Cardiac conditions - ischaemic heart disease
Description
IHD in the older patient - the disease is the same; the presentation, the evidence base and the risk-benefit calculation are not.
- Spectrum: stable angina - unstable angina - NSTEMI - STEMI - ischaemic cardiomyopathy - sudden cardiac death
- Type 1 MI = plaque rupture/erosion with thrombus
- Type 2 MI = supply-demand mismatch without plaque rupture - the dominant mechanism in older inpatients
- Sepsis, anaemia, GI bleed, tachyarrhythmia, hypotension, hypoxia, severe AS
- *Treating the precipitant, not antiplatelets and angiography, is the treatment*
Presentation in the older patient - why it is missed
- Chest pain is frequently ABSENT (~1/3 of MIs over 75 are painless)
- Presents instead as: dyspnoea (the commonest anginal equivalent), delirium, falls, syncope, fatigue, nausea, epigastric pain, sudden functional decline, "off legs"
- Silent infarction is common in diabetes, dementia and the very old
- Functional limitation from arthritis, COPD or frailty masks exertional angina - the patient never walks far enough to get it
Epidemiology
- Leading single cause of death in Australia; ~2/3 of MI deaths occur in people over 75
- Prevalence rises steeply with age: >20% of those over 80 have established IHD
- Over-75s are systematically under-represented in trials - most evidence is extrapolated
- Aboriginal and Torres Strait Islander people: IHD onset 10-20 yr earlier, higher mortality
- Women present later, with more atypical symptoms, and are less often revascularised
Aetiopathogenesis
- Atherosclerosis: endothelial injury -> LDL retention and oxidation -> macrophage foam cells -> fibrous plaque -> rupture or erosion -> platelet-rich thrombus
- Vulnerable plaque = large lipid core, thin fibrous cap, inflammation - not necessarily the most stenotic
- Ageing-specific contributors
- Arterial stiffening -> inc systolic BP, wide pulse pressure, inc afterload and LVH -> inc myocardial O2 demand with dec coronary perfusion pressure in diastole
- Microvascular dysfunction and endothelial ageing - angina with unobstructed arteries (ANOCA/INOCA) is common in older women
- dec beta-adrenergic responsiveness -> blunted tachycardic response, dec exercise capacity
- Coronary calcification -> harder PCI, more complications
- Risk factors: age, male sex, smoking, hypertension, diabetes, dyslipidaemia, CKD, family history, obesity, inactivity
- In the very old, the relative risk conferred by lipids attenuates while absolute event rates rise - the absolute benefit of treatment is often greater, not smaller
Diagnosis
A. History
- Character, radiation, duration, precipitants and relieving factors; anginal equivalents in the frail
- Prior events: MI, PCI (stent type and date), CABG (graft anatomy), previous reperfusion, ejection fraction
- Precipitants of a type 2 event: GI bleed, infection, anaemia, new arrhythmia, dehydration, drug change
- Baseline function and cognition; premorbid exercise tolerance; goals of care - establish these before, not after, deciding on invasive management
B. Examination
- Haemodynamics, signs of heart failure, new murmur (acute MR from papillary muscle dysfunction, or VSD), pericardial rub
- Femoral/radial puncture sites, bruising (antithrombotics), infusions running (heparin, nitrate, inotrope, antiarrhythmic)
- Pacemaker/ICD, peripheral and carotid vascular disease, AAA
- Aortic stenosis - a frequent coexisting cause of angina in this age group
C. Troponin - interpret with age in mind
- High-sensitivity troponin: a RISE AND/OR FALL with at least one value above the 99th percentile is required for MI
- *Chronically elevated troponin is the norm in older patients with CKD, heart failure, AF or LVH - a single raised value is not an MI*
- Elevated without ACS: PE, myocarditis, sepsis, tachyarrhythmia, heart failure, renal failure, stroke, contusion
D. ECG
- Serial and comparative; LBBB, paced rhythm and LVH obscure ST analysis (use Sgarbossa criteria)
- Posterior leads if ST depression V1-V3
E. Further investigation - after an event
- Echocardiography: LV function, regional wall motion, mechanical complications (acute MR, VSD, LV thrombus, free wall rupture), valve disease
- Residual ischaemia: exercise or stress echo, CT coronary angiography (high calcium score limits interpretability in the old), stress perfusion MRI/MPI, or invasive angiography
- Functional imaging is often preferable in the frail - avoids contrast nephropathy and vascular access complications
- Bloods: FBE (anaemia), UEC, HbA1c, lipids, TFT, iron studies
Management
A. Acute coronary syndrome
- STEMI: primary PCI regardless of age where the goals of care support it - absolute benefit is greatest in the old
- NSTEMI: an early invasive strategy benefits older patients, but bleeding and contrast risk are higher
- Age alone is never the reason to withhold angiography; frailty, cognition, comorbidity and the patient's goals are
