Instagram Threads

Bay Four

          Patterns, pearls and practical medicine

Chronic Coronary Syndromes

Definitions

  • Chronic coronary syndromes include:
      • Asymptomatic with abnormal tests (coronary imaging or functional)
      • Angina/ischaemia with non-obstructive coronaries
      • Typical or atypical angina
      • Post-ACS or intervention
      • HF secondary to ischaemia
  • Mechanisms can be
      • Epicardial (eg atherosclerosis, coronary aneurysm, vasospasm)
      • Microvascular (less likely to present with typical angina)
  • Angina
      • Constricting/squeezing/heavy discomfort in chest, neck, shoulders, jaw or arms
      • Tends to last 5-10 minutes if triggered (continuous pain of long duration suggests other diagnoses)
      • Typical vs Atypical
          • Typically precipitated by exertion, relieved by rest or GTN (If these 3 features present – typical angina. If not – atypical)
          • Other atypical features include GI discomfort, SOB and nausea
          • Perhaps only 20% presents typically, 65% atypically, 15% have exertional dyspnoea rather than pain (esp in long standing DM and very sedentary patients)
      • Other than exertion, triggers include cold weather, heavy meals, emotional distress (and is not typically precipitated by specific movements or breathing/coughing)
      • Pre-test probability of CAD depends on symptomatology, age and number of the 5 main risk factors (family hx, smoking, hyperlipidaemia, HTN and DM)
      • Outcome pretty good with medical management and control of risk factors
  • Angina equivalent
      • SOB, sweating, fatigue or pain away from chest – can all be due to myocardial ischaemia.
      • Diabetics especially can get silent ischaemia or angina-equivalents, very rare in non-diabetics who almost always get chest pain.
  • Unstable angina
      • Angina at rest may indicate unstable angina (see ACS) but can also occur with coronary vasospasm (which can be epicardial or microvascular)
      • Suspect UA if increasing frequency or intensity of previous stable angina
      • Not included in detail here, see ACS section

Investigation tips

  • As a general rule, unless there are symptoms, don’t go looking for Coronary Artery Disease
  • If very low likelihood (<5%) of obstructive CAD, only investigate further if symptoms persist and non-cardiac causes have been excluded
  • If severely frail and comorbid, and revascularisation futile, can make a clinical diagnosis
  • Sequential testing often needed (i.e. functional testing after CTCA, or vice versa), especially in the moderate risk group
  • Can use a CAD probability calculator like this to help guide investigation
      • Adding results of previous calcium scores and imaging can provide alternative scores
      • A ‘positive family history’ is defined as 1st degree relative with CAD aged <55 (men) or <65 (women)
  • Investigate based on pre-test probability (taking into account local availability and patient preference) and results of subsequent testing
      • <5% (very low) – can defer further testing
      • 5-15% (low) – consider CTCA
      • 15-50% (moderate) – CTCA best, functioning imaging can also be used
      • 50-85% (high) – functional imaging best
      • >85% (very high) – invasive angio best
  • Bloods – include a trop, TFTs, lipids, Hba1c or fasting glucose, CRP, consider BNP
  • ECG
      • Typically no ST segment changes post-angina, and non-dynamic
      • May suggest undiagnosed CAD however:
          • Q waves (especially)
          • LBBB
          • Impaired AV conduction
          • AF
          • ST and T wave abnormalities (however ST depression during an SVT is not a strong predictor of CAD)
  • Consider CxR and pulmonary function tests if SOB is the main problem

CTCA (CT coronary angio)

  • Useful as non-invasive, low dose of radiation, also can tell you about the chambers and valves
  • Useful if history suggestive of angina, or they have non-ischaemic sounding chest pain with resting ECG changes (ST or Q waves)
  • Used when pre-test likelihood is low or moderate (5-50%)
  • Also used if functional imaging is non-diagnostic
  • A good rule out test – if normal, stable angina extremely unlikely.
      • Sensitivity 99% in detecting significant CAD
      • Specificity 64%
      • Negative prediction value of 99%
  • Contraindications
      • Tachycardia eg fast AF – a slow and regular heart rate required (tachycardia impacts on image quality)
      • Inability to cooperate with breath holding commands (necessary to achieve good image quality)
      • eGFR <30
      • Decompensated HF
      • Extensive coronary calcification
  • Significant coronary artery disease (CAD) is:
      • ≥ 70% diameter stenosis of at least one major epicardial artery segment or
      • ≥ 50% diameter stenosis in the left main coronary artery
  • Less severe lesions can cause angina though anaemia, spasm, tachycardia, LVH, long lesion
  • Very severe lesions can be asymptomatic if well-developed collaterals, or small area of ischaemia (eg distal lesion, or old infarction)
  • CTCA has a 30% rate of incidental findings
  • CTCA doesn’t lead to more downstream invasive angiograms compared to functional imaging
  • If negative – the patient could still have microvascular angina (functional imaging may help diagnose here)
  • The Calcium Score
      • A score of zero has a >95% negative predictive value for obstructive CAD
      • Careful in young patients – if aged <40 and found to have obstructive CAD, 58% have a calcium score of zero
      • Score should be interpreted alongside nature of symptoms and risk factors

