Non Atherosclerotic angina

1. Non-atherosclerotic
angina
BY DR. DOHA RASHEEDY
ASSOCIATE PROFESSOR OF
GERIATRICS
AIN SHAMS UNIVERSITY

2. Contents
▪ Definition of angina and its types.
▪ Pathophysiology of angina.
▪ Causes of non-atherosclerotic angina and their characteristics.

3. Angina
▪ Typical / atypical
▪ Stable/ unstable
▪ Walk through angina
▪ Warm up angina
▪ Occlusive CAD vs. non-occlusive (INOCA)

4. Pathophysiology

5. Causes of non-atherosclerotic angina:
1. Vasospastic angina:
2. Coronary artery embolism
3. Spontaneous coronary artery dissection
4. Microvascular dysfunction
5. Tako-Tsubo cardiomyopathy
6. Vasculitis
7. Coronary vessels anomaly: (myocardial bridging, fistula,
abnormal origin of coronary vessels, coronary artery ectasia
/ aneurysm)
8. Angina due to mismatch in supply and demand of oxygen (
severe anemia, severe aortic stenosis, uncontrolled
hypertension, pulmonary disease)

6. Coronary artery vasospasm(CAVS)
▪ women < 50 years
▪ epicardial /microvascular
▪ partial / complete
▪ May be due to:
1. Impaired parasympathetic
activity.
2. Endothelial dysfunction.
3. Enhanced smooth muscle
vasoconstriction.
4. Chronic inflammation.
5. Oxidative stressors.
Triggers:
1. Cigarette smoking
2. Psychological stress
3. Cold exposure
4. Hyperventilation
5. Alcohol consumption
6. Magnesium deficiency
7. Stimulants (e.g., cocaine)
8. chemotherapies (including 5-fluorouracil and
capecitabine)
9. Kounis syndrome
10. Infectious myocarditis
11. Catheter induced vasospasm

7. ▪ Diagnosis:
A representative case of coronary artery
vasospasm documented by pharmacologic
spasm provocation test during invasive
coronary angiography: focal
vasoconstriction (arrow, A) resulting in
total occlusion of proximal left anterior
descending coronary artery developed with
ergonovine injection (E2, A), which was
normalized with nitroglycerin
administration (N, B). [13]

8. Avoid Triggers
Beta blockers, aspirin in large dose
contraindicated
CCBs First line
long-acting nitrates or nicorandil
sublingual nitrates may be useful for relieving
acute episodes of angina
If resistant occlusive use stenting with continued
CCBs, Nitrates
Statins, ACEIs, Vitamin C, E, Mg may have a
preventive role

9. Coronary artery embolism
▪ Direct, paradoxical, and iatrogenic.
▪ Risk factors:
▪ Atrial fibrillation
▪ Prosthetic Aortic, mitral valve
▪ Infective endocarditis
▪ Intracardiac thrombi or tumors
▪ Hypercoagulable states
▪ Patent foramen ovale
▪ Atrial septal defect

10. Diagnosis
▪ Distinguishing embolism from atherosclerotic disease
clinically is difficult.
▪ Angiography together with clinical suspicion in risky patients.
▪ Transthoracic and trans-esophageal echocardiography for the
cause.

11. Angiographic features
▪ An abrupt (cutoff)
occlusion of a coronary
artery.
▪ Multiple occlusions
(raise the level of
suspicion).
▪ Normal appearance of
the remaining coronary
vessels.
▪ No collateral vessels to
the occluded artery.

12. Treat the cause e.g. prosthetic valve thrombosis, AF
If indicated, angioplasty or stent placement should be considered, ensuring
adequate procedural anticoagulation and antiplatelet therapy
aspiration thrombectomy may restore flow in some cases
The initial management of coronary embolism is similar to that of other
forms of ACS, and includes antiplatelet therapy and targeted reperfusion
therapy

13. Spontaneous coronary artery dissection
(SCAD)
▪ 4% of all cases of ACS.
▪ Causes (arteriopathy)
1. Fibromuscular dysplasia
2. Peripartum Status
3. Connective tissue diseases,
such as Marfan syndrome,
vascular Ehlers–Danlos
syndrome.
Predisposing factors:
▪ Extreme emotion or exercise
▪ Intense Valsalva-like activities (e.g.
vaginal delivery, coughing,
vomiting, bowel movement)
.
myocardial ischaemia by obstruction
of coronary blood flow
subsequent luminal compression
deeper intramural haematoma
accumulation
formation of a false lumen
intima–media dissection

14. Investigations of SCAD
▪ In coronary angiography,
SCAD can appear as a
classic double lumen with
contrast filling into the
dissection plane
▪ intravascular
ultrasonography (IVUS) or
optical coherence
tomography (OCT)
▪ Cardiac CT angiography

15. Treating SCAD
Hemodynamically and clinically stable
Conservative medical management
(antiplatelet therapy, β- blockade and
statins)
Careful use of anticoagulants
Better outcome
Occluded blood flow or worsening
clinical status, hemodynamic instability,
or left main dissection
Revascularization with percutaneous
coronary intervention (PCI) (can be
unsuccessful in 50% of cases)
Stents may cause the dissection to
progress to adjacent coronary
segments
CABG surgery might need to be
considered.
the patency of bypass grafts at follow
up coronary angiography is very low).

