5. Ischemic Heart Disease Stable Angina (1).ppt

Ischemic Heart Disease Chronic Stable Angina CAD, coronary artery disease; INOCA, ischaemia and no obstructive coronary artery disease; MINOCA, myocardial infarction with no obstructive coronary artery disease. Thomas J Ford et al. Heart 2018;104:284-292 Copyright © BMJ Publishing Group Ltd & Br...

Ischemic Heart Disease Chronic Stable Angina CAD, coronary artery disease; INOCA, ischaemia and no obstructive coronary artery disease; MINOCA, myocardial infarction with no obstructive coronary artery disease. Thomas J Ford et al. Heart 2018;104:284-292 Copyright © BMJ Publishing Group Ltd & British Cardiovascular Society. All rights reserved. Angina pectorisdefinition     Angina pectoris- is a clinical manifestation of acute myocardial ischemia Heberden- ”sense of strangling and anxiety” and “a painful and most disagreeable sensation in the chest” discomfort usually located in the retrosternal area, but may radiate to the jaw, throat, right or left arm, wrist or back; epigastric discomfort in conjunction with chest pain Other associated symptoms: dyspnea, fatigue, syncope (particularly common in the elderly). Duration     Typical angina usually characterized by a crescendo increase in the intensity of pain over minutes Precipitated by exercise, exposure to cold temperatures or carbohydrate- rich meals Relieved within minutes by rest and nitroglycerin If pain not relieved within 5- 10 min. after rest or Ntg.= severe ongoing ischemia is present (unstable angina or AMI). Etiology of myocardial ischemia      Coronary atherosclerotic narrowing (the common cause) Nonatherosclerotic coronary disease: coronary spasm, coronary thrombembolism, congenital anomalies, coronary vasculitis Valvular heart disease: AoS and/or Ao Insuf., MS with pulmonary hypertension, mitral valve prolapse, pulmonic stenosis Pulmonary hypertension Hypertrophic or dilated cardiomyopathies Stable Angina Pectoris Stable = there has been no change in the frequency, duration, precipitating factors or ease of relief of angina attacks during the last 60 days. Pathophysiology – myocardial ischemia occurs when an increase in myocardial oxygen demand occurs in the presence of fixed myocardial oxygen supply. - occurs when the patient walks rapidly or climbs a slight incline. Stable Angina Pectoris Factors that affect myocardial oxygen demand: - heart rate, - myocardial contractility - myocardial wall stress ( determined by LV pressure, volume and wall thickness). The Canadian Cardiovascular Society Classification of Angina Pectoris 1. 2. Ordinary physical activity does not cause angina, such as walking and climbing stairs. Angina with strenuous or rapid or prolonged exertion at work or recreation. Slight limitations of ordinary activity. Walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, or in cold, or in wind, or under emotional stress, or only during the few hours after awakening. Walking more than two blocks on the level and climbing more than one flight of ordinary stairs at a normal pace and in normal conditions/ The Canadian Cardiovascular Society Classification of Angina Pectoris 3. Marked limitation of ordinary physical activity. Walking one to two blocks on the level and climbing one flight of stairs in normal conditions and at normal pace. 4. Inability to carry on any physical activity without discomfort- angina syndrome may be present at rest. Physical Examination  Brief episodes of angina can result in transient LV and papillary muscle dysfunction, characterized by S3, loud S4, pulmonary rales and apical systolic murmurs. Physical Examination   Evidence of peripheral vascular disease (diminished pulses, carotid bruits ) Patients with angina may have a completely normal physical examination. Other differential diagnosis        Acute myocardial infarction Aortic dissection Pulmonary embolism Acute pericarditis Gastro esophageal reflux Cholecystitis Costosternal chondritis and Tietze syndrome Diagnostic Testing Biochemical Tests      Fasting lipid profile and fasting glucose ( to screen for dyslipidemias and insulin resistance). Other markers of increased atherogenicity: lipoprotein Lp (a), small dense LDL, apolipoprotein B High- sensitive C-reactive protein (CRP) can be used to prognosticate patients with established CAD. B-type natriuretic peptide (BNP) = strong predictor of morbidity and mortality; suggests LV failure. Cell blood count, creatinine, thyroid function. Usual Diagnostic Tests     Resting ECG: normal in approx. one-half of patients During an angina episode, ECG becomes abnormal in about 50% of patients with normal baseline ECG. detection of repolarization abnormalities, mainly in the form of ST-segment depressions an ECG can demonstrate indirect signs of CAD, such as signs of previous MI (pathological Q waves) or conduction abnormalities [mainly left bundle branch block (LBBB) and impairment of atrioventricular conduction. Holter ECG monitoring   24-h Holter monitoring: helpful in evaluating the total ischemic burden = episodes of painful and painless myocardial ischemia./recommended in pt with chest pain and suspected arrhythmias and in vasospastic angina. The presence of nonspecific ST-segment changes has been associated with unfavorable outcome, especially in combination with ventricular arrhythmias. Echocardiography   An echocardiographic study will provide important information about cardiac