Coronary artery disease and Hypertension Flashcards
Discuss differences between indications for beta-blockers in the surgical vs non surgical setting
indications for beta-blockers in non surg setting:
- hypertension
- svt
- vt
- angina
- ami
surgical indication
- conflicting evidence (small trials with differing methodology)
- POISE trial - large trial looking into topic (>45 undergoing noncardiac surg with CAD, PVD, stroke, prior CCF admission)
- Theory: stress response increase catecholamines lead to increase HR/BP/fatty acids - betablockers can attenuate this
- outcome from trial, treatment group had less non fatal MI and primary outcome of (CV death) but metoprolol had higher mortality and increased stroke and more hypotension/bradycardia
- downgraded periop betablockers post poise AHA
- all decreased non fatal MI in followup and increased stroke/hypo/brady
class 1 indication - continue in those who have been on them chronically - if recognised preop don't start or should start well before e.g. delay surgery.
What are some of the effects of beta blockers?
- b1 selective and nonselective
(atenolol, metoprolol, bisoprolol are all beta 1 selective)
Classic effects
- reduce myocardial O2 suppler/demand mismatch
- rapid onset
Non Classic effects
- complex interaction between heart, sympathetic nervous system and inflammatory system ?plaque stabilisation (specifically bisoprolol)
- slower onset
What is the outcomes of studies looking at perioperative outcomes of clonidine and aspirin?
Clonidine
- theory: decreased noradrenergic CNS transmission (anxiolysis, analgesia) suppress normal post op increase in fibrinogen and antagonise adrenaline induced platelet aggregation. May reduce stress response
- did not reduce atherosclerotic disease but did cause hypotension and increase in nonfatal cardiac arrest
Aspirin
- POISE 2 stratified based on continuation or initiation
- aspirin did not reduce nonfatal MI but did increase major bleeding
- result confounded by other forms of anticoagulation
What are the two types of stents? What are some considerations for each?
Bare metal stent
- cobalt and chrome or platinum chrome (thinner struts)
- restenosis due to smooth muscle cell proliferation and neointimal hyperplasia
- peaks between 3-6mths
- required repeat PCI in 12-20% (balloon angioplasty, re-stent, brachytherapy)
Drug eluting stent
- stent coated with thin polymer (drug carrier) with antiproliferative agent
- now 80% are DES now (>60% off label)
- lipo-philic molecule that are distributed into arterial wall
- reduce need for PCI from 20 to 5%
- stent remains uncovered therefore late thrombosis and need DAPT - length increases over years
- changing landscape 1st gen (sirolimus/paclitaxel) whereas new use everolimus and cobalt.
What are some complications from stenting?
bare metal stent thrombosis
- 2 weeks after stenting
- risk diminishes after endothelialization (4-6weeks)
bare metal stent restenosis
- peaks at 3-6mths
5-7 days clopidogrel post
6-12weeks post BMS can wait for surgery
What are some guidelines for surgery post PCI?
DES - delay for 1 year (clopidogrel therapy)
BMS - delay for 3-45days (6weeks)
Balloon angioplasty <14 days
wait for completion of clopidogrel therapy in elective
if semi-urgent take case by case basis
- risk of thrombosis and low risk bleeding intraop continue aspirin and clopidogrel and vice versa (e.g. intracranial surg/TURP stop aspirin)
if grey zone stop clopidogrel and continue aspirin
restart clopidogrel asap post surgery with loading dose if possible (>300mg 6hrs, >600mg 2hrs)
no evidence for bridging techniques currently but many case reports.
- monitor until anti-platelets re-established
- should be performed in centre with urgent PCI facilities
How do you determine risk of bleeding vs thrombosis?
- consider myocardium at risk (Left main, proximal LAD stent?)
- ?previous stent thrombosis
- ?multi-vessel or long/overlapping stents
Associated risk factors
- DM, CKD, low ejection fraction, advanced age
discussion with surgeon/cardio/home team
What is the common mechanism of myocardial injury perioperatively? What is the outcomes in these people?
