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20 Cardiovascular Diseases — Comprehensive Clinical Reference

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1. HYPERTENSION (Essential)

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2. HEART FAILURE WITH REDUCED EF (HFrEF)

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3. HEART FAILURE WITH PRESERVED EF (HFpEF)

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4. ACUTE MYOCARDIAL INFARCTION (STEMI)

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5. UNSTABLE ANGINA / NSTEMI

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6. STABLE ANGINA (Chronic Coronary Syndrome)

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7. ATRIAL FIBRILLATION (AF)

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8. VENTRICULAR TACHYCARDIA (VT)

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9. COMPLETE HEART BLOCK (Third-Degree AV Block)

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10. AORTIC STENOSIS

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11. MITRAL REGURGITATION (MR)

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12. DILATED CARDIOMYOPATHY (DCM)

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13. HYPERTROPHIC CARDIOMYOPATHY (HCM)

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14. INFECTIVE ENDOCARDITIS (IE)

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15. PERICARDITIS (Acute)

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16. DEEP VEIN THROMBOSIS (DVT) / PULMONARY EMBOLISM (PE)

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17. AORTIC DISSECTION

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18. PERIPHERAL ARTERIAL DISEASE (PAD)

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19. CARDIAC TAMPONADE

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20. DYSLIPIDAEMIA

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Quick-Reference Summary Table

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30 Cardiovascular Diseases — Comprehensive Clinical Reference

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1. ESSENTIAL HYPERTENSION

• BP measurements on ≥ 2 separate occasions
• Urinalysis (proteinuria, haematuria)
• Serum electrolytes, creatinine, eGFR
• Fasting glucose, HbA1c
• Fasting lipid profile
• ECG (LVH: Sokolow-Lyon criteria)
• Echocardiogram (if clinical LVH suspected)
• 24-hr ambulatory BP monitoring (to exclude white-coat or masked HTN)

• LVH on ECG/echo, hypertensive retinopathy (AV nicking, cotton wool spots, papilloedema in grade 4), proteinuria, elevated creatinine, hypertensive nephrosclerosis

• White-coat hypertension
• Renal artery stenosis (fibromuscular dysplasia in young women; atherosclerotic in elderly)
• Primary hyperaldosteronism (Conn syndrome) — hypokalaemia, hypertension, suppressed renin
• Phaeochromocytoma — episodic hypertension, headache, sweating, palpitations
• Cushing syndrome — moon face, buffalo hump, striae
• Coarctation of aorta — radio-femoral delay, rib notching on CXR
• Thyroid disorders (hypo/hyperthyroidism)
• Sleep apnoea (OSA)

• Lifestyle: DASH diet, weight loss, salt restriction (<2.3 g/day), aerobic exercise ≥30 min/day, limit alcohol
• Step 1: ACE inhibitor OR ARB OR thiazide-like diuretic OR CCB
• Step 2: Two-drug combination (CCB + ACE-I/ARB is preferred)
• Step 3: Three-drug combination
• Step 4 (resistant): Add spironolactone 25–50 mg or beta-blocker or alpha-blocker

• Amlodipine 5–10 mg OD
• Ramipril 5–10 mg OD
• Indapamide 1.5 mg OD
• Losartan 50–100 mg OD (if ACE intolerant)
• Bisoprolol 5–10 mg OD (if coexisting IHD/HF)

• ACE-I/ARB: bilateral renal artery stenosis, pregnancy, hyperkalaemia >6 mmol/L
• Thiazides: gout (relative), hypokalaemia
• Beta-blockers: asthma, COPD, heart block, decompensated HF
• Aldosterone antagonists: eGFR <30, K⁺ >5.0

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2. HEART FAILURE WITH REDUCED EF (HFrEF)

• NT-proBNP / BNP (BNP >400 pg/mL strongly supports HF)
• Echocardiogram (LVEF, wall motion, dimensions, valves)
• ECG (LBBB, AF, LVH, Q waves)
• CXR (cardiomegaly, interstitial oedema, Kerley B lines, pleural effusions)
• CBC, LFT, RFT, TFT, iron studies, HbA1c
• Cardiac MRI (if cause uncertain)
• Coronary angiography (if ischaemic aetiology suspected)

• Displaced apex beat, S3 gallop, bibasilar crackles, raised JVP, peripheral oedema, ascites
• Echo: dilated, hypokinetic LV, functional MR, elevated filling pressures
• BNP >400 pg/mL, hyponatraemia (poor prognosis), elevated creatinine

• HFpEF (EF ≥ 50%)
• Cardiac tamponade
• Constrictive pericarditis
• Nephrotic syndrome (oedema without cardiac cause)
• Hepatic cirrhosis (ascites, oedema)
• Cor pulmonale (right heart failure from lung disease)
• Severe anaemia

• ACE-I or ARNI (sacubitril/valsartan) — reduces mortality
• Evidence-based beta-blocker (bisoprolol, carvedilol, metoprolol succinate)
• Mineralocorticoid receptor antagonist (spironolactone/eplerenone)
• SGLT2 inhibitor (empagliflozin/dapagliflozin — quadruple therapy)
• Diuretics (furosemide) for symptomatic congestion
• ICD (LVEF <35%, NYHA II-III, on GDMT ≥3 months)
• CRT (LVEF ≤ 35%, LBBB, QRS ≥ 150 ms)

• Sacubitril/Valsartan 49/51 mg BD (titrate to 97/103 mg BD)
• Bisoprolol 2.5 → 10 mg OD (titrate slowly)
• Spironolactone 25–50 mg OD
• Empagliflozin 10 mg OD
• Furosemide 20–80 mg OD (symptom-guided)
• Iron carboxymaltose IV (if ferritin <100 or 100–299 with TSAT <20%)

• Initiate beta-blocker during acute decompensation — avoid until euvolaemic
• ACE-I + ARB + ARNI triple combination — nephrotoxic, hypotension
• NSAIDs — cause fluid retention, antagonise diuretics
• Thiazolidinediones (pioglitazone) — worsen HF
• Verapamil/diltiazem — negative inotropes

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3. HEART FAILURE WITH PRESERVED EF (HFpEF)

• Echo with tissue Doppler (E/e' ≥ 15 = raised filling pressures), diastolic dysfunction grading
• NT-proBNP (often moderately elevated)
• Cardiac MRI (for infiltrative disease — amyloidosis, sarcoidosis)
• Sleep study (OSA in >50%)
• HbA1c, TFTs
• Technetium pyrophosphate scan (for ATTR amyloidosis)

• LVH, concentric remodelling, impaired relaxation, elevated E/e' ratio, preserved LVEF, LA dilatation, pulmonary hypertension

• Cardiac amyloidosis (ATTR or AL) — thickened walls, "sparkling" echo appearance
• HCM
• Constrictive pericarditis
• Hypertensive heart disease
• Fabry disease (young men, angiokeratomas)

