6b IHD - Ischemic Heart Disease PDF

To prevent ACS and death Alleviate acute symptoms of angina Prevent recurrent symptoms of angina Desired Outcome Prevent progression of the disease • Reduce complications of IHD Avoid or minimize adverse effect General Treatment Strategy Nicotine replacement therapy (Patches) Smoking Bupropion S...

To prevent ACS and death Alleviate acute symptoms of angina Prevent recurrent symptoms of angina Desired Outcome Prevent progression of the disease • Reduce complications of IHD Avoid or minimize adverse effect General Treatment Strategy Nicotine replacement therapy (Patches) Smoking Bupropion SR , Varenicline Cause suicidal tendencies Variety of fruits, vegetables, whole grains, fish, nuts, and legumes. Phytosterols (1–3 g/day) and/or Dietary modifications Lifestyle Modifications Soluble/viscous fiber (3.0–12.0 g/day) Physical activity Must be increased Caloric restriction and increased physical activity Weight loss Limit cholesterol intake to less than 200 mg/day. Limit saturated fat to less than 7% Specific dietary recommendations Limit trans fatty acids to less than 1% of total calories. Limit daily sodium intake to less than 1500 mg for BP control. Limit alcohol to one drink/day for women unless otherwise contraindicated. one to two drinks/day for men 30 ml = one unit 1st option Short acting: Glyceryl trinitrate (GTN) Nitrates Sublingual 30 seconds fast action Long acting: Isosorbide dinitrate; Isosorbide mononitrate Bisoprolol B-blockers (2nd option) Nebivolol Betaxol Carpidalol Veraparnil and Diltiazem Calcium channel blockers Nifedipine Dihydropyridines: Drugs for IHD Amlodipine Blocks sodium-calcium exchange Ranolazine Potassium channel openers Nicorandil Trimetazidine Others Ivabradine Oxyphedrine Interventional Approaches to Revascularization Cause destruction of muscle fibers Statins Myocytise Myolytice Ezetimibe, Dyslipidemia bile acid sequestrants, and proprotein convertase subtilisin/ kexin type 9 (PCSK9) inhibitors Target BP of 130/80 mm Hg or less. Prevention of ACS-Risk factors β-Blockers, ACE inhibitors, or ARBs First-line therapy: Hypertension + calcium channel blocker DHPs, thiazide diuretics, Other agents: and/or mineralocorticoid receptor antagonists (MRAs) DM with ASCVD: Pharmacological Therapy GLP-1 receptor agonists: DM SGLT2 inhibitor alone liraglutide Semaglutide or with GLP-1 Reduce Renin flow ↓ myocardial oxygen consumption: B-blockers Management of Stable IHD By ↓ in resting and exercise HR ↓ in heart rate allows for greater time spent in diastole, and ↓ in myocardial contractility. thereby promoting greater coronary perfusion and myocardial oxygen supply. reduced LV systolic function, First-line therapy in patients with SIHD who have concomitant with ACE inhibitors. Hypotension: BP < 100 mmHg Bradycardia: HR < 50 bpm Contraindications Chronic bronchitis, Asthma Severe chronic renal insufficiency B - Adrenergic Blockers β blockers should not be used alone in unstable angina risk of worsening coronary vasospasm if present. Dilate blood vessels What does it dilate ? More veins than arteries Dilate veins more → Peripheral pooling of Preload reduction blood → ↓ venous return After load reduction Redistribution of coronary blood flow Collateral blood flow Bronchi, Other tissues: Biliary tract Esophagus also relaxed Nitrites Throbbing headache, Flushing, sweating, palpitation, dizziness and fainting Vasodilatation: 6b IHD Orthostatic Hypotension Tachycardia: baroreceptor reflex Methemoglobinemia caution in severe anaemia common with pentaerythritol tetranitrate Rashes: rare. Adverse effects: Tolerance: if continuously in blood Sign no denitrations Due to low glutathione = cGRP sudden withdrawal – coronary spasm Dependence: potentially dangerous hypotension Sildenafil, vardenafil, tadalafil: Drug interactions: Hypo-perfusion of critical organs: PDE 5 Inhibitors Vasodilators: In the Smooth muscles: Relaxation MI Death additive hypotension PVR decreased Negative chronotropic Negative inotropic In the Heart: Calcium Channel Blockers: for Angina Negative dromotropic (conduction velocity of the AV node) despite treatment with betablockers Used when symptoms persist or when beta-blockers are contraindicated. Also used in Prinzmetal angina with or without nitrates. Cardiac depression, cardiac arrest, bradycardia, atrioventricular block, and heart failure Very Rare but serious: not seen Facial Flushing, dizziness, nausea Side effects: Headaches Common but not troublesome: Non-pitting ankle edema Constipation (common) It is a metabolic modulators • pFOX inhibitors Fatty-acid oxidation inhibitors (pFox Inhibitors) Trimetazidine partially inhibit the fatty acid oxidation pathway in myocardium and shift it to more of glucose Partial inhibition of the enzyme long-chain 3-ketoacyl thiolase (LC-3KAT) appears to improve the S/E: Gait, Restless leg, parkinsonism Other uses: It reduces myocardial contractility Tinnitus dizziness. By blockade of a late sodium current that facilitates: calcium entry via the sodium-calcium exchanger Use: approved for chronic angina in the USA. Ranolazine for angina S/E: ↑ QT interval. Verapamil & diltiazem-QT prolongation CYP 3A4 substrate and inhibit CYP 2D6 D/I: With simvastatin- risk of rhabdomyolysis a) Tachycardia due to nitrate is blocked by β blocker. β blocker + long acting nitrate b) β blocker causes ventricular dilatation – c) β blocker reduces total coronary flow- it is counteracted by nitrate. it is opposed by nitrate. A slow acting DHP in place of nitrates with β blocker Verapamil and Diltiazem should not be used with β blocker Nitrates decrease preload, while CCBs have a greater effect on afterload. Rational Drug Combinations Nitrates + CCBs Their concurrent use may decrease cardiac work to an extent not possible with either drug alone. Valuable in severe vasospastic angina. Nitrates primarily decrease preload. Nitrates + CCBs + β blocker CCBs mainly reduce afterload + increase coronary flow. β blocker decrease cardiac work primarily by : ❖Verapanfil /diltiazem should be avoided in such combinations. Treatment algorithm for ischemic heart disease: direct action on heart. metabolic status of ischemic tissue.