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Chronic forms of ischemic heart disease PowerPoint Presentation

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Description : Check out this medical presentation on Angina, which is titled "Chronic forms of ischemic heart disease", to know about the chronic forms of ischemic heart disease (Angina, Cardiosclerosis, and Silent myocardial ischemia).

Tags : Angina, Chronic forms, ischemic heart disease, Cardiosclerosis, Silent myocardial ischemia

Published on : May 25, 2021 | Views : 3112 | Downloads : 9

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Slide 1-

Chronic forms of ischemic heart disease Taras V. Chendey, MD, PhD
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Classification of chronic IHD Angina Stable angina pectoris Vasospastic angina Coronary X-syndrome Cardiosclerosis (cardiofibrosis) Focal cardiosclerosis (post-MI) LV aneurysm Diffuse cardiosclerosis (atherosclerotic c/s) Silent myocardial ischemia (“painless form if IHD”)
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Physiology of coronary circulation Heart is supplied by two major coronary arteries, originating from the aortic root Major branches of coronary arteries lie on the epicardial surface of the heart so the direction of repfusion is from epicardium to endocardium. Subendocardial layers of the LV are most susceptible to ischemia Coronary ostia are being blocked while valve opens – no coronary blood flow during systole During diastole blood is forced into coronary arteries. Driving force of coronary perfusion is diastolic blood pressure. Heart rate determines the duration of diastole: the lower the HR the longer the duration of coronary perfusion
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Determinants of myocardial metabolic needs and myocardial blood supply Needs Systolic BP HR Myocardial contractility Myocardial stress (Laplace equation T=(p*R)/2*t) Supply Diameter of coronary artery Blood O2 capacity – Hb concentration “double product”
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ECG patterns of myocardial ischemia Fixed, stable obstructive coronary lesion (>60% stenosis) – no ischemia at rest, subendocardial ischemia on exertion Downsloping ST segment depression Horizontal ST segment depression J point J point
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Measuring ST segment depression Upsloping ST segment depression is not indicative for myocardial ischemia and usually occurs with tachycardia
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ECG patterns of myocardial ischemia Complete artery occlusion by spasm or clot (ACS) – transmural myocardial ischemia regardless of level of myocardial needs
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Stable angina pectoris (I 20.8) The most common form of chronic IHD Prevalence: 20-40 cases per 1000 adults, 10-20% of men aged 65-74 yrs Average annual mortality 0.9-1.4%, annual MI rate is around 2.0%
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Symptoms of Angina Abrams J. N Engl J Med 2005;352:2524-2533. 9
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Classification and Severity of Angina (Canadian classification) Abrams J. N Engl J Med 2005;352:2524-2533. 11 Abrams,NEJM,2005;352:2524-2533
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Common Stress-Testing Procedures for the Evaluation of Chest Pain Abrams J. N Engl J Med 2005;352:2524-2533. 12
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Typical result of positive stress test
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Coronary angiography: gold standard for diagnosis and risk stratification in chronic IHD. Indications for coronary angiography: Class III-IV angina (disabling angina), esp. despite treatment Prior MI Prior VF/resuscitated sudden cardiac death Exercise testing result compatible with high risk Recurrence of angina after revascularization
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From the angiography standpoint coronary lesions can be classified into: Single-vessel disease Two-vessel disease Multi-vessel disease Left main disease
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Stable angina management: general measures Smoking cessation Weight loss, diet and physical activity Control of blood pressure and diabetes Lipid management - statins. LDL-C goal is <1.8 mmol/L or >50% reduction from the baseline
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Pharmacological treatment of stable angina: drugs for prognosis improvement (prevention of MI and death) Low-dose (75-100 mg) aspirin – on the reglar basis Clopidogrel if not tolerant to aspirin Statins (simva, atorva, rosuva) ACEis in patients with HTN, DM or heart failure Beta-blockers in patients with prior MI
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Pharmacological treatment of stable angina: drugs for symptom relief (antianginal drugs) Short-acting nitroglycerine (NG) – sublingual tablets or spray Mode of action: donator of NO (needs SH-groups for the reaction) → mostly venodilatation → ↓ return of blood to the heart → reduced preload and pressure in ventricles → reduced myocardial oxygen needs, enhanced subendocardial perfusion. Onset of action – up to 1 minute, duration of action – up to 5 minutes. Daily multiple doses are safe.
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Long-acting nitrates & sydnonimines Extended-release NG (Sustac, Nitrong, Nitrogranulong) Isosorbide dinitrite: regular and extended-release formulations (Isoket, Isoket-ret., Cardiket) Isosorbide-5-mononitrite: regular and extended-release formulations (Olicard retard, Monosan, Mononitrosid) Pentaerythrytol tetranitrate (Erynit) Sydnonimine derivate – molsidomine (Sydnopharm)
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Nitrates: PK features Low oral bioavailability due to first passage effect (high inactivation in liver) – better with ER formulations Presence of nitrates in blood >24h leads to exhaustion of SH-pool and development of tolerance In order to prevent tolerance allow at least 12-14 hours nitrate-free interval per day. Usually first dose of long-acting nitrates is given in the morning, second – at noon (if needed), then no nitrates (except short-acting NG on demand) Molsidomine doesn’t need SH-groups for releasing NO – no tolerance. Side effects: headaches (most common), hypotension. Not indicated in valvular stenoses
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Beta-blockers First-line antianginal therapy Mode of action: negative chronotropic effect → ↓HR → prolonged diastolic perfusion time (increased supply) negative inotropic effect → ↓contractility → decreased myocardial metabolic needs ↓SBP → ↓afterload → decreased myocardial metabolic needs ↑tone of intact coronary arteries → “reversed steal” phenomenon (increased flow is affected artery) All beta-blockers are equally effective in preventing anginal episodes
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Calcium channel blockres Verapamil & Diltiazem Negative chrono- and inotropic effects Vasodilatation Combination with beta-blockers prohibited! (risk of profound bradycardia and complete heart block) Dihydropiridines (amlodipine, felodipine) Mostly vasodilatation, less negative inotropic effect Useful in vasospastic angina Well combined with beta-blockers
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Ivabradine (Coraxan) Selective If channel blocker Selective negative chronotropic effect No effect on BP, LV contractility and conduction May be first-line antianginal if beta-blocker is contraindicated Can be combined with any other antianginal
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Trimetazidine (Preductal MR) Oral 3-ketoacylthiolaze (3-KAT) inhibitor 3-KAT activity is responsible for fatty acid oxidation in muscles Inhibition of 3-KAT switches metabolism from aerobic fatty acid oxidation to anaerobic glycolisis, thus favorably influencing myocardial O2 demands and ATP balance in cell. No effect on BP, HR, contractility and conduction Well tolerated, few side effects Usually added to haemodynamic antianginals as a second-line therapy
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Revascularization in angina
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Single or two-vessel disease Preserved LV EF technical suitability Multi-vessel or left main stem disease Depressed LV EF technical inability to perform PCI