• Control HTN (most important modifiable factor)
• Diuretics for congestion
• SGLT2 inhibitors (empagliflozin/dapagliflozin — EMPEROR-Preserved/DELIVER trials)
• Treat AF aggressively (rate/rhythm control)
• Exercise rehabilitation

• Empagliflozin 10 mg OD
• Furosemide 20–40 mg OD PRN
• Amlodipine 5–10 mg OD (HTN control)
• Bisoprolol 5 mg OD (rate control if AF)
• Spironolactone 25 mg OD (some evidence for benefit)

• Aggressive diuresis (preload-dependent — can cause low output state)
• Excessive afterload reduction with vasodilators — precipitate hypotension
• Negative inotropes in severe diastolic dysfunction

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4. ST-ELEVATION MYOCARDIAL INFARCTION (STEMI)

• 12-lead ECG immediately (serial every 30 min if first non-diagnostic)
• High-sensitivity troponin I/T at 0, 1 (or 3) hours
• Echocardiogram (wall motion abnormality, EF, complications)
• CXR (pulmonary oedema, aortic widening to exclude dissection)
• CBC, coagulation (PT/APTT), RFT, LFT, lipids, glucose
• Coronary angiography (primary PCI)

• Hyperacute T waves (earliest), ST elevation, pathological Q waves (later), T-wave inversion
• Troponin rise + fall, elevated CK-MB
• Regional wall motion abnormality on echo
• Possible complications: MR, VSD, free wall rupture, pericarditis, RV infarction

• NSTEMI (no ST elevation, troponin positive)
• Aortic dissection (type A — tearing chest pain, BP differential)
• Acute pericarditis (saddle ST elevation, PR depression, no Q waves)
• Myocarditis (diffuse ST changes, young patient)
• Prinzmetal/vasospastic angina (transient ST elevation, no fixed stenosis)
• PE with right heart strain (S1Q3T3, not ST elevation)
• LBBB (Sgarbossa criteria to assess)
• Benign early repolarisation

• MONA (with caution): Morphine (judicious use), O₂ (if SpO₂ <90%), Nitrates (sublingual), Aspirin 300 mg stat
• Antiplatelet loading: Aspirin 300 mg + Ticagrelor 180 mg (or Clopidogrel 600 mg)
• Primary PCI (preferred, within 90 min of first medical contact)
• Fibrinolysis (if PCI unavailable within 120 min): Alteplase or Tenecteplase
• Anticoagulation: UFH bolus + infusion (during PCI) or Enoxaparin
• Post-MI: Dual antiplatelet (DAPT 12 months), statin, beta-blocker, ACE-I
• Secondary prevention: cardiac rehabilitation

• Thrombolytics: prior haemorrhagic stroke ever, ischaemic stroke <3 months, active internal bleeding, suspected aortic dissection, BP >185/110 (relative), recent major surgery <3 weeks
• Nitrates: RV infarction (ST elevation in II, III, aVF + V4R), recent sildenafil/tadalafil use
• Morphine: delays P2Y12 absorption, may increase mortality in STEMI (CRUSADE data)
• Prasugrel: prior TIA/stroke, age >75 years, weight <60 kg (relative)

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5. NON-STEMI / UNSTABLE ANGINA (ACS without ST elevation)

• Serial 12-lead ECG (ST depression, T-wave inversion, or normal)
• High-sensitivity troponin (positive in NSTEMI, negative in UA)
• GRACE score / TIMI score for risk stratification
• Echo (wall motion, EF)
• Coronary angiography (timing based on risk: <2 hrs immediate, <24 hrs early, <72 hrs delayed)
• Lipid profile, HbA1c, CBC, RFT

• ST depression ≥ 0.5 mm, T-wave inversion; troponin rise (NSTEMI); normal ECG also possible
• Wall motion abnormality on echo (if significant ischaemia)

• STEMI, stable angina, aortic dissection, PE, myocarditis, oesophageal spasm/GORD, musculoskeletal, panic disorder

• Dual antiplatelet: Aspirin 300 mg + Ticagrelor 180 mg (preferred) or Clopidogrel
• Anticoagulation: Fondaparinux 2.5 mg SC OD (preferred, less bleeding) or Enoxaparin
• Beta-blocker for rate/ischaemia control
• Statin (high-intensity), ACE-I
• Coronary angiography ± PCI/CABG based on anatomy

• GPIIb/IIIa inhibitors (eptifibatide/tirofiban): thrombocytopenia <100,000, recent major surgery, active bleeding
• Prasugrel: prior TIA/stroke; do not use before angiography (anatomy unknown)
• Fondaparinux as sole anticoagulant during PCI (catheter thrombosis risk — add UFH)

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6. STABLE CORONARY ARTERY DISEASE (Chronic Coronary Syndrome)

• Resting ECG, CBC, lipids, HbA1c, TFT
• Exercise ECG (Bruce protocol) — positive if >1 mm ST depression
• Stress echo or myocardial perfusion imaging (MPI) — preferred if baseline ECG abnormal
• CT coronary angiography (CTCA) — first-line non-invasive imaging in many guidelines
• Invasive coronary angiography + FFR (Fractional Flow Reserve) for revascularisation decision

• Reproducible exertional chest pain/discomfort, relieved by GTN or rest
• Positive stress test, coronary stenosis ≥70% (or ≥50% for LM) on angiography
• FFR ≤ 0.80 = haemodynamically significant stenosis

• GORD / oesophageal spasm (burning, associated with meals)
• Costochondritis (Tietze syndrome — reproducible on palpation)
• Musculoskeletal chest pain
• Anxiety/panic disorder
• PE (pleuritic, with dyspnoea)
• Pleural/pericardial disease

• Antianginal: Beta-blocker (1st line), CCB, nitrates
• Revascularisation: PCI for symptom relief; CABG preferred for left main, multi-vessel CAD with reduced EF, diabetes
• Antiplatelet: Aspirin 75 mg OD indefinitely
• Statin: high-intensity, LDL target <1.8 mmol/L (or <1.4 if very high risk)
• ACE-I: if co-existing DM, CKD, or HF
• PCSK9 inhibitor (evolocumab/alirocumab): if LDL remains elevated on max statin + ezetimibe

• Short-acting nifedipine alone (without beta-blocker) — reflex tachycardia worsens angina
• Diltiazem + verapamil combination — severe bradycardia, heart block
• Abrupt withdrawal of beta-blockers — rebound angina/MI risk

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7. ATRIAL FIBRILLATION (AF)

• 12-lead ECG (absent P waves, irregularly irregular RR intervals, fibrillatory baseline)
• 24–72 hr Holter monitor (paroxysmal AF)
• Echo (LA size, LV function, valvular disease, thrombus)
• TOE (before cardioversion if AF >48 hrs)
• TFT, CBC, LFT, RFT, CRP
• CHA₂DS₂-VASc score (anticoagulation threshold)

