NUR 635 Topic 6 DQ 2

Sample Answer for NUR 635 Topic 6 DQ 2 Included After Question

Keith is 68-year-old male who is diagnosed with stable ischemic heart disease. His medication list includes aspirin 81mg daily, clopidogrel 75mg daily, metoprolol tartrate 75mg bid, and atorvastatin 10mg daily. Use the guidelines and relevant literature in your topic Resources to discuss the following:

  • Briefly explain the pathophysiology associated with stable ischemic heart disease (SIHD).
  • Based on the mechanism of action, how do beta blockers and calcium channel blockers treat SIHD. Which class is considered first-line therapy?
  • Explain the purpose of antiplatelet therapy for the treatment of SIDH.
  • Compare the antiplatelet therapies for SIHD, monotherapy with aspirin or clopidogrel versus dual antiplatelet therapy with clopidogrel and aspirin.
  • In the event Keith requires immediate angina relief, what agent would you prescribe? How does the mode of action treat angina? What dose/frequency will you write on the prescription? What counseling points would educate the patient regarding the prescribed medication?
  • What is the purpose of atorvastatin in Keith’s medication regimen?
  • Describe the classifications of statins: Low intensity versus moderate intensity versus high intensity. Is atorvastatin 10mg daily an appropriate dose for a SIHD patient?
  • After a month of being on atorvastatin, Keith’s LFTs have risen 2 times normal upper limit. What is an alternative lipid lowering agent, and is it as effective as a statin (i.e., compare LDL percentage decrease potential)?
  • Explain the purpose of antiplatelet therapy for the treatment of SIDH.
  • What are some non-pharmacologic treatments Keith may benefit from?

American Association of Colleges of Nursing Core Competencies for Professional Nursing Education 

This assignment aligns to AACN Core Competencies 1.2, 2.2, 2.5. 4.2, 6.4, 9.2

A Sample Answer For the Assignment: NUR 635 Topic 6 DQ 2

Title: NUR 635 Topic 6 DQ 2

Stable Ischemic Heart Disease

Briefly explain the pathophysiology associated with stable ischemic heart disease (SIHD).

Stable Ischemic Heart Disease (SIHD) is a common cardiovascular condition characterized by reduced blood flow to the heart muscle due to the narrowing of coronary arteries. The narrowing, typically caused by atherosclerosis, results from the accumulation of plaque deposits composed of cholesterol, fat, and inflammatory cells within the arterial walls (Severino et al., 2020). As these plaques gradually obstruct blood flow, the heart muscle may not receive an adequate supply of oxygen and nutrients, leading to chest pain or angina.

Based on the mechanism of action, how do beta blockers and calcium channel blockers treat SIHD. Which class is considered first-line therapy?

 Beta blockers, like metoprolol tartrate in Keith’s medication list, primarily act by reducing the heart’s workload and oxygen demand. They achieve this by blocking the effects of stress hormones like adrenaline on the heart, leading to a slower heart rate and decreased contractility (Jamil et al., 2023). This helps to lower blood pressure, reduce the heart’s oxygen requirements, and improve the heart’s oxygen supply-demand balance. On the other hand, CCBs, such as amlodipine or diltiazem, primarily work by relaxing the smooth muscles in the arteries, leading to vasodilation. The dilation reduces the resistance against which the heart pumps blood, subsequently lowering blood pressure and improving blood flow to the heart muscle.

In terms of first-line therapy for SIHD, beta blockers are typically considered the first-line choice. According to guidelines and relevant literature, beta blockers have shown consistent benefit in reducing the risk of angina (chest pain), improving exercise tolerance, and lowering the risk of adverse cardiovascular events in patients with SIHD. They are especially beneficial in patients with a history of heart attacks or who have impaired left ventricular function.

Explain the purpose of antiplatelet therapy for the treatment of SIDH.