function and anatomy. LV ejection fraction (LVEF) is often normal in patients with CCS. A decreased LV function and/or regional wall motion abnormalities may increase the suspicion of ischaemic myocardial damage. Magnetic resonance imaging   Cardiac magnetic resonance (CMR) may be considered in patients with suspected CAD when the echocardiogram is inconclusive. CMR will provide useful information on cardiac anatomy and systolic cardiac function Assessment of LV function (Echocardiography or CMR)is important for risk stratification and should therefore be performed in all symptomatic patients with suspected CAD. Usual Diagnostic Tests   Exercise stress testing (treadmill protocol) – helpful in individuals in whom the pretest probability of coronary atherosclerosis is intermediate Stress testing is not needed, and should not be used as a diagnostic procedure, when the pretest probability of stable angina pectoris is 90%. Exercise stress testing (treadmill protocol)    Exercise ECG has inferior diagnostic performance compared with diagnostic imaging tests, and has limited power to rule-in or rule-out obstructive CAD use of an imaging diagnostic test instead of exercise ECG as the initial test for to diagnose obstructive CAD. exercise ECG assessment of symptoms, ST-segment changes, exercise tolerance, arrhythmias, blood pressure (BP) response. Usual Diagnostic Tests  Exercise echocardiography and pharmacological stress echocardiography important in assessing LV wall motion abnormalities and systolic function. Exercise echocardiography Stress testing  Myocardial perfusion imaging (a nuclear medicine procedure). A radiotracer is injected and scans are acquired showing the relative amounts of radioisotope within the heart muscle, can identify area of reduced blood flow/ combined with stress. Myocardial perfusion imaging Usual Diagnostic Tests Coronary angiography indicated for :  patients with stable angina who are clinically determined to be at high risk for future cardiac events (ischemia at low workload, reduced ejection fraction);  whose angina pectoris is poorly controlled by medication;  in whom coronary spasm is suspected. Anatomical non-invasive evaluation  Anatomical non-invasive evaluation, by visualizing the coronary artery lumen and wall using an intravenous contrast agent, can be performed with coronary Ct angiography, which provides high accuracy for the detection of obstructive coronary stenoses TREATMENT Treatment Medical management: treat conditions which can exacerbate previously stable angina:  anemia,  thyrotoxicosis,  fever,  infection,  tachycardia,  avoid drugs that can activate the sympathetic nervous system. Reduction of coronary risk factors  Hypertension: the risk for ischemic heart disease doubles for every 20 mm Hg increase among individuals between 40 to 70 years. Pharmacological treatment of mildmoderate HTN demonstrates a reduction in CAD events Reduction of Coronary Risk Factors Dyslipidemia: ↑LDL cholesterol: several clinical trials have demonstrated that administrations of statins significantly reduce subsequent cardiovascular events; statins have also shown to improve endothelial function, lower circulating levels of Creactive protein, reduce thrombogenicity, stabilize atherosclerotic plaques.  ↓HDL cholesterol seems to be a challenging aim of therapy for CAD patients. Exercise: the conditioning effect of exercise lowers the heart rate and increases the cardiac output at any given level of myocardial O2 consumption.  Specific Pharmacological Management of Angina Pectoris Nitrates   Nitrates induce endotheliumindependent vasodilatation, relax systemic arteries and veins; the venodilator effect predominates. In the coronary circulation, nitrates also dilate epicardial stenosis and alleviate endothelial dysfunction, thus improving blood flow across obstructed regions. Nitroglycerin Tablets    Sublingual nitroglycerin remains to be the treatment of choice for acute angina episodes. The half- life of NTG is brief, and within 30-60 min hepatic breakdown abolishes the hemodynamic and clinical effect. Sublingual NTG, when taken prophylactically prior to physical activities, can prevent angina for up to 40 min. Nitroglycerin Transdermal Patches The release rate varies from 0.1 mg/hour to 0.8 mg/hr. Can prolong exercise duration and offer sustained antianginal effects for 12 hours without significant nitrate tolerance or rebound phenomena. Isosorbide Dinitrate   Undergoes rapid hepatic metabolism and thus has low bioavailability after oral adm. Partial or complete nitrate tolerance develops with doses at 30 mg 3-4x daily; hence, a dosage schedule which includes a 10 to 12 hour nitrate- free interval should be implemented to prevent tolerance. Isosorbide 5-Mononitrate    Is the active metabolite of dinitrate which does not undergo first-pass hepatic metabolism. It reaches peak level between 30 min to 2 hours after ingestion, with a plasma half-life of 4-6 hours. Given once daily; nitrate tolerance has not been demonstrated with once a day dosing intervals. Β- Adrenergic Receptor Blocking Agents    Β-blockers antagonize the effect of circulating and neuronal released catecholamine B- blockers slow the heart rate and increase diastole, which allow more coronary perfusion. By blocking the surges of sympathetic activity during exercise, β-blockers reduce contractility and LV wall tension, resulting in lower myocardial O2 