• Irregularly irregular pulse, absent P waves, variable QRS rate, ±LVH, ±LA enlargement
• LA thrombus on TOE (commonest site — left atrial appendage)

• Atrial flutter (sawtooth flutter waves, regular 2:1 or 3:1 block)
• Multifocal atrial tachycardia (≥3 distinct P-wave morphologies — COPD patients)
• Frequent atrial ectopics giving irregular pulse
• AF secondary to: thyrotoxicosis, infection, PE, alcohol, post-surgery

• Rate control (resting HR 60–110): Bisoprolol (1st line), digoxin (low activity patients), diltiazem/verapamil (if no HF)
• Rhythm control (if symptomatic, young, 1st episode): Flecainide (pill-in-pocket for paroxysmal), amiodarone (structural heart disease), DC cardioversion
• Anticoagulation: Apixaban 5 mg BD or Rivaroxaban 20 mg OD (DOAC preferred over warfarin) — if CHA₂DS₂-VASc ≥ 2 (men) / ≥ 3 (women)
• Catheter ablation (pulmonary vein isolation — if symptomatic paroxysmal AF refractory to drugs)

• Flecainide/propafenone: structural heart disease, HF, post-MI — pro-arrhythmic
• Digoxin: WPW syndrome (conducts via accessory pathway → VF), avoid as monotherapy in active lifestyle patients
• Anticoagulation: active major bleeding, haemorrhagic stroke; HAS-BLED score guides bleeding risk
• Verapamil/diltiazem: decompensated HF, pre-excitation syndromes

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8. ATRIAL FLUTTER

• 12-lead ECG (sawtooth flutter waves at ~300/min in inferior leads, commonly 2:1 block → ventricular rate ~150/min)
• Holter, TOE, echo, TFT, CBC

• Regular tachycardia at 150 bpm (2:1 flutter), flutter waves best seen in II, III, aVF, V1
• Carotid sinus massage/adenosine unmasks flutter waves (reveals sawtooth)

• AF (irregular), SVT, atrial tachycardia (distinct P waves different from sinus)

• Rate control: same as AF (beta-blockers, CCBs)
• Cardioversion (electrical or pharmacological) — often very responsive
• Cavotricuspid isthmus (CTI) ablation — highly curative (>95% success)
• Anticoagulation: same principles as AF (thromboembolic risk similar)

• Class IC drugs without AV nodal blocker (may convert to 1:1 flutter with dangerous rate)
• Adenosine for definitive treatment (only diagnostic/temporary effect)

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9. VENTRICULAR TACHYCARDIA (VT)

• 12-lead ECG (wide QRS ≥ 120 ms, AV dissociation, fusion/capture beats)
• Serum electrolytes (K⁺, Mg²⁺), troponin
• Echo (LV function, structural disease)
• Cardiac MRI (scar, infiltration, ARVC)
• Electrophysiology study (EPS) for inducibility and ablation planning

• AV dissociation (pathognomonic), fusion beats, capture beats, concordance in chest leads, Brugada sign (RS interval >100 ms in any chest lead)
• Cannon A waves in JVP (random timing of atrial contraction)

• SVT with aberrant conduction (RBBB/LBBB pattern)
• AF with pre-excitation (WPW — irregular wide complex)
• Hyperkalaemia (peaked T waves, widened QRS)
• Sodium channel blocker toxicity (TCA, flecainide overdose)

• Pulseless VT: CPR + unsynchronised DC shock (200 J biphasic), IV adrenaline, amiodarone 300 mg IV
• Stable VT: IV amiodarone 150 mg over 10 min then 1 mg/min infusion OR synchronised cardioversion
• Long-term: ICD implantation; catheter ablation (especially scar-related VT); treat reversible causes (ischaemia, electrolyte imbalance)

• Verapamil in wide complex tachycardia of unknown origin — haemodynamic collapse risk
• Class IC agents (flecainide) in structural heart disease / post-MI — pro-arrhythmic (CAST trial)
• Amiodarone: pulmonary toxicity, thyroid dysfunction, hepatotoxicity with long-term use

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10. VENTRICULAR FIBRILLATION (VF)

• ECG: irregular, chaotic electrical activity without identifiable QRS complexes
• Post-resuscitation: Troponin, ECG (exclude STEMI — may require immediate angiography), echo, electrolytes, blood glucose, toxicology screen

• No cardiac output, absent pulse, chaotic ECG baseline

• Pulseless VT (also requires defibrillation)
• Asystole (flat line)
• PEA (pulseless electrical activity — organised ECG, no output)
• Artefact/motion on monitor

• Immediate unsynchronised defibrillation (200 J biphasic) — every 2 minutes
• High-quality CPR between shocks
• IV adrenaline 1 mg every 3–5 min (after 3rd shock)
• IV amiodarone 300 mg (after 3rd shock), 150 mg after 5th shock
• Post-ROSC: targeted temperature management (36°C), urgent coronary angiography (if STEMI or suspected ischaemic trigger), ICD implantation

• Delaying defibrillation for any non-essential intervention
• Synchronised cardioversion (reserved for organised rhythms only)

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11. COMPLETE HEART BLOCK (Third-Degree AV Block)

• 12-lead ECG (P waves and QRS complexes completely dissociated, ventricular rate <40 bpm)
• Holter monitor (if intermittent)
• Echo (LV function, aetiology)
• Electrolytes, digoxin level, Lyme serology (if endemic area), ANA, anti-Ro/La (neonatal CHB)
• Coronary angiography (if inferior MI-related)

• Bradycardia, syncope/Stokes-Adams attacks, variable S1 intensity, cannon A waves
• ECG: no relationship between P waves and QRS; narrow escape if junctional, wide if ventricular origin

• Mobitz II (intermittent dropped QRS, consistent PR interval)
• High-degree AV block (2:1, 3:1)
• Inferior STEMI (transient high-degree block)
• Drug toxicity (digoxin, beta-blockers, CCBs)
• Sarcoidosis, Lyme disease, post-surgical (TAVI, valve surgery)

• Haemodynamically unstable: IV atropine 0.5–1 mg (often ineffective in infranodal block)
• Transcutaneous pacing (bridge)
• Transvenous temporary pacing
• Permanent pacemaker (Class I indication — dual-chamber DDD preferred)

• AV nodal blocking drugs (digoxin, verapamil, diltiazem, beta-blockers) — must be withheld
• Atropine unreliable in Mobitz II / complete infranodal block
• Isoprenaline infusion: risk of VF, use only as extreme bridge

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12. SUPRAVENTRICULAR TACHYCARDIA (SVT — AVNRT/AVRT)

• 12-lead ECG (narrow complex tachycardia, rate 150–250, retrograde P waves in AVNRT — RP short)
• Holter, EP study (if ablation planned)
• Echo (exclude structural disease in AVRT)

