• 9. HFpEF. (6) • 10. Infective endocarditis – Etiology, diagnosis & treatment. (20) • 11. Define pulmonary hypertension. Discuss classification, diagnosis & management of PAH. (20) • 12. Narrow QRS tachycardia & its management. (6) • 13. ARNI. • 14. Differentiate between constrictive pericarditis & restrictive cardiomyopathy. (20) • 15. Atrial fibrillation – Etiopathogenesis & management. (20) • 16. Recent diagnostic modifications for IHD. (6) • 17. Acute rheumatic fever – Clinical features, diagnosis & treatment. (20) Kindly prepare answers as per MD medicine university examination add flowcharts and diagrams as needed and make good quality notes ,take 20 for long answer and 6 for short notes

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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)

FeatureDetail
HemodynamicElevated LVEDP/PCWP at rest or with exertion; normal LVEF
Obesity/ComorbiditiesHTN, DM, obesity, CKD, AF, sleep apnea
Age/SexOlder women predominantly
FibrosisLV hypertrophy, concentric remodeling, myocardial fibrosis
SymptomsDyspnea 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

CategoryDrug/Intervention
Proven benefitSGLT2 inhibitors (empagliflozin, dapagliflozin) - ↓HF hospitalization
DiureticsFor congestion relief (symptomatic)
Comorbidity controlAggressive HTN/DM/AF/obesity management
Exercise trainingImproves functional capacity
IneffectiveACEi, ARB, beta-blockers (no mortality benefit proven)
AvoidPDE5 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

RiskExamples
HighProsthetic valve, prior IE, unrepaired cyanotic CHD
ModerateRheumatic HD, bicuspid aortic valve, MVP with regurgitation
Low/NegligibleASD (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

  1. Positive blood cultures (≥2 separate cultures with typical IE organisms, OR persistent bacteremia)
  2. Evidence of endocardial involvement:
    • Echo: oscillating vegetation, abscess, new dehiscence of prosthetic valve
    • New valvular regurgitation

Minor Criteria

  1. Predisposing heart condition or IVDA
  2. Fever ≥38°C
  3. Vascular phenomena (emboli, Janeway lesions, mycotic aneurysm, conjunctival hemorrhage)
  4. Immunologic phenomena (Osler nodes, Roth spots, RF positive, GN)
  5. Microbiological evidence (positive culture not meeting major criteria)

Classification

ClassificationCriteria
Definite IE2 major; OR 1 major + 3 minor; OR 5 minor
Possible IE1 major + 1 minor; OR 3 minor
RejectedFirm 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

TestFindings
Blood cultures3 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
CBCLeukocytosis, normocytic anemia
ESR/CRPElevated
UrinalysisHematuria, proteinuria (GN)
CT/PET-CTFor 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)

ClassDescription
FC INo limitation; ordinary activity causes no symptoms
FC IISlight limitation; comfortable at rest; ordinary activity causes dyspnea/fatigue
FC IIIMarked limitation; comfortable at rest; less than ordinary activity causes symptoms
FC IVInability 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

InvestigationFinding/Purpose
EchoScreening; TAPSE <18mm (RV dysfunction)
RHCDiagnostic gold standard; hemodynamic profile
CT-PAPulmonary emboli, parenchymal disease
V/Q scanCTEPH (more sensitive than CT-PA for chronic thrombi)
6MWTPrognosis and therapy monitoring
BNP/NT-proBNPSeverity marker; RV stress
Cardiac MRIRV 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

ArrhythmiaRateP wavesRP interval
AVNRT (typical)150-250Buried in QRS or pseudo-r' in V1Short RP (<70ms)
AVRT (orthodromic)150-250Inverted P after QRSShort RP
Atrial tachycardia100-250P before QRS (abnormal axis)Long RP
Atrial flutter250-350 (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

  1. HFrEF (LVEF ≤40%): NYHA Class II-IV, already on stable ACEi/ARB
  2. 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 EffectImportant Points
HypotensionMost common; start at low dose
Angioedema2-3x more common than ACEi (due to bradykinin accumulation via neprilysin inhibition)
HyperkalemiaMonitor K+
Renal impairmentMonitor creatinine
ContraindicatedWith 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

FeatureConstrictive PericarditisRestrictive Cardiomyopathy
EtiologyTB (commonest globally), viral pericarditis, post-cardiac surgery, post-radiation, connective tissue diseaseAmyloidosis, sarcoidosis, hemochromatosis, Löffler's eosinophilic, idiopathic, post-radiation
PathophysiologyFibrotic, calcified pericardium limits diastolic fillingMyocardial disease causes ↑stiffness; filling restriction
Ventricular interdependenceMARKED (hallmark) - pericardial constraint couples ventriclesAbsent or mild
PericardiumThickened (>4mm by CT/MRI), may be calcifiedNormal thickness
MyocardiumNormalAbnormal (infiltration, fibrosis)
Systolic functionUsually normalUsually normal early; impaired late (esp. amyloid)