Antiplatelet therapy, such as aspirin and clopidogrel in Keith’s medication list, is crucial in the treatment of SIHD to reduce the risk of blood clot formation within the coronary arteries (Mangieri et al., 2020). These clots can partially or completely block blood flow, leading to acute myocardial infarctions (heart attacks) or unstable angina episodes. Aspirin works by inhibiting platelet aggregation, making it less likely for platelets to stick together and form clots. Clopidogrel, another antiplatelet agent, further reduces the risk of clot formation by inhibiting platelet activation. In combination, they provide a dual antiplatelet effect, preventing the formation of potentially life-threatening clots in the coronary arteries.

Compare the antiplatelet therapies for SIHD, monotherapy with aspirin or clopidogrel versus dual antiplatelet therapy with clopidogrel and aspirin.

Monotherapy with aspirin has been a traditional option for SIHD patients, as it inhibits platelet aggregation and reduces the risk of cardiovascular events (Bittl & Laine, 2022). Clopidogrel, on the other hand, is a P2Y12 receptor antagonist that works synergistically with aspirin to provide stronger antiplatelet effects when used in combination. Dual antiplatelet therapy (clopidogrel and aspirin) is typically considered for patients at higher risk of recurrent cardiovascular events, such as those with recent coronary stent placement. The decision should be made after careful consideration of the patient’s clinical profile and the potential risks and benefits of each therapy.

In the event Keith requires immediate angina relief, what agent would you prescribe? How does the mode of action treat angina? What dose/frequency will you write on the prescription? What counseling points would educate the patient regarding the prescribed medication?

In the event that Keith requires immediate angina relief, I would prescribe nitroglycerin. Nitroglycerin works by relaxing and dilating the blood vessels, which leads to increased blood flow to the heart muscle (Udom et al., 2020). This helps relieve angina by reducing the heart’s workload and oxygen demand. The typical prescription for nitroglycerin includes sublingual tablets or spray, with instructions to take one tablet or spray under the tongue at the onset of angina symptoms, and if the pain persists after 5 minutes, a second dose can be taken. Patients should be counseled on the proper administration technique, potential side effects such as headache or dizziness, and the importance of seeking immediate medical attention if angina symptoms are not relieved after three doses, as this may indicate a more serious cardiac event.

What is the purpose of atorvastatin in Keith’s medication regimen?

Atorvastatin helps in lowering cholesterol levels, specifically LDL cholesterol, in the blood. Elevated LDL cholesterol is a significant risk factor for atherosclerosis and the progression of coronary artery disease, which underlies SIHD. By reducing LDL cholesterol levels, atorvastatin helps to stabilize and potentially regress atherosclerotic plaques in the coronary arteries, thus lowering the risk of future cardiovascular events, including angina episodes and heart attacks (Ishii, 2022).

Describe the classifications of statins: Low intensity versus moderate intensity versus high intensity. Is atorvastatin 10mg daily an appropriate dose for a SIHD patient?

Low-intensity statins typically lower LDL cholesterol by less than 30%, moderate-intensity statins lower it by 30-50%, and high-intensity statins lower it by more than 50% (Thongtang et al., 2020). Atorvastatin 10mg daily is considered a low-intensity statin therapy, and it may be an appropriate starting dose for a patient with stable ischemic heart disease (SIHD), as the goal is to balance the benefits of cholesterol reduction with potential side effects.

After a month of being on atorvastatin, Keith’s LFTs have risen 2 times normal upper limit. What is an alternative lipid lowering agent, and is it as effective as a statin (i.e., compare LDL percentage decrease potential)?

When a patient experiences such elevations, it is crucial to consider alternative lipid-lowering agents. One effective alternative is ezetimibe, which is a non-statin medication that works in the intestines to reduce the absorption of cholesterol (Bardolia et al., 2021). Ezetimibe can be effective in lowering LDL cholesterol levels and may be considered for Keith, especially if he experiences statin-related side effects. It is important to note that while ezetimibe is not as potent as high-intensity statins, it can still contribute to significant reductions in LDL cholesterol levels

Explain the purpose of antiplatelet therapy for the treatment of SIDH.