• Regular narrow complex tachycardia, pseudo R' in V1 (AVNRT), retrograde P waves in ST segment
• AVRT (WPW): delta wave visible in sinus rhythm, short PR, wide QRS

• AF (irregular), atrial flutter (sawtooth, slower rate), sinus tachycardia (gradual onset), VT (if wide complex)

• Vagal manoeuvres (Valsalva — modified supine position with passive leg raise, carotid sinus massage)
• IV adenosine 6 mg rapid bolus → 12 mg → 18 mg (drug of choice for acute termination)
• IV verapamil 5–10 mg (if adenosine fails, no WPW/pre-excitation)
• DC cardioversion (if haemodynamically unstable)
• Long-term: radiofrequency catheter ablation (curative — >95% for AVNRT)

• Adenosine: WPW/pre-excitation with AF (may accelerate ventricular rate → VF); severe asthma; heart transplant patients (extreme bradycardia)
• Verapamil/diltiazem: WPW with AF, pre-excitation, decompensated HF
• Digoxin in WPW: enhances accessory pathway conduction

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13. WPW SYNDROME (Wolff-Parkinson-White)

• ECG: delta wave, short PR (<120 ms), widened QRS, secondary ST-T changes
• EP study (for accessory pathway localisation and ablation)
• Exercise stress test (intermittent pre-excitation)
• Holter (AF burden assessment)

• Pre-excitation on ECG; tachycardia episodes; if AF occurs — irregular wide complex tachycardia (due to rapid conduction via AP → VF risk)

• LBBB, RBBB, Brugada syndrome, LVH with strain, hyperkalaemia

• Radiofrequency catheter ablation (first-line curative treatment)
• Acute AF with WPW: IV procainamide or flecainide (blocks accessory pathway); DC cardioversion if unstable
• Prophylactic treatment (if ablation declined): flecainide, propafenone, amiodarone

• Adenosine, digoxin, verapamil, diltiazem, beta-blockers: all enhance accessory pathway conduction in WPW — risk of inducing VF
• Class IA drugs (quinidine) now rarely used

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14. AORTIC STENOSIS

• Echocardiogram: valve area <1.0 cm² (severe), mean gradient >40 mmHg, peak velocity >4 m/s
• ECG: LVH, LBBB
• CXR: post-stenotic ascending aortic dilatation, calcified aortic valve, cardiomegaly late
• Exercise stress test (asymptomatic severe AS — safety monitored)
• Coronary angiography (pre-operatively or pre-TAVR)
• Low-dose dobutamine stress echo (if low-flow low-gradient AS with reduced EF)
• CT aortogram (TAVR planning — annulus sizing, access)

• Harsh crescendo-decrescendo systolic murmur (right 2nd ICS), radiates to carotids
• Slow-rising, small-volume pulse (pulsus parvus et tardus)
• Narrow pulse pressure, heaving undisplaced apex
• Syncope, angina, dyspnoea = classic symptom triad (SADs)
• Average survival after symptoms: angina 5 yrs, syncope 3 yrs, dyspnoea 2 yrs

• HOCM (murmur increases with Valsalva, decreases with squatting)
• Aortic sclerosis (no gradient, calcification without obstruction)
• Subaortic membrane
• Mitral regurgitation (pansystolic, different location)

• Symptomatic severe AS: TAVR (preferred, age >65 or high surgical risk) or SAVR (surgical, <65 or complex anatomy)
• No medication slows progression
• Asymptomatic severe AS: close monitoring, surgery if LVEF <50% or rapid progression

• Vasodilators (ACE-I, nitrates, hydralazine): severe hypotension — afterload reduction without compensatory increase in cardiac output
• Aggressive diuresis: preload-dependent physiology
• Anticoagulation for AF — use with caution (increased bleeding at valve)

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15. MITRAL STENOSIS

• Echo: mitral valve area (MVA <1.5 cm² = significant, <1 cm² = critical), Wilkins score (calcification + mobility assessment), PAP
• ECG: P-mitrale (bifid P wave), AF, RVH
• CXR: LA enlargement (double right heart border, elevated left mainstem bronchus), pulmonary oedema, Kerley B lines
• TOE (pre-PMBV, assess subvalvular apparatus)
• Cardiac catheterisation (haemodynamic assessment if non-invasive inconclusive)

• Loud S1, opening snap, mid-diastolic rumbling murmur (apex, left lateral decubitus), presystolic accentuation (if sinus rhythm)
• Malar flush (mitral facies — peripheral vasoconstriction with low CO)
• LA enlargement, AF (common complication), pulmonary hypertension
• Haemoptysis (rupture of thin-walled pulmonary veins)

• Mitral regurgitation (pansystolic murmur), HOCM, ASD (fixed splitting), Austin Flint murmur (AR simulating MS), left atrial myxoma (tumour plop)

• Medical: diuretics (congestion relief), beta-blockers/rate-limiting CCBs (rate control in AF)
• Anticoagulation: mandatory if AF present (Wilkins) — DOAC or warfarin
• Percutaneous Mitral Balloon Valvotomy (PMBV): Wilkins score ≤8, pliable non-calcified valve, minimal MR — preferred intervention
• Mitral valve surgery (repair or replacement): if PMBV not suitable, severe MR coexists

• PMBV: significant mitral regurgitation (MR ≥2+), left atrial thrombus, heavy calcification (Wilkins >8), severe subvalvular disease
• Aggressive diuresis: may cause low output state
• Digoxin alone for rate control in AF: inadequate at exercise; combine with beta-blocker

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16. MITRAL REGURGITATION

• Echo (colour Doppler: vena contracta width, EROA, regurgitant volume)
• Cardiac MRI (quantitative regurgitant fraction — gold standard)
• ECG: LA enlargement, AF, LVH
• Exercise stress test (symptoms masked at rest in chronic MR)
• Coronary angiography (pre-surgery)

• Pansystolic murmur (apex, radiates to axilla/back)
• S3, hyperdynamic displaced apex
• Echo: LA/LV enlargement, EF appears falsely elevated (due to low afterload)
• Ruptured papillary muscle (acute MR) — flash pulmonary oedema, haemodynamic collapse

• Tricuspid regurgitation (increases with inspiration — Carvallo's sign)
• VSD (harsh, left sternal edge)
• AS (systolic, different location/radiation)
• HOCM

• Chronic severe MR with symptoms OR EF <60% OR LVESD >40 mm: Mitral valve repair (preferred) or replacement
• MitraClip (transcatheter edge-to-edge repair): for high surgical risk or functional MR
• Acute severe MR: IV nitroprusside + IABP → emergency surgery
• Medical: ACE-I if EF reduced; diuretics for congestion; anticoagulation if AF

• Vasoconstrictors (increase afterload, worsen regurgitant fraction)
• Delay surgery beyond EF <60% — myocardial fibrosis occurs
• Warfarin bridging interruption perioperatively without clear indication

