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Ciclosporin is a calcineurin inhibitor widely used in immunosuppressive therapy since 1984 to prevent rejection in solid organ transplants. It works by suppressing T lymphocyte activation, which plays a crucial role in allograft rejection and the immune response to infections. Ciclosporin is typically used alongside antiproliferative agents (such as azathioprine or mycophenolate mofetil) and corticosteroids like prednisolone.
Due to variations in bioavailability between generic formulations, ciclosporin must be prescribed by brand name to ensure consistent therapeutic levels. Neoral® is the preferred brand for liver transplant patients. The drug requires careful dose titration and regular monitoring of blood levels to avoid toxicity and ensure efficacy. Clinicians must be mindful of drug interactions and recommend vaccinations like pneumococcal and annual influenza, while avoiding live vaccines due to the patient's immunocompromised state.
Ciclosporin's immunosuppressive effects increase the risk of infections (e.g., listeriosis) and malignancies in transplant recipients. Its suppression of T-cell responses weakens immune defense, making patients more susceptible to infections and impairing immune surveillance against cancer. Long-term use is associated with a higher risk of post-transplant malignancies, requiring careful management and alternative immunosuppressive strategies for high-risk patients or those with a history of cancer.
Aspect | Details |
---|---|
Indication | Immunosuppressive therapy- prevention of organ rejection |
Formulations and Strengths Available | Neoral® microemulsion soft gel capsules (10, 25, 50, 100mg) and liquid (100mg/ml) |
Dosage | 1-2mg/kg daily in two divided doses, adjusted by trough blood levels |
Usual Dose Range | 50mg bd to 300mg bd, based on blood levels and time from transplant |
Duration of Treatment | Lifelong unless switched by transplant unit |
Contraindications | Known hypersensitivity to ciclosporin |
Warnings | Breastfeeding is contraindicated. Avoid live vaccines (yellow fever, BCG, MMR). May be used in planned pregnancy under specialist advice. |
Common Side Effects | Nephrotoxicity, hypertension, hyperlipidaemia, hirsutism, gingival hypertrophy, tremor, increased infection risk, malignancy |
Drug Interactions | Inhibited by: macrolide antibiotics, azole antifungals, calcium antagonists, grapefruit juice. Induced by: anticonvulsants, rifampicin, St John’s Wort. Enhanced nephrotoxicity with NSAIDs and sirolimus. |
Monitoring | Regular blood tests, reviewed by transplant unit. Dose adjustment by transplant unit only. |
Ciclosporin is effective but carries a risk of **nephrotoxicity** due to its vasoconstrictive effects, which can worsen renal ischemia and cause kidney damage. Monitoring drug levels to stay within the therapeutic range (200–300 ng/mL initially, then 100–200 ng/mL) is crucial to minimize toxicity. Additionally, variations in bioavailability between generic formulations highlight the importance of prescribing specific brands for consistent outcomes.
In summary, ciclosporin plays a pivotal role in the management of transplant patients by preventing allograft rejection and improving graft survival. However, its use is accompanied by significant risks, including nephrotoxicity and increased susceptibility to infections and malignancies. Ongoing research and clinical vigilance are essential to optimize its use and mitigate associated risks in the transplant population.
