STABLE ISCHEMIC HEART DISEASE 1.0 Flashcards
SIHD
What is “angina” OR “angina pectoris”?
What is “chronic stable angina” or “stable angina”?
What is “Ischemic heart disease” (IHD)?
angina OR angina pectoris:
• term used for the symptoms of chest pain believed to
be of cardiac origin
chronic stable angina or table angina:
• term used for predictable angina symptoms that
occurs with exertion/emotional stress and are
relieved by rest / medications
schemic heart disease (IHD):
• Ischemia = inadequate blood supply = tissue hypoxia
(low O 2 )
• term used to describe narrowing of coronary arteries
that affects the blood supply to the heart
• IHD = coronary artery disease with ischemia (clinical
CAD = symptoms or event)
• Not all patients with IHD have symptoms of angina
(e.g. completed MI)
SIHD
NOMENCLATURE
What are the 2 Coronary Syndrome?
Stable Coronary Syndrome:
• Obstructive CAD
• INOCA
Acute Coronary Syndrome:
• MINOCA
• UA /NSTEMI
• STEMI
INOCA – ischemia / no obstructive disease;
MINOCA – MI / no obstructive disease
Dfferent Entities of Ischemic Heart Disease
see slide 14
Spectrum of Coronary Atheroscerosis
Stable / chronic angina = initial manifestation of CAD in 50% of patient
• Plaque ➡ incr flow limiting stenosis ➡ stable angina
• Plaque rupture ➡ temporary thrombus ➡ unstable
angina
• Plaque rupture ➡ permanent thrombus ➡ MI
(see slide 15 for reference)
Lipids deposited
Can start to look like plaue
Pushes out blood vessel
Plaque causes obstruction with increases exertion and can bring on signs of ischemia
Label ISD –> having symtpoms of ischemia
Rupture can lead to unstable angina
New Terminology: Chronic Coronary Syndromes (CCS)
see slide 16
Actue event once in blue
Green: angina fine for rest of life
CCS when there is no event
ACS when there is an acute eve
CCS is 12 months post ACS
Why does it only cause chest Pain some of the time?
Coronary Blood Flow in Exercise
• Blood flow to the myocardium is controlled
microcirculation (dilating/constricting) rather than the
large coronary arteries (under normal conditions)
• > 50-75% occlusion is required to cause ischemia with
exertion
• > 90% occlusion is required to affect resting blood flow
(see slide 18 for reference)
Blood vessels dilate in exercise
Atherosclerotic: very little dilation can occur
Cause chest pain
When you stop chest pain will go away
Ischemia at resting blood flow 90% obstruction
Why does it only cause chest Pain some of the time?
Coronary Blood Flow in Exercise
• Myocardial “economics”
• Myocardial homeostasis regulated by O 2 supply and demand (MVO 2 )
• balance between “delivery” and “needs”
• imbalance results in angina – demand > supply in
SIHD
(see slide 19 for reference)
Why does it only cause chest Pain some of the time?
Factor Affecting Supply and Demands
see slide 20
What tests aid in the diagnosis of SIHD?
ECG & Exercise Test (EST):
May or may not show ischemia
Treadmill, watch ECG changes
Myocardial Perfusion Imaging:
• Nuclear medicine scan
• MIBI / PET scan
- Radiotracers
- uptake in the muscle
• Image heart at rest and during stress
- Difference in uptake
Stress Echocardiograph:
• Transthoracic echocardiography (ultrasound)
- Exercise
- pharmacologuc (dobutamine)
• No radiation exposure
• Image heart at rest and under stress
- Looks for wall motion abnormalities
Ultradone during exercise
Watch how walls of heart move
No radiation
Can visualize heart structures
CT Coronary Angiography:
• Anatomy
• Stenosis
• Calcium score
Coronary Angiography:
• Gold standard – direct visualization are arteries
- 2D, not inside lumen
• Access through femoral or radial artery
• Contrast dye + X-ray
• Invasive
- Risk of: MI, stroke, arrhythmia, perforation, bleeding
see slide 29 for Diagnosis Table
What is the general approach to treating SIHD?
