95% rheumatic; 5% congenital (RARE) ^[1]

This percentage reflects the lecture's traditional teaching and is not universal: the cause of MS is strongly geography- and age-dependent. Rheumatic disease remains dominant globally, while degenerative mitral annular calcification is increasingly important in older patients in high-income settings ^[8].

Gross specimen on the slide: rheumatic MS produces a narrowed “fish-mouth/buttonhole” orifice. Commissural fusion forms the slit-like opening; leaflet thickening and shortening/fusion of the chordae create the rigid funnel below it. This anatomy explains both the opening snap (while leaflets remain mobile) and why heavy calcification predicts poor balloon-commissurotomy results.

Obstruction to LV inflow → ↑LA pressure → ↑pulmonary venous pressure → ↑thickness of pulmonary vascular beds → pulmonary arterial hypertension ("second stenosis") → right heart failure. ^[1]

From first principles: The stenotic mitral valve acts like a dam between the LA and LV. Blood backs up into the LA, then into the pulmonary veins, then the pulmonary capillaries (causing oedema), and eventually the pulmonary arteries remodel (reactive pulmonary hypertension = "second stenosis"). This irreversible pulmonary vascular change further burdens the right ventricle, which eventually fails.

1. Respiratory symptoms — SOB on exertion, PND; 2. Chronic RV failure — congestive cardiac failure; 3. Atrial fibrillation — 50–75% of MS patients develop AF because of ↑LA size; AF is an important cause of cardiac decompensation because: (a) normal LA contraction contributes 20% of LV filling, which becomes more important in MS ("atrial kick"), (b) ↑ventricular rate reduces diastolic filling time, reducing SV and CO; 4. Systemic embolisation — LA enlarged leading to stasis of blood. ^[1]

Mechanism of AF in MS (from senior notes ^[4]): LA dilatation distorts the pulmonary vein–LA junction. Micro-reentrant circuits develop in the dilated, stretched atrial tissue, initiating and sustaining AF.

Malar flush (pulmonary hypertension); (1) Pulse — small volume, irregular if in AF; (2) Venous — loss of 'a' wave in AF, ↑JVP if RHF; (3) Precordium — parasternal heave / tapping apex, loud S1, opening snap (OS), mid-diastolic rumbling murmur (may be enhanced with exercise, lying on left side); (4) Signs of complications — pulmonary oedema, embolisation (peripheral vessels, stroke). ^[1]

Clinical severity indicators:

Duration of murmur; Interval between S2 and OS ^[1]

• A shorter S2–OS interval means higher LA pressure (valve opens sooner) = more severe MS.
• A longer murmur duration means significant gradient persists through more of diastole = more severe MS.

CXR: ↑LA (straight left heart border), pulmonary oedema, Kerley A and B lines. ECG: if sinus — P mitrale (bifid P wave); AF; RVH. Echo: thickened + doming leaflets, parallel diastolic movement of MV, measure MV opening (significant MS if < 1.5 cm²). Cardiac catheterisation: unnecessary if pure MS; to assess associated CAD. ^[1]

Reading the slide images:

• On the paired CXRs, LA enlargement straightens or bulges the left heart border; pulmonary venous congestion and septal lines show the upstream pressure load.
• In parasternal long axis, rheumatic MS shows thickened leaflet tips with restricted opening and anterior-leaflet diastolic doming. In parasternal short axis, trace the smallest orifice at the leaflet tips in mid-diastole—not an oblique cut through the funnel.
• The planimetry example traces an area of about 0.78 cm², an unequivocally severe anatomical narrowing. Valve area must still be integrated with mean gradient, heart rate, flow, symptoms and pulmonary pressure.

1. Diuretics; 2. Rate control if in AF; 3. Anticoagulation (valvular AF) — warfarin. Indications: history of embolisation, paroxysmal or sustained AF. ^[1]

1. Percutaneous balloon valvuloplasty; 2. Valvotomy (closed or open); 3. MVR — if valve calcified or badly destroyed. ^[1]

Balloon valvuloplasty is the procedure of choice for patients with pliable, non-calcified valves with minimal MR and no LA thrombus.

