Chronic Stable Angina Study Guide 2025 PDF
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Drake University
2025
Natalie Gadbois-Mincks
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Summary
This study guide provides learning objectives, references, and questions on chronic stable angina, a type of heart disease, for a Wednesday class on January 29, 2025. The document covers topics including pathophysiology, clinical presentation, risk factors, and treatment.
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**Chronic Stable Angina -- Therapeutics I** **Study Guide for Wednesday, January 29, 2025** **Natalie Gadbois-Mincks, PharmD, MPA, BCACP** Assistant Professor of Pharmacy Practice natalie.gadboismincks\@drake.edu ** ** **[Note:]** *This section is titled "Chronic Stable Angina" however there a...
**Chronic Stable Angina -- Therapeutics I** **Study Guide for Wednesday, January 29, 2025** **Natalie Gadbois-Mincks, PharmD, MPA, BCACP** Assistant Professor of Pharmacy Practice natalie.gadboismincks\@drake.edu ** ** **[Note:]** *This section is titled "Chronic Stable Angina" however there are multiple similar and overlapping terms to describe this condition that may be used throughout this study guide. Angina symptoms can be a result of ischemic heart disease (IHD) which is a type of chronic coronary disease (CCD).* **[Learning Objectives]** 1. Define chronic coronary disease and different types of ischemic heart disease 2. Relate the pathophysiology of ischemic heart disease to medication therapy options 3. Understand the clinical presentation of ischemic heart disease 4. Identify risk factors that contribute to the development of ischemic heart disease 5. Recall the classification of angina symptoms 6. Recall the treatment goals of stable ischemic heart disease 7. Recommend appropriate non-pharmacologic & pharmacologic therapy for chronic stable angina 8. Describe indications, mechanisms, adverse effects, monitoring parameters and clinical pearls of medication therapy options for chronic stable angina 9. Create a care plan for a patient with chronic stable angina utilizing patient-specific information and applying evidence-based literature **[Required References]** [Textbook:] ***Chapter 8: Stable Ischemic Heart Disease*** in ***Pharmacotherapy Principles and Practice**, 6^th^ edition*. Chisolm-Burns MA, et al. 2022. ISBN: 978-1260460278. - Access through **Access Pharmacy** on the [Drake Library Pharmacy & Health Science Home Page](https://library.drake.edu/phs) [Guideline:] ***2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients with Chronic Coronary Disease (CCD)*.** Virani SS, et al. 2023.. [Drug Information:] *Drug Information Handbook*, 30^th^ edition. 2020. ISBN: 978-1-59195-385-2. - Access through **Lexidrug** on the [Drake Library Pharmacy & Health Science Home Page](https://researchguides.drake.edu/phs) **[Optional/Supplemental References]** [Video:] Angina Pectoris -- Symptoms and Pathology (6:07 min) - [Top 200/300 Medications:] Top 200 Drug List from ClinCalc - Access directly through [ClinCalc](https://clincalc.com/DrugStats/Top200Drugs.aspx) Top 300 Drug Flashcards (Utilize as resource to review medications) - Access through **Top Drugs** on the [Drake Library Pharmacy & Health Science Top Drugs Page](https://library.drake.edu/phs/topdrugs)**[\ ]** **[Medications]** The table below lists medications you will be responsible for knowledge related to as outlined in the study guide questions. - Brand Names Required: None - Dosing Required: Aspirin Of note, at least 1 RAT question (and possibly exam questions) will pertain to the [Top 200 Medications](https://clincalc.com/DrugStats/Top200Drugs.aspx) (indicated with a \* below). You will be responsible for knowledge related to the following areas, even if there are no specific associated study guide questions. Areas that may be tested on include: - Mechanism of action - Pharmacokinetic/dynamic properties (i.e. t1/2, ADME) - Adverse reactions - Monitoring parameters - Contraindications - Black box warnings - Major drug interactions - Available dosage formulations - Key patient counseling points - Clinical pearls +-----------------------------------+-----------------------------------+ | **Class of Agents** | **Specific