Antiplatelet therapy is commonly used in the treatment of stable ischemic heart disease to reduce the risk of blood clot formation and subsequent cardiovascular events (Gibler, 2018). Keith is currently taking aspirin and clopidogrel, which are both antiplatelet agents. Aspirin is a low-dose antiplatelet agent that helps prevent the aggregation of platelets, reducing the risk of clot formation in the coronary arteries. Clopidogrel is another antiplatelet medication that further inhibits platelet activation. The combination of these two antiplatelet agents is often prescribed to SIHD patients to lower the risk of heart attacks and strokes by preventing blood clots in the coronary arteries.

What are some non-pharmacologic treatments Keith may benefit from?

In addition to medications, there are several non-pharmacologic treatments that Keith may benefit from to manage his stable ischemic heart disease. Lifestyle modifications such as regular exercise, a heart-healthy diet low in saturated fats and cholesterol, weight management, smoking cessation, and stress reduction techniques can all contribute to improved cardiovascular health (Ghodeshwar, Dube & Khobragade, 2023). Cardiac rehabilitation programs can also provide structured exercise and education to help patients like Keith manage their condition. These non-pharmacologic interventions, combined with appropriate medications, can have a significant positive impact on Keith’s overall heart health and quality of life.

References 

Bardolia, C., Amin, N. S., & Turgeon, J. (2021). Emerging non-statin treatment options for lowering low-density lipoprotein cholesterol. Frontiers in Cardiovascular Medicine8, 789931.

Bittl, J. A., & Laine, L. (2022). Gastrointestinal Injury caused by aspirin or clopidogrel monotherapy versus dual antiplatelet therapy. Journal of the American College of Cardiology79(2), 129-131.

Ghodeshwar, G. K., Dube, A., & Khobragade, D. (2023). Impact of Lifestyle Modifications on Cardiovascular Health: A Narrative Review. Cureus15(7).

Gibler, W. B. (2018). Advances in the treatment of stable coronary artery disease and peripheral artery disease. Critical Pathways in Cardiology17(2), 53.

Ishii, H. (2022). Cardiovascular events and atherosclerosis in patients with type 2 diabetes and impaired glucose tolerance: What are the medical treatments to prevent cardiovascular events in such patients?. Journal of diabetes investigation13(7), 1114-1121.

Jamil, Y., Park, D. Y., Chongthammakun, V., Al Damluji, A., & Nanna, M. (2023). D-22| Trajectories of Patients Treated With Beta Blockers and Calcium Channel Blockers for Stable Ischemic Heart Disease and Diabetes Mellitus (from the Bypass Angioplasty Revascularization Investigation 2 Diabetes Trial). Journal of the Society for Cardiovascular Angiography & Interventions2(3).

Mangieri, A., Gallo, F., Sticchi, A., Khokhar, A. A., Laricchia, A., Giannini, F., & Colombo, A. (2020). Dual antiplatelet therapy in coronary artery disease: from the past to the future prospective. Cardiovascular intervention and therapeutics35, 117-129.

Severino, P., D’Amato, A., Pucci, M., Infusino, F., Adamo, F., Birtolo, L. I., … & Fedele, F. (2020). Ischemic heart disease pathophysiology paradigms overview: from plaque activation to microvascular dysfunction. International journal of molecular sciences21(21), 8118.

Thongtang, N., Piyapromdee, J., Tangkittikasem, N., Samaithongcharoen, K., Srikanchanawat, N., & Sriussadaporn, S. (2020). Efficacy and safety of switching from low-dose statin to high-intensity statin for primary prevention in type 2 diabetes: a randomized controlled trial. Diabetes, Metabolic Syndrome and Obesity, 423-431.