Functional testing 

  • Includes MPS/SPECT, stress echo, stress/perfusion MRI – depends on the centre
  • Indications
      • CT angiogram is undiagnostic or shows CAD of uncertain significance
      • Useful in old patients with heavily calcified coronaries (as this presents a technical challenge to CTCA)
  • If CT coronary angio abnormal (or non-diagnostic) – do a stress test if uncertainty about whether pain caused by ischaemia. If this is normal, angina becomes less likely.
  • If these are abnormal – do an angiogram
  • Non-obstructive coronary atherosclerosis not linked with ischaemia is undetected by functional testing
  • Stress echo
      • Stress testing precipitates wall-thickening abnormalities in the perfusion territory of narrowed coronary arteries
      • Can use exercise, dobutamine or vasodilators with atropine
      • Underestimates ischaemia in patients with microvascular disease, and image quality may be poor in obesity or COPD
      • Ultrasound contrast agents (microbubbles) often used to improve accuracy
  • MPS/SPECT (Myocardial perfusion scintigraphy / single-photon emission computed tomography)
      • Relies on the myocardial uptake and retention of a radiopharmaceutical Technetium-99m
      • Can find myocardial hypoperfusion
      • Used alongside physical exercise, dobutamine or vasodilators to induce ischaemia
  • PET-CT
      • Uses short-lived radionuclides, in combination with dobutamine or vasodilators
      • Better image quality and lower radiation than SPECT, and also provides quantitative measure of myocardial blood flow
      • Can be useful in
          • Those with diffusely impaired myocardial blood flow eg multivessel CAD or microvascular dysfunction
          • Young patients (less radiation than SPECT)
          • Obesity
      • Probably the most accurate functional imaging, but less available
      • Can also provide a calcium score
  • Stress CMR
      • Can be used, but less available, and may be contraindications/claustrophobia
      • Doesn’t provide information regarding calcifications

Invasive coronary angiogram

  • Indicated if:
      • Very high likelihood of CAD (>85%) or new / severe symptoms at minimal exertion that are highly suggestive
      • Those with LV dysfunction thought to be ischaemic in aetiology
      • If non-invasive assessment suggests high event risk eg ≥50% left main stenosis, or ≥70% proximal LAD stenosis with single or two-vessel CAD, or ≥70% proximal three-vessel CAD on CTCA, or when any stress test shows moderate to severe inducible ischaemia
  • Specific tests can help diagnose non-obstructive microvascular disease (eg index of microcirculatory resistance)
  • Risk of major complications around 0.1-0.2%
  • Identifying the artery responsible for ischaemia can be hard in multivessel CAD or coronary stenoses of intermediate severity (useful to assess functional severity of intermediate lesions eg using fractional flow reserve)

Notes on other investigations

  • Echo
      • RWMA or reduced LV function (which is the strongest predictor of long-term survival) might suggest previous ischaemic damage
      • HOCM can cause angina-like pain without CAD
      • Valvular HD and pericardial effusions/inflammation can sometimes cause CP
  • Plain CT
      • The presence of coronary artery calcium can also be evaluated qualitatively by visually inspecting the coronary arteries on a previous non-cardiac chest CT scan, if available
  • Exercise ECG
      • Has very little role in the diagnosis of angina if no known CAD. Superseded by modern functional imaging and CTCA due to its low sensitivity and specificity (both around 60%)
      • Sometimes used for risk stratification
      • Can be useful if limited access to other methods, or for patients with a low pre-test likelihood of CAD
      • Not useful if abnormal resting ECG (eg LBBB< paced, WPW, ST depression on resting ECG, digoxin tx)
  • Previous USS or CTs showing atherosclerotic disease in non-coronary arteries increases likelihood of CAD

