificity for ischemia
- Late Gadolinium Enhancement (LGE): Detects myocardial infarction (subendocardial pattern), fibrosis, viability
- Distinguishes ischemic vs. non-ischemic cardiomyopathy
5. Fractional Flow Reserve (FFR) & iFR
- FFR: Invasive pressure wire; FFR <0.80 = hemodynamically significant stenosis → revascularize
- iFR (instantaneous wave-free ratio): Without adenosine; iFR ≤0.89 = significant
- DEFER, FAME, FAME-2 trials: FFR-guided PCI improves outcomes vs. angiography-alone
6. Stress Echocardiography and Nuclear Imaging
- Dobutamine stress echo: Detects wall motion abnormalities; viable myocardium (low-dose: "biphasic response")
- SPECT/PET: Myocardial perfusion imaging; hibernation vs. stunning
7. TIMI, HEART, GRACE Scores
- Risk stratification tools; guide disposition and timing of angiography
Q.17 - Acute Rheumatic Fever: Clinical Features, Diagnosis & Treatment (20 marks)
Definition
ARF = Inflammatory disease occurring as a complication of Group A beta-hemolytic Streptococcal (GAS) pharyngitis, typically in children (5-15 years), involving the heart, joints, skin, and CNS.
Etiopathogenesis
GAS (Strep. pyogenes) THROAT INFECTION
↓
Molecular mimicry mechanism:
Streptococcal M-protein antigens cross-react
with cardiac, joint, brain, skin antigens
↓
Autoimmune reaction
(NOT direct bacterial invasion)
↓
┌────────────────────────────────────────────────────┐
│ ORGANS INVOLVED │
│ Heart: Pancarditis (endocardium → valves most) │
│ Joints: Migratory polyarthritis │
│ Brain: Chorea (Sydenham's) │
│ Skin: Erythema marginatum, Subcutaneous nodules │
└────────────────────────────────────────────────────┘
CLINICAL FEATURES
Major Criteria (J-JONES Mnemonic: J SAFE)
1. Joints (Migratory Polyarthritis) - Most Common (75%)
- Migratory, fleeting, asymmetric
- Affects large joints (knees, ankles, elbows, wrists)
- Exquisitely tender; often disproportionate to fever
- Responds dramatically to salicylates
- Does NOT cause permanent damage
2. Carditis - Most Serious (40-60%)
RHEUMATIC CARDITIS - PANCARDITIS
├── PERICARDITIS: Friction rub, chest pain, effusion
├── MYOCARDITIS: Tachycardia, cardiomegaly, CCF, prolonged PR
└── ENDOCARDITIS: Valvular involvement
├── Mitral valve most common (MC)
├── MR (acute) → MS (chronic - fibrosis, fusion)
├── Aortic regurgitation (2nd most common)
└── Carey Coombs murmur (mid-diastolic): acute MR
3. Chorea (Sydenham's Chorea / "St. Vitus' Dance") - 10-30%
- Involuntary, purposeless movements; emotional lability
- "Milkmaid's grip" - irregular hand contractions
- Appears late (weeks-months after strep infection); may be sole feature
- ASO titres may be normal by this time
- Self-limiting (weeks to months)
4. Erythema Marginatum - <5%
- Evanescent, non-pruritic pink rash
- Central clearing with irregular advancing edge
- Trunk and proximal limbs; never face
- Heat-sensitive (exacerbated by hot bath)
5. Subcutaneous Nodules - <5%
- Small (0.5-2 cm), firm, painless
- Overlying bony prominences (elbows, wrists, knees, occiput, vertebral spinous processes)
- Associated with severe carditis
Minor Criteria
| Minor Criteria | Details |
|---|
| Clinical | Arthralgia (only if arthritis NOT counted as major); Fever ≥38.5°C |
| Lab | Elevated ESR (≥60mm/hr), CRP (≥3mg/dL) |
| ECG | Prolonged PR interval (AV block) |
REVISED JONES CRITERIA (AHA 2015)
Population-based Application
| Population | Definition |
|---|
| Low-risk (developed countries, incidence <2/100,000/year) | Standard criteria |
| Moderate/High-risk (developing countries, incidence ≥2/100,000/year) | Modified criteria (lower threshold) |
Requirements for Diagnosis
EVIDENCE OF PRECEDING GAS INFECTION (mandatory):
├── Positive throat culture for GAS
├── Rapid strep antigen test
├── Elevated/rising streptococcal antibodies:
│ ├── ASO titre: >200 IU/mL (adults >150)
│ └── Anti-DNase B
PLUS:
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
2 MAJOR OR 1 MAJOR + 2 MINOR OR 3 MINOR (for chorea/carditis alone)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
Subclinical Carditis (2015 Update)
- Doppler echocardiography detects valvular regurgitation not clinically audible
- Doppler carditis counts as a major criterion
Modified Criteria for High-Risk Populations
- Monoarthritis/arthralgia counts as major criterion
- Fever threshold lowered to 38°C
INVESTIGATIONS
| Investigation | Finding |
|---|