1. Algan, M., Jonon, B., George, J., Lion, C., Kessler, M., & Burdin, J. (1990). *Listeria monocytogenes* endophthalmitis in a renal-transplant patient receiving ciclosporin. **Ophthalmologica**, 201(1), 23-27. https://doi.org/10.1159/000310120
2. Esposito, C., Semeraro, L., Bellotti, N., Fasoli, G., Fornoni, A., Rampino, T., … & Canton, A. (2000). Risk factors for chronic renal dysfunction in cardiac allograft recipients. **Nephron**, 84(1), 21-28. https://doi.org/10.1159/000045534
3. Günay, A., Ünal, A., Demirpolat, E., & Yerer, M. (2023). Risk factors for early onset acute kidney injury after allogeneic haematopoietic stem cell transplantation and the role of drug–drug interactions. **European Journal of Hospital Pharmacy**, ejhpharm-2023-003703. https://doi.org/10.1136/ejhpharm-2023-003703
4. Nankivell, B., Borrows, R., Fung, C., O’Connell, P., Chapman, J., & Allen, R. (2004). Calcineurin inhibitor nephrotoxicity: longitudinal assessment by protocol histology. **Transplantation**, 78(4), 557-565. https://doi.org/10.1097/01.tp.0000128636.70499.6e
5. Pascual, J., Fernandez, A., Marcén, R., & Ortuño, J. (2006). Conversion to everolimus in a patient with arterial hypertension and recurrent cutaneous neoplasia—a case report. **Nephrology Dialysis Transplantation**, 21(suppl_3), iii38-iii41. https://doi.org/10.1093/ndt/gfl299
6. Wong, W., Venetz, J., Tolkoff-Rubin, N., & Pascual, M. (2005). 2005 immunosuppressive strategies in kidney transplantation: which role for the calcineurin inhibitors? **Transplantation**, 80(3), 289-296. https://doi.org/10.1097/01.tp.0000168436.76784.45
7. Wormser, C., Mariano, A., Holmes, E., Aronson, L., & Volk, S. (2014). Post‐transplant malignant neoplasia associated with cyclosporine‐based immunotherapy: prevalence, risk factors and survival in feline renal transplant recipients. **Veterinary and Comparative Oncology**, 14(4). https://doi.org/10.1111/vco.12120
Kidney transplant recipients are particularly vulnerable to a range of health complications due to their immunosuppressed state, which is necessary to prevent graft rejection but also increases their susceptibility to infections and other medical conditions. As primary care clinicians, pharmacists, and nurses often encounter these patients, it is critical to understand the complexities of their management and the specific risks associated with their post-transplant care.
This guide covers some of the most common and dangerous clinical scenarios in kidney transplant patients, including acute abdominal pain, respiratory infections, cardiovascular issues, and medication interactions. The unique physiology of kidney transplant patients means that these conditions can present atypically and may have significantly higher morbidity and mortality rates than in the general population. Management strategies need to be tailored, often requiring the coordination of care between primary care, nephrology, and other specialists.
Understanding the management of these issues is essential to ensure timely interventions, prevent graft loss, and improve patient outcomes.
The skin can often be a window to underlying haematological diseases, manifesting with various dermatological signs. These manifestations can range from subtle rashes to more severe, systemic skin lesions that may indicate malignancies or immune system dysregulation. Recognizing these signs in primary care is essential, as they can guide the diagnosis of serious underlying conditions such as leukemia, lymphoma, or other hematologic abnormalities. The following table provides a concise overview of common skin presentations linked to haematological diseases, aiding clinicians in their evaluation and decision-making process.
Condition | Presentation | Significance |
---|---|---|
Mycosis Fungoides (Cutaneous T-Cell Lymphoma) | Erythematous, scaly patches and plaques, typically on non-sun-exposed areas like the buttocks or thighs. Tumor formation and widespread skin involvement may occur in later stages. | Most common form of cutaneous T-cell lymphoma. Early diagnosis is crucial as it may progress over time. |
Leukemia Cutis | Red to violaceous papules, nodules, or plaques that may ulcerate, occurring anywhere on the body and may mimic infections or inflammatory dermatoses. | Often indicates disease progression, occurring when leukemic cells infiltrate the skin. |
Sweet's Syndrome (Acute Febrile Neutrophilic Dermatosis) | Sudden onset of painful, erythematous plaques or nodules, often on the face, neck, and upper extremities. Accompanied by fever and systemic symptoms. | Associated with haematological malignancies like acute myeloid leukemia (AML); can be an early sign of leukemia relapse. |
Paraneoplastic Pemphigus | Painful erosions on mucosal surfaces, particularly in the mouth, with flaccid blisters on the skin. | Often associated with lymphomas or chronic lymphocytic leukemia (CLL); early recognition is vital due to its severe autoimmune nature. |
Cutaneous Small Vessel Vasculitis | Palpable purpura, often on the lower extremities. Lesions may ulcerate or become necrotic. | Commonly associated with lymphoma or multiple myeloma, can also be drug-induced in patients with malignancies. |
Amyloidosis | Waxy, translucent papules or plaques, often on the face, eyelids, and neck. Purpura and bruising common in areas of minimal trauma. | Associated with multiple myeloma and other plasma cell dyscrasias. |
Plasma Cell Leukemia and Paraproteinaemia-associated Skin Lesions | Purpuric macules, plaques, ulcers, or infiltrative lesions. | May occur due to plasma cell infiltration or secondary to paraproteinemia. |
Kaposi Sarcoma (in HIV or Post-transplant Patients) | Red, purple, or brown patches and nodules, often seen in immunocompromised patients, especially on the skin. | Associated with human herpesvirus 8 (HHV-8), often found in HIV-positive or immunosuppressed individuals. |
Disseminated Intravascular Coagulation (DIC) | Petechiae, purpura, and widespread bruising due to bleeding disorders. | Life-threatening condition, common in patients with advanced malignancies or severe infections, requiring urgent intervention. |
1. Cerroni, L. (2018). "Mycosis fungoides—clinical and histopathologic features, differential diagnosis, and treatment." *Seminars in Cutaneous Medicine and Surgery*.
