give ansewers as per md medicine university exam and add flow charts and diagrams and make good quality notes

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long answer questions 1)Discuss the etiopathogenesis, classification, clinical presentation, diagnosis & treatment of CHF. (20 marks ) 2)Discuss recent advances in investigation & treatment of CAD. (20 marks)

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MD MEDICINE UNIVERSITY EXAM NOTES

QUESTION 1: CONGESTIVE HEART FAILURE (CHF) — 20 Marks

DEFINITION

Heart failure (HF) is a clinical syndrome resulting from the inability of the heart to meet the metabolic requirements of the body at normal filling pressures. The term "congestive heart failure" (CHF) is still widely used, though "heart failure" is preferred because fluid congestion may not always be present.

I. ETIOPATHOGENESIS

A. Etiology (Causes)

Category	Common Causes
Ischemic	CAD, MI (most common cause ~70%)
Pressure Overload	Systemic HTN, aortic stenosis, coarctation of aorta
Volume Overload	MR, AR, VSD, PDA
Cardiomyopathy	Dilated, hypertrophic, restrictive, PPCM
Metabolic	Diabetes mellitus, hypothyroidism, hyperthyroidism
Toxins	Alcohol, anthracyclines (adriamycin), cobalt
Infections	Viral myocarditis (coxsackie B), Chagas disease, diphtheria
Infiltrative	Amyloidosis, sarcoidosis, hemochromatosis
High-output causes	Anaemia, thyrotoxicosis, beriberi, AV malformations, Paget's disease
Arrhythmias	AF, complete heart block, sustained VT
Pericardial	Constrictive pericarditis, cardiac tamponade
Congenital	Septal defects, complex CHD

B. Pathogenesis — Neurohormonal Model (Current Concept)

The old hemodynamic model (pump failure only) has been replaced by the neurohormonal model incorporating LV remodeling.

Step-by-step pathogenesis:

INITIAL CARDIAC INJURY
(MI / HTN / Valvular disease / Cardiomyopathy)
            |
            v
    LV DYSFUNCTION
(Reduced CO / Increased filling pressures)
            |
            v
  COMPENSATORY MECHANISMS ACTIVATED
      /              \
   RAAS              SNS
  activated         activated
(Ang II, Aldosterone) (↑ Norepinephrine)
      \               /
       \             /
        v           v
   ┌─────────────────────────────────────┐
   │       LV REMODELING                 │
   │  - Myocyte hypertrophy              │
   │  - Myocyte apoptosis                │
   │  - Interstitial fibrosis            │
   │  - Chamber dilation                 │
   │  - Collagen deposition (↑ MMPs)     │
   └─────────────────────────────────────┘
            |
            v
   ↓ LV function → ↑ Wall stress
            |
            v
   PROGRESSIVE CARDIAC DECOMPENSATION
   (↑ EDV, ↑ EDP, Pulmonary congestion)
            |
            v
       CLINICAL HF

Key neurohormonal mediators:

Mediator	Source	Effect
Angiotensin II	RAAS	Vasoconstriction, myocyte apoptosis, aldosterone secretion, fibrosis
Aldosterone	Adrenal cortex	Na+ retention, K+ loss, myocardial fibrosis
Norepinephrine	SNS	Vasoconstriction, tachycardia, direct myocardial toxicity, down-regulation of β-receptors
Endothelin-1	Vascular endothelium	Vasoconstriction
BNP / ANP	Ventricles/atria	Counter-regulatory (vasodilation, natriuresis)
TNF-α / IL-6	Myocardium	Cytokine-mediated myocardial depression

RAAS and SNS neurohormonal activation in CHF - targets of pharmacotherapy

II. CLASSIFICATION

A. ACC/AHA Staging (Progressive, irreversible)

Stage	Description	Equivalent NYHA	Management
A	At risk (HTN, DM, CAD, FH) - NO structural disease	-	Risk factor modification
B	Structural disease, NO symptoms	NYHA I	ACEi/ARB + Beta blocker
C	Structural disease WITH symptoms	NYHA II-III	Full GDMT
D	Refractory symptoms at rest	NYHA IV	Advanced therapies (VAD, transplant)