| ASO titre | >200 Todd units (rises 3-6 weeks post-infection; peaks 4-6 weeks) |
| Anti-DNase B | More sensitive than ASO (especially for skin infection) |
| Throat culture | GAS (positive in only ~25% at time of ARF) |
| Rapid antigen test | Lower sensitivity |
| ESR | Elevated (>60mm/hr); may be normal in pure chorea |
| CRP | Elevated; good for monitoring activity |
| Leukocytosis | Neutrophilia |
| ECG | Prolonged PR interval, sinus tachycardia |
| Echo (2D+Doppler) | Valvular regurgitation (MR, AR), wall motion abnormality, effusion |
| Chest X-ray | Cardiomegaly (carditis) |
TREATMENT
1. Eradication of GAS (Primary Prevention/Eradication)
- Benzathine Penicillin G (BPG): 1.2 million units IM (single dose; 0.6 MU if <30kg) - Preferred
- Phenoxymethyl Penicillin (Penicillin V): 500mg BD x 10 days (oral alternative)
- Amoxicillin: 50mg/kg/day x 10 days (oral)
- Penicillin-allergic: Azithromycin 12mg/kg/day x 5 days; Clindamycin x 10 days
2. Anti-inflammatory Treatment
Arthritis (without carditis)
- Aspirin (Salicylates): 80-100mg/kg/day in children; 4-8g/day adults (in divided doses)
- Dramatic response within 24-48 hours (diagnostic clue)
- Continue until symptoms resolve and inflammatory markers normalize
Carditis (without cardiomegaly/CCF)
- Aspirin: As above for 8-12 weeks
Severe Carditis (with cardiomegaly, CCF, or pericarditis)
- Prednisolone: 2mg/kg/day (max 80mg) x 2-3 weeks, then taper over 6-8 weeks
- Overlap with aspirin during steroid taper (to prevent rebound)
Chorea
- Mild: Reassurance, avoid stimulation
- Moderate-Severe: Carbamazepine or Valproic acid
- Refractory: Haloperidol, Corticosteroids
3. Management of Heart Failure
- Bed rest, digoxin, diuretics, vasodilators (ACEi/ARB for MR)
- Surgical valve repair/replacement: For severe valvular disease
SECONDARY PROPHYLAXIS (Long-term Prevention of Recurrence)
Drug
- Benzathine Penicillin G: 1.2 million units IM every 3-4 weeks (every 3 weeks in high-risk)
- Oral Penicillin V 250mg BD (less effective)
- Penicillin-allergic: Sulfadiazine 0.5-1g OD
Duration of Prophylaxis
┌─────────────────────────────────────────────────────────────┐
│ DURATION OF SECONDARY PROPHYLAXIS (AHA/RHD Guide) │
├─────────────────────────────┬───────────────────────────────┤
│ Condition │ Duration │
├─────────────────────────────┼───────────────────────────────┤
│ ARF without carditis │ 5 years OR until 21 years │
│ │ (whichever is longer) │
├─────────────────────────────┼───────────────────────────────┤
│ ARF with carditis, │ 10 years OR until 21 years │
│ no persistent valvular HD │ (whichever is longer) │
├─────────────────────────────┼───────────────────────────────┤
│ Persistent valvular HD │ 10 years OR until 40 years │
│ │ (whichever is longer) │
├─────────────────────────────┼───────────────────────────────┤
│ Severe valvular disease │ LIFELONG │
│ or post-valve surgery │ │
└─────────────────────────────┴───────────────────────────────┘
PROGNOSIS
- Arthritis: Complete recovery; no permanent damage
- Chorea: Self-limiting; full neurological recovery
- Carditis: Determines long-term prognosis
- Mild carditis (only subclinical): Often resolves
- Severe carditis → Rheumatic heart disease (RHD): Mitral stenosis (chronic), MR, AR → requires valve intervention
- Recurrence (without prophylaxis): Very high risk; each recurrence worsens valvular damage
SUMMARY QUICK REFERENCE CARD
┌─────────────────────────────────────────────────────────────────────┐
│ CARDIOLOGY EXAM SUMMARY - KEY NUMBERS │
├──────────────────────────────┬──────────────────────────────────────┤
│ HFpEF LVEF definition │ ≥ 50% │
│ PH definition (new 2022) │ mPAP > 20 mmHg │
│ PAH definition │ mPAP ≥20, PAWP ≤15, PVR ≥2 WU │
│ Adenosine dose (SVT) │ 6mg IV bolus; repeat 12mg │
│ BPG dose (ARF eradication) │ 1.2 MU IM single dose │
│ ARNI washout from ACEi │ 36 hours │
│ AF cardioversion threshold │ 48 hours (anticoagulation protocol)│
│ CACS high risk threshold │ > 400 Agatston │
│ FFR cutoff for significance │ < 0.80 │
│ hs-cTn rule-out (0h) │ < 5 ng/L (hs-cTnT) │
│ ASO titre positive │ > 200 Todd units │
└──────────────────────────────┴──────────────────────────────────────┘
Sources: Braunwald's Heart Disease 12e, Harrison's Principles of Internal Medicine 22E (2025), Fuster & Hurst's The Heart 15e, Goldman-Cecil Medicine, Goodman & Gilman's Pharmacology 14e. References verified against medical library database.