The Daphne Rogers Case — Cardiac Presentation

The Daphne Rogers Case — Cardiac Presentation

Case Introduction

Daphne Rogers is a 68-year-old woman with a background of hypertension, type 2 diabetes, and hyperlipidaemia who presents to the emergency department with central chest pain radiating to her left jaw, of 90 minutes duration. She is diaphoretic, nauseous, and anxious. Vital signs: BP 145/88 mmHg, HR 98/min, RR 18/min, SpO2 94% on air. ECG shows 2 mm ST elevation in leads II, III, aVF and reciprocal ST depression in I, aVL.

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Acute Coronary Syndrome Spectrum

Acute coronary syndrome (ACS) encompasses a spectrum of myocardial ischaemia from unstable angina to acute MI:

Stable angina:

• Fixed atherosclerotic plaque causes flow-limiting stenosis during increased demand (exertion, emotional stress)
• No plaque rupture; no troponin rise
• ECG: ST depression or T-wave changes during pain (reversible); normal at rest
• Management: sublingual GTN (acute), risk factor modification, antianginals (beta-blockers, calcium channel blockers, nitrates, ranolazine), revascularisation (PCI/CABG if symptoms not controlled)

NSTEMI (non-ST elevation MI):

• Partial occlusion of coronary artery (or dynamic occlusion with spontaneous recanalisation); subendocardial ischaemia/infarction
• ECG: ST depression and/or T-wave inversion (dynamic — resolve or evolve), NO persistent ST elevation; new LBBB may represent equivalent
• Troponin: raised (typically rises within 3–6h; high-sensitivity troponin detects earlier)
• Management: MONA-B + DAPT + early invasive strategy (coronary angiography within 24–72h)

STEMI (ST elevation MI):

• Complete occlusion of epicardial coronary artery → transmural ischaemia
• ECG: ≥1 mm ST elevation in ≥2 contiguous limb leads OR ≥2 mm in ≥2 contiguous chest leads; new LBBB; posterior MI (tall R in V1-V2 + ST depression = posterior STEMI equivalent)
• Troponin: rises within 3–6h, peaks 24h (cTnI) or 12–24h (cTnT)
• Daphne: inferior STEMI — ST elevation in II, III, aVF → right coronary artery (RCA) territory (supplies posterior-inferior LV and usually AV node)
• Reperfusion is mandatory and time-critical: "time is muscle"

ECG localisation of STEMI:

• II, III, aVF → Inferior → RCA (85%) or LCx
• V1-V4 → Anterior → LAD (left anterior descending)
• I, aVL, V5-V6 → Lateral → LCx
• V1-V2 ST depression + tall R → Posterior → wrap-around LCx or RCA
• V4R (right-sided lead) ST elevation → Right ventricular MI (complication of inferior STEMI — haemodynamic significance)

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Troponin Kinetics

Cardiac troponin I (cTnI) and troponin T (cTnT) are structural proteins in the troponin-tropomyosin complex that regulate actin-myosin interaction. They are highly cardiac-specific (cTnI is cardiac-exclusive; cTnT has high-sensitivity assays).

• Onset of elevation: ~3–6h after myocyte necrosis begins (time for release from damaged cells into bloodstream); high-sensitivity (hs-cTn) assays detect rise earlier (~1–3h)
• Peak: cTnI peaks at ~24h; cTnT peaks ~12–24h; may rise with reperfusion (wash-out phenomenon)
• Return to normal: cTnI by ~5–7 days; cTnT may remain elevated up to 14 days (useful for late presenters)
• Serial troponin: ESC recommends 0h/1h or 0h/2h algorithm with hs-cTn; rising trend (delta troponin) + absolute value used for rule-in/rule-out of NSTEMI
• Non-ACS causes of troponin rise: Pulmonary embolism (RV strain), myocarditis, sepsis, renal failure, cardiac contusion, cardioversion, Takotsubo cardiomyopathy, hypertensive emergency

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Initial Management: MONA-B

Mnemonic (now partially superseded but useful framework):

• M — Morphine: IV morphine 2.5–5 mg for pain/anxiety; reduces sympathetic activation and cardiac work; use cautiously (may cause nausea, may delay P2Y12 inhibitor absorption, associated with worse outcomes in observational studies — use judiciously, not reflexively)
• O — Oxygen: Target SpO2 94–98%; avoid hyperoxia (increased ROS, may worsen myocardial injury); only give if SpO2 <94%
• N — Nitrates: Sublingual GTN (glyceryl trinitrate) for pain; vasodilator (venous > arterial); reduce preload and myocardial O2 demand; CONTRAINDICATED if SBP <90 mmHg, RV MI (dependent on preload), or recent PDE5 inhibitor use (e.g., sildenafil — dangerous hypotension)
• A — Aspirin: 300 mg loading dose (chewed for rapid absorption) → irreversibly inhibits COX-1 in platelets → reduced TXA2 → reduced platelet activation; reduces mortality in ACS (ISIS-2 trial)
• B — Beta-blockers: Oral metoprolol (if HR elevated, no contraindications); reduce heart rate and contractility → decrease O2 demand; reduce VF risk; improve mortality in STEMI; contraindicated in acute LVF, Killip class ≥3, bradycardia, severe bronchospasm

Dual antiplatelet therapy (DAPT):