Treatment

  • There has been a switch over time from early revascularisation to medical management which is used first today (the initial risks of the surgery/procedures outweigh the benefit of slightly fewer events down the line)
  • Symptoms are very important. We don’t tend to treat asymptomatic ischaemia (even if the ischaemia has caused LV dysfunction). PCI may carry no more benefit than medical tx in stable CAD
  • Lifestyle advice – diet and weight, smoking, drug use, exercise, psychosocial stress, sleep, alcohol
  • All should get statin, GTN, aspirin unless contraindications
      • GTN – take up to 2 doses, 5 mins apart. If pain ongoing – call ambulance
      • Aspirin confers a relative risk reduction of around 30% for a future MI (if used in secondary prevention). Clopidogrel can be used instead of aspirin, as monotherapy.
      • DAPT indicted post PCI (usually 1-6 months, with 6/12 standard, and less if high bleeding risk or lower ischaemic risk)
      • If on DOAC for AF – often get DAPT for 1-4 weeks, then SAPT (clopidogrel best) and DOAC to continue
      • Consider additional lipid-lowering therapy if not hitting targets (more here)
      • Consider SGLT2i and GLP-1RA if hx of DM and angina
      • Low dose colchicine (500mcg OD) reduces risk of CV events in patients with known atherosclerotic CAD, but not given routinely
  • Some get ACEI – if CCF, CKD, DM, previous MI or HTN
  • Anti-anginals
      • No evidence that any antianginal medication may improve long-term cardiovascular outcomes, except beta-blockers if administered within 1 year after an acute MI
      • No large RCT head to head trials of the older anti-anginals
      • Patients may get anginal symptoms through more than one mechanism (eg obstruction, vasospasm, microvascular dysfunction)
      • First line: Beta-blocker or a calcium-channel blocker
          • Choose betablocker if previous MI or HF (less evidence of benefit if normal LV function post ACS), choose CCB if HTN or hx of vasospasm
          • Aim to reduce resting HR to 55-60 with a betablocker
      • If poor control of symptoms (review response at 2-4 weeks)
          • Switch to, or add, a long-acting dihydropyridine CCB eg amlodipine, modified-release nifedipine, or MR felodipine (caution in HF)
          • Do not combine a beta-blocker with a rate-limiting CCB (diltiazem or verapamil), as severe bradycardia and heart failure can occur.
      • If 1st line drugs contraindicated or not tolerated, consider adding (or using as monotherapy)
          • A nitrate (ISMN, avoid in HCM)
          • Nicorandil (if not hypotensive or hx of HCM)
          • Ivabradine (if heart rate is > 70 beats, only combine with dihydropyridine CCB not a rate-limiting one. Might avoid if normal EF)
          • Ranolazine (can be used in hypotension and bradycardia)
          • Diltiazem or verapamil (rate-limiting CCBs, avoid in HFrEF)
      • If still getting angina despite 3 anti-anginals – consider PCI or CABG for symptomatic benefit
  • No role for TENS or acupuncture
  • Re-evaluate coronaries if LV function deteriorates (assuming no reversible cause)
  • If new or worsening symptoms – consider stress testing
  • If refractory symptoms – consider invasive angio. If previous CABG or PCI, and symptoms refractory – consider CTCA
  • Consider CABG or PCI if symptoms not controlled on drugs
      • Intervention indicated if symptoms persist despite medical tx, or for certain patterns of coronary disease
      • CABG indicated in left main or 3 vessel disease, esp if reduced LV function. Can also consider if proximal LAD involved.
      • PCI more cost effective, and preferred if high surgical risk
      • Better survival advantage for CABG if multivessel disease and DM or aged >65.
      • Incidence of stroke similar in both procedures.
      • Lower rate of repeat procedure with CABG
      • CABG generally preferred in surgical candidates with reduced EF
      • CABG surgical risk calculator
      • One in five revascularized patients needs a repeat revascularization within the first 5 years, with higher risk after PCI compared with CABG. Can be due to in-stent restenosis, progression of CAD, stent thrombosis or graft failure

Non-symptomatic atheroma

  • A risk factor for having a coronary event (but only a risk factor)
  • Calculate 10 years Q risk score
  • Lifestyle. Lifestyle!
  • Consider statin (esp if other risk factors) and aspirin (though evidence very sketchy for the latter)
  • No evidence for PCI
  • We don’t screen for this with CT coronaries because we don’t know what to do with the result. Therefore non-symptomatic atheroma will be picked up incidentally, often on chest CT scans order by respiratory or oncology, especially if surgery is planned and unclear if it’s safe given atheroma on CT
  • Problematic, because the finding could potentially delay lifesaving treatment of other disease
  • Consider stress echo

Microvascular angina

  • Sometimes called Angina/ischaemia with non-obstructive coronary arteries (ANOCA/INOCA). Previously Cardiac syndrome X
  • Anginal symptoms with normal coronary angiogram – but that doesn’t mean they don’t have angina (it’s the microvasculature which is affected)
  • A bit more common in women (60% of cases)
  • Patients have an increased morbidity/mortality
  • Underdiagnosed
  • Trial data on management a bit lacking
  • Risk factors similar to obstructive CAD (as well as systemic inflammatory disorders and psychosocial stress)
  • Investigations
      • Non-invasive tests (stress echocardiography, PET, perfusion CCTA, and CMR) allow diagnosing ANOCA/INOCA by measuring the Coronary Flow Reserve
      • PET-CT myocardial perfusion imaging is the best modality if available (quantifies myocardial blood flow and, crucially, myocardial flow reserve. MFR <2.5 is abnormal)
      • The endotype of ANOCA/INOCA can be determined though invasive functional coronary testing using Ach and adenosine
  • Management
      • Usual lifestyle advice
      • Optimise treatment of comorbidities (eg DM, HTN, hyperlipidaemia)
      • Drugs to reduce CV risk are not routine
      • Continue anti-anginals only if helpful – they definitely help in some
      • Treat the endotype
          • If abnormal vasodilation – consider BB, CCB, ranolazine, ivabradine
          • If abnormal microvascular vasoconstriction consider CCB, 2nd CCB, nitrates
          • If abnormal epicardial vasoconstriction, consider CCB, nitrates, nicorandil

 

Scroll to Top

Comments and corrections

Help us improve by reporting your comments and corrections.

Thank you!

Your comment has been sent. We review all submissions carefully.