Microvascular angina Flashcards
define angina pectoris
Angina is traditionally defined as central chest discomfort (pain or tightness) of less than 10 minutes’ duration. This discomfort is provoked by exertion or emotional stress and is relieved by rest or by administration of nitroglycerin. In this typical form, angina is suggestive of obstructive coronary artery disease
What does NICE define stable angina as?
- Constricting discomfort in the front of the chest, neck, shoulders, jaw, or arms.
- Precipitated by physical exertion.
- Relieved by rest or GTN within about 5 minutes.
People with typical angina have all three of the above
People with atypical angina have two, and people with non-anginal chest pain have one or none of the above
what is a strong predictor of the presence of coronary artery disease?
Typical chest pain is a strong predictor of the presence of coronary artery disease.
Non-anginal chest pain (i.e pain unrelated to activity, not relieved by rest or GTN, and not suggestive of angina) is an important predictor for ruling out CAD.
what is the term angina pectoris synonymous with?
obstructive atherosclerotic epicardial CAD (coronary artery disease).
The main cause for myocardial ischaemia in clinical practice is considered to be obstructive CAD
Current diagnostic and therapeutic strategies for angina are based on this paradigm
what is considered the angina universe?
Coronary atheroma: STEMI, NSTEMI, ACS, CSA, graft stenosis, stent stenosis.
Vasospastic angina: variant angina
what does myocardial ischemia result from?
a mismatch between myocardial oxygen demand and coronary blood flow (supply limited by coronary atherosclerosis)
Patients and physicians frequently view coronary artery stenosis as a mechanical problem that can be “fixed” by mechanical means.
what is the management of IHD based on?
the paradigm that myocardial ischaemia is almost always caused by atheromatous CAD-
[angiogram] CAD in the absence of myocardial ischaemia= false negative
Ischaemia in the absence of CAD= false positive
Orbita study showed that in stable angina patients: angioplasty is not better than placebo! (not the case for acute coronary syndrome- angioplasty may be required)
if the plaque is not the centre of the “universe” (occlusive CAD), what can trigger myocardial ischaemia?
Problems with the coronary microcirculation:
•Structural mechanisms--> o Adverse arteriolar remodelling: - Increased medial wall thickness - Intimal thickening - Reduced wall/lumen ration
o Intravascular plugging
o Perivascular fibrosis
o Capillary rarefaction
•Functional mechanisms–>
o Microvascular spasm
o Abnormal vasodilation
o Endothelial dysfunction and/or VSMC dysfunction
Microvascular angina as a cause of chest pain with angiographically normal coronary arteries
what are the myocardial factors affecting microvascular function?
- Left ventricular hypertrophy
- Reduced diastolic time
- Calcium overload
- Amyloidosis
- Increased intramyocardial pressure
- Increased intracavitary pressure
- Tissue edema
Coronary microvascular dysfunction leads to transient myocardial ischaemia- “Microvascular angina”:
the coronary microcirculation has remained elusive to conventional imaging techniques for decades
what is microvascular angina?
Markedly increased resistance to coronary blood flow at the site of the coronary microvasculature can trigger myocardial ischaemia, as shown by ECG shifts, myocardial perfusion defects and LV dysfunction in patients who otherwise have patent epicardial coronary arteries.
Hermann J, Kaski JC, Lerman A. Eur Heart J 2012.
microvascular angina (Cardiac syndrome X) is mainly seen in who?
menopausal women
- Typical exertional/rest chest pain*
- Transient ischaemic ECG changes
- Normal coronary arteriograms
More prevalent in women in most series; >50% have documented myocardial ischaemia and >50% coronary microvascular endothelial dysfunction leading to abnormal MV dilatation and ischaemia
JC Kaski. Circulation 2004
Estrogen deficiency must have also played a part as mainly in women
what did Jaskanwal D. Sara et al’s study on the prevalence of coronary microvascular dysfunction among patients with chest pain and non-obstructive coronary artery disease show?
- 60% of people who were sent for angiography due to angina= had normal arteries
- What proportion of those had abnormalities in the coronary microvessels?
- Showed that 60% of those with normal arteries + angina had abnormalities in the coronary microvessels
what is the diagnostic criteria for microvascular angina?
COVADIS (Coronary Vasomotion Disorders International Study Group)
- Signs/symptoms of angina
- Absence of obstructive CAD*
- Objective evidence of myocardial ischaemia
- Coronary microvascular dysfunction (CFR <2.5/MV spasm)
Ong P, Camici PG, Beltrame JF, Crea F, Shimokawa H, Sechtem U, Kaski JC, Bairey Merz N, International standardization of diagnostic criteria for microvascular angina. Int J Cardiol 2017
Coronary microvascular dysfunction (CMD) is one reason why there is a high prevalence of angina/myocardial ischaemia which is not caused by obstructive CAD. Describe its presentation
No CAD - “Primary MVA” (“Cardiac Syndrome X”):
- Systemic hypertension, dyslipidaemia, smoking, diabetes, oestrogen deficiency, Cardiomyopathies, LVH- left ventricular hypertrophy, amyloid disease, AS.
- Amyloid disease: can have deposits of the abnormal protein in the microvessels–> embolus
- Left ventricular hypertrophy: have less capillaries than normal + have compressive effect on the microvessels
SLE and Rheumatoid Arthritis:
Inflammation–> vasoconstriction–> endothelial damage–> ischaemia (even in the absence of CAD)–> affect microvessels
ACS (acute coronary syndrome)– MINOCA, Takotsubo syndrome, no reflow:
- Arteries are normal in some cases
- Ventricle has a peculiar shape: takotsubo syndrome
does PCI (Percutaneous Coronary Intervention- formerly known as angioplasty with stent) help microvascular angina?
(Li Y et al. Can J Cardiol 2015):
- Coronary flow reserve (CFR) and hyperaemic index of myocardial resistance (IMR) assessed in 39 patients with chest pain and 12 asymptomatic patients after PCI-stenting; all without restenosis. The culprit vessel and a reference artery were assessed.
- Symptomatic patients had lower CFR* and higher IMR in both, culprit and reference arteries (*54% with CFR <2.5).
Mechanisms:
- Microembolism (platelets / microparticles)
- Ischemia-reperfusion injury (endothelial damage due to increase in proinflammatory molecules)
- Increase in reactive oxygen species
- Decreased NO activity
- Abnormal microvascular remodeling
