Atherosclerosis and Stable Ischemic Heart Disease

1. Atherosclerosis and Stable Ischemic Heart Disease MartinHorváth Department of Cardiology, Charles University in Prague, 2nd Faculty of Medicine and Motol University Hospital

2. Overview Atherosclerosis • Pathogenesis • Epidemiology • Clinical presentation • Risk-factors Stable ischemic heart disease • Clinical presentation • Diagnostics • Treatment options

3. Atherosclerosis • Definition: focaldiseaseoftheinnerlayeroflargeand medium-sizedarteries.

4. Why is it important? Epidemiology • Single most common “killer” • In 2008 17,3 million deaths (7,3 MI, 6,2 stroke) • About ½ of deaths in developed countries • Involves many vascular beds and thus causes various diseases

6. Pathogenesis

7. Stableplaque • Unstable“vulnerable” plaque

8. Clinical presentation?

9. Cerebrovascular disease • Stroke • TIA • Coronaryarterydisease • MI • Angina • Peripheral artery disease • AAA • abdominal angina • renal artery disease • Intermittent claudication

10. George et al. Circulation. 2015;132:1320-1328.

11. Risk factors of atherosclerosis • Atherosclerosisis a systemicdisease, butcanbeprevented. • Primarypreventionis a keyapproach.

12. Risk factorsofatherosclerosisdevelopment Non modifiable • Age • Gender • Genetic Modifiable • Hyperlipidemia • Smoking • Arterial hypertension • Physical inactivity • Diabetes mellitus • Obesity

14. Dyslipidemia • Primary vs. secondary • Prevalence and mortality of CVD positivelycorrelateswiththeleveloftotal cholesterol and LDL • LDL • Total cholesterol • HDL • TAG

15. Dyslipidemia

16. Dyslipidemia • Treatmentoptions • Non-pharmacological • Diet • Exerciseand avoidance of sedentary behaviors • Pharmacological • Statins • Ezetimibe • Fibrates • PCSK9 inhibitors

17. Smoking • Activeandpassive smoking is a veryimportant risk-factor • Nicotinepromotes LCL-C oxydization, causesendothelialdysfunction, isprothrombogenic, promotes insulin resistance • Smoking cessationisthe most effectivemeanof CV diseasepreventionandmayleed to 36% reductionof MI mortality

18. Smoking Between 1985 and 2008 there was a decline in cigarette smoking among men (from 45% to 30.5%; p <0.001) in women there was no change. Cífková R et al. Atherosclerosis. 2010;211:676-81.

19. Obesity BMI 27....29 BMI 27....27 Cífková R et al. Atherosclerosis. 2010;211:676-81.

20. Arterial hypertension

23. Invasive methods Non invasive methods Intravascular ultrasound (IVUS) Lower the incidence of CVD related deaths Computed tomography (CT) Optical coherence tomography (OCT) Magnetic resonance (MRI) Near infrared spctroscopy (NIRS) Identification in vivo Prevention of rupture Biomarkers

24. IVUS

25. NIRS and IVUS Plaque burden MLA EEM Lumen IVUS cross-section NIRS chemogram External elastic membrane Minimal lumen area Pullback legth (mm) Yellow = high probability of lipids Lumen diameter / area Plaque burden Circumefential position (°) Lipid core burden index (LCBI)

26. Optical coherence tomography

27. Stable ischemic heart disease

28. Stable ischemic heart disease • Characterised by transient myocardial ischemia • Most commonly caused by obstruction of the coronary arteries by atheromatous plaque

29. Physiology of coronary circulation • Coronarybloodflowisphasicwithmaximalflow in diastole. • 75% ofthe oxygen delivered by coronaryarteriesisextracted by LV → limited oxygen extractionreserve in coronarycirculation. • At 85% lumen diameterreductionat rest (85% at maximum exercise), vasodilatorreserveisexhausted → inadequatepressuredistal to thestenosis → rest orexertionalmyocardialischemia

30. Classification • Chronic stable angina pectoris • Variant angina pectoris • Microvascular AP and syndrome X • Asymptomatic myocardial ischemia

31. What are the characteristics???

32. Variant anginapectoris Chronicstableanginapectoris • Typicalanginapectorisand/orothersymptoms • Angina at rest associated with transient ST-segment elevation, both resolving with the administration of nitrate.

33. Asymptomaticmyocardialischemia Microvascular AP and syndrome X • AP caused by coronarymicrovasculardysfunctionin patientswhohavenonstenoticarteries on coronaryangiography. • The objective evidence of myocardial ischemia (ECG) in the absence of chest pain.

35. Grading of angina pectoris

36. Evaluation • History- typical symptoms • Laboratory evaluation • dyslipidemia, hyperglycemia, renal disease etc. • biomarkers- hs-CRP, MMP-1, PAPP-A • Resting ecg • ECHO • Stress testing • CT angio • Coronarography

37. Evaluation

39. Rest ECG in CHD LBBB T negativity Pathological Q wave

40. Biochemistry • Total cholesterol • LDL • HDL • TAG • hs-CRP • hs-TnI • fasting plasma glucoselevel • HBA1C

42. Echocardiography • Evaluation of LV function, localized kinetic defect • Evaluation of other disease causing angina pectoris (AS, HKMP). • LV function= strongest predictor of long-term survival • A patient with an LVEF <50% is already at high risk for CV death

43. Evaluation

46. Stress tests

47. Stress tests

48. Stress tests

49. Coronary CTA  + • shows anatomical detail as well as the burden of CAD • has reasonable sensitivity and specificity in detecting severe CAD as well as an excellent negative predictive value in excluding significant CAD - • owerpositive predictive value • greater radiation doses to the patient compared to invasive coronary angiograph • does not give validinformation about the functional significance of coronary atherosclerotic lesions

50. Selectiveinvasivecoronaryangiography • the gold standard in assessing the severity of CAD • excellent reliability in assessing severe and mild disease • determine the functional significance of any given coronary stenosis with measurement of fractional flow reserve (FFR) • Intravascular ultrasound (IVUS) can also be used at the time of coronary angiography to assess plaque morphology and vessel size in order to guide decisions regarding the approach to PCI or whether a patient may be better served with medical therapy or CABG.