Medication(s)** | +===================================+===================================+ | Antiplatelet Agents | Aspirin\* | | | | | | Clopidogrel\* | +-----------------------------------+-----------------------------------+ | B-Blocker (Beta-Blocker) | Metoprolol succinate\* | +-----------------------------------+-----------------------------------+ | CCB (Calcium Channel Blocker) | Amlodipine\* | | | | | | Diltiazem\* | +-----------------------------------+-----------------------------------+ | Nitrates | Nitroglycerin\* | | | | | | Isosorbide Mononitrate\* | +-----------------------------------+-----------------------------------+ | Miscellaneous | Ranolazine | +-----------------------------------+-----------------------------------+ \*Top 200 Medication *[Note:] Medications in this table do not encompass all drugs within each class or all drugs utilized to treat this condition. What is included represents medications commonly used in clinical practice and/or with specific indications for this condition.* **[\ ]** **[Study Guide Questions]** 1. **What is chronic coronary disease (CCD)?** *(Guideline, 2. Epidemiology & General Principles, Pg 842 Obj 1)* Chronic Coronary Disease (CCD) is a heterogenous group of conditions that includes: - obstructive and non obstructive CAD with or without previous myocardial infarction (MI) or revascularization - ischemic heart disease diagnosed only by noninvasive testing - chronic angina syndrome with varying underlying causes 2. **What occurs in the body when a patient has ischemic heart disease (IHD)?** *(Textbook Ch 8, Introduction, Pg 1, Obj 2)* - When a pt has IHD, there is reduced supply of oxygenated blood to the heart. IHD is caused by stenosis (narrowing) in one or more of the major coronary arteries that supply blood to the heart due to atherosclerotic plaques. - IHD results from an imbalance between myocardial oxygen supply and oxygen demand. - In patients without IHD, coronary blood flow increases in response to increased myocardial oxygen demand. - However in pts with IHD, coronary blood flow cannot sufficiently increase (and may decrease) in response to increased oxygen demand, resulting in angina. 3. **What are common clinical manifestations of IHD?** *(Textbook Ch 8, Introduction, Pg 1, Obj 3)* Common clinical manifestations include chronic stable angina and the acute coronary syndromes (ACS) of unstable angina (UA), non-ST- segment elevation myocardial infarction (NSTEMI), and ST segment elevation myocardial infarction (STEMI) 4. **What is the most common symptom of IHD?** *(Textbook Ch 8, Introduction, Pg 2, Obj 3)* Angina pectoris/ Angina is the most common symptom. Angina is discomfort in the chest that occurs when the blood supply to the myocardium is compromised. Chronic stable angina is a chronic occurrence of chest discomfort due to transient myocardial ischemia with physical exertion or other conditions that increase myocardial oxygen demand. 5. **What are major risk factors for IHD? Which risk factors are modifiable versus nonmodifiable?** *(Textbook Ch 8, Epidemiology & Etiology, Pg 4, Table 8-2, Obj 4)* Pts with multiple risk factors, particularly those with diabetes, are at greatest risk for IHD, experiencing 5-7 times higher risk compared to indicviduals without risk factor [Modifiable Risk Factors:] - Cigarette smoking - Dyslipidemia Elevated LDL or total cholesterol Reduced HDL cholesterol - Diabetes mellitus - Hypertension - Physical inactivity - Obesity (body mass index ≥ 30 kg/m^2^) - Low daily fruit and vegetable consumption - Alcohol overconsumption [Nonmodifiable Risk Factors:] - Age ≥ 45 years for men, age ≥ 55 years for women - Gender (men and postmenopausal women) - Family history of premature cardiovascular disease, defined as cardiovascular disease in a male first-degree relative (ie, father or brother) \< 55 years or a female first-degree relative (ie, mother or sister) \< 65 years 6. **What is the difference in pathophysiology of stable IHD versus acute coronary syndrome (ACS)?