Contraindications for PMC ^[1]:

• MVA > 1.5 cm²
• Left atrial thrombus
• More than mild MR
• Severe or bi-commissural calcification
• Absence of commissural fusion
• Severe concomitant aortic valve disease, or severe combined tricuspid stenosis and regurgitation requiring surgery
• Concomitant CAD requiring bypass surgery

High thromboembolic risk: history of systemic embolism, dense spontaneous contrast in the LA, or new-onset AF. High risk of haemodynamic decompensation: systolic pulmonary pressure > 50 mmHg at rest, need for major non-cardiac surgery, or desire for pregnancy ^[1].

1. Atrial fibrillation; 2. Chest infection; 3. Pregnancy — ↑intravascular volume by 30%. ^[1]

1. Rheumatic — 50% associated with MS; 2. Mitral valvular prolapse; 3. Ruptured chordae tendinae — degenerative/collagen disease (e.g., Marfan's), IE, active rheumatic heart disease; 4. Papillary muscle dysfunction — ischaemia or MI; 5. LV dilatation — enlarged MV ring leading to regurgitation. ^[1]

Causes 1–3 are primary (organic) MR — the valve apparatus itself is diseased. Causes 4–5 are secondary (functional) MR — the valve is structurally normal but doesn't coapt properly because the ventricle is dilated or ischaemic. This distinction matters for treatment: primary MR is fixed by repairing/replacing the valve; secondary MR is addressed by treating the underlying LV dysfunction.

↑LA pressure only during systole, ∴ pulmonary hypertension usually a late feature. Volume overload of LV can lead to LV enlargement and failure. ^[1]

Why pulmonary HTN is late in chronic MR but early decompensation occurs in acute MR: In MS, the LA pressure is elevated throughout diastole. In chronic MR, LA/LV compliance increases gradually. In acute MR (e.g., chordal or papillary-muscle rupture), the normal-sized, non-compliant LA cannot accommodate the regurgitant volume, so LA pressure rises abruptly → flash pulmonary oedema and low forward output. Calling this simply “acute LV failure” (as on the slide) misses the key mechanism.

LV dilatation; S1 not increased; S2 obscured by murmur; S3 usual; pansystolic murmur radiating to axilla. ^[1]

CXR: LV enlargement. Echo: define cause of MR. Cardiac catheterisation: assess severity, associated CAD. ^[1]

1. If symptomatic → repair or MVR; 2. Asymptomatic: ↑heart size or ↓LV function → consider surgery; 3. Functional MR, poor LV and refractory HF. ^[1]

Repair is preferred over replacement when a durable repair is expected because it preserves the native valve and subvalvular apparatus. Transcatheter edge-to-edge repair (TEER) is an option for anatomically suitable patients when surgery is inappropriate/high risk; it is not interchangeable with surgery for every MR phenotype ^[8].

What the procedure diagrams show: surgical repair commonly restores annular geometry with an annuloplasty ring, whereas replacement removes/bypasses the diseased valve with a prosthesis. TEER reaches the LA through a femoral venous–transseptal route and grasps the anterior and posterior leaflets edge-to-edge, reducing the regurgitant orifice without open surgery.

• LA dilatation defined as volume index ≥ 60 mL/m² or diameter ≥ 55 mm in sinus rhythm ^[1]
• Extended HF treatment includes CRT, ventricular assist devices, and heart transplantation ^[1]
• TEER = transcatheter edge-to-edge repair (e.g., MitraClip)

2025 update: the familiar LV-dysfunction triggers for asymptomatic severe primary MR remain important (LVEF ≤60% or LVESD ≥40 mm). The newer guideline also supports earlier expert repair in selected low-risk asymptomatic patients when several adverse markers cluster, reinforcing referral to a high-volume repair centre rather than waiting for overt LV failure ^[8].

Rheumatic — often associated with MS. Non-rheumatic — congenital (bicuspid), subvalvular, supravalvular, calcific. By age: < 60 rheumatic or congenital (bicuspid/unicuspid); 60–75 calcified bicuspid valve (usually male); > 75 degenerative calcification (usually female). ^[1]

Gradient develops across AV obstructing aortic outflow. Compensatory LVH (no cavity dilatation until HF develops). Inadequate increase in CO during exercise. ^[1]

Current haemodynamic definition: severe high-gradient AS is supported by a mean gradient ≥40 mmHg, peak velocity ≥4.0 m/s, and valve area ≤1.0 cm²; discordant low-flow states require integrated assessment rather than applying one number in isolation ^[8]. The slide's “> 50 mmHg” mean-gradient threshold is outdated.