Memory tip: A = At risk, B = Before symptoms, C = Clinical HF, D = Death approaching

B. NYHA Functional Classification (Symptomatic, reversible)

Class	Symptoms	MVO2 (mL/kg/min)
I	No symptoms with ordinary activity	>20
II	Slight limitation; comfortable at rest, symptoms on ordinary exertion	16-20
III	Marked limitation; symptoms on less than ordinary activity	10-16
IV	Unable to carry on any activity; symptoms at rest	<10

C. By Ejection Fraction

Type	EF	Mechanism
HFrEF (Systolic HF)	<40%	Impaired contractility
HFmrEF (Mildly reduced)	40-49%	Mixed
HFpEF (Diastolic HF)	≥50%	Impaired relaxation/filling; increased stiffness

D. By Onset

Acute HF - new onset or rapid decompensation
Chronic HF - stable, persistent symptoms

E. By Side

Left HF - pulmonary congestion (dyspnea, orthopnea, PND)
Right HF - systemic venous congestion (edema, JVD, hepatomegaly)
Biventricular HF (most common in clinical practice)

F. By Output

Low-output HF - most cases (CAD, cardiomyopathy, HTN)
High-output HF - thyrotoxicosis, beriberi, anaemia, Paget's disease

III. CLINICAL PRESENTATION

Symptoms

LEFT HEART FAILURE                    RIGHT HEART FAILURE
     |                                       |
Dyspnea on exertion (earliest)         Ankle swelling / pitting edema
Orthopnea (2-3 pillow)                 Right upper quadrant pain
Paroxysmal nocturnal dyspnea (PND)     Anorexia, nausea, bloating
Cardiac cough (dry, nocturnal)         Weight gain (fluid)
Fatigue, exercise intolerance          Abdominal distension
Haemoptysis (pink frothy - severe)     Oliguria (daytime), nocturia

Signs on Examination

Vital signs:

Tachycardia (compensatory)
Low BP or narrow pulse pressure
Pulsus alternans (severe LV dysfunction)
Cheyne-Stokes respiration (severe)

Cardiovascular exam:

Displaced apex beat (LVE - shifted down and out)
S3 gallop (ventricular filling sound) - pathognomonic
S4 gallop (stiff/hypertrophied ventricle)
Murmurs of underlying cause (AS, MR, AR)
Raised JVP (right HF)
Hepatojugular reflux positive

Respiratory exam:

Bibasilar fine crepitations (pulmonary oedema)
Dullness at bases (pleural effusion - usually right-sided)

Abdomen:

Hepatomegaly (tender, pulsatile in TR)
Ascites (chronic RHF)
Splenomegaly (portal hypertension)

Periphery:

Pitting pedal edema (bilateral)
Cold extremities, cyanosis (peripheral)
Cardiac cachexia (severe, chronic)

IV. DIAGNOSIS

A. Investigations

Flowchart - Diagnostic Approach:

CLINICAL SUSPICION OF HF
(Dyspnea + Edema + Fatigue)
            |
            v
INITIAL WORKUP (All patients)
    |               |               |
  ECG           CXR           BNP/NT-proBNP
(LVH, AF,      (Cardiomegaly,  BNP >100 pg/mL
ischemia,       pulmonary       NT-proBNP >300
BBB, QRS        congestion,     pg/mL → HF
duration)       Kerley B lines, likely
                pleural eff)
            |
            v
ECHOCARDIOGRAPHY (Key test)
- Systolic function (EF)
- Diastolic function
- Wall motion abnormalities
- Valvular disease
- LV dimensions
            |
     ┌──────┴──────┐
  EF <40%      EF >50%
  (HFrEF)      (HFpEF)
     |              |
  GDMT        Control rate,
  (see Rx)    BP, risk factors
            |
            v
ADDITIONAL TESTS (As indicated)
- CBC (anaemia)
- RFT/EFT (renal/liver function)
- TFT (thyroid)
- Iron studies (ferritin, TSAT)
- Serum electrolytes, creatinine
- Cardiac MRI (myocarditis, amyloid, sarcoid)
- Coronary angiography (if ischemic etiology suspected)
- Radionuclide ventriculography (RNVG) - MUGA scan
- 6-minute walk test (exercise tolerance)
- Cardiopulmonary exercise testing (CPET) - gold standard for transplant evaluation
- Sleep study (OSA co-morbidity common)