- Antithrombotics
- Aspirin + a P2Y12 inhibitor; DAPT for 12 months by default if not at high bleeding risk
- *Prasugrel is contraindicated over 75 and under 60 kg or with prior stroke/TIA[[c2]]; clopidogrel is often the safer P2Y12 inhibitor in the frail elderly*
- De-escalation strategies are explicitly endorsed: shortened DAPT in high bleeding risk, or transition to ticagrelor monotherapy from 1 month post-PCI in those who tolerate it
- Add a PPI where there is GI bleeding risk - almost everyone over 75 on DAPT
- Dose-adjust anticoagulants for weight and renal function - the commonest iatrogenic bleed in geriatric cardiology is an unadjusted enoxaparin dose
- Triple therapy (DAPT + anticoagulant) should be as short as possible - usually a week, then dual therapy
B. Secondary prevention - the prognostic drugs
- Aspirin indefinitely
- High-intensity statin for everyone - atorvastatin 40-80 mg or rosuvastatin 20-40 mg
- Target LDL <1.4 mmol/L; add ezetimibe, and then a PCSK9 inhibitor or inclisiran, if not achieved - the 2025 guideline moved from "maximally tolerated statin" to "statin plus non-statin to target"
- Statin benefit persists into the ninth decade in secondary prevention - do not stop a statin for age alone; do review it when life expectancy is under ~1 year
- Beta blocker - clear benefit with reduced EF; benefit after uncomplicated MI with preserved EF is now questioned and long-term continuation is not mandatory
- ACE inhibitor or ARB - LV dysfunction, diabetes, hypertension, CKD
- MRA if EF <=40% with heart failure or diabetes
- SGLT2 inhibitor if heart failure or diabetes
- Cardiac rehabilitation - refer everyone; exercise, diet, weight, smoking cessation, psychological support
- *Uptake in older patients is ~half that of younger patients despite equal or greater benefit*
- Influenza and COVID vaccination; influenza vaccine reduces cardiovascular events post-MI
C. Chronic stable angina
- Symptom control: beta blocker or calcium channel blocker first; long-acting nitrate, ivabradine, nicorandil, ranolazine, perhexiline as add-ons
- Revascularisation improves symptoms; in stable disease it does not reduce mortality over optimal medical therapy (ISCHEMIA)
- Ask what the angina actually limits - in a housebound 92-year-old, medical therapy may be all that is needed
D. Geriatric-specific considerations
- Correct the precipitant in type 2 MI - transfuse, treat sepsis, rate-control AF, stop the offending drug
- Deprescribe and rationalise - dual antiplatelets + anticoagulant + NSAID + SSRI is a GI bleed waiting to happen
- Postural hypotension and falls - measure lying and standing BP after every uptitration; falls risk does not outweigh the benefit of secondary prevention, but the dose may need to
- Delirium prevention during the admission; early mobilisation
- Renal protection - hydrate before contrast, minimise contrast volume, hold nephrotoxins
- Frailty assessment (Clinical Frailty Scale) to inform, not to ration - it predicts outcome better than age
- Advance care planning, ICD deactivation discussions, and a clear ceiling of care documented
Associations
- Heart failure (ischaemic cardiomyopathy), atrial fibrillation, ventricular arrhythmia
- Peripheral arterial disease, carotid disease, abdominal aortic aneurysm, renovascular disease
- Diabetes, CKD, obstructive sleep apnoea, anaemia, iron deficiency
- Depression and anxiety after MI - independently predict worse outcome; screen
- Cognitive impairment and delirium
- Aortic stenosis and amyloidosis (both cause exertional chest pain in the elderly)
- Frailty, sarcopenia, polypharmacy
Natural history & complications
- Post-MI mortality rises steeply with age - in-hospital mortality over 85 is several times that under 65
- Outcomes after MI in the elderly are driven by: LV function, renal function, revascularisation, frailty and cognition - frailty adds prognostic information beyond ejection fraction
- Higher rates of re-infarction, heart failure, stroke, bleeding and delirium; longer stay and higher rates of new institutionalisation
Complications to look for
- Arrhythmia (AF, VT/VF, heart block - especially inferior MI), heart failure and cardiogenic shock
- Mechanical: acute MR (papillary muscle rupture), VSD, free wall rupture, LV aneurysm and thrombus - days 2-7; a new murmur with haemodynamic deterioration
- Pericarditis (early) and Dressler syndrome (weeks)
- Bleeding, contrast nephropathy, hospital-acquired delirium and deconditioning
Monitor
- Symptoms, BP (lying and standing), heart rate, weight, renal function and potassium after ACEi/MRA changes
- Lipids at 4-12 weeks then annually; HbA1c; FBE if on antithrombotics
- Echo at 6-12 weeks if EF was reduced - reassess for ICD eligibility
- Function, cognition, falls and medication burden at each review
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