Ischaemic Heart Disease

This page covers the perioperative management of patients with known ischaemic heart disease, including previous acute coronary syndromes and stent insertion.

There is a separate, albeit closely interrelated, page on (de novo) perioperative myocardial infarction.

There was a CRQ in March 2020 (75% pass rate) focussing specifically on drug-eluting stents, with only positive feedback from the examiners.

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IHD is the commonest cause of death un the UK, and also the commonest cause of premature death
60% of patients who die within 30 days of surgery have evidence of ischaemic heart disease

Non-modifiable	Modifiable
Age: ↑ incidence with age	Smoking: ↑ incidence 60%
Gender: 5x ↑ risk in males ≥50yrs	Serum cholesterol: incidence ↑↑ once LDL:HDL ratio >4:1
Family history of IHD	Hypertension (systolic or diastolic)
	Diabetes mellitus
	Obesity

Deposition of lipid and smooth muscle proliferation causes atheromatous plaques within the coronary vasculature
This causes luminal narrowing and restricts coronary blood flow
Subsequently, when myocardial oxygen demand increases there is an inability for supply to concurrently increase, leading to ischaemia
Furthermore, plaque rupture may precipitate thrombosis, vessel occlusion and MI

Factors affecting myocardial oxygen supply/demand

Oxygen supply	Oxygen demand
Heart rate: a low/normal HR is ideal for max. diastolic CBF	Heart rate: tachycardia causes ↑ demand and a ↓ diastolic filling time
Coronary perfusion pressure (= AoDP - LVEDP)	Contractility: ↑ demand in stress due to neurohumoral activation
Coronary artery diameter: as per Hagen-Poiseuille eqn.	Afterload / ventricular wall tension
Arterial oxygen content i.e. [Hb] and P_aO₂	Tissue mass e.g. higher in hypertrophy
	Temperature e.g. cold cardioplegic solutions ↓ myocardial O₂ consumption

Coronary stents are inserted to reduce coronary artery re-stenosis following balloon angioplasty, which otherwise occurs in up to 40%
Stents can be broadly classified as:

Bare metal stents (BMS)
Drug-eluting stents (DES)

Stent re-stenosis

A feared complication of coronary stents is re-stenosis

As part of the normal healing process, there is neo-intimal hyperplasia with growth of the scar tissue around the stent mesh
On some occasions, the growth leads to occlusion of the coronary lumen
This process peaks in the third month post-stent insertion and plateaus at six months post-procedure
For bare metal stents, re-stenosis requiring repeat intervention occurs in 15%, hence the creation of drug-eluting stents

Drug eluting stents

The stent's metal struts are coated in a thin polymer coating of anti-proliferative substance e.g. sirolimus or paclitaxel, which inhibit neointimal hyperplasia
Reduce the incidence of re-stenosis to <2%
However, once the polymer coating dissolves there is bare metal uncovered, especially as the polymer coating delays re-endothelialisation of the stent struts
This leads to a longer-term risk of stent thrombosis

Stent thrombosis

The presence of exposed metal struts in the coronary arteries is highly thrombogenic
Stent thrombosis is a potentially devastating complication, leading to MI (50%) or mortality (20-45%)
Both BMS and DES are at risk of thrombosis, necessitating the use of anti-platelet regimens

Anti-platelet regimens reduce the incidence of stent thrombosis to <1%, typically consisting of:

Aspirin, often lifelong
P2Y₁₂ inhibiting drug (e.g. prasugrel, ticagrelor or clopidogrel) for 1yr following ACS

In order to reduce the bleeding risk associated with DAPT, some patients undergo:

DAPT de-escalation i.e. switching from a potent P2Y₁₂ inhibitor to clopidogrel after 3 months
Abbreviated DAPT therapy i.e. only 3-6 months of DAPT before anti-platelet monotherapy thereafter

Premature cessation of anti-platelet therapy is the strongest predictor of subsequent stent thrombosis

Stopping clopidogrel in the high-risk period increases the risk of stent thrombosis by 30x
Stopping all antiplatelet agents increases the relative risk of coronary thrombosis by 90x

Risk factors for thrombosis:

Clinical factors	Procedural factors
Premature DAPT cessation	Long or overlapping stents
Renal failure	Multiple or complex lesions
Diabetes mellitus	Small coronary vessels
EF <30%	Suboptimal angiographic results

The risk-balance equation is between ceasing or continuing anti-platelet therapy

Ceasing anti-platelet therapy risks stent thrombosis

This is especially so in the oft-hypercoagulable state post-operatively, which lasts at least seven days following major surgery

Continuing anti-platelet therapy risks peri-operative bleeding

Other sequelae may include requirement for blood transfusion, prolonged ICU & hospital length of stay, or need for repeat surgical intervention

Assessing risk

Bleeding risk	Thrombotic risk
Nature of surgery	Type, number and location of stents
Perceived haemorrhagic risk	Duration since stent insertion
Consequences of excessive bleeding	Previous re-stenosis or thrombosis
Other patient factors increasing risk	Other risk factors for thrombosis
Urgency of surgery	Antiplatelet regimen and duration
Available alternatives

The highest risk period for discontinuing DAPT is within:

2 weeks of balloon angioplasty
6 weeks of BMS insertion
6 weeks of MI
6-12 months of DES insertion

Perioperative management of DAPT

Overall requires an individualised, MDT-led approach including Cardiology, Surgical, Anaesthetic and Haematology input

Aspirin is generally continued, except:

For procedures associated with high risk of bleeding or complications of bleeding (e.g. spinal surgery, neurosurgery, some ophthalmological procedures)
For patients in whom methods of managing major bleeding is more complex e.g. Jehovah's witnesses refusing blood transfusion

For patients on DAPT who are in the high risk period (see above) requiring;