B. Key Diagnostic Criteria

Framingham Criteria for CHF:

Major criteria (≥2 major OR 1 major + 2 minor):

PND or orthopnea
Neck vein distension
Rales
Cardiomegaly on CXR
Acute pulmonary oedema
S3 gallop
Increased venous pressure (>16 cmH2O)
Hepatojugular reflux
Pulmonary oedema on CXR
Weight loss ≥4.5 kg in 5 days with treatment

Minor criteria:

Bilateral ankle oedema
Nocturnal cough
Dyspnoea on exertion
Hepatomegaly
Pleural effusion
HR >120/min
Decrease in VC by 1/3 from maximum

C. CXR Findings (Ordered by increasing severity)

Mild → Moderate → Severe
  |         |          |
Cardiomegaly  Kerley B lines   Bat-wing / Butterfly
(CT ratio     (septal lines)   pulmonary oedema
>0.5)
              Peribronchial     Pleural effusions
              cuffing           (bilateral)
              Cephalization     Air-space opacities
              of vessels

V. TREATMENT

A. General / Non-Pharmacological Measures

Salt restriction (<2 g/day Na+)
Fluid restriction (1.5-2 L/day if severe)
Daily weight monitoring (report if gain >2 kg/week)
Cardiac rehabilitation and regular exercise (NYHA I-III)
Smoking cessation, alcohol abstinence
Vaccinations (influenza, pneumococcus)
Avoid NSAIDs, CCBs (verapamil, diltiazem), class I antiarrhythmics

B. Pharmacological Treatment - HFrEF (EF <40%)

"FOUR PILLARS" of GDMT for HFrEF:

┌─────────────────────────────────────────────────────────────────┐
│               FOUR PILLARS OF GDMT (HFrEF)                     │
├──────────────────┬──────────────────┬──────────────┬────────────┤
│  RAAS Blocker    │  Beta-Blocker    │   MRA        │  SGLT2i   │
│  (ACEi/ARB/ARNI) │                  │              │            │
├──────────────────┼──────────────────┼──────────────┼────────────┤
│ Sacubitril/      │ Carvedilol       │Spironolactone│Dapagliflozin│
│ Valsartan (ARNI) │ Metoprolol XL    │Eplerenone    │Empagliflozin│
│ Ramipril/Enalapril│ Bisoprolol      │              │            │
│ Losartan/Valsartan│                 │              │            │
├──────────────────┼──────────────────┼──────────────┼────────────┤
│ ↓ Mortality 20%  │ ↓ Mortality 34%  │↓ Mortality   │↓ HHF+CV   │
│ (PARADIGM-HF)    │ (MERIT-HF,       │25-30%        │death 25%  │
│                  │  CIBIS-II)       │(RALES,       │(DAPA-HF,  │
│                  │                  │EMPHASIS-HF)  │EMPEROR-R) │
└──────────────────┴──────────────────┴──────────────┴────────────┘

Additional medications:

Drug	Class	Indication
Furosemide / Torsemide	Loop diuretic	Fluid overload (symptom relief)
Hydralazine + Isosorbide dinitrate	Vasodilators	ACEi/ARB intolerant (cough, renal failure), Black patients
Ivabradine	If-channel blocker	HR ≥70 bpm, sinus rhythm, LVEF ≤35%
Digoxin	Cardiac glycoside	Persistent symptoms, AF rate control, reduce HHF
Vericiguat	sGC stimulator	High-risk symptomatic HFrEF (VICTORIA trial)
Tafamidis	TTR stabilizer	TTR-amyloid cardiomyopathy
IV Iron (ferric carboxymaltose)	Iron supplementation	Iron deficiency (TSAT <20%, ferritin <100)

C. Treatment of HFpEF (EF ≥50%)

Note: Unlike HFrEF, fewer proven mortality-reducing therapies exist.