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17. DILATED CARDIOMYOPATHY (DCM)

• Echo (dilated LV, EF <45%, functional MR, functional TR)
• Cardiac MRI (mid-myocardial or epicardial LGE pattern — fibrosis; non-ischaemic pattern)
• Genetic testing (TTN, LMNA, MYH7, SCN5A mutations)
• Endomyocardial biopsy (if giant cell myocarditis, eosinophilic myocarditis, sarcoidosis suspected)
• TFT, alcohol history, drug history (anthracyclines, trastuzumab)
• Coronary angiography / CTCA (exclude ischaemic aetiology)

• Dilated, globally hypokinetic LV; EF markedly reduced; functional MR
• Mid-myocardial LGE on MRI (distinguishes from ischaemic — which has subendocardial/transmural LGE)
• LBBB on ECG (associated with LMNA mutation — poor prognosis, early ICD)

• Ischaemic cardiomyopathy (coronary artery disease)
• Myocarditis (acute onset, elevated troponin, viral prodrome)
• Alcohol-induced cardiomyopathy
• Peripartum cardiomyopathy (last month of pregnancy to 5 months postpartum)
• Tachycardia-induced cardiomyopathy (persistent rapid AF/SVT)
• Takotsubo (stress) cardiomyopathy — apical ballooning, trigger event

• GDMT as HFrEF (ARNI, beta-blocker, MRA, SGLT2-i)
• ICD (LVEF <35% despite GDMT ≥3 months)
• CRT-D (if LBBB, QRS ≥150 ms)
• Urgent re-assessment at 3–6 months (some cases recover — especially myocarditis, peripartum, tachycardia-induced, alcohol-related)
• Bromocriptine (peripartum DCM — if no severe haemodynamic compromise)
• Heart transplant (refractory cases)

• Alcohol (direct myocardial toxin) — must abstain completely
• NSAIDs, thiazolidinediones
• Class I antiarrhythmics (flecainide, propafenone) — pro-arrhythmic
• Verapamil/diltiazem — negative inotropes

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18. HYPERTROPHIC CARDIOMYOPATHY (HCM)

• Echocardiogram (septal wall thickness ≥15 mm [or ≥13 mm + family history/genetic], SAM of mitral valve, LVOTO gradient ≥30 mmHg resting, ≥50 mmHg provoked)
• Cardiac MRI with gadolinium LGE (fibrosis extent — SCD risk)
• 24–48 hr Holter (NSVT = SCD risk factor)
• Genetic testing (MYBPC3, MYH7 — most common mutations)
• Exercise stress test (abnormal BP response — SCD risk factor)
• HCM Risk-SCD calculator (5-yr SCD risk: >6% → ICD recommended)

• Jerky carotid upstroke (due to midsystolic obstruction), double apical impulse
• Systolic ejection murmur increases with Valsalva/standing, decreases with squatting/handgrip
• Mitral regurgitation murmur (due to SAM)
• Asymmetric septal hypertrophy on echo; myocyte disarray on histology

• Aortic stenosis (fixed obstruction, calcified valve)
• Athlete's heart (symmetric hypertrophy, EF normal, no SAM, no gradient)
• Hypertensive LVH
• Storage diseases (Fabry disease — angiokeratoma, no mutation in sarcomere)
• Cardiac amyloidosis (biventricular thickening, "sparkling" echo, typical MRI pattern)

• Symptom control: Bisoprolol or verapamil (first-line, reduce obstruction, improve relaxation)
• Mavacamten (cardiac myosin inhibitor — reduces obstruction; EXPLORER-HCM trial)
• Disopyramide (adjunct for refractory LVOTO)
• Septal reduction: surgical myectomy (gold standard — centres of excellence) or alcohol septal ablation (higher surgical risk)
• ICD (primary or secondary prevention based on SCD risk score)
• Avoid competitive sports/intense exertion

• Nitrates, diuretics, ACE-I/ARBs — worsen LVOTO, reduce preload
• Digoxin — positive inotropy worsens obstruction
• Vasodilating CCBs (nifedipine/amlodipine) — worsen outflow obstruction
• Mavacamten + strong CYP2C19 inhibitors (fluconazole, omeprazole) — elevated drug levels
• Disopyramide alone without AV nodal blocker (increases AV conduction — dangerous)

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19. RESTRICTIVE CARDIOMYOPATHY (RCM)

• Echo (normal or mildly reduced EF, biatrial enlargement, impaired diastolic filling, "speckled" pattern in amyloidosis)
• Cardiac MRI (diffuse subendocardial LGE — amyloid; patchy LGE — sarcoidosis)
• Technetium pyrophosphate scan (ATTR amyloidosis — highly sensitive/specific)
• Endomyocardial biopsy (Congo red stain — apple-green birefringence in amyloid; non-caseating granulomas in sarcoidosis)
• Serum protein electrophoresis, light chains, bone marrow biopsy (AL amyloid)
• Genetic testing (TTR gene mutation — hereditary ATTR)

• Marked biventricular diastolic dysfunction, severely elevated filling pressures
• Prominent x and y descents in JVP, Kussmaul sign (JVP rises on inspiration)
• Conduction disease common (amyloid infiltrates AV node)

• Constrictive pericarditis (surgically correctable — most critical distinction): respiratory variation >25% in MV E velocity on Doppler, absence of tissue annular reversal on MRI
• HFpEF, haemochromatosis, Fabry disease, Löffler endocarditis

• Treat underlying cause:
  • ATTR amyloidosis: Tafamidis (TTR stabiliser — reduces mortality/morbidity, ATTR-ACT trial)
  • AL amyloidosis: haematology (chemotherapy ± autologous stem cell transplant)
  • Sarcoidosis: corticosteroids
  • Haemochromatosis: venesection, chelation
• Diuretics for congestion (cautious — preload dependent)
• Heart transplant (end-stage, selected cases)

• Digoxin in cardiac amyloidosis — binds amyloid fibrils, accumulates → toxicity at therapeutic levels
• Calcium channel blockers in amyloid — profound hypotension
• Aggressive diuresis — preload dependent, may precipitate low output state
• Anticoagulation in AL amyloid — factor X deficiency may coexist

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20. INFECTIVE ENDOCARDITIS (IE)

• Blood cultures ×3 from separate sites before antibiotics (critical)
• Echocardiography: TTE (initial), TOE (superior sensitivity — detects vegetations >2mm, abscesses, prosthetic valve involvement)
• CBC (leucocytosis, anaemia, elevated ESR/CRP)
• Urinalysis (haematuria — immune complex deposition)
• CT chest/abdomen/brain (embolic complications)
• Modified Duke criteria (2 major = definite IE)

• Fever + new or changed murmur
• Peripheral stigmata: Osler nodes (painful, fingers), Janeway lesions (painless, palms/soles), Roth spots (retina), splinter haemorrhages
• Vegetations on echo (most commonly mitral > aortic > tricuspid valve)
• Positive blood cultures (Staph. aureus, Strep. viridans most common)