Udom, G. J., Effiong, D. E., Onyeukwu, N. J., Obot, D. N., Alozie, M., & Yemitan, O. K. (2020). Recent Trends in the Pharmacotherapy of Angina Pectoris. IOSR J Pharm10(5), 01-13.

A Sample Answer 2 For the Assignment: NUR 635 Topic 6 DQ 2

Title: NUR 635 Topic 6 DQ 2

  • Stable ischemic heart disease (SIHD), as described by Dababneh E., & Goldstein S. (2023), includes a number of disorders that ultimately lead to a recurrent mismatch between myocardial oxygen supply and demand. It is sometimes used interchangeably with chronic coronary artery disease (CAD). This phenomenon is often seen when there is a chronic blockage caused by atherosclerosis in the coronary arteries, leading to inadequate blood flow and subsequent ischemia in the distal regions. Nevertheless, this is not the only process. Chronic recurrent ischemia may arise from a range of pathophysiologic processes, including coronary artery vasospasm, microcirculation dysfunction, and congenital defects. These mechanisms can all contribute to a supply-demand mismatch, leading to the development of ischemic conditions. According to the guidelines established by the American College of Cardiology (ACC) and the American Heart Association (AHA) in 2012, the category of stable ischemic heart disease encompasses adults who have a confirmed diagnosis of ischemic heart disease (IHD) and experience stable pain syndromes, such as chronic angina. Additionally, this category also includes individuals who have recently developed low-risk chest pain, referred to as low-risk, unstable angina (UA). Patients who do not exhibit symptoms and have been identified through non-invasive techniques, or have effectively managed their symptoms by medical intervention or revascularization procedures, are also classified as having stable ischemic heart disease.
  • According to Tarkin, J. M., & Kaski, J. C. (2013), calcium-channel blockers and beta-blockers of the -adrenergic receptor are first-line anti-anginal medications that have been proved in several trials to prevent angina and myocardial ischemia. The anti-anginal effects of beta-blockers are attributed to their ability to decrease heart rate, contractility, and heart rate, leading to a reduction in myocardial oxygen demands. Moreover, the reduction in heart rate leads to an elongation of the diastolic phase of the cardiac cycle, therefore enhancing myocardial perfusion. To achieve optimal effectiveness, it is preferable to use long-acting beta-blockers that are cardioselective and devoid of intrinsic sympathomimetic action. In order to get a desired resting heart rate of 50-60 beats per minute, it is necessary to adjust the dosage accordingly. The potential prognostic advantage of beta-blockers in the context of angina has been inferred from research conducted on patients who have had a myocardial infarction, but its efficacy in treating stable angina has not yet been empirically shown. Calcium channel blockers exert their effects by targeting L-type calcium receptors, resulting in the dilation of both systemic and coronary blood vessels. This mechanism ultimately leads to a decrease in afterload and an enhancement in the flow of blood to the myocardium. Similar to beta-blockers, non-dihydropyridines such as verapamil and diltiazem have supplementary anti-anginal effects by decreasing heart rate and contractility.
  • According to Jourdi et al. (2022), antiplatelet medications are essential elements of antithrombotic therapies, primarily used for the management and prophylaxis of atherothrombotic conditions such as acute coronary syndromes (ACS) and stable coronary artery disease (CAD).  Antiplatelet drugs exert their effects by several mechanisms, including the inhibition of second messenger production, modulation of intracellular signaling pathways, blockade of membrane receptors, and direct inhibition of platelet aggregation. The mechanism by which ASA exerts its antithrombotic effects involves the irreversible inhibition of cyclooxygenase (COX)-1, leading to a reduction in the production of thrombi. This inhibition results in the suppression of platelet thromboxane A2 (TXA2) synthesis. ASA is often recommended for those with stable coronary artery disease (CAD). In the context of acute coronary syndrome (ACS), the administration of acetylsalicylic acid (ASA) is recommended in conjunction with a P2Y12 receptor antagonist for a duration of 6 to 12 months, taking into consideration the delicate balance between the risks of bleeding and ischemia. In patients who are at a high risk of experiencing ischemic events, it is possible to prolong the duration of dual antiplatelet treatment (DAPT) for a period of up to three years. Subsequently, it is advised to provide acetylsalicylic acid (ASA) continuously as a sole antiplatelet treatment (SAPT). ASA is often recommended for people who have stable coronary artery disease (CAD). Clopidogrel may be correlated with a duration of up to 12 months in individuals who are having elective coronary percutaneous intervention (PCI). 