SGLT2i (dapagliflozin, empagliflozin) - EMPEROR-Preserved, DELIVER trials - reduce HHF
Diuretics - symptom relief
Control underlying causes: HTN, AF, CAD, DM, obesity
Spironolactone - some benefit (TOPCAT trial, borderline)

D. Device Therapy

Device	Indication
ICD (Implantable cardioverter defibrillator)	LVEF ≤35%, NYHA II-III, >3 months optimal medical therapy, life expectancy >1 year
CRT (Cardiac resynchronization therapy)	LVEF ≤35%, LBBB, QRS ≥150 ms, NYHA II-IV, sinus rhythm
CRT-D	Combined CRT + ICD
LVAD (Left ventricular assist device)	NYHA IV / INTERMACS 1-3, bridge to transplant or destination therapy

E. Treatment of Acute Decompensated HF (ADHF)

ACUTE HF → ASSESS: Wet/Dry + Warm/Cold Profile
                    (Stevenson Classification)
    |
    v
┌──────────┬────────────┐
│          │            │
Wet-Warm   Wet-Cold     Dry-Cold
(Most      (Cardiogenic (Low output,
common)    shock)       no congestion)
    |           |           |
 Diuretics   Inotropes   Volume
 Vasodilators +Diuretics  challenge
(IV Nitrates) (Dobutamine,
              Dopamine)

Immediate management:

Positioning - sit upright (reduces preload)
O2 - maintain SpO2 >94%; NIV (CPAP/BiPAP) for respiratory failure
IV furosemide - 40-80 mg IV bolus (decongestive)
IV nitrates - sublingual/IV GTN (if SBP >90 mmHg) - reduces preload/afterload
Morphine - 2-4 mg IV (reduces anxiety, mild venodilation) - use with caution
Vasopressors - norepinephrine if cardiogenic shock (MAP <65)
Inotropes - Dobutamine/Dopamine for low-output shock

F. Surgical and Advanced Therapies

Revascularization (CABG/PCI) - ischemic HF with viable myocardium
Valve repair/replacement - valvular cause
Cardiac transplantation - Gold standard for end-stage HF (NYHA IV, LVEF <20%, VO2 max <10 mL/kg/min)
LVAD - Bridge to transplant or destination therapy
Ultra-filtration - diuretic-resistant fluid overload
Cardiac contractility modulation (CCM) - newer device for non-LBBB patients

Overall Treatment Algorithm (Summary Flowchart)

CHF pathophysiology, diagnosis, and therapy - complete overview

G. Precipitating Factors (Must identify and treat) - Mnemonic: "FAILURE"

Letter	Factor
F	Forgot to take medications / Fast AF
A	Anaemia / Arrhythmia
I	Ischemia / Infarction
L	Lifestyle - Na+/fluid excess
U	Uncontrolled HTN
R	Renal failure (cardiorenal syndrome)
E	Embolism (PE) / Endocarditis / Exertion

QUESTION 2: RECENT ADVANCES IN INVESTIGATION & TREATMENT OF CAD — 20 Marks

DEFINITION

Coronary artery disease (CAD) is atherosclerotic obstruction of the coronary arteries resulting in myocardial ischemia. It encompasses stable angina, unstable angina, NSTEMI, STEMI, and sudden cardiac death.

PART A: RECENT ADVANCES IN INVESTIGATION OF CAD

1. Coronary CT Angiography (CCTA)

Key advances:

Feature	Details
Indication	Intermediate pre-test probability of CAD (10-70%), low-risk acute chest pain
Technique	Multi-detector CT (64-slice, 256-slice, dual-source CT)
Sensitivity/Specificity	~95-99% sensitivity for significant stenosis
Calcium scoring	Agatston score; CAC=0 near-zero event risk
Advantage	Non-invasive, rapid, no arterial puncture
SCOT-HEART trial	CCTA-guided strategy reduced MI at 5 years vs standard care
PROMISE trial	CCTA non-inferior to functional testing for outcomes