Anatomy in the illustrations: a bicuspid valve has two functional cusps and an eccentric “fish-mouth” systolic opening, whereas congenital valvar stenosis may leave a small central triangular opening. The parasternal-long-axis echo points to thickened/calcified cusps with restricted separation; concentric LVH is the chamber response to the pressure load.

Why LVH develops without dilatation initially: Pressure overload triggers concentric hypertrophy — new sarcomeres are laid in parallel to generate more wall tension to overcome the high afterload. The cavity stays the same size or even shrinks. This is in contrast to volume overload lesions (MR, AR) where the cavity dilates.

Why gradient may be low in HF: If the LV is failing and can't generate adequate flow, the transvalvular gradient will be deceptively low despite severe stenosis. This is "low-flow, low-gradient AS" — echocardiography with low-dose dobutamine can unmask the true severity by increasing flow and revealing the gradient.

1. Exertional dyspnoea; 2. Angina pectoris; 3. Congestive cardiac failure. When AS becomes symptomatic, mortality 50% in 3 years. 4. Syncope or sudden death. ^[1]

Why angina occurs without CAD in AS: The massively hypertrophied LV has increased myocardial oxygen demand. Simultaneously, the elevated LV end-diastolic pressure compresses subendocardial coronary vessels during diastole, reducing coronary perfusion. Supply-demand mismatch → angina.

Why syncope occurs: During exercise, peripheral vasodilation lowers SVR, but the fixed obstruction prevents the necessary increase in cardiac output. Blood pressure drops → cerebral hypoperfusion → syncope. Arrhythmias (from the hypertrophied myocardium) can also cause syncope.

Slow-rising pulse; LVH; ↓A2 (if calcified and severely stenotic); thrill + ejection systolic murmur at aortic area, radiating to neck. ^[1]

Symptomatic → aortic valve replacement. LV impairment may reverse. ^[1]

Options include surgical AVR (SAVR) and transcatheter aortic valve implantation (TAVI/TAVR). The choice is not “old versus young” alone: it integrates age/life expectancy, transfemoral and valve/root anatomy, operative risk, concomitant surgical disease, patient preference and lifetime re-intervention strategy ^[8].

Surgical approaches for SAVR ^[1]: conventional median sternotomy, or minimally invasive approaches (mini-thoracotomy, hemi-sternotomy). The procedural montage contrasts these with TAVI and shows catheter crossing, balloon/valve positioning and stent-frame deployment. Transfemoral access is preferred when feasible; transapical and direct-aortic access shown on the older slide are now uncommon alternatives. The 2025 ESC/EACTS guideline lowered the age favouring TAVI for suitable tricuspid AS from 75 to 70 years, while anatomy, surgical risk, life expectancy and lifetime re-intervention strategy remain Heart-Team decisions ^[8].

1. Rheumatic; 2. Non-rheumatic: IE (diseased or previously normal valve), syphilitic aortitis, bicuspid aortic valve, heritable aortopathy (e.g. Marfan syndrome), inflammatory aortitis, aortic dissection and trauma. ^[1]

Causes can be broadly divided into valve leaflet disease (rheumatic, IE, bicuspid) and aortic root dilatation (Marfan's, syphilis, dissection, seronegative arthropathies). This distinction matters because root dilatation often requires composite graft repair (valve + ascending aorta), not just valve replacement.

Regurgitant volume → ↑LVEDV (with initially normal LVEDP). ↑SV in compensated case by LV dilatation. Deterioration of LV function → ↑LVEDP → SOB + heart failure → early mitral valve closure. Impaired LV function → ↓SV. ^[1]

Acute and chronic AR differ: chronic AR permits eccentric LV remodelling, a large total stroke volume and wide pulse pressure before decompensation. Acute severe AR (IE, dissection or trauma) abruptly raises LV diastolic pressure and can cause pulmonary oedema, hypotension and early mitral closure without time to develop a large LV or dramatic peripheral signs.