• Aspirin 300 mg load → 75–100 mg daily maintenance
• P2Y12 inhibitor (in addition to aspirin): ticagrelor 180 mg load (preferred for STEMI; reversible, faster onset) OR prasugrel 60 mg load (post-PCI, if no prior stroke/TIA) OR clopidogrel 300–600 mg load (less potent, requires hepatic conversion to active metabolite via CYP2C19 — poor metabolisers respond poorly)
• Duration: 12 months DAPT after ACS; then aspirin monotherapy

Reperfusion decision:

• Primary PCI (percutaneous coronary intervention): Preferred if available within 120 min of first medical contact (FMC); direct catheterisation and stenting of culprit artery; superior to thrombolysis for mortality, reinfarction, and stroke
• Fibrinolysis (thrombolysis): If primary PCI not available within 120 min AND within 12h of symptom onset; tenecteplase (TNK-tPA) or alteplase (tPA) — plasminogen activators; assess for reperfusion at 60–90 min (>50% ST resolution = success); transfer to PCI centre for rescue PCI or routine coronary angiography within 3–24h

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Heart Failure: Classification and Pathophysiology

Daphne's inferior STEMI may be complicated by acute heart failure. Heart failure is defined as a clinical syndrome resulting from structural or functional cardiac abnormality.

Systolic (HFrEF — heart failure with reduced ejection fraction):

• EF <40%; impaired LV contractility
• Causes: MI (commonest), dilated cardiomyopathy, myocarditis, valvular disease
• Pathophysiology: reduced CO → RAAS activation (angiotensin II → aldosterone → Na+/water retention → volume overload → cardiac remodelling); SNS activation (noradrenaline → increased HR/contractility acutely, but chronic catecholamine exposure → β-receptor downregulation → cardiomyocyte apoptosis, hypertrophy)
• Treatment: ACEi/ARB (reduce afterload, reverse remodelling), beta-blocker, mineralocorticoid receptor antagonist (spironolactone/eplerenone), SGLT2 inhibitor, diuretics (symptom relief), ARNI (sacubitril-valsartan)

Diastolic (HFpEF — heart failure with preserved ejection fraction):

• EF ≥50%; impaired LV relaxation and filling (diastolic dysfunction)
• Causes: hypertension (LV hypertrophy → stiff ventricle), diabetes, obesity, ageing — all relevant to Daphne
• Pathophysiology: impaired myocardial relaxation → elevated LV filling pressures → pulmonary venous hypertension → dyspnoea, pulmonary oedema
• Treatment: SGLT2 inhibitors (empagliflozin, dapagliflozin) — only class proven to reduce HHF/CV death in HFpEF (EMPEROR-Preserved, DELIVER); diuretics for congestion; target underlying hypertension, AF, diabetes

Killip classification (in-hospital mortality in STEMI):

• Killip I: No HF signs — mortality ~6%
• Killip II: S3 gallop, bibasal crackles — mortality ~17%
• Killip III: Frank pulmonary oedema — mortality ~38%
• Killip IV: Cardiogenic shock (SBP <90 + end-organ hypoperfusion) — mortality ~80%

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Neurohormonal Activation in Heart Failure

RAAS: Low renal perfusion → juxtaglomerular cells release renin → cleaves angiotensinogen → Ang I → ACE → Ang II → (1) vasoconstriction (AT1 receptors on vascular smooth muscle); (2) aldosterone release from adrenal cortex → Na+/water retention; (3) ADH/AVP release → water retention; (4) fibrosis, inflammation, cardiomyocyte hypertrophy. ACEi/ARBs block this pathway.

SNS: Reduced CO → baroreceptor unloading → increased SNS tone → noradrenaline release → acute: increased HR (β1), contractility (β1), vasoconstriction (α1); chronic: maladaptive — β-receptor downregulation, oxidative stress, arrhythmias, hypertrophy, apoptosis. Beta-blockers block chronic SNS harm.

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Cardiogenic Shock

Daphne could deteriorate into cardiogenic shock (Killip IV).

Definition: Persistent hypotension (SBP <90 mmHg) + signs of end-organ hypoperfusion (oliguria, confusion, cool/clammy peripheries, lactate >2 mmol/L) despite adequate filling pressure.

Haemodynamic profile: High PCWP (pulmonary capillary wedge pressure) > 18 mmHg (high LV filling pressure), low cardiac output/index (CI <2.2 L/min/m²), high SVR (compensatory vasoconstriction). Distinguishes from other shock types on right heart catheterisation (Swan-Ganz).

Management:

• Immediate reperfusion (PCI — most effective intervention; reduces mortality)
• Inotropes: dobutamine (β1 + mild β2 agonist → positive inotropy + vasodilation → increased CI + reduced afterload; 2.5–20 mcg/kg/min IV); milrinone (PDE3 inhibitor)
• Vasopressors if profound hypotension: noradrenaline (α1 + β1; maintains MAP while inotrope titrated)
• Intra-aortic balloon pump (IABP): Mechanical support device inserted into descending aorta; inflates in diastole → augments coronary perfusion pressure; deflates in systole → reduces afterload. IABP-SHOCK II trial: did not reduce 30-day mortality vs optimal medical therapy — now reserved for selected patients. Newer devices: Impella (LVAD — rotary blood pump, percutaneous), VA-ECMO (venoarterial extracorporeal membrane oxygenation) for refractory cardiogenic shock.