2. CT-Derived Fractional Flow Reserve (FFR-CT / HeartFlow)

CCTA Images → 3D coronary model → Computational fluid dynamics
                                              |
                                              v
                                    FFR-CT value per vessel
                                    (≤0.80 = hemodynamically significant)
                                              |
                        ┌─────────────────────┴────────────────┐
                    FFR-CT >0.80                        FFR-CT ≤0.80
                   (Medical therapy)               (Proceed to invasive
                                                    coronary angiography)

PLATFORM trial: FFR-CT reduced unnecessary invasive angiography by 61%
DISCOVER-FLOW, DeFACTO, NXT trials: FFR-CT more accurate than anatomical CTA

3. Invasive Coronary Physiology

Test	Principle	Cut-off	Use
FFR (Fractional Flow Reserve)	Pd/Pa during maximal hyperaemia (adenosine)	≤0.80 = significant	Guides revascularization in intermediate stenoses
iFR (Instantaneous Wave-Free Ratio)	Diastolic pressure ratio, no adenosine	≤0.89 = significant	Equivalent to FFR (DEFINE-FLAIR, iFR-SWEDEHEART trials)
CFR (Coronary Flow Reserve)	Hyperaemic vs resting flow	<2.0 = abnormal	Microvascular disease
IMR (Index of Microvascular Resistance)	Distal pressure × transit time	>25 = abnormal	Microvascular disease post-PCI
Resting Full-cycle Ratio (RFR)	Resting Pd/Pa	≤0.89	Avoids adenosine

4. Intravascular Imaging

Modality	Principle	Resolution	Key Use
IVUS (Intravascular Ultrasound)	Sound waves	100-150 μm	Plaque burden, stent sizing, stent expansion, calcium
OCT (Optical Coherence Tomography)	Near-infrared light	10-15 μm (10x better than IVUS)	Plaque morphology, thrombus, fibrous cap thickness, stent apposition
NIRS (Near-Infrared Spectroscopy)	Lipid detection	-	Lipid-rich plaque (NIRS-IVUS combined)

ILUMIEN IV trial (2022): OCT-guided PCI superior to angiography-guided PCI for stent expansion. ULTIMATE trial: IVUS-guided PCI reduced MACE vs angiography-guided.

5. Advanced Non-Invasive Imaging

Test	Key Feature	Recent Advance
Cardiac MRI	Gold standard for viability, function, scar	T1 mapping, ECV fraction - quantify diffuse fibrosis
PET (Myocardial Perfusion PET)	Absolute flow quantification	Rb-82 or N-13 ammonia PET; detects microvascular disease
SPECT (Myocardial Perfusion Imaging)	Perfusion defects	CZT cameras - higher resolution, lower dose, faster
Echocardiography	Wall motion	Strain imaging (GLS); 3D echo; contrast echo (LVO, perfusion)

6. Novel Biomarkers

Biomarker	Significance
High-sensitivity Troponin I/T (hs-cTnI/T)	Detects MI at 0h/1h (0h/1h rule-out algorithm) - ESC 2023 guidelines
Copeptin	Combined with troponin - rapid rule-out in <2 hours
BNP/NT-proBNP	Identifies concurrent HF in ACS
hsCRP / IL-6	Inflammatory risk markers
Lp(a)	Emerging genetic risk marker; target for newer therapies
PCSK9 levels	Target biomarker for lipid-lowering therapy
GDF-15	Prognostic marker in NSTE-ACS

7. Wearable Technology and AI

Continuous ECG wearables (Apple Watch, Zio Patch) - detect silent AF, ischemia
AI-based ECG interpretation - detect LV dysfunction, CAD, HF from 12-lead ECG
Deep learning applied to CCTA - automated stenosis quantification
Remote monitoring - implantable hemodynamic sensors (CardioMEMS for HF-CAD overlap)