16. Takotsubo Cardiomyopathy (TTC)
▪ 90 % postmenopausal women.
▪ typically following an emotional or physical
stressor.
▪ Most common symptom is chest pain (75%),
▪ Apical ballooning in 70%,
▪ transient ST-segment elevation.
▪ increased levels of troponin and BNP .
▪ reduced ejection fraction.
▪ transient systolic ventricular dysfunction with
regional wall motion abnormalities extending
beyond a single vascular territory and in the
absence of significant obstruction in the
epicardial coronary vessels
Many pathways may be involved:
1. Multivessel epicardial spasm
2. Microvascular dysfunction
3. Catecholamines
cardiotoxicity
4. Neurogenic stunned
myocardium.
5. Role of estrogen deficiency

17. ▪ Treatment: is largely supportive and continues until the
spontaneous return of left ventricular function (within 21 days of
the onset of the syndrome in 95% of cases)
pulmonary
congestion
Venodilators (such as nitroglycerin, nitroprusside, or nesiritide) and
diuretics
In presence of hypertension (ACEis, ARBs, ARNI, spironolactone)
cardiogenic
shock
urgent ECHO
with left ventricular
outflow tract
obstruction (LVOTO)
Avoid inotropes
IV fluids, Beta-blockers, if tolerated, to reduce
basal contractility, and vasopressors
Extracorporeal membrane oxygenation (ECMO)
may be necessary in severe cases of cardiogenic
shock with LVOTO
without obstruction Inotropes such as milrinone, dobutamine, and
dopamine can be used.
Vasopressors and left ventricular assist devices
for refractory cases.
Initiate anticoagulation if large area of hypokinesia

18. Coronary Microvascular Dysfunction
▪ 30% to 50% of non-obstructive CAD on invasive coronary angiography.
▪ more commonly seen in women and patients with cardiovascular risk
factors (e.g. increasing age, diabetes mellitus, hypertension, smoking,
or dyslipidemia).
▪ Diagnosis 3 criteria: ischemic chest discomfort, non-obstructive
coronary arteries, and an impaired coronary flow.
▪ Primary microvascular angina, Secondary microvascular angina
(myocardial diseases , obstructive CAD, iatrogenic).
▪ Pathophysiology:
▪ Endothelial dysfunction
▪ Smooth muscle cell (SMC) dysfunction
▪ Vascular remodeling
▪ Luminal obstruction
▪ Autonomic dysfunction

19. Impaired coronary flow can be determined by
any of the following during angiogram:
Invasive angiogram
1. Coronary flow reserve
<2.0
2. Microvascular spasm
diagnosed during Acetyl
choline provocative
spasm testing.
3. coronary slow flow
phenomenon
Non invasive
1. Coronary MRI.
2. PET Scan.
3. CT coronary angiography.

20. Management
▪ No role for revascularization
▪ Nitrates are less effective
▪ CCBs, BBs beneficial
Other treatments:
1. improving endothelial function (e.g. l-arginine, statins therapy,
enalapril).
2. Microvascular vasodilation (ranolazine).
3. Endotheline receptor antagonist (Bosentan).
4. visceral analgesic effect (imipramine).

21. Pathophysiology of CMD in COVID-19

22. Congenital coronary artery anomalies
(CCAAs)
▪ Uncommon <1% of general population.
▪ a common cause of sudden cardiac death
among young athletes.
▪ The clinical symptoms range from asymptomatic
carrier, angina, dyspnea, palpitations, syncope,
cardiomyopathy, arrhythmia, myocardial
infarction and sudden cardiac death.

23. ▪ The anomalies with significant risk of include:
▪ Ectopic origin of LCA from PA or the right sinus.
▪ Ectopic origin of RCA form the PA or left sinus.
▪ coronary artery fistula.
▪ atresic or hypoplastic coronary artery.
▪ Investigations:
1. Coronary CT
2. Cardiac MRI
3. invasive angiography
4. TEE
▪ Treatment options:
▪ Medical treatment/observation (namely β-blockers, calcium channel
blockers, nitrates, and antiarrhythmic drugs).
▪ Avoiding severe exercise.
▪ Surgical repair with variable outcomes.

24. Coronary fistula
▪ It is a communication between the termination of a coronary
artery or its branches and a cardiac chamber, a great vessel
or other vascular structure.
▪ Mostly, fistulae are congenital .
▪ May be secondary to:
▪ infective endocarditis
▪ trauma of previous surgery, endomyocardial biopsy, coronary
angioplasty and bypass surgery, valve replacement, cardiac
transplantation, or permanent pacemaker placement.