  • As a healthcare provider, I will prescribe and instruct Keith on how to utilize Nitroglycerin 0.4 Sublingual to immediately treat his chest discomfort in the event that Keith had acute angina. When an acute anginal attack initially appears, Keith will be told to place one pill under the tongue or in the buccal pouch. Without swallowing, let the pill dissolve. An extra pill may be used at intervals of 5 minutes until the desired relief is achieved. It is advised to limit the intake of pills to a maximum of three within a duration of 15 minutes. In the event that the pain endures after the consumption of a cumulative total of three pills within a span of fifteen minutes, or if the pain deviates from the customary experience, it is advisable to promptly seek medical assistance. Additionally, according to Drugs.com (2023), nitroglycerin sublingual tablets may be used as a preventative measure, 5 to 10 minutes before participating in activities that have the potential to trigger an acute attack. It is recommended to take the medication when at rest, ideally in a seated posture.
  • Atovastatin 10 mg HS is a component of Keith’s treatment plan. According to Gabara et al. (2022), statins prevent the production of cholesterol by inhibiting the enzyme HMG-CoA reductase. Statins exhibit additional effects known as ‘pleiotropic effects’, including the augmentation of nitric oxide, stabilization of atherosclerotic plaques, reduction in the synthesis of proinflammatory cytokines and reactive oxygen species, inhibition of platelet reactivity, and prevention of the progression of cardiac hypertrophy and fibrosis. Therefore, these medications are indeed disease-modifying. Given that statin medication lowers cardiovascular events by around 23%, it is recommended for all patients with CAD, including the elderly and those with ‘normal’ blood cholesterol.
  • According to AHA/ACC guidelines, based on estimated LDL level reductions, statins can be classified into high-intensity, moderate-intensity, and low-intensity statins (Sizar O, Khare S, Jamil RT. 2023)
  •  
  • High-intensity statin(LDL-C lowering > 50%): rosuvastatin 20 mg, rosuvastatin 40 mg, atorvastatin 40 mg, atorvastatin 80 mg
  • Moderate-intensity statin(LDL-C lowering 30% to 49%): atorvastatin 10 mg, atorvastatin 20 mg, pravastatin 40 mg, pravastatin 80 mg, lovastatin 40 mg, lovastatin 80 mg, fluvastatin XL 80 mg,  fluvastatin 40 mg BID, pitavastatin 1–4 mg
  • Low-intensity statin(LDL-C lowering < 30%): simvastatin 10 mg,  pravastatin 20 mg, pravastatin 10 mg, lovastatin 20 mg, fluvastatin 20 mg, fluvastatin 40 mg. 
  • Although statins have a proven safety and effectiveness profile, they have apparently been linked to a number of side effects that force patients to stop taking them suddenly without first contacting a healthcare professional, a condition known as statin intolerance. Raju et al. (2013) identified many significant side effects associated with statin use, including muscle-related issues such as myalgia, myopathy, and rhabdomyolysis, as well as hepatotoxicity, nephrotoxicity characterized by proteinuria, headache, rash, and gastrointestinal discomfort. For Keith, who has experienced an elevation of liver function tests (LFT) after one month of statin therapy, as a healthcare professional, the management of statin intolerance may involve various strategies. These include switching to an alternative therapy, adopting alternate day dosing, and considering non-statin lipid-lowering drugs. Non-statin lipid-lowering drugs encompass a range of options, such as bile acid sequestrants (e.g., colesevelam), intestinal cholesterol absorption inhibitors (e.g., ezetimibe), fibrates, and niacin. These medications can be used alone or in combination. Additionally, lipid lowering nutraceuticals, which consist of dietary interventions, have been utilized in patients who are unable to tolerate statins. These interventions involve consuming foods low in saturated fat and high in viscous fibers (e.g., oats and barley), incorporating plant sterols, consuming vegetable protein foods (e.g., soy), and incorporating nuts (e.g., almonds) into the diet.
  • Stable ischemic heart disease therapy aims to restrict the course of atherosclerotic disease, avoid or lessen consequences like mortality, and almost entirely eradicate ischemia symptoms to improve quality of life and restore functional ability. The non-pharmacological interventions for Keith include risk control, which starts with personalized lifestyle modifications such as changes in eating habits, weight management, cessation of smoking, and regular physical activity. It is also fair for Keith and other patients to proactively avoid stressors and cultivate effective coping methods to manage symptoms of sadness and anxiety, if appropriate. Education pertaining to medication adherence and meticulous self-monitoring is also necessary. It is of great significance to prioritize the optimization of hypertension, diabetes, and dyslipidemia treatment, as these conditions have a direct impact on the outcomes of stable ischemic heart disease and contribute to an increased risk of future occurrences (Dababneh E., & Goldstein S. (2023).