PART B: RECENT ADVANCES IN TREATMENT OF CAD

1. Pharmacological Advances

A. Lipid-Lowering Therapy

LDL-C Reduction Strategy (Escalating approach)
            |
    Statin therapy (first-line)
    (Atorvastatin 40-80mg, Rosuvastatin 20-40mg)
            |
    If LDL not at goal (< 1.4 mmol/L in very high risk)
            |
    Add Ezetimibe 10mg (IMPROVE-IT trial)
            |
    If still not at goal
            |
    PCSK9 inhibitors
    (Evolocumab 140mg Q2W - FOURIER trial)
    (Alirocumab 75-150mg Q2W - ODYSSEY OUTCOMES trial)
    ↓LDL by 50-60% additional; ↓MACE by 15-20%
            |
    Inclisiran (siRNA) - 2x yearly injection (ORION-10, ORION-11)
            |
    Bempedoic acid - ACL inhibitor, oral, for statin-intolerant
    (CLEAR Outcomes trial - ↓MACE 13%)

B. Antiplatelet Therapy Advances

Strategy	Evidence
Dual Antiplatelet Therapy (DAPT) - Aspirin + P2Y12i	Standard post-ACS/PCI
Ticagrelor (90 mg BD) vs Clopidogrel	PLATO trial: ↓ mortality 19% in ACS
Prasugrel (10 mg OD) vs Clopidogrel	TRITON-TIMI 38: ↓ CV death/MI/stroke (↑ bleeding)
De-escalation of DAPT	TROPICAL-ACS, HOST-REDUCE: potent → clopidogrel after 1 month
DAPT duration	1-3 months in high bleed-risk (ARC-HBR); 6-12 months standard
P2Y12 monotherapy after 1-3 months DAPT	TWILIGHT, TICAGRELOR-SOLO trials
Cangrelor (IV P2Y12i)	Bridging therapy, peri-PCI
Vorapaxar (PAR-1 antagonist)	TRACER: reduces recurrent MI in stable CAD (↑ ICH risk)

C. Anticoagulation in CAD

Drug	Indication	Trial
Rivaroxaban 2.5 mg BD + Aspirin	Stable CAD / PAD (vascular dose)	COMPASS trial - ↓MACE 24%
Betrixaban, Apixaban	Post-ACS extended VTE prophylaxis
Reviparin / LMWH	ACS bridge to PCI

D. Anti-Anginal Drugs

Drug	Mechanism	Evidence
Ranolazine	Late Na+ channel blocker	Reduces angina frequency without affecting HR/BP (CARISA trial)
Ivabradine	If-channel blocker (HR reduction)	SIGNIFY trial (CAD with angina, HR ≥70)
Trimetazidine	Metabolic (shifts to glucose oxidation)	Reduces angina, improves LV function
Nicorandil	K-ATP opener + nitrate	IONA trial: ↓ coronary events
Colchicine 0.5 mg OD	Anti-inflammatory	COLCOT trial: ↓MACE 23% post-MI; LoDoCo2: stable CAD

E. Diabetes Drugs with CV Benefit

Drug	Trial	Benefit
SGLT2 inhibitors (Empagliflozin, Canagliflozin, Dapagliflozin)	EMPA-REG, CANVAS, DECLARE	↓ CV death, HHF, renal outcomes
GLP-1 RAs (Liraglutide, Semaglutide, Dulaglutide)	LEADER, SUSTAIN-6, REWIND	↓ MACE, CV death

2. Interventional Advances (PCI)

A. Generation of Coronary Stents

Bare Metal Stents (BMS) - 1st gen
    ↓  (high restenosis - 20-30%)
Drug Eluting Stents (DES) 1st gen - Sirolimus, Paclitaxel
    ↓  (reduced restenosis to 5-10%; late ST concern)
DES 2nd gen - Everolimus, Zotarolimus, Biolimus
(Thinner struts, biocompatible/biodegradable polymer)
    ↓  (current standard)
Bioresorbable Vascular Scaffolds (BVS/BRS)
- Absorb BVS (Abbott) - fully dissolves in 3 years
- Concern: ↑ late scaffold thrombosis - use cautious
Drug-coated balloons (DCB) - no permanent implant
- For ISR, small vessels, bifurcations