CLINICAL FEATURES

FeatureConstrictive PericarditisRestrictive Cardiomyopathy
HistoryPrior pericarditis, TB, cardiac surgery, radiationSystemic disease (amyloid, sarcoid)
JVP↑↑ with Kussmaul's sign (JVP rises on inspiration)↑ with Kussmaul's sign (also present)
Pericardial knockPresent (early diastolic sound)Absent
3rd heart soundAbsentMay be present
RegurgitationRareCommon (esp. amyloid - bilateral AV valve involvement)
Peripheral edema, ascitesProminentPresent
CachexiaCommonLess common
AFCommonCommon (amyloid)

INVESTIGATIONS

ECG

Constrictive PericarditisRestrictive Cardiomyopathy
VoltageMay be lowLow voltage (esp. amyloid) - QRS voltage inversely proportional to amyloid infiltration
ConductionNon-specificAV block, bundle branch block (amyloid, sarcoid)
PatternNon-specificPseudo-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 PericarditisRestrictive Cardiomyopathy
CTPericardial thickening >4mm, calcificationNormal pericardium
Cardiac MRIPericardial enhancement (gadolinium), thick pericardiumLate 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

TestFinding
Serum amyloid/SPEPAmyloid (light chains)
Ferritin/transferrin saturationHemochromatosis
ACE levelsSarcoidosis
Congo Red staining (biopsy)Amyloid (apple-green birefringence)
Endomyocardial biopsyDefinitive for RCM (e.g., amyloid fibrils)

TREATMENT

Constrictive PericarditisRestrictive Cardiomyopathy
DefinitivePericardiectomy (surgical decortication) - potentially curativeNo cure for most (treat underlying cause)
MedicalDiuretics (temporary); anti-TB for tuberculosis etiologyDiuretics; treat underlying (e.g., tafamidis for ATTR amyloid)
PrognosisGood post-surgery if done earlyPoor, 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

TypeDefinition
Paroxysmal AFSelf-terminating within 7 days (usually <48h)
Persistent AFLasting >7 days or requires cardioversion
Long-standing persistentContinuous AF >12 months; rhythm control strategy chosen
Permanent AFAF accepted; no further rhythm control attempts
First diagnosed AFFirst 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

  1. Hemodynamic: Loss of atrial kick (15-20% reduction in CO); tachycardia-induced cardiomyopathy
  2. Thromboembolic: LA appendage thrombus → stroke (2-7x risk); AF causes 25% of strokes in elderly
  3. 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 FactorScore
Congestive heart failure1
Hypertension1
Age ≥752
Diabetes mellitus1
Stroke/TIA (prior)2
Vascular disease (prior MI, PAD, aortic plaque)1
Age 65-741
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

DrugRouteUse
Beta-blockers (metoprolol, bisoprolol, carvedilol)Oral/IVFirst line, especially with HFrEF
Diltiazem/VerapamilOral/IVEffective; avoid in HFrEF (negative inotropy)
DigoxinOral/IVAdd-on therapy; useful in HF, sedentary patients; less effective during exercise
AmiodaroneIV/OralRefractory 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

SituationManagement
Acute AF + WPWIV Procainamide or cardioversion; avoid adenosine, digoxin, verapamil
Acute AF + hemodynamic compromiseEmergency DC cardioversion
Thyrotoxicosis-related AFTreat hyperthyroidism first; beta-blockers for rate control
Post-operative AFUsually 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 CriteriaDetails
ClinicalArthralgia (only if arthritis NOT counted as major); Fever ≥38.5°C
LabElevated ESR (≥60mm/hr), CRP (≥3mg/dL)
ECGProlonged PR interval (AV block)

REVISED JONES CRITERIA (AHA 2015)

Population-based Application

PopulationDefinition
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

InvestigationFinding
ASO titre>200 Todd units (rises 3-6 weeks post-infection; peaks 4-6 weeks)
Anti-DNase BMore sensitive than ASO (especially for skin infection)
Throat cultureGAS (positive in only ~25% at time of ARF)
Rapid antigen testLower sensitivity
ESRElevated (>60mm/hr); may be normal in pure chorea
CRPElevated; good for monitoring activity
LeukocytosisNeutrophilia
ECGProlonged PR interval, sinus tachycardia
Echo (2D+Doppler)Valvular regurgitation (MR, AR), wall motion abnormality, effusion
Chest X-rayCardiomegaly (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.
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