- majority are ST depression in 24-48hrs (NSTEMI) post surgery (rare within a procedure)
- implies myocardial o2 supply/demand mismatch
- often silent (pain distractors, analgesia, nausea, baseline ECG changes (LBBB, paced), missed without trop level
Outcomes
- 10-15% mortality from cardiac complications, >50% are due to STEMI
- plaque fissure/rupture and thrombus
- Non cardiac surgery troponin rise predict prognosis for long term morbidity/mortality
What is the definition of an AMI? Prior MI?
- detection of a rise/fall of cardiac biomarkers (troponin) gold standard
- evidence of myocardial ischaemia (ECG changes, sxs, imaging evidence of loss of viable myocardium/regional wall abnormality)
- exclude alternative for trop increase
Prior MI:
- new pathological Q waves with or without prior symptoms
- imaging evidence of region of loss of viable myocardium
What are some downfalls of raised cardiac troponin?
- all patients with AMI is not the same
categorise associated prognostic factors/other causes:
- ablation, pacing, DCR, biopsy
- CCF (acute/chronic)
- aortic dissection
- tachy/bradyarrhythmias
- PE
- severe pul HTN
- Renal failure
- infiltrative disease (amyloid, sarcoid, scleroderma)
- inflammatory conditions (myocarditis)
- drug toxicity (snake, chemo)
- critically ill patients
- burns
What is the difficulty of measuring troponin in renal failure?
normally both trop T and I comparable for diagnostic accuracy
- in renal failure higher troponin T compared to troponin I
- chronic elevation secondary to presumed myocardial injury resulting from some aspect of renal failure
- troponin T carries prognostic significance
- an increase from baseline distinguishes acute IHD
What is highly sensitive troponin? What are some difficulties with its interpretation?
- 5th gen, in theory should have higher diagnostic rates and a higher negative predictive value
- in practice have lower specificity and lower positive predictive value
Guidelines for interpreting (MJA 2012)
- needs to be a dynamic change
- report conditions e.g. haemolysed sample/circulating antibodies
- should have pre-test probability (rule out rather than rule in AMI) - not elevated in 6hrs of symptom onset very low likelihood.
What is the management of MI? Can you stratify this management?
NSTEMI
- medical stabilisation/risk stratification
- O2,morph, GTN
- antiplatelet therapy (aspirin) ideally clopidogrel (CURE trial 20% reduction in death)
- anticoagulation (heparin/clexane)
- beta-blockade (if HR >50, nil CCF decompensation, no severe COPD and no major CI with improved mortality/cardiac arrest/re-infarction)
- ace-inhibitors - continue in long term with low EF, significant MR
- statin
STEMI
- acute re-perfusion (fibrinolytics/PCI)
- peri-operatively PCI recommended due to reduced bleeding risk (still require anticoag tirofiban and DAPT)
- consider risks and benefits in each patient.
What is a hypertensive crisis/emergency? What do you do in this sceanario?
SBP >180 or DBP >110
HTN emergency
- progressive organ dysfunction (encephalopathy, ICH, stroke, acute renal failure, infarct, dissection)
- reduce BP quickly to prevent end organ damage (10-15% over first hour and aim towards 160/1000 over next 2-4hrs)
HTN urgencies
- no end organ dysfunction
- control over days-weeks
What is the SBP targets for patients?
Based on 2014 JNC-8 guidelines
- CKD/DM aim <130/80 increased to <140/90
- contradict other guidelines
relaxed goals - producing a minority report
impact of change is large
- 8.5% increase in MI over 10 years
Currently following JNC 7 guideline
What are some contributing factors to HTN peri-operatively? When should you delay surgery?
- anxiety
- essential
- rarely secondary
- peri-op HTN lability in elderly (as age vasculature less compliant)
Provided DBP <110 proceed with surgery
- uncontrolled HTN only a minor risk factor (ACC/AHA guidelines)
- old studies not considering subtypes
- more recent studies more important to focus on haemodynamic stability rather than BP target.
- DBP data suggest >110 is associated with periop complications.
Pulse pressure
- > 80mmHg stronger predictor of ischaemic outcomes rather than each individually.