** *(Textbook Ch 8, Pathophysiology, Pg 5-6 & Figure 8-3, Obj 2)* **Stable IHD:** - Hallmark feature of stable IHD is an established atherosclerotic plaque in one or more of the major coronary arteries that impedes blood flow such that myocardial oxygen supply can no longer meet myocardial oxygen demand. - Stable IHD consists of a small lipid core surrounded by a thick fibrous cap - Diagram of a structure of the human body Description automatically generated - Hallmark feature is atherosclerotic plaque rupture with subsequent thrombus formation. - Plaque rupture refers to fissuring (breaking/ crack) of the fibrous cap and the exposure of the plaque contents to the blood. - Consists of a thin, weak fibrous cap covering a large lipid-core that makes the plaque vulnerable to rupture - Transformation of a stable plaque into an unstable plaque involves degradation of the fibrous cap by substances released from macrophages. Usually pt with unstable plaque is asymptomatic ![Diagram of a diagram showing the structure of the body Description automatically generated](media/image3.png) 7. **What is Prinzmetal or variant angina?** *(Textbook Ch 8, Pathophysiology, Pg 6, Obj 1)* - Variant angina results from vasoconstriction or spasm of a coronary artery in absence of significant atherosclerosis. - Usually occurs at rest, during early morning hours. - Although transient (exists only for a short time), it may persist long enough to cause myocardial ischemia and subsequent infarction. - Pts with variant angina are typically younger than those with chronic stable angina and often do not possess the classic risk factors of IHD. 8. **What are the classes of angina in the Canadian Cardiovascular Society Classification System and how are these utilized in clinical practice?** *(Textbook Ch 8, Clinical Presentation & Diagnosis, Pg 8, Table 8-4, Obj 5)* - [Class I] -- Able to perform ordinary physical activity (eg, walking, climbing stairs) without symptoms. Strenuous, rapid, or prolonged exertion causes symptoms. - [Class II] -- Symptoms slightly limit ordinary physical activity. Walking rapidly or for more than two blocks, climbing stairs rapidly, or climbing more than one flight of stairs causes symptoms. - [Class III] -- Symptoms markedly limit ordinary physical activity. Walking less than two blocks or climbing one flight of stairs causes symptoms. - [Class IV] -- Angina may occur at rest. Any physical activity causes symptoms The Canadian Cardiovascular Society Classification System is commonly used to assess the degree of disability resulting from IHD. Pts are divided into 4 classes depending on the extent of activity causing angina. In clinical practice, this categorization is used to assess changes in IHD severity over time and effectiveness of pharmacological therapy. 9. **What are the goals and desired outcomes for treatment of stable IHD?** *(Textbook Ch 8, Treatment, Pg 9, Obj 6)* - Prevent ACS and death - Alleviate acute symptoms of angina - Prevent recurrent symptoms of angina - Prevent progression of the disease - Reduce complications of IHD - Avoid or minimize adverse treatment effects 10. **When are percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG) surgery indicated for patients with stable IHD?** *(Textbook Ch 8, Treatment, Pg 13-14, Obj 7)* - In patients with SIHD, optimal medical therapy is equivalent to PCI in reducing major adverse cardiac events (MACE) - Therefore, medical therapy is preferred as the initial treatment strategy. However, when optimal medical therapy fails, symptoms are unstable, or extensive coronary atherosclerosis is present (eg, \> 70% occlusion of coronary lumen), PCI is often performed to restore coronary blood flow and relieve symptoms. 11. **What are the general treatment recommendations for stable IHD?** *(Textbook Ch 8, Treatment, Pg 11, Figure 8-5, Obj 7)* A diagram of a patient\'s flowchart Description automatically generated 12. **What are the recommendations for type and duration of antiplatelet therapy in the following clinical scenarios?