Chronic ischemic heart

disease
dr. Cut Aryfa Andra, Sp.JP(K)

Program Studi Magister Kedokteran Klinik

Fakultas Kedokteran Universitas Sumatera Utara | 2020
Sharhay S, Libby P. Atherosclerosis. In: Lilly LS, editor. Pathophysiology of heart disease: a collaborative project of medical students and faculty. 6th ed. Philadelphia: Wolters Kluwer; 2016.
 Global burden of the disease

Camm J, et al. International Journal of Cardiology. 2015 p200-207

Ischemic Heart Disease: where are we now?

Most prevalent manifestation of Patients with CAD & angina have

ischemic heart disease: Angina higher rates of future
~5% of adult population over age cardiovascular event compared
40y with patients without angina

Up to 1/3 patients continue to

have angina despite a successful
PCI and medical therapy

EAPCI Expert Consensus Document on Ischaemia with Non Obstructive Coronary Arteries in Collaboration with European Society of Cardiology Working Group on Coronary
Pathophysiology & Microcirculation Endorsed by Coronary Vasomotor Disorders International Study Group
https://eurointervention.pcronline.com/doi/10.4244/EIJY20M07_01
Economical and Personal Burden
Ford TJ, et al. BMJ 2017. Stable coronary syndromes: pathophysiology, diagnostic advances and therapeutic need
http://dx.doi.org/10.1136/ heartjnl-2017-311446
The balance of myocardial O2 supply vs demand
 Coronary Artery Disease
• A pathological process characterized by atherosclerotic plaque
accumulation in the epicardial arteries, whether obstructive or
non-obstructive.
• The disease can have long, stable periods but can also become
unstable at any time, typically due to an acute atherothrombotic
event caused by plaque rupture or erosion.
• However, the disease is chronic, most often progressive, and
hence serious, even in clinically apparently silent periods.
• The dynamic nature of the CAD process results in various clinical
presentations, which can be conveniently categorized as either
acute coronary syndromes (ACS) or chronic coronary
syndromes (CCS).
 Stable vs Vulnerable
Plaque

Wilder JS, Sabatine MS, Lilly LS. Ischemic heart disease. In: Lilly LS, editor. Pathophysiology of heart disease:
a collaborative project of medical students and faculty. 6th ed. Philadelphia: Wolters Kluwer; 2016.
Viviany R Taqueti. JACC 2018; 72: 2625-2641
Ford TJ, et al. BMJ 2017. Stable coronary syndromes: pathophysiology, diagnostic advances and therapeutic need
http://dx.doi.org/10.1136/ heartjnl-2017-311446
 Rethinking stable ischemic heart disease

Bala Christina et al. Treatment of Angina: Where Are We?. Cardiology 2018;140:52–67
http://dx.doi.org/10.1016/j.jacc.2012.04.046
Myocardial cellular mechanism
Grading severity of Angina
Multiple “faces” of angina
 Transmission of
cardiac ischemic pain

Source: ESC Textbook of Cardiovascular Medicine. 2004

TREATMENT
Antiplatelet
Ischaemic event vs Bleeding risk assessment

10.1093/eurheartj/ehz425
Medical therapy of ischemia
 Statin, ACE-i/ARB, BB
2019 ESC Guideline for CCS
• Patients with established CAD are
regarded as being at very high risk
for cardiovascular events and statin
treatment must be considered,
irrespective of LDLC levels.
• Goal: LDL-C to <1.8 mmol/L (<70
mg/dL) or at least to reduce it by
50% if the baseline LDL-C level is
1.83.5 mmol/L (70-135 mg/dL).

2011 ESC Guideline for Dislipidemia:

Very high risk , Subjects with any of the following:
• Documented CVD by invasive or non-invasive testing (such as coronary angiography, nuclear imaging, stress echocardiography, carotid
plaque on ultrasound), previous myocardial infarction (MI), ACS, coronary revascularization [percutaneous coronary intervention (PCI),
coronary artery bypass graft (CABG)] and other arterial revascularization procedures, ischaemic stroke, PAD.
• Patients with type 2 diabetes, patients with type 1 diabetes with target organ damage (such as microalbuminuria).
• Patients with moderate to severe CKD [glomerular filtration rate (GFR) ,60 mL/min/1.73 m2 ).
• A calculated 10 year risk SCORE ≥10%.
THANK YOU
Patophysiology

Source: Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 11 th Ed

 Normal artery wall

Wilder JS, Sabatine MS, Lilly LS. Ischemic heart disease. In: Lilly LS, editor. Pathophysiology of heart disease: a collaborative project of medical students and faculty. 6th ed. Philadelphia: Wolters Kluwer;
2016.
 Endothelial and Arterial cells

Wilder JS, Sabatine MS, Lilly LS. Ischemic heart disease. In: Lilly LS, editor. Pathophysiology of heart disease: a collaborative project of medical students and faculty. 6th ed.
Philadelphia: Wolters Kluwer; 2016.
 Atherosclerosis plaque formation

Wilder JS, Sabatine MS, Lilly LS. Ischemic heart disease. In: Lilly LS, editor. Pathophysiology of heart disease: a collaborative project of medical students and faculty. 6th ed. Philadelphia:
Wolters Kluwer; 2016.
 Plaque Formation

Wilder JS, Sabatine MS, Lilly LS. Ischemic heart disease. In: Lilly LS, editor. Pathophysiology of heart disease: a collaborative project of medical students and
faculty. 6th ed. Philadelphia: Wolters Kluwer; 2016.
https://doi.org/10.1016/j.jcin.2020.04.040
 TERAPI ANTIPLATELET DAN
ANTIKOAGULAN
Figure 6
Antithrombotic
treatments in non-ST-
segment elevation acute
coronary syndrome
patients: pharmacological
targets. Drugs with oral
administration are shown
in black letters and drugs
with preferred parenteral
administration in red.
Abciximab (in brackets) is
not supplied anymore.

©ESC
2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without
www.escardio.org/guidelines
persistent ST-segment elevation (European Heart Journal 2020 - doi/10.1093/eurheartj/ehaa575)