B. Complex PCI Techniques

Technique	Use
Rotational atherectomy (Rotablator)	Heavily calcified lesions, undilatable plaque
Orbital atherectomy	Calcified CAD
Intravascular lithotripsy (Shockwave IVL)	Severe calcification - sonic pressure waves
Laser atherectomy (EXCIMER)	Ostial lesions, ISR, SVG lesions
Bifurcation PCI	"Provisional T" stenting vs DK-Crush
CTO-PCI	Chronic total occlusion - retrograde approach, ADR
CHIP (Complex High-risk Indicated PCI)	Protected PCI with hemodynamic support (Impella)

C. Hemodynamic Support Devices (for High-Risk PCI)

Device	Mechanism	CO support
IABP (Intra-aortic balloon pump)	Counterpulsation	0.5-1.0 L/min
Impella (CP, 5.0, 5.5)	Axial flow catheter, LV to aorta	2.5-5.5 L/min
TandemHeart	Extracorporeal centrifugal pump, LA to femoral artery	3.5-5.0 L/min
VA-ECMO	Full cardiopulmonary bypass	4-6 L/min

PROTECT II trial: Impella superior to IABP for high-risk PCI outcomes.

3. Surgical Advances - CABG

Advance	Details
Off-pump CABG (OPCAB)	Avoids cardiopulmonary bypass; less systemic inflammation
Minimally invasive CABG (MIDCAB, TECAB)	Smaller incisions, robotic-assisted
Bilateral IMA grafting (BIMA)	Better long-term patency vs single IMA; ART trial
Radial artery grafts	Superior to saphenous vein at 10 years (RAPS trial)
Hybrid revascularization	LIMA-LAD (surgical) + PCI of non-LAD
No-touch saphenous vein harvesting	Better vein conduit quality, ↓ atherosclerosis

EXCEL trial: PCI with 2nd-gen DES vs CABG for left main CAD (comparable outcomes at 5 years). SYNTAX trial: CABG superior in complex 3VD (SYNTAX score >32).

4. Cardiac Rehabilitation (CR)

Exercise-based CR reduces all-cause mortality by ~20% post-MI/PCI
Telecardiac rehabilitation and digital CR platforms (new development)

5. Emerging / Future Therapies

Therapy	Mechanism	Stage
Inclisiran	siRNA targeting PCSK9, 2x/year injection	Approved (FDA/EMA)
Pelacarsen	Antisense oligonucleotide against Lp(a)	Phase 3 (OCEAN(a)-OUTCOMES trial)
Obicetrapib (CETP inhibitor)	↑ HDL, ↓ LDL	Phase 3
Gene therapy	PCSK9 CRISPR editing, single lifetime dose	Early trials
CAR-T for HF/CAD	Anti-fibrotic immune cells	Preclinical
Coronary gene therapy	Angiogenesis (VEGF, HGF)	Trials ongoing
Colchicine 0.5 mg	Anti-NLRP3 inflammasome	Practice-changing (COLCOT, LoDoCo2)
Ziltivekimab (IL-6 inhibitor)	Anti-inflammatory in CKD+CAD	Phase 3

KEY TRIALS SUMMARY (CAD - for exam)

Trial	Drug/Intervention	Key Finding
PLATO	Ticagrelor vs Clopidogrel	Ticagrelor ↓ mortality 19% in ACS
TRITON	Prasugrel vs Clopidogrel	Prasugrel ↓ MACE but ↑ bleeding
FOURIER	Evolocumab	↓ LDL 59%, ↓ MACE 15%
ODYSSEY	Alirocumab	↓ LDL 62%, ↓ all-cause mortality
COMPASS	Rivaroxaban 2.5mg + ASA	↓ MACE 24% in stable CAD
IMPROVE-IT	Ezetimibe + Statin	↓ MACE 6.4%; lower LDL = better
COLCOT	Colchicine post-MI	↓ MACE 23%
LoDoCo2	Colchicine stable CAD	↓ MACE 31%
ISCHEMIA	PCI vs Medical therapy (stable CAD)	No difference in outcomes (landmark)
SYNTAX	CABG vs PCI in 3VD/LM	CABG superior in complex disease
EXCEL	PCI vs CABG left main	Comparable 5-year outcomes
PARADIGM-HF	Sacubitril/Valsartan	↓ CV death 20% in HFrEF
DAPA-HF	Dapagliflozin	↓ CV death/HHF 26% in HFrEF
EMPEROR-R	Empagliflozin	↓ CV death/HHF 25% in HFrEF