** *(Guideline, 4. Treatment, Pg 879-881 & Figure 9, Obj 7, 9)* - [CCD with No Indication for Anticoagulation] -- Low dose aspirin 81 mg (75-100 mg) is recommended to reduce atherosclerotic events - [PCI] -- dual antiplatelet therapy (DAPT) consisting of aspirin and clopidogrel for 6 months post PCI followed by single antiplatelet therapy (SAPT) is indicated to reduce MACE and bleeding events - [PCI and High Bleeding Risk] -- DAPT from month 1-3, P2Y12 inhibitor from month 3-12, followed by SAPT for month 12 and beyond. - [PCI with Indication for Anticoagulation] -- DAPT for 1 to 4 weeks followed by clopidogrel alone for 6 months should be administered in addition to DOAC ACS indicates acute coronary syndrome; ASA, aspirin; CCD, chronic coronary disease; DAPT, dual antiplatelet therapy; DES, drug-eluting stent; DOAC, direct oral anticoagulant; MI, myocardial infarction; OAC, oral anticoagulants; PCI, percutaneous coronary intervention; SAPT, single antiplatelet therapy 13. **What is the recommended dose for aspirin to reduce atherosclerotic events?** *(Guideline, 4. Treatment, Pg 879, Obj 7, 9)* Low dose aspirin 81 mg (75 mg- 100 mg) 14. **What if aspirin is contraindicated or not tolerated?** (*Textbook Ch 8, Treatment, Pg 15, Obj 7, 9)* **Clopidogrel 75 mg daily** 15. **Why is dual antiplatelet therapy (DAPT) required after stent placement?** (*Textbook Ch 8, Treatment, Pg 16, Obj 8)* - Antiproliferative drugs in DES reduce the risk of in-stent restenosis but delay endothelialization. Until endothelialization occurs, platelets are exposed to the foreign surface of the stent and can stimulate platelet adhesion, activation, aggregation, and eventual thrombus formation within the implanted stent resulting in acute ischemia 16. **What are patient characteristics or risk factors should be evaluated when considering extending or shortening the duration of DAPT?** (*Textbook Ch 8, Treatment, Pg 16, Obj 7, 9)* - [Prolonged/Extended Duration of DAPT] -- Select patients with IHD who have not experienced a bleeding complication on DAPT and are not at high risk for bleeding (eg, prior bleeding on DAPT, coagulopathy, oral anticoagulant use) may be considered for "prolonged" or "extended" duration of DAPT - [Shorter Duration of DAPT] -- patients who experience a significant bleeding complication are at high risk for bleeding or have a high risk of severe bleeding complications (eg, major intracranial surgery) may be considered for a shorter duration of DAPT 17. **The following risk calculators can be used to assess bleeding risk and duration of antiplatelet therapy. List the factors within each of these scoring systems. *Do not need to indicate specific scores for individual factors.*** (*Textbook Ch 8, Treatment, Pg 17, Table 8-5, Obj 9)* +-----------------------------------+-----------------------------------+ | **PRECISE-DAPT** | **DAPT** | | | | | Use During PIC with Stent | Use After 12 Months of Event-Free | | Implantation | DAPT | +===================================+===================================+ | Hgb | Age\>/= 75 | | | | | WBC | Age 65- 75 years | | | | | Age | Age \< 65 years | | | | | CrCl | Current cigarette smoker | | | | | Prior bleed | Diabetes mellitus | | | | | | MI at presentation | | | | | | Prior PCI | | | | | | Stent diameter | | | | | | Paclitaxel eluting stent | | | | | | Heart failure or LVEF | | | | | | PCI of saphenous vein graft | +-----------------------------------+-----------------------------------+ 18. **Medications for angina work via two general mechanisms. Which medication classes work through the following mechanisms?** *(Guideline, 4. Treatment, Pg 889, Obj 8)* - [Decreasing Myocardial Oxygen Demand] -- Beta blockers, non dihydropyridine CCBs, and ivabradine - [Increasing Myocardial Arterial Blood Supply] -- Nitrates and dihydropyridine CCBs 19. **What medication is recommended for short-term relief of acute angina symptoms?** *(Guideline, 4. Treatment, Pg 889, Obj 7, 9)* Short acting nitrates 20. **What counseling points would you provide a patient who is prescribed sublingual nitroglycerin tablets?** (*Textbook Ch 8, Treatment, Pg 20, Obj 8)* - [Typical Dosing] -- 0.3- 0.4 mg (tablet or spray) - [Administration] -- administered sublingually and repeated every 5 minutes up to three times or until symptoms resolve. Standing enhances venous pooling and may contribute to hypotension, dizziness, or light-headedness. So make sure to sit down. - [Storage] -- Keep nitroglycerin tablets in the original glass container and close the cap tightly after use. Nitroglycerin should not be stored in the same container as other medications because this may reduce nitroglycerin's effectiveness - [Drug Interactions] -- Nitroglycerin should not be used within 24 hours of taking sildenafil or vardenafil or within 48 hours of taking tadalafil because of the potential for life-threatening hypotension. - [When to Call 911] -- if symptoms are unimproved or worsen 5 minutes after the first dose. 21. **What medications are recommended first line for long-term prevention of angina symptoms?