demand. Β- Adrenergic Receptor Blocking Agents    B-blockers decrease the frequency of angina episodes and raise the angina threshold. B- blockers reduce mortality and re-infarction in post-MI patients Abrupt withdrawal of β-blockers can precipitate unstable angina and MI in patients with chronic CAD. ACE Inhibitors    ACE inhibitors reduce LVH, vascular hypertrophy, plaque rupture and thrombosis risk. ACE inhibition also enhances coronary endothelial vasomotor function and decreases inflammatory changes in animal models of atherosclerosis ACE inhibitors should be recommended for all patients with CAD in conjunction with diabetes and/or impaired LV function, HT. Calcium Channel Antagonists Three subclasses: 1. dihydropyridines (e.g., nifedipine) 2. phenylalkylamines (e.g., verapamil) 3. benzothiazepines (e.g., diltiazem) They reduce myocardial O2 demand and enhance myocardial O2 supply. - very useful in the treatment of vasospastic angina and angina of small coronary arteries. - potential to worsen heart failure in pts. with LV dysfunction  TREATMENT ANGINA RELIEF   1. Nitroglicerine for immediate relief of angina 2. Betablockers or calcium channel blockers  3. Combination beta blocker -DHP calcium channel blocker  4. Add Long acting nitrates TREATMENT EVENT PREVENTIONANTIPLATELET DRUGS Platelet activation and aggregation is the driver for symptomatic coronary thrombosis, forming the basis for the use of antiplatelet drugs. TREATMENT EVENT PREVENTIONANTIPLATELET DRUGS   Low-dose aspirin. Aspirin acts via irreversible inhibition of platelet cyclooxygenase-1 and thus thromboxane production. Aspirin ( 75- 325 mg/ day) reduced the rate of subsequent MI, stroke, and death, improved endothelial function and reduced the circulating levels of Creactive protein TREATMENT EVENT PREVENTION ANTIPLATELET DRUGS    Oral P2Y12 inhibitors. P2Y12 inhibitors block the platelet P2Y12 receptor, which plays a key role in platelet activation and thrombus formation. Clopidogrel and prasugrel that irreversibly block P2Y12 via active metabolites. Ticagrelor is a reversibly-binding P2Y12 inhibitor that does not require metabolic activation TREATMENT EVENT PREVENTION ANTIPLATELET DRUGS    Aspirin 75-100 mg daily Or Clopidogrel 75 mg daily is recommended as an alternative to aspirin in patients with aspirin intolerance and may be considered in preference to aspirin in PAD or a history of ischaemic stroke ANTIPLATELET THERAPY (dual)    Adding a second antithrombotic drug to aspirin for long-term secondary prevention in patients with a high risk of ischaemic events and without high bleeding risk Aspirin 75-100 mg daily is recommended following stenting. Clopidogrel 75 mg daily following appropriate loading is recommended, in addition to aspirin, for 6 months following coronary stenting ANTIPLATELET THERAPY  Prasugrel or ticagrelor may be considered, in specific high-risk situations of stenting (associated with high risk of stent thrombosis, complex left main lesion, or multivessel stenting) . TREATMENT EVENT PREVENTION Statins and other lipidlowering drugs   Dyslipidaemia should be managed with pharmacological and lifestyle intervention. 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. TREATMENT EVENT PREVENTION ACE INHIBITORS  ACE inhibitors be considered for the treatment of patients with stable angina with coexisting hypertension, heart failure, diabetes. Revascularization treatment (in stable angina) EXTENT OF CAD For prognosis For symptoms Left main stenosis > 50% Proximal LAD stenosis > 50% 2 or 3 vessel disease with LVEF <35% Large area of ischemia (>10%LV) Single remaining patent artery with stenosis>50% The presence of limiting Therapy No Longer Recommended in the Treatment of Chronic CAD Estrogenic Replacement  Randomized, controlled secondary prevention trials have suggested that hormone therapy does not reduce cardiovascular events or mortality. Antioxidants  vitamin C, vitamin E and beta-caroten. Variant (Prinzmetal’s) Angina Pectoris     Episodes of myocardial ischemia that last several minutes, occur at rest, frequently worse in the morning, associated with transient ST- segment elevation It is believed that coronary vasospasm is responsible for episodes of myocardial ischemia Local endothelial changes may be responsible for the hyperactivity of coronary artery segments The majority of patients also have atherosclerotic coronary artery disease Variant (Prinzmetal’s) Angina Pectoris  The coronary arteries may develop spasm as a result of exposure to cold weather, exercise, or a substance that promotes vasoconstriction as alphaagonists (pseudoephedrine). Recreational drug use, for example, cocaine use, is associated with the development of vasospastic angina, especially when used concurrently with cigarette smoking. Usual Diagnostic Tests  24 h Holter monitoring  Coronary arteriography in all patients  During cardiac catheterization, coronary spasms can be visualized spontaneously or under drug induction. If no significant stenosis, attempt to provoke vasospasm by iv ergonovine (only in the cath lab). Treatment     In the absence of significant atherosclerotic CAD, nitrates and Ca antagonists are the mainstay of medical therapy Beta blockers may, theoretically exacerbate variant angina if unopposed alphareceptor- mediated vasoconstriction occurs. Exposure to cold environment should be avoided Interventional treatment imposed by coronary anatomy