• Rheumatic fever (Jones criteria, migratory arthritis, erythema marginatum)
• Marantic (non-bacterial thrombotic) endocarditis — hypercoagulable state, malignancy
• Libman-Sacks endocarditis (SLE — antiphospholipid antibody)
• Atrial myxoma (constitutional symptoms, "tumour plop")
• Systemic vasculitis

• IV antibiotics for 4–6 weeks (organism and sensitivity guided)
• Native valve, Strep. viridans (MIC <0.125): Benzylpenicillin 1.2 g 4-hrly × 4 wks ± Gentamicin
• Staph. aureus (MSSA): Flucloxacillin 2 g 6-hrly × 6 wks
• MRSA: Vancomycin × 6 wks
• Prosthetic valve: add Rifampicin
• Surgery indications: HF, uncontrolled infection, abscess, large vegetation >10 mm + embolic event, prosthetic valve dehiscence

• Oral antibiotics alone — insufficient bioavailability for established IE
• Routine prophylaxis for all dental procedures no longer recommended (NICE — only for patients with prior IE, prosthetic valves, congenital HD)
• Anticoagulation with vegetations on native valve — no evidence of benefit; may increase haemorrhagic transformation of embolic strokes

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21. RHEUMATIC HEART DISEASE (RHD)

• Echo (mitral stenosis most common — "hockey stick" deformity of anterior mitral leaflet, commissural fusion; other valve involvement)
• ASO titre (elevated), anti-DNase B
• Throat swab culture (Group A Strep)
• CRP, ESR, CBC
• ECG (prolonged PR interval in acute rheumatic fever)

• Mitral stenosis features (as above); also aortic regurgitation, mitral regurgitation, tricuspid involvement
• Aschoff bodies on histology (pathognomonic of rheumatic carditis)
• Jones criteria for acute rheumatic fever: Major (carditis, migratory polyarthritis, chorea, erythema marginatum, subcutaneous nodules); Minor (fever, raised CRP, prolonged PR)

• Degenerative valve disease (elderly), bicuspid aortic valve, mitral valve prolapse, IE, SLE

• Secondary prophylaxis: Benzathine penicillin G 1.2 million units IM every 3–4 weeks (duration: 10 years or age 25 if no carditis; lifelong if moderate-severe carditis)
• Treat valvular lesions as appropriate (surgical/PMBV)
• Anticoagulation if AF present

• Penicillin allergy → azithromycin or erythromycin as alternatives
• PMBV contraindicated if significant MR present
• Aspirin in children <16 yrs (Reye syndrome) — use paracetamol for fever

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22. CARDIAC TAMPONADE

• Echocardiogram (pericardial effusion, RV diastolic collapse — most sensitive sign, RA systolic collapse, IVC plethora, respiratory variation in Doppler velocities >25%)
• ECG (sinus tachycardia, low QRS voltage, electrical alternans — pathognomonic)
• CXR (globular enlarged cardiac silhouette — >200 mL fluid)
• CT chest (if echo inconclusive, complex/loculated effusion)

• Beck's triad: hypotension + raised JVP + muffled heart sounds
• Pulsus paradoxus >10 mmHg (inspiratory fall in SBP)
• Kussmaul sign absent (present in constrictive pericarditis)
• RV collapse on echo

• Constrictive pericarditis (Kussmaul sign +, pericardial knock, no effusion)
• RV infarction (elevated JVP, hypotension, ST elevation in V4R)
• Tension pneumothorax (absent breath sounds, tracheal deviation)
• Cardiogenic shock (HF signs, no pulsus paradoxus)

• Pericardiocentesis (emergency echo-guided — subxiphoid approach)
• IV fluid resuscitation to maintain preload
• Pericardial drain (leave in situ for effusion >1L or malignant effusion)
• Surgical pericardial window (recurrent malignant effusions)
• Treat underlying cause (malignancy, TB, uraemia, post-cardiac surgery)

• Vasodilators (reduce preload → cardiovascular collapse)
• Aggressive diuresis (same reason)
• Positive pressure ventilation if possible (reduces venous return — worsens haemodynamics)
• Avoid pericardiocentesis if haemorrhagic/traumatic tamponade — may need open surgery

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23. CONSTRICTIVE PERICARDITIS

• Echo with Doppler (respiratory variation in mitral E velocity >25%, tissue Doppler: medial e' > lateral e' — reversal = pathognomonic "annulus reversus")
• Cardiac MRI (pericardial thickness >4 mm, real-time respiratory variation)
• CT chest (pericardial calcification — particularly in TB aetiology)
• Cardiac catheterisation ("square root sign" in RV/LV diastolic waveform, equalisation of end-diastolic pressures)

• Kussmaul sign (JVP rises on inspiration), pericardial knock (early S3), prominent x and y descents ("M" or "W" pattern in JVP)
• Ascites out of proportion to peripheral oedema (mimics liver disease)
• Pericardial calcification on CXR/CT

• Restrictive cardiomyopathy (most important — CT/MRI differentiation; catheterisation; discordant septal motion with respiration on echo)
• Hepatic cirrhosis, nephrotic syndrome, cor pulmonale

• Definitive: Surgical pericardiectomy (complete — "radical decortication")
• Anti-inflammatory (NSAIDs + colchicine) if inflammatory/subacute — may resolve without surgery
• Anti-TB treatment (if tuberculous aetiology — 6–9 months rifampicin-based)
• Diuretics for symptomatic congestion (temporary)

• Digoxin, beta-blockers (patients are rate-dependent for cardiac output)
• Aggressive diuresis before surgery (causes hypovolaemia)

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24. AORTIC DISSECTION

• CT aortogram with contrast (gold standard — 98% sensitivity/specificity)
• CXR (widened mediastinum >8 cm, left pleural effusion, obliteration of aortic knuckle — only ~60% sensitive)
• TOE (for Type A unstable patients — performed in OR)
• ECG (exclude MI, check for pericardial tamponade/haemopericardium)
• Troponin, CBC, coagulation, group & crossmatch, renal function

• Acute onset tearing/ripping chest pain radiating to back (interscapular)
• BP differential between arms >20 mmHg, pulse deficit
• Aortic regurgitation murmur (Type A — ascending aorta involves aortic root)
• Neurological deficits (carotid/spinal artery involvement)
• Intimal flap on CT, true vs false lumen

• STEMI (troponin elevation, ECG changes — may coexist if dissection involves coronary ostia)
• PE, acute pericarditis, pneumothorax, acute aortic syndrome (intramural haematoma, penetrating atherosclerotic ulcer)