Pathology images: rheumatic AR shows thickened, shortened cusps with a triangular central coaptation defect. The historical syphilitic-aortitis plate shows a dilated, scarred ascending aorta and widened annulus pulling otherwise taut cusps apart; ostial narrowing and “tree-bark” medial scarring are classic but now rare findings. Chronic AR produces eccentric LV hypertrophy/dilatation from volume overload—not purely concentric hypertrophy.

1. Collapsing pulse (pulse pressure > 50 mmHg); 2. LV dilatation; 3. Early blowing diastolic murmur following S2. ^[1]

1. Austin-Flint murmur — diastolic murmur across MV (AR jet impinges on anterior mitral leaflet); 2. Duroziez sign — to-and-fro murmur over femoral arteries; 3. Quincke's pulse — capillary pulsation in fingertips or mucous membranes; 4. Traube's sign — pistol-shot (systolic and diastolic) sounds over femoral artery; 5. De Musset's sign — head bobbing with each heartbeat; 6. Corrigan's pulse — rapid upstroke and collapse of carotid artery. ^[1]

These signs reflect the wide pulse pressure of chronic severe AR. They support the diagnosis but neither a pulse pressure > 50 mmHg nor any eponym alone establishes severity; echocardiography is required.

Key surgical thresholds for asymptomatic severe AR: LVEF ≤ 50%, LVESD > 50 mm (or > 25 mm/m² BSA), or significant ascending aortic enlargement ^[1].

A disease caused by microbial infection of the endocardial lining of the heart (or blood vessels). ^[1]

Valvular: MR > MS, AR > AS; prosthetic valves; normal valves in people who inject drugs. Shunts: congenital or post-surgical (VSD, PDA, AV fistula). ^[1]

Why regurgitant lesions predispose more than stenotic lesions: Regurgitant jets create high-velocity flow that damages the endothelium on the low-pressure side of the valve. This damaged endothelium accumulates fibrin and platelets (non-bacterial thrombotic endocarditis / NBTE), which serves as a nidus for bacterial colonisation during transient bacteraemia. Stenotic valves, while damaged, have less jet-stream endothelial injury.

The prophylaxis cartoon makes this sequence visible: endothelial trauma/turbulence → platelet–fibrin nidus → transient bacteraemia → microbial adhesion and vegetation. An intact normal valve is relatively resistant, not immune; virulent organisms such as S. aureus can infect a previously normal valve.

Why people who inject drugs can develop IE on normal valves: injected bacteria enter the venous circulation and can seed the tricuspid valve; particulate/endothelial injury and repeated bacteraemia add risk. S. aureus is prominent, but left-sided and polymicrobial infection also occur—do not assume every case is isolated tricuspid IE.

Clinical features of IE are classified into: (A) Systemic infection, (B) Manifestations of intravascular lesions, (C) Manifestations of immunological reactions. ^[1]

Janeway lesions — macular, non-painful, erythematous, on palms and soles. Osler's nodes — tender papulopustules on the pulp of the finger. ^[1]

Other signs:

• Splinter haemorrhages — linear dark streaks in the nail bed (micro-emboli to nail bed capillaries)
• Roth spots — retinal haemorrhages with a pale centre (immune complex vasculitis of retinal vessels)
• Petechiae — conjunctival, oral mucosa, skin (micro-emboli)

1. Clinical features; 2. Blood cultures — 3 venous cultures before antibiotics; 3. Echocardiograms — vegetations; TOE better delineation of vegetation. ^[1]

Blood-culture sequence: ESC 2023 advises at least three peripheral sets at 30-minute intervals before antibiotics, with aerobic and anaerobic bottles. Do not wait for a fever spike. In haemodynamic instability, obtain them promptly without materially delaying treatment. The 2023 Duke-ISCVID diagnostic criteria removed mandatory timing and separate-venepuncture wording from the criterion itself, so distinguish bedside sampling practice from the formal diagnostic definition [9,10].

TTE vs. TOE: TTE is first-line. TOE is usually required when TTE is positive or non-diagnostic, suspicion remains high despite a negative TTE, or prosthetic material/device infection is possible. A negative echo does not exclude early IE; repeat imaging is appropriate when suspicion persists. Cardiac CT is complementary for peri-annular abscess/pseudoaneurysm, and FDG-PET/CT or WBC-SPECT/CT can materially improve assessment of prosthetic-valve/device infection [9,10].