Goals of Therapy
see slide 31 and slide 32
improve prognosis
- prevent MACE
improve symptoms/QOL
- minimized ischemia/prevent symptoms
- improve exercise tolerance/func capacity
Treatment Approach: SIHD
Risk factor modification
|
Medical Therapy
|
|——————————-|
Medical alone Revascularization
|
|—————————————|
Percutaneous Coronary Artery
Coronary Bypass Grafting
Intervention (PCI) (CABG)
/ “stenting”
See slide 34 for pictures on PCI / “stenting” & CABG
What determines the approach to treatment?
see slide 36
low risk (annual CV mort <1%) --> med tx intermediate (1-2%) --> med tx +/- coronary angiography depending on level of symptoms and clinical judgement high risk (>2%): med tx + coronary angiogrpahy for better risk stratification --> if high risk coronary anatomy --> revasculatization regardless of symptoms
otherwise coronary angiography + revasc if symptomatic control unsatisfactory
“Stents” don’t fix the problem, why?
- Atherosclerosis is a progressive disease
- Atherosclerosis is typically diffuse
- Multiple coronary arteries
- Multiple vascular beds (e.g. CVA, PAD)
• Obstructive coronary lesions cause more events than
non-obstructive lesions, but non-obstructive lesions are
more common
• Medical Therapy vs. PCI
- All on background medical therapy
- Most have not shown improvement in hard outcomes
(MI, death, etc.)
* Improvement in symptoms of angina consistently
* Some benefits in certain circumstances /
populations
• Medical therapy is considered to be lifelong
Medical Treatment Approach
see slide 38
risk factor mod: healthy weight, active, smoking cess, HTN, gyslipidemia, diabetes
disease progression: antiplatelet, ACE/ARB, statin
- high risk: low dose rivaroxaban DAPT (post MI/PCI), SGLT2i, PCSK-9i, icosapent ethyl
symptom control: BB, CCB, NTG (short, long acting), ranolazine
Medical Therapy
Thrombosis Prevention
see slide 41
Medical Therapy - Disease Progression
Thrombosis Prevention
Antiplatelet Agents: Acetylsalicylic Acid (ASA, ASPIRIN®)
• Antithrombotic Trialists’ Collaboration Meta-analysis
- High risk patients
- 1º outcome: non-fatal MI, non-fatal stroke, death from
vascular cause or unknown cause
- RRR = 30%, ARR = 4.2, NNT = 24
- ADE – ↑ risk of major intracranial and GI hemorrhage
• Place in therapy:
- all patients unless contraindicated, first line
- Dosage: 80-325mg daily (“low dose” preferred)
Medical Therapy - Disease Progression
Thrombosis Prevention
Antiplatelet Agents:
Clopidogrel (PLAVIX®)
• CAPRIE RCT (n=19,185)
- ASA 325mg daily vs. clopidogrel 75mg daily
- High risk with vascular disease
- ↓ stroke, MI or vascular death
- RRR = 3.7%, ARR = 0.5, NNT = 200
- ADE – ↑ risk of major intracranial and GI hemorrhage
• Place in therapy:
- ASA intolerance/contraindication
- Dosage: 75mg daily
Decrease stroke, mi death
Small benefit compared to risk
Clopidogrel as secondary agent for contra of aspirin
Medical Therapy - Disease Progression
Thrombosis Prevention
Antiplatelet Agents:
Dual Antiplatelet therapy (DAPT)
see slide 44
see slide 45
Bottom line:
• Not indicated in most patients for stable disease
• Option:
- High risk individuals with low risk of bleeding where
benefits are thought to outweigh risks
- Multiple events
- Younger age
- Disease in multiple vascular beds: CAD, CVA, PAD
• Common post ACS (12 mos; “extended” up to 36
mos) and post PCI (6-12 mos)
Medical Therapy - Disease Progression
Thrombosis Prevention
Antiplatelet Agents:
Dual Pathway Approach: ASA + RIVAROXABAN
see slide 47
Dual pathway approach
ASA + rivaroxaban
Inhibiting on both sides
Left: coagulation cascade, thrombin
Right:antiplatelet agents
Aspirin block platet agg and adhesion
Riva: blockpathways of coagulation
Agents alone: no cardio benefit
Increase in bleeding
Best: low dose rivaroxaban + ASA
Consider pt at low risk of bleeding