Elective surgery - should have surgery delayed until after the high risk period
Emergency surgery - should proceed with consideration of platelet transfusion to reverse the actions of aspirin and clopidogrel
Urgent surgery - depends on bleeding risk:

Low surgical bleeding risk; continue DAPT
Intermediate surgical bleeding risk: continue aspirin but consider stopping clopidogrel, or switching clopidogrel monotherapy to aspirin monotherapy
High bleeding risk; stop clopidogrel ± aspirin and consider bridging therapy

Bridging therapy may be used in scenarios where clopidogrel is held, using a reversible, short-acting agent in lieu of an irreversible, long-acting agent
No strong evidence for one regimen over another, although options include

Unfractionated heparin infusion targeted to APTTr
Gp IIb/IIIa inhibitor infusion (e.g. tirofiban), which may be titrated to maximum amplitude on TEG/ROTEM
LMWH subcutaneously
NSAIDs e.g. the reversible, short-acting COX inhibitor flurbiprofen

Perhaps counterintuitively, a recent study (BJA, 2018) found neither withdrawal nor partial discontinuation of antiplatelet therapy increased the risk of perioperative major adverse cardiac events
Indeed, the predictors for major cardiac events were:

Recent myocardial infarct
Lack of any preoperative antiplatelet therapy
Perioperative major bleeding events
CKD
Diabetes mellitus requiring insulin

Patients with a history of ischaemic heart disease are often on multiple agents
In general, all drugs (except ACE-I) should be continued in the perioperative period

Anti-anginal agents

Nitrates: reduce myocardial oxygen demand and improve myocardial perfusion
Calcium channel blockers: reduce coronary vascular resistance and systemic vascular resistance (afterload)
β-blockers: reduce myocardial oxygen demand and provide mortality benefit

Anti-platelet agents

Aspirin, which reduces platelet activation and may reduce death in unstable by 50%
Clopidogrel, which may act synergistically
± anti-thrombotic agents e.g. LMWH

Lipid lowering agents

Statins: reduce fatal and non-fatal MI rates

ACE-inhibitors

The HOPE trial demonstrated ACE-I can reduce cardiovascular mortality & revascularization rates, especially for those with concurrent HTN or DM

Perioperative management of the patient with ischaemic heart disease

The peri-operative period may provoke myocardial ischaemia by increasing myocardial oxygen demand and/or reducing supply
Regardless of DAPT management, patients with stented ischaemic heart disease are at high risk of:

Major bleeding events during admission (≤37%)
Major adverse cardiac events within 90 days post-operatively (≤15%)
Mortality (≤3%), with a higher risk from major vascular surgery

History and examination

Full history, focusing on:

Current anginal or other cardiac symptoms
Current medications
Previous myocardial events
Previous coronary revascularisation, including type of stents, or CABG

Investigations

Bloods including FBC, U&E, LFT and clotting
Group and save, especially if DAPT is to be continued
Up-to-date ECG
CXR
TTE
Assessment of functional capacity

Timing of surgery

Patients who've had a prior myocardial event are at high risk of re-infarct if surgery within 3 months

For patients who've had prior drug-eluting stents, delay surgery where possible for 6 - 12 months

Optimisation

Cardiology opinoin

Especially if high risk e.g. cardiac event or intervention within past six weeks, recurrent or unstable disease
Optimisation of drugs

Drug management

See section above re: management of DAPT
Typically beneficial to continue anti-anginal medications, acknowledging that they may contribute to hypotension intra-operatively

Premedication with benzodiazepines may help reduce anxiety-related tachycardia

The overall goal is to ensure myocardial oxygen delivery exceeds demand

Monitoring and access

AAGBI as standard
Arterial line insertion prior to induction
May require CVC, depending on nature of surgery and need for vasoactive drugs
Intra-operative TOE may help monitor ventricular function, RWMA, cause of hypotension

Anaesthetic technique

Most IV agents cause direct myocardial depression ± reduced SVR
Therefore slowly and carefully titrate induction agents with concurrent use of vasopressors
Conversely, there's also the need to attenuate the pressor response to intubation with opioids and full neuromuscular relaxation

Volatile anaesthetic agents may have a cardioprotective benefit

They cause negative inotropy and chronotropy, which may improve myocardial oxygen supply/demand balance

Also have a direct cardioprotective effect whcih mimics ischaemic pre-conditioning

Effect is maximal at 1.5-2 MAC but may occur at 0.25 MAC
Associated with lower troponin concentrations, ↓ inotrope reqirement, ↓ length of stay and better cardiac indices in those undergoing CABG
Xenon, adenosine, nicorandil, and norepinepherine are also felt to have pre-conditioning effects

Volatiles also have a post-conditioning effect by inhibiting neutrophil-mediated ROS generation responsible for reperfusion injury

Historic concerns about coronary steal phenomenon, particularly with isoflurane, are not felt to be significant at clinically relevant concentrations

Homeostasis

Avoid ischaemic precipitants

Pain (see below)
Tachycardia
Hypoxia
Hypotension
Shivering
Anaemia

Analgesia

Regional techniques may avoid the depressant effects of GA and attenuate the pain response
Conversely, neuraxial techniques can reduce preload and afterload, leading to hypotension

Neither thoracic epidural or spinal techniques have been shown to reduce incidence of myocardial ischaemia

Opioids attenuate the surgical stress response

Morphine, via its DOP effect, has a myocardial pre-conditioning effect which is synergistic with that of volatiles

Clonidine may have myocardial protective properties in the perioperative period, reducing myocardial ischaemia

Ensure appropriate tissue oxygen delivery e.g. oxygenation, treatment of anaemia
Multi-modal analgesia to avoid pain, tachycardia
HDU or ITU as needed