- theory: SBP high therefore myocardial work required higher and myocardial O2 high. Indicates lower diastolic therefore diastolic perfusion pressure for coronary arteries higher.
- longitudinal >90 better predictor of CAD
- still being evaluated
Poorly controlled HTN (SBP>180 or PP >80)
- look for evidence of subclinical organ dysfunction (GFR, LVH, ECG)
- risk factors (DM, smoking)
- delay surgery for 2-3mths to determine treatment and commence of therapy to control BP and modification of risk factors
What is the peri-operative management of anti-hpypertension medication?
- just be aware of potential adverse effects
- ace-inhibitor for HTN then continue, CCF and baseline BP low withhold.
- rebound postop HTN vs hypotension intraop
How do you treat post op HTN? What contributes to this?
- pain, agitation, hypercarbia, hypoxia, bladder distension
Treatment:
- re-institute normal meds
- treat if marked increase from baseline
Outline the recommendations for cardiac meds peri-operatively
Aspirin
- withhold at least 3 days before surg and restart when the risk of bleeding has passed (8-10days after major non cardiac surgery)
- increased major risk of bleeding but did not impact non fatal MI at 30 days
- if a closed space procedure (e.g. intracranial, intramedullary, intraocular, prostate) then hold for 5-10days and restart postop asap if for secondary prevention (e.g. prior PCI within 12 mths or DM and >50male>60females +one other risk factor) - see flow diagram
Beta-blocker
- continue during periop period if the systolic BP is low then consider withholding or decreasing dose
- type of beta-blocker consideration (bisoprolol >atenolol >metoprolol) for cardioprotective benefits
- see POISE trial for preop initiation (decrease non fatal MI increase nonfatal stroke, hypotension, bradycardia and increased mortality)
ACEI/ARB
- withhold 24hrs before non cardiac surg and restart 2 days after if stable
- risk of AKI/hypotension if continued
- 3 small randomised control trials but no large RCT - case by case basis
Alpha 2- adrenoceptor agonists (e.g. clonidine - non selective, dexmedetomidine (alpha 2 specific)
Statins
- HMG CoA reductase to reduce cholestrol but also anti-inflammatory/vasodilatory/plaque stabilising effects by reducing coronary calcium
- continue and start preop if high risk (e.g. start if undergoing vascular surgery)
- favour statins with long half life or extended release formulation
What are the indications for coronary revascularisation?
Symptom benefit
- limiting function despite optimal medical management
- active patient prefers PCI for QoL improvement (e.g. intolerant of medical management)
Survival benefit
- > 50% left main stenosis
- multivessal CAD (>75% left ant descending, double vessel disease)
after PCI the ORBITA trial 2018 showed there was no real difference in exercise tolerance/angina/QoL 6weeks post proceudre but slight improvement in dobutamine stress ECHO
What helps determine the choice between CABG and PCI in management of a patient?
patient comorbidities
complexity
location of stenoses
SYNTAX score
general principles:
- CABG preferred in DM, multivessel disease and high SYNTAX score due to reduced need for revascularisation.
- left main >50% requires CABG
- lower complexity lesions undergo PCI/single vessel disease and high surgical mortality.
What is a strategy to detect and manage MINS?
- assess probability of CAD
- high risk should undergo perioperative monitoring (ECG via telemtery during anaesthesia)
- due to long plasma half life of cardiac troponins checking day 1-4 post op will detect >90% of periop MIs
- if MINS is present CCS 2016 guidelines recommend long term aspirin and statin therapy with smoking cessation/BP optimistion and glycemic control.
- recent trial in Lancet (MANGAGE) showed dabigatran didn’t increase bleeding but reduced mortality in MINS for 2yrs therapy
recommendations vary - canada states daily troponin measurement for 48-72hrs after noncardiac surgery with a baseline risk >5%
e.g. elevated NT-proBNP before surgery
What is the sensitivity of ECG findings for MI?
Horizontal/downsloping ST depression of >1mm suggests subendocardial ischaemia
ST elevation = transmural ischaemia
T wave changes/QRS changes and new arrhythmias also suggest ischaemia