Key point: the slide's 2015 flowchart captures the TTE→TOE escalation, but current evaluation is multimodality. Prosthetic valves and intracardiac devices warrant a low threshold for TOE plus CT/nuclear imaging when echocardiography is inconclusive [9,10].

Definite IE: 2 major, or 1 major + 3 minor, or 5 minor. Pathologic criteria: (1) microorganisms demonstrated in a vegetation, (2) pathologic lesions confirmed by histology. ^[1]

The two yellow organism tables are useful as a source-and-association map, but their frequency and “sensitivity” columns are historical. Do not infer treatment from organism name alone: use valve type, acquisition setting, species, MIC/susceptibility, renal function and Endocarditis-Team/microbiology advice ^[9].

A large 2009 international cohort shown on the slide reported the following distribution (historical cohort, not a universal present-day prevalence table):

The figure's main visual message is that S. aureus was the largest single slice (31%), followed by oral/viridans streptococci (19%), with sizeable CoNS and enterococcal groups. Current distributions vary by geography, referral pattern, age, prosthetic material and healthcare exposure; ESC 2023 explicitly cautions against treating one registry as universal ^[9].

The slide reviews haemolysis and Lancefield grouping. Group A S. pyogenes causes pharyngitis, scarlet fever, invasive disease and rheumatic fever; group B S. agalactiae causes neonatal and adult invasive infection. ^[1]

These are microbiology reminders, not the common “subacute IE” pair. Group A/B/C/G streptococcal IE is relatively rare, and “SBE” is an imprecise legacy label ^[9].

Causes: (1) prior antibiotics or sampling problems; (2) organisms not recovered by routine culture; (3) non-bacterial mimics.

Current work-up: prior antibiotics are the commonest reason. Inform microbiology early and obtain targeted serology/PCR according to exposure and epidemiology—especially Coxiella burnetii, Bartonella spp. and Tropheryma whipplei, with consideration of Brucella, fungi and other rare agents. Modern automated culture usually detects HACEK organisms, and the correct acronym is Haemophilus/Aggregatibacter, Cardiobacterium, Eikenella, Kingella (not Capnocytophaga) [9,10]. Also reconsider non-bacterial thrombotic endocarditis when cultures and microbiology remain negative.

Obtain blood cultures first, then start prompt empiric treatment when IE is suspected; tailor immediately when the organism and susceptibility are known. Combine antimicrobial therapy with source/device control, complication imaging and surgery when indicated. ^[9]

Follow temperature and haemodynamics, repeat cultures until clearance, monitor renal/hepatic function and blood counts/drug toxicity, and repeat echo or cross-sectional imaging when complications or treatment failure are suspected. ^[9]

Vegetations contain dense organisms within platelet–fibrin material and are difficult to sterilise, which explains prolonged high-exposure regimens. But “only bactericidal drugs work” is too absolute: pathogen-specific IE such as Q-fever endocarditis uses doxycycline-based therapy. Persistent/recurrent fever is not passively accepted for 1–2 weeks; reassess cultures, drug reactions, embolic/metastatic foci, abscess and surgical indications.

• Partial oral/OPAT completion is selective: only after an initial in-hospital IV phase, clinical stability and control of heart failure, abscess, embolic and surgical issues; it is not simply triggered by one satisfactory TOE.
• IE itself is not an indication for anticoagulation or antiplatelets. If the patient already has an indication, continuation/interruption and peri-operative bridging are individualised. Thrombolysis is not recommended for IE-related stroke; thrombectomy may be considered for selected large-vessel occlusion.
• Stroke does not impose one fixed surgical delay: do not delay clearly indicated surgery after TIA or uncomplicated non-haemorrhagic stroke solely because a stroke occurred. Significant intracranial haemorrhage often favours delay, but timing is case-by-case with repeat neuroimaging and the Endocarditis Team.
• Complete CIED-system removal is recommended for confirmed lead/device infection. Surgery is considered for heart failure, uncontrolled infection, peri-annular extension/prosthetic dehiscence and high embolic risk—not from vegetation length alone.