2. Kuo, T. T., et al. (2019). "Leukemia cutis: a review." *Journal of the American Academy of Dermatology*.
3. Cohen, P. R. (2018). "Sweet's syndrome: a review of the literature." *The American Journal of Clinical Dermatology*.
4. Anhalt, G. J., et al. (1990). "Paraneoplastic pemphigus: an autoimmune mucocutaneous blistering disease associated with neoplasia." *The New England Journal of Medicine*.
5. Sontheimer, R. D. (2005). "Cutaneous small vessel vasculitis." *Dermatologic Clinics*.
6. Merlini, G., et al. (2013). "Systemic amyloidosis: a review." *The New England Journal of Medicine*.
7. Palumbo, A., et al. (2014). "Plasma cell leukemia: a review." *Blood*.
8. Whitby, D., et al. (2000). "Kaposi's sarcoma-associated herpesvirus (KSHV) and the pathogenesis of Kaposi's sarcoma." *Nature Reviews Cancer*.
9. Levi, M., et al. (2004). "Disseminated intravascular coagulation." *The Lancet*.
Acute migraine management involves the prompt treatment of migraine attacks with the goal of reducing pain, restoring normal function, and minimizing recurrence. Treatments are generally categorized into migraine-specific and non-specific therapies.
Migraine-specific medications include triptans (such as sumatriptan and rizatriptan), ergot derivatives, and more recently, calcitonin gene-related peptide (CGRP) antagonists. These therapies have been shown to be effective in relieving migraine symptoms by targeting the mechanisms that drive migraine pathophysiology (Buse et al., 2015; Marzoughi & Spacey, 2023; Marmura et al., 2015).
However, it is important to note that ergot derivatives and opioids are not recommended by NICE Clinical Knowledge Summaries (CKS) for routine use in the management of acute migraine. This is due to concerns about their efficacy, side effects, and the risk of medication overuse headaches. NICE recommends focusing on more effective and safer alternatives, such as triptans, NSAIDs, and CGRP antagonists, to manage acute migraine episodes.
Calcitonin gene-related peptide (CGRP) antagonists are a newer class of medications specifically designed for the treatment and prevention of migraines. CGRP is a neuropeptide that plays a crucial role in migraine pathophysiology by promoting inflammation and dilating blood vessels in the brain, which contributes to the pain and other symptoms associated with migraines.
CGRP antagonists work by blocking the activity of CGRP, either by inhibiting its receptor or by directly binding to CGRP itself. By doing so, these medications help prevent or relieve the vasodilation and inflammation that trigger migraines.
Key Points about CGRP Antagonists:
CGRP antagonists represent a significant advancement in migraine management, offering both acute relief and preventive options with a novel mechanism that directly targets migraine pathology
Non-specific treatments for acute migraine attacks include non-steroidal anti-inflammatory drugs (NSAIDs), acetaminophen, and dopamine antagonists such as metoclopramide and prochlorperazine. These medications help in reducing inflammation and managing associated symptoms like nausea and vomiting (Buse et al., 2015; Burch, 2024; Gelfand & Goadsby, 2012).