References

 
 Choi, K. H., Song, Y. B., Jeong, D. S., Jang, Y. H., Hong, D., Lee, S. Y., Youn, T., Bak, M., Min, K. M., Lee, J. M., Park, T. K., Yang, J. H., Hahn, J.-Y., Choi, J.-H., Choi, S.-H., Chung, S. R., Cho, Y. H., Sung, K., Kim, W. S., …Lee, Y. T. (2021). Differential effects of dual antiplatelet therapy in patients presented with acute coronary syndrome vs. stable ischaemic heart disease after coronary artery bypass grafting. European Heart Journal: Cardiovascular Pharmacotherapy, 7(6), 517+. https://link-gale com.lopes.idm.oclc.org/apps/doc/A690097961/AONE?u=canyonuniv&sid=ebsco&xid=d07bb8ff

Dababneh E, & Goldstein S. (2023). Chronic Ischemic Heart Disease Selection of Treatment Modality.  In: StatPearls [Internet]. Treasure Island (FL) https://www.ncbi.nlm.nih.gov/books/NBK507703/

        
Drugs.com. (2023). Nitroglycerin sublingual tablet prescribing information. 

Gabara, L., Olsen, S., Alaour, B., & Curzen, N. (2022). Ischemic heart disease: stable angina. Medicinehttps://doi-org.lopes.idm.oclc.org/10.1016/j.mpmed.2022.04.004

Jourdi G, Godier A, Lordkipanidzé M, Marquis-Gravel G and Gaussem P. (2022). Antiplatelet Therapy for Atherothrombotic Disease in 2022—From Population to Patient-Centered Approaches. Front. Cardiovasc. Med. 9:805525. doi: 10.3389/fcvm.2022.805525

Raju, S. B., Varghese, K., & Madhu, K. (2013). Management of statin intolerance. Indian journal of endocrinology and metabolism, 17(6), 977–982. https://doi.org/10.4103/2230-8210.122602

Sizar O, Khare S, Jamil RT. (2023).  Statin Medications.  In: StatPearls [Internet]. Treasure Island (FL). https://www.ncbi.nlm.nih.gov/books/NBK430940/#

Tarkin, J. M., & Kaski, J. C. (2013). Pharmacological treatment of chronic stable angina pectoris. Clinical medicine (London, England), 13(1), 63–70. https://doi.org/10.7861/clinmedicine.13-1-63