** *(Guideline, 4. Treatment, Pg 889, Obj 7, 9)* Beta blockers, Calcium channel blockers, long acting nitrates. 22. **If angina symptoms are not improved with one agent what is recommended?** *(Guideline, 4. Treatment, Pg 889, Obj 7, 9)* addition of a second antianginal agent from a different therapeutic class (beta blockers, CCB, long-acting nitrates) is recommended for relief of angina or equivalent symptoms 23. **When is ranolazine typically used to treat anginal symptoms? When would you use it over a beta-blocker or calcium channel blocker?** *(Guideline, 4. Treatment, Pg 889, AND Textbook, Ch 8, Treatment, Pg 26, Obj 7, 9* In patients with CCD, ranolazine is recommended in patients who remain symptomatic despite treatment with beta blockers, CCB, or long- acting nitrate therapies. Ranolazine has minimal effects on heart rate or BP; thus, it may be an option in SIHD patients with low baseline BP or heart rate. 24. **What type of beta-blockers should be avoided as antianginal agents and why?** *(Textbook Ch 8, Treatment, Pg 21, Obj 7, 9)* β-Blockers with intrinsic sympathomimetic activity (eg, acebutolol, pindolol, and penbutolol) have partial β-agonist effects and cause lesser reductions in heart rate at rest. As a result, β-blockers with intrinsic sympathomimetic activity may produce lesser reductions in myocardial oxygen demand and should be avoided in patients with SIHD. 25. **What type of calcium channel blockers are typically more effective antianginal agents and why?** (*Textbook Ch 8, Treatment, Pg 23, Obj 7, 9)* - The nondihydropyridine CCBs, verapamil and diltiazem, slow sinoatrial and AV nodal conduction, decrease heart rate, and further decrease myocardial oxygen demand. - Because of their negative [chronotropic](https://ppp-mhmedical-com.cowles-proxy.drake.edu/content.aspx?bookid=3114§ionid=261459981#chisppp6_ch8gloss17) effects, verapamil and diltiazem are generally more effective antianginal agents than the dihydropyridine CCB 26. **If used in combination with a beta-blocker what type of calcium channel blocker is preferred and why?** (*Textbook Ch 8, Treatment, Pg 23, Obj 7, 9)* combination should be used with caution because both drugs decrease AV nodal conduction, increasing the risk for severe bradycardia or AV block when used together. If combination therapy is warranted, a long-acting dihydropyridine CCB is preferred. - Because of their negative [inotropic](https://ppp-mhmedical-com.cowles-proxy.drake.edu/content.aspx?bookid=3114§ionid=261459981#chisppp6_ch8gloss18) effects, CCBs may cause or exacerbate heart failure in patients with bradycardia. Amlodipine and felodipine have less negative inotropic effects compared to other CCBs 27. **Can long-acting nitrates be used as monotherapy, why or why not?** (*Textbook Ch 8, Treatment, Pg 25, Obj 7, 8, 9)* Monotherapy with nitrates for the prevention of ischemia should generally be avoided. Reflex increases in sympathetic activity and heart rate, with resultant increases in myocardial oxygen demand, may occur secondary to nitrate-induced venodilation. 28. **What is a major limitation of long-acting nitrate therapy and what can be done to help reduce this?** (*Textbook Ch 8, Treatment, Pg 25, Obj 8, 9)* The major limitation of nitrate therapy is the development of tolerance with continuous use. Loss of antianginal effects may occur within the first 24 hours of continuous nitrate therapy. - The most effective method to avoid tolerance and maintain the antianginal efficacy of nitrates is to allow a daily nitrate-free interval of at least 8 to 12 hours. 29. **What are the preferred and nonpreferred treatments for variant angina?** (*Textbook Ch 8, Treatment, Pg 27, Obj 7, 9)* Preferred: CCBs, immediate release nitrate/ nitroglycerin Nonpreferred: Beta blockers should be avoided in patients with variant angina because of their potential to worsen vasospasm due to unopposed α-adrenergic receptor stimulation