• Type A (ascending): Emergency cardiac surgery (in-hospital mortality 1–2% per hour untreated)
• Type B (descending): Aggressive medical management: IV beta-blocker (esmolol/labetalol) → target HR <60, SBP 100–120 mmHg
• Complicated Type B (malperfusion, rupture, progression): TEVAR (thoracic endovascular aortic repair)
• Long-term: strict BP control, serial imaging (MRI/CT at 1, 3, 6, 12 months)

• Thrombolytics — absolutely contraindicated (catastrophic haemorrhage)
• Vasodilators before beta-blockade (reflex tachycardia → increased aortic wall shear stress)
• Anticoagulation unless necessary (e.g., ECMO during surgery)
• Balloon aortic counterpulsation (worsens proximal dissection)

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25. PULMONARY HYPERTENSION (PAH)

• Echo (elevated RVSP estimated from TR jet velocity — Doppler; RV enlargement, IVS flattening "D-sign")
• Right heart catheterisation (diagnostic gold standard: mPAP ≥25 mmHg, PCWP ≤15 mmHg, PVR ≥3 Wood units — for Group 1 PAH)
• CT pulmonary angiography (CTPA) — rule out CTEPH (Group 4)
• V/Q scan (CTEPH: multiple mismatched defects)
• PFTs, polysomnography, ANA, anti-Scl-70, HIV, LFTs
• 6-minute walk test (functional capacity, prognosis)

• Exertional dyspnoea, fatigue, syncope (right heart compromise)
• Loud P2, RV heave, TR murmur, raised JVP, peripheral oedema
• Echo: dilated RV, flattened IVS, pericardial effusion (poor prognosis)

• HFpEF (Group 2 PH — most common globally)
• CTEPH (Group 4 — surgically correctable by pulmonary endarterectomy)
• Interstitial lung disease/COPD (Group 3)
• Portopulmonary hypertension, HIV, connective tissue disease (Group 1)

• Phosphodiesterase-5 inhibitors: Sildenafil 20 mg TDS or Tadalafil 40 mg OD
• Endothelin receptor antagonists (ERA): Ambrisentan 5–10 mg OD or Macitentan 10 mg OD
• Prostanoids: IV Epoprostenol (most effective), inhaled Iloprost, SC Treprostinil
• Riociguat (soluble guanylate cyclase stimulator — PAH and CTEPH)
• Combination therapy: ERA + PDE5-i
• CTEPH: Surgical pulmonary endarterectomy (curative) or Riociguat if inoperable

• PDE5-inhibitors + nitrates — profound hypotension
• ERA drugs: hepatotoxicity risk; teratogenic — mandatory contraception in women
• Calcium channel blockers: only in vasoreactive patients (acute vasoreactivity test positive — ~10%); harmful in non-vasoreactive PAH
• Anticoagulation in SSc-PAH — increased bleeding risk outweighs benefit (unlike idiopathic PAH)

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26. PERIPHERAL ARTERIAL DISEASE (PAD)

• Ankle-Brachial Pressure Index (ABPI): normal 1.0–1.4; 0.7–0.9 = mild PAD; 0.4–0.69 = moderate; <0.4 = critical limb ischaemia
• Duplex Doppler USS (location and severity of stenosis)
• CT angiography (pre-revascularisation planning)
• MR angiography (no contrast — renal impairment)
• Lipid profile, HbA1c, CBC, coagulation

• Intermittent claudication (reproducible exertional calf pain), rest pain, non-healing ulcers, gangrene
• Absent/reduced pedal pulses, pallor on elevation, dependent rubor, venous guttering
• Critical limb ischaemia: ABP <50 mmHg, ABPI <0.4

• Neurogenic claudication (spinal stenosis — worse standing, relieved by forward flexion)
• DVT (acute, unilateral swelling, warmth)
• Popliteal artery entrapment syndrome (young active males)
• Buerger's disease (thromboangiitis obliterans — young smokers, small vessels)
• Diabetic neuropathy (burning/numbness rather than claudication)

• Risk factor modification: smoking cessation, HbA1c control, statin, BP control
• Supervised exercise programme (50% improvement in walking distance)
• Antiplatelet: Clopidogrel 75 mg OD (preferred over aspirin alone)
• Statin: Atorvastatin 80 mg
• Cilostazol 100 mg BD (phosphodiesterase inhibitor — improves claudication)
• Revascularisation: angioplasty ± stenting (short stenoses), bypass surgery (long-segment disease)
• Critical limb ischaemia: urgent revascularisation ± amputation

• Cilostazol: heart failure (any class) — absolute contraindication (class effect of phosphodiesterase inhibitors)
• Vasoconstrictors (ergotamine, triptans) — worsen ischaemia
• Beta-blockers: use with caution in severe PAD (may worsen claudication — but generally safe if cardioprotection needed)

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27. DEEP VEIN THROMBOSIS (DVT)

• Wells DVT score (risk stratification before imaging)
• D-dimer (sensitive but not specific — if low probability + negative D-dimer, DVT excluded)
• Compression Duplex Ultrasound (gold standard — non-compressibility of vein = DVT)
• Venography (rarely needed)
• Thrombophilia screen (if unprovoked, recurrent, or strong family history — test after stopping anticoagulation): Factor V Leiden, Prothrombin G20210A, Protein C/S, Antithrombin III, APLA
• Malignancy screen (if unprovoked DVT >50 yrs)

• Unilateral leg swelling, erythema, warmth, tenderness along deep vein distribution
• Homan's sign (unreliable — do not use)
• Phlegmasia cerulea dolens (massive DVT → venous gangrene — blue, painful, severe oedema)

• Cellulitis (skin warmth, erythema, no venous distribution)
• Ruptured Baker's cyst (posterior knee — US confirms)
• Muscle tear/haematoma
• Superficial thrombophlebitis
• Lymphoedema (bilateral, non-pitting)
• Post-thrombotic syndrome (previous DVT history)

• DOAC: Rivaroxaban 15 mg BD × 21 days then 20 mg OD, or Apixaban 10 mg BD × 7 days then 5 mg BD
• Duration: 3 months (provoked/reversible risk factor); 6 months (unprovoked); indefinite (recurrent/active cancer — use LMWH or DOAC)
• Compression stockings (reduce post-thrombotic syndrome)
• IVC filter: anticoagulation absolutely contraindicated + PE high risk (temporary filter preferred)
• Catheter-directed thrombolysis: extensive iliofemoral DVT with limb-threatening ischaemia

• DOACs: severe renal impairment (CrCl <15 mL/min) — use warfarin
• LMWH: CrCl <30 mL/min — reduce dose or use UFH
• Anticoagulation: active haemorrhage, haemorrhagic stroke <3 months, major trauma/surgery (relative)
• IVC filter alone: does not treat existing DVT — anticoagulate as soon as safe

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28. PULMONARY EMBOLISM (PE)

