Microvascular Angina Flashcards
Angina Pectoris - Definition (3)
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
angina pectoris synonymous
w/ obstructive atherosclerotic epicardial
CAD (2)
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
The Angina Universe
The “classical” approach:
Focus on the atherosclerotic plaque
ANGINA PECTORIS: THE PARADIGM
Myocardial ischemia results from a
mismatch between myocardial oxygen
demand and coronary blood flow (supply
limited by coronary atherosclerosis)
The Dogma
Patients and physicians frequently view
coronary artery stenosis as a mechanical
problem that can be “fixed” by mechanical means
management of IHD (3)
based on the paradigm that myocardial ischaemia is almost always caused by atheromatous CAD
CAD in the absence of myocardial ischaemia = false negative
Ischaemia in the absence of CAD = false positive
OVERUSE OF
PCI ORBITA study:
PCI=Placebo in
stable angina
Changes in
Angina Management
Optical Medical treatments - trials (4)
- Courage
- Orbita
- Ischemia
- ESC Guidelines 2019
Microvascular Angina
definition
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
Microvascular Angina (Cardiac Syndrome X) (4)
Typical exertional/rest chest pain*
Transient ischaemic ECG changes
Normal coronaries
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
CPNCA: A REAL &
Common Condition
398,978 patients
with suspected CAD
Age, 61 years,
53% men,
26% with diabetes,
70% hypertensive,
Non-invasive testing
in 84% (69% +ve)
60% had coronary
stenoses <50%
Prevalence of Coronary Microvascular Dysfunction Among Patients With Chest Pain and Nonobstructive Coronary Artery Disease
Functional Causes of Microvascular Angina
Impaired coronary microvascular dilatation reduces CFR and
causes exertional angina. Microvascular spasm can cause rest
angina
Endothelial dysfunction: Conventional risk factors for CAD, Oestrogen deficiency
Chronic Inflammation i.e. RA / SLE, dyslipidaemia
Diagnostic Criteria for Microvascular Angina - COVADIS (4)
Signs/symptoms of angina
Absence of obstructive CAD*
Objective evidence of myocardial ischaemia
Coronary microvascular dysfunction (CFR <2.5/MV spasm)
Stable angina (5)
High Prevalence of Angina/Myocardial Ischaemia that is not caused by obstructive CAD
No CAD -No CAD - “Primary MVA”“Primary MVA” (“Cardiac Syndrome X”)
Systemic hypertension, dyslipidaemia, smoking, diabetes, oestrogen deficiency
Cardiomyopathies, LVH, amyloid disease, AS
SLE and Rheumatoid Arthritis
CAD patients and post-revascularization angina
ACS (2)
– MINOCA, Takotsubo syndrome, no reflow
Coronary Microvascular Dysfunction (CMD)
1/3 patients undergoing successful PCI has recurrent angina and
a positive ECG exercise test one month after complete and successful PCI
graphs
Ach high response in stable angina + unobstructed coronary arteries test (3)
124 (86%) of the patients with NCA underwent i.c. ACH
testing.
Main findings: ~ 50% of patients undergoing diagnostic angiography for stable angina had NCA
and
the ACH test
triggered epicardial or microvascular spasm in > 60 %
Myocardial Ischaemia Triggered by Coronary Microvascular Spasm
In patients with Ach induced epicardial or microvascular spasm ECG shifts and chest pain were associated with reversible ischemic
changes on SPECT and Echo, and increased high sensitivity cTn
Data from the WISE
project - women
The presence of
coronary microvascular
dysfunction is
associated with
impaired cardiac
outcomes in women, contrary to initial
views
The Need to Identify Ischemia In Patients INOCA (5)
Poor quality of life
MACE, 2.5% annual rate
10% have prior subclinical MI which predicts MACE
Healthcare spending similar to that in obstructive CAD
Patients receive
inappropriate treatment
Microvascular angina in the angina universe
INOCA- The Rationale for Adjunctive
Testing of Coronary Vascular Function (3)
- A normal angiogram does not exclude ischaemia caused by coronary vascular dysfunction. Hence angiography is an “incomplete” study
without adjunctive diagnostic tests of coronary vascular function - Functional testing in INOCA patients allows the cardiologist to make the correct diagnosis, offer therapy that can improve QOL and gather prognostic information
- Functional testing providing a diagnosis also “empowers the patient who is often in limbo regarding the cause of their symptoms”
What is the effective management of angina based on?
largely dependent on
efficiently targeting the prevailing pathogenic mechanism
Stable angina treatment pre-referral for revascularisation (6)
Identify the prevailing
pathogenic mechanism
Tailor treatments to individual needs
Improve endothelial function (Risk
factors, statins, exercise, ACEI, Oestrogen)
Angina/Ischaemia – CCB and BB useful in
effort-induced MVA and vasodilators (nitrates, nicorandil, CCB) for
microvascular spasm
Tackle cardiometabolic issues
(Metformin, ranolazine and trimetazidine)
Pain management (Imipramine,
aminophylline, TENS, SCS)
Primary Microvascular Angina: Treatment Targets
Increased MVO2 demand
(High BP- Tachycardia) : BB, CCBs, Ivabradine
Coronary artery spasm: Nitrates, CCBs, Nicorandil, Rho-K I
Impaired coronary microvascular
dilatation -Nitrates - CCBs, Nicorandil, HRT
Heart metabolic abnormalities
Effects of ischaemia per se
(microvascular compression) : Ranolazine, Metformin, Trimetazine
Inflammation: statins, colchicine (biologicals?)
Summary (5)
The current paradigm (“plaque-centred”) is flawed. A mechanistic, ischaemia-centred- working hypothesis is
required
Prevalence of CMD and microvascular spasm is higher
than originally thought
MVA may affect ~50% of patients undergoing
diagnostic angiography
CMD is both a risk factor and a target for treatment
MVA patients need to be identified and treated rationally