QUICK REVISION - HIGH-YIELD POINTS

CHF

Most common cause: CAD/IHD
Best initial test: Echocardiography
Best biomarker: BNP/NT-proBNP
Pathognomonic sign: S3 gallop
Drug reducing mortality most: Beta-blocker (carvedilol, metoprolol XL)
Newest 4th pillar: SGLT2 inhibitor (dapagliflozin/empagliflozin)
Best for LBBB + EF<35%: CRT-D
End-stage treatment: Cardiac transplant

CAD - Recent Advances

Best investigation for intermediate risk: CCTA
Gold standard for ischemia physiology: FFR (≤0.80 = significant)
Best intravascular imaging resolution: OCT
Strongest new anti-anginal: Ranolazine
Newest statin-independent lipid drug: Inclisiran (2x/year siRNA)
Anti-inflammatory proven: Colchicine 0.5 mg (COLCOT/LoDoCo2)
Best for complex 3VD: CABG (SYNTAX score >32)
SGLT2i benefit in CAD: Empagliflozin reduces CV death in T2DM+CAD

Sources: Braunwald's Heart Disease (11e), Fuster and Hurst's The Heart (15e), Textbook of Family Medicine (9e), Goodman & Gilman's Pharmacology (13e), Katzung Pharmacology (16e), ACC/AHA 2022 HF Guidelines, ESC 2023 ACS Guidelines. Recent PubMed: DAPA ACT HF-TIMI 68 (2025, PMID 40884036), Inclisiran ORION trials, CLEAR Outcomes (bempedoic acid).

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1. Discuss recent advances in acute stroke management. (20) * 2. Recent advances in management of epilepsy. (6) * 3. Newer antiepileptic drugs. (6) * 4. Draw a labelled diagram of brainstem and explain the applied anatomy of various brainstem syndromes. (20) * 5. Explain formation and circulation of CSF and its clinical applications. (6) * 6. Discuss the approach to a patient with acute flaccid quadriparesis. Discuss the management of acute demyelinating polyradiculopathy (GBS). (20) * 7. Myasthenia gravis. (6) Page 2 * 8. Chronic fatigue syndrome. (6) * 9. Discuss seizure disorder – pathophysiology, classification, clinical features, investigations and management. (20) * 10. Discuss various types of inflammatory myopathies, diagnostic approach, differential diagnosis and treatment of inflammatory myopathy. (20) * 11. Deep brain stimulation. (6) * 12. Discuss clinical anatomy and correlation of cerebellar dysfunction. (20) * 13. Channelopathies in neurology. (6) * 14. Ataxic paraparesis. (6) * 15. Eating disorders. (6) * 16. Define ataxia. Discuss classification, clinical features, diagnosis and management. (20) * 17. Primary headache disorders. (6) * 18. Circle of Willis. (6) Page 3 * 20. Discuss the pathophysiology of sleep and describe various sleep disorders. (20) * 21. Bell's palsy. (6) * 22. Abernethy syndrome. (6) * 23. Clinical features of GBS. Write in brief about newer modalities of treatment of GBS. (20) * 24. What are the different aphasias? Write in brief the development of aphasias with respect to the structure and physiology involved. What is conduction aphasia? (20) * 25. What are the stages of sleep? Write in brief about pathophysiology and management of OSA. (20) * 26. TB meningitis – manifestations and management. (6) Page 4 * 27. Inflammatory muscle disease. (6) * 28. Parkinsonism. (6) * 29. Membranous nephropathy / nephrotic syndrome in pulmonology (handwriting unclear). (20) * 30. Treatment of epilepsy with emphasis on mechanism of newer third-generation antiseizure medications. (20) * 31. Discuss antiepileptic drugs. (6) * 32. Motor neuron disease (MND): genetics, clinical features and diagnosis. (20) * 33. Approach to reperfusion therapy for acute ischemic stroke. (6)

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