25. ▪ The vast majority of patients are asymptomatic.
▪ However, it may present with SCD, myocardial ischemia, pulmonary
hypertension, heart failure, arrhythmia, or rupture.
▪ Symptomatic patients with large fistulae should undergo closure of
the fistulae at the drainage site by transcatheter approach or
surgical ligation.
▪ There is no consensus whether asymptomatic coronary fistulae
should be treated or not.
▪

26. Coronary artery ectasia/ aneurysm
▪ Found in up to 5% of patients undergoing coronary
angiography.
▪ The right coronary artery is usually the most affected artery
(40%)
▪ Risk factors:
▪ Genetic predisposition.
▪ Atherosclerosis in 50% of cases.
▪ Vasculitis
▪ Connective tissue disease e.g. Marfan, Ehler Danlos syndromes.
▪ Local wall injury following intracoronary manipulation
(angioplasty, stenting).
▪ mycotic aneurysm.

27. Presentations
▪ Detected incidentally during coronary angiography or
computed tomography.
▪ Distal embolization and acute myocardial infarction.
▪ local compression of adjacent structure (pulmonary artery,
tricuspid valve, etc.).
▪ can also eventually rupture, producing life-threatening cardiac
tamponade or fistulous communications.

28. Management
▪ Currently no guidelines to aneurysmal management.
▪ Atherosclerosis is implicated in the pathogenesis of a large
proportion of CAA especially in older patients; therefore, it is
important to aggressively modify risk factors.
• Vasodilators such as nitrates have been shown to exacerbate myocardial
ischemia in patients with an isolated large CAA or CAE, and therefore their
avoidance is recommended.
▪ Lines of treatment depend on clinical presentations and may include:
▪ Antiplatelet (dual).
▪ Anticoagulants in multivessel ectasia.
▪ Angiotensin-converting enzyme inhibitors may slow the progression of
CAA.
▪ Percutaneous covered stent or coil embolization, or surgical excision can
be considered.

29. Myocardial bridging (MB)
▪ a congenital anomaly in which a segment of a coronary artery
takes a “tunneled” intramuscular course under a “bridge” of
overlying myocardium.
▪ The most affected region is the mid-segment of the left
anterior descending artery.
▪ Investigations:
▪ coronary computed tomography angiography.
▪ Fractional flow reserve at baseline and with dobutamine
provocation.
▪ Intracoronary Doppler.
▪ Intravascular ultrasound.

30. Consequences
▪ In some patients it may have no consequences.
▪ may be associated with angina, myocardial ischemia, acute
coronary syndrome, left ventricular dysfunction, arrhythmias,
and even sudden cardiac death.

31. ▪ First-line therapy of symptomatic bridging
remains medical treatment with beta-blockers
and non-dihydropyridine calcium-channel
blockers.
▪ Nitrates are contraindicated.
▪ Surgical interventions include:
▪ Myotomy.
▪ Intracoronary stenting: serious complications such
as stent fracture, and coronary perforation have
been reported.
▪ Coronary artery bypass graft surgery have been
used for refractory symptoms, but long-term
outcomes remain uncertain.

32. Coronary arteries vasculitis
▪ Primary: Polyarteritis Nodosa (PAN), Kawasaki’s Disease (KD), Takayasu’s
Arteritis (TA) and Giant Cell Arteritis (GCA).
▪ Secondary to another autoimmune disease (SLE, RA) or can be associated
with other precipitants such as drugs (hydralazine and penicillamine),
infections (HBV, HCV)
▪ Consequences:
▪ Coronary artery aneurysms
▪ Coronary stenotic lesions (diffuse, focal)
▪ Microvascular dysfunction
▪ Spontaneous dissection of large coronaries,
▪ or thrombosis
All may result in acute coronary syndromes.
Moreover, it can manifest as pericarditis or myocarditis.
▪

33. Investigations
▪ Laboratory investigations include:
▪ inflammatory markers such as C-reactive protein,
Erythrocyte Sedimentation Rate,
▪ high sensitivity troponin assay,
▪ ANCA, Rheumatoid factor, Complement (C3 and C4).
▪ Imaging modalities include :
▪ Cardiac magnetic resonance imaging,
▪ Computed tomography coronary angiography,
▪ Fluorodeoxyglucose-positron emission tomography,
▪ Conventional coronary angiogram with intravascular
ultrasound.

34. Treatment
▪ All patients with known vasculitis should be treated with
aspirin with needed immune-suppressive according to the
diagnosis.
▪ percutaneous interventions are recommend in patients
with either a single vessel involvement or focal
multivessel disease.
▪ CABG is recommended in these patients after induction of
immunosuppression.
▪ Coronary artery aneurysms can be occluded by coiling or
implantation of covered graft stents,
resection/thrombectomy and by-pass surgery are also
available options.

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