The slide's fixed penicillin/gentamicin, vancomycin and prosthetic-valve combinations are historical examples, not a safe stand-alone prescription. ^[1]

Treatment depends on native versus prosthetic valve, species, MIC, allergy phenotype, kidney function, complications and local resistance. The 2-week beta-lactam/aminoglycoside option applies only to selected uncomplicated susceptible streptococcal NVE with normal renal function. Aminoglycosides are not recommended in staphylococcal NVE because toxicity outweighs unproven benefit, and enterococcal IE does not automatically require gentamicin. Once identification is available, empiric therapy should be narrowed promptly with infectious-disease/microbiology input ^[9].

Think in three indications: (1) heart failure from valve dysfunction, (2) uncontrolled infection/local extension, and (3) prevention of embolism in selected high-risk vegetations. ^[9]

An abnormal valve with turbulence → bacterial adherence → infection. A normal valve → no bacterial adherence → no infection. Antibiotic prophylaxis aims to kill bacteria during the transient bacteraemia caused by a procedure, covering the period when bacteria are in the blood. ^[1]

The lecture shows a pharmacokinetic graph ^[1]: 2 g oral amoxicillin taken 30–60 minutes before a dental procedure produces serum levels above the MIC for streptococci during the entire period of transient bacteraemia.

Primary reasons: (1) IE is much more likely to result from frequent random bacteraemia from daily activities (brushing teeth, chewing) than from procedure-related bacteraemia; (2) Prophylaxis may prevent an exceedingly small number of IE cases; (3) Risk of antibiotic-associated adverse events exceeds the benefit; (4) Maintaining optimal oral health/hygiene is more important than prophylactic antibiotics. ^[1]

The deck reproduces an AHA 2007 four-category list. ESC 2023 recommends dental prophylaxis for patients at high risk, especially ^[9]:

1. previous IE;
2. a surgically or transcatheter-implanted prosthetic valve, or material used for valve repair;
3. untreated cyanotic CHD or CHD repaired with prosthetic material/conduits/shunts (the first 6 months after complete repair when there is no residual defect; longer when a residual defect/prosthetic valve remains).

ESC says prophylaxis should be considered after transcatheter mitral/tricuspid repair and may be considered in heart-transplant recipients; local/AHA recommendations may categorise these differently. Isolated MVP, bicuspid aortic valve and uncomplicated native valve disease do not qualify for routine dental prophylaxis.

At-risk dental procedures manipulate gingival tissue, the periapical region, or perforate oral mucosa. ^[9]

The AHA approach remains primarily dental and does not recommend prophylaxis solely for routine GI/GU procedures. ESC 2023 introduced a weak “may be considered” option for high-risk patients undergoing invasive respiratory, GI, GU, skin or musculoskeletal procedures; evidence is observational, so follow local policy ^[9].

All regimens are a single dose given 30–60 minutes before the procedure.

* Or other first- or second-generation oral cephalosporin in equivalent dosage.
† Cephalosporins should not be used in patients with a history of anaphylaxis, angioedema, or urticaria with penicillins or ampicillin ^[9].

The tutorial uses a 50-year-old man with MVP, 2-week fever, displaced apex, pansystolic murmur at apex, painful red raised lesion on palm (Osler's node), Roth spots on fundoscopy, RBC 2+ in urine, Hb 10.5, WCC 15. This is a textbook IE presentation and directly mirrors the lecture content. Learning objectives include: DDx of reduced exercise capacity/SOB, pathophysiology of HF, presentation + Duke criteria + common pathogens of IE, complications, and treatment ^[2].

• 2023 Fourth Summative Minicase (Case 3): Blood culture growing Staph. aureus, persistent fever, lower limb weakness → infective spondylitis as a complication of bacteraemia/IE. Asks about neurological examination, organisms causing infective spondylitis, and management principles ^[5].
• 2024 Fourth Summative SAQ Q7: Septic arthritis in a child — overlaps with the concept of bacteraemia from a distant source (otitis media) seeding to joints/bone, which shares the same pathogenic mechanism as IE (bacteraemia → seeding of vulnerable site) ^[6].
• Various MCQs test Modified Duke criteria, IE prophylaxis indications, and valve lesion auscultatory findings.