• ECG (sinus tachycardia most common; S1Q3T3 — right heart strain; new RBBB)
• D-dimer (if PERC negative + Wells score low → exclude PE; if elevated → CTPA)
• CTPA (gold standard for diagnosis)
• V/Q scan (if CTPA contraindicated — pregnancy, renal failure, dye allergy)
• Troponin + BNP (right heart strain markers — risk stratification)
• Echocardiogram (RV dysfunction — intermediate/high-risk PE)
• PESI score or sPESI (haemodynamic risk classification)

• Pleuritic chest pain, dyspnoea, haemoptysis, tachycardia
• Hampton's hump (wedge-shaped opacity on CXR — pulmonary infarction)
• Westermark sign (oligaemia distal to PE on CXR)
• Pleural effusion (exudate — infarction)
• RV strain on echo, elevated troponin/BNP = high-risk intermediate PE

• STEMI (ECG — ST elevation not S1Q3T3), Pneumonia, Pleuritis, Aortic dissection, Acute HF, Pneumothorax, Musculoskeletal

• Low-risk: Outpatient DOAC (Rivaroxaban or Apixaban) — OUTRIGHT/HOME-PE trial criteria
• Intermediate-risk (RV dysfunction + elevated troponin): Anticoagulate fully; consider catheter-directed thrombolysis vs conservative
• High-risk/Massive PE (haemodynamic compromise, SBP <90): Systemic thrombolysis (Alteplase 100 mg IV over 2 hrs) or surgical embolectomy/catheter-directed therapy
• Anticoagulate immediately if high clinical suspicion before imaging confirmed

• Systemic thrombolysis: active major internal bleeding, haemorrhagic stroke ever, ischaemic stroke <3 months, recent major surgery <10 days, head trauma <3 months
• DOACs: antiphospholipid antibody syndrome (triple positive) — use warfarin
• LMWH alone in massive PE: insufficient for rapid thrombus dissolution

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29. AORTIC ANEURYSM (Thoracic/Abdominal)

• USS abdomen (AAA screening — sensitivity >95%; ≥3 cm = aneurysm; ≥5.5 cm (men)/≥5 cm (women) = surgical threshold for AAA)
• CT aortogram (gold standard for size, morphology, iliac involvement, planning repair)
• MRI (radiation-free monitoring — for thoracic aortic aneurysm/connective tissue disease)
• Genetic testing (Marfan: FBN1; Ehlers-Danlos type IV: COL3A1; Loeys-Dietz: TGFBR1/2)
• ECG, TTE (aortic root in Marfan, bicuspid AV)

• Usually asymptomatic — incidental finding
• Pulsatile, expansile abdominal mass (AAA)
• Ruptured AAA: sudden severe back/abdominal pain, hypotension, pulsatile mass (Grey-Turner/Cullen signs — late)
• Thoracic: hoarseness (recurrent laryngeal nerve), dysphagia, back pain, superior vena cava syndrome

• Aortic dissection, renal colic, mesenteric ischaemia, retroperitoneal haematoma, pancreatitis (for ruptured AAA presentation)

• Surveillance (AAA <5.5 cm): USS every 3–6 months if 4.5–5.4 cm; annually if 3–4.4 cm
• Statin + antiplatelet + BP control (reduce expansion rate)
• Elective repair (AAA ≥5.5 cm men/≥5 cm women, or rapid growth >1 cm/year): EVAR (endovascular) preferred over open surgery
• Ruptured AAA: emergency EVAR (if anatomically suitable) or open repair; IV access, O-negative blood, minimal BP resuscitation (permissive hypotension SBP ~70–80 mmHg until surgical control)
• Marfan with TAA: ACE-I/ARB (losartan reduces aortic root dilation rate)

• Aggressive IV fluid resuscitation in ruptured AAA (increases aortic wall stress before surgical control)
• Anticoagulation in AAA without clear indication (may precipitate rupture risk)
• Surgical repair of small asymptomatic AAA (<5.5 cm) — operative risk outweighs benefit

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30. CARDIAC AMYLOIDOSIS

• Echo: biventricular hypertrophy, "granular sparkling" texture, diastolic dysfunction, biatrial enlargement, thickened valves, pericardial effusion
• Cardiac MRI: diffuse subendocardial or transmural LGE with abnormal T1 mapping — highly specific
• ⁹⁹mTc-pyrophosphate (PYP) scan: Grade 2–3 cardiac uptake = ATTR amyloidosis (distinguishes from AL with 97% specificity if serum FLC normal)
• Serum free light chains (FLC), SPEP/UPEP, bone marrow biopsy (AL amyloidosis)
• Genetic testing (TTR mutation — Val30Met most common hereditary ATTR)
• Fat pad or endomyocardial biopsy (Congo red stain → apple-green birefringence under polarised light)
• ECG: low voltage despite thick walls ("voltage-mass discordance") — pathognomonic combination
• 24-hr Holter (AV block, AF common — amyloid infiltrates conduction system)

• Low QRS voltage on ECG + thickened walls on echo (voltage-mass discordance)
• Progressive HF, conduction disease, orthostatic hypotension (autonomic neuropathy — ATTR)
• Carpal tunnel syndrome (often bilateral, years before cardiac involvement — ATTR)
• Macroglossia, periorbital purpura ("raccoon eyes"), easy bruising (AL amyloid)
• Low blood pressure despite previous hypertension ("history of treated hypertension" — clue to ATTR)

• HCM (gene mutation, younger, LVOTO, different MRI pattern)
• Hypertensive LVH (no amyloid features, responds differently on MRI)
• Fabry disease (X-linked, angiokeratomas, renal failure, mid-myocardial LGE posterolateral)
• Sarcoidosis (young, non-caseating granuloma, patchy LGE, AV block)
• Glycogen storage disease (Danon, Pompe)

• ATTR-CM (wild-type or hereditary):
  • Tafamidis 61 mg OD (TTR stabiliser — ATTR-ACT trial: significant reduction in mortality and CV hospitalisations)
  • Acoramidis (recently approved)
  • Patisiran / Eplontersen (RNA interference — reduce TTR production; mainly polyneuropathy indication)
  • Device therapy: pacemaker (AV block), ICD (selected cases — benefit uncertain in amyloid)
• AL amyloidosis: Haematology-led chemotherapy (cyclophosphamide-bortezomib-dexamethasone — CyBorD); autologous SCT (eligible patients)
• Diuretics (cautious) for congestion
• AF: anticoagulation (high thromboembolic risk) — DOAC preferred

• Digoxin: binds amyloid fibrils → drug accumulation → toxicity at therapeutic doses (absolute avoid)
• Calcium channel blockers (verapamil, diltiazem): bind amyloid fibrils → profound hypotension, haemodynamic collapse
• Nitrates: severe orthostatic hypotension in autonomic neuropathy
• Beta-blockers: patients are chronotropically dependent due to diastolic dysfunction — use with extreme caution
• Aggressive rate control in AF — compensatory tachycardia maintains output

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MASTER QUICK-REFERENCE TABLE

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