The choice of treatment is guided by the severity of the attack, the patient’s medical history, and potential drug side effects. It is essential to tailor the treatment based on individual needs to ensure optimal outcomes.
Timely intervention plays a critical role in improving outcomes for patients with acute migraines. Studies suggest that administering acute treatments early in the course of the attack results in better pain control and a quicker return to normal function (Taylor, 2010; Burch, 2024). Fast-acting formulations, such as subcutaneous or intranasal delivery methods, can provide more rapid relief compared to oral routes, particularly in cases of severe attacks or when gastrointestinal symptoms are prominent (Burch, 2024; Marmura et al., 2015).
Step | Action | Rationale |
---|---|---|
1. Assess Severity and Frequency | Evaluate severity of headache, associated symptoms, and comorbidities. | Tailors treatment based on the patient's specific migraine presentation and history. |
2. First-Line Monotherapy | Offer aspirin (900 mg), ibuprofen (400–600 mg), or a 5HT1-receptor agonist (triptan) such as sumatriptan (50–100 mg). | Early administration increases effectiveness and prevents escalation of symptoms. |
3. Treat at Onset of Headache | Advise patients to take medication at the start of the headache (not the aura phase). | Timely treatment can abort the migraine or reduce its severity. |
4. Alternative Tripans | If sumatriptan is ineffective, try alternative triptans (almotriptan, eletriptan, etc.). | Response to different triptans can vary between individuals. |
5. Combination Therapy | If monotherapy fails, use combination therapy: triptan + NSAID (e.g., naproxen) or triptan + paracetamol. | Enhances therapeutic effect by targeting different pain pathways. |
6. Non-Oral Options | For patients with early vomiting, offer subcutaneous sumatriptan or nasal zolmitriptan. | Avoids limitations of oral administration in patients with nausea or vomiting. |
7. Use of Antiemetics | Offer metoclopramide or prochlorperazine for nausea, even in the absence of vomiting. | Reduces nausea and enhances the effectiveness of analgesic or triptan therapy. |
8. Follow-Up and Review | Arrange follow-up within 2–8 weeks to assess treatment effectiveness, frequency of attacks, and side effects. | Ensures that treatment remains effective, prevents medication overuse, and allows consideration of preventive therapies. |
9. Consider Preventative Treatment | For patients with frequent attacks or treatment failure, consider preventive therapy. | Prevents frequent migraine episodes and reduces dependency on acute treatment. |
10. Avoid Medication Overuse | Limit acute treatment to 2 days per week and advise against opioids and ergots. | Prevents medication-overuse headache, which can worsen migraine frequency and severity. |
Effective migraine management requires not only addressing the acute symptoms but also considering comorbid conditions such as anxiety, depression, and medication overuse headaches, which can complicate the treatment process (Pozo-Rosich, 2024; Yang et al., 2022). A comprehensive approach tailored to each patient’s needs, taking into account both migraine and associated conditions, is essential for optimal care.
Regular monitoring and follow-up are crucial in evaluating the effectiveness of treatment plans. Clinicians should assess symptom recurrence, the need for rescue medications, and patient adherence to prescribed therapies. Additionally, patient education regarding potential side effects and the importance of consistent treatment use can enhance long-term outcomes (Cady et al., 2022; Yang et al., 2022). By combining individualized treatment plans with thorough follow-up, clinicians can improve overall management and quality of life for patients with migraines.
Burch, R. (2024). Acute treatment of migraine. *Continuum Lifelong Learning in Neurology*, 30(2), 344-363. https://doi.org/10.1212/con.0000000000001402
Buse, D., Serrano, D., Reed, M., Kori, S., Cunanan, C., Adams, A., … & Lipton, R. (2015). Adding additional acute medications to a triptan regimen for migraine and observed changes in headache‐related disability: results from the American Migraine Prevalence and Prevention (AMPP) study. *Headache: The Journal of Head and Face Pain*, 55(6), 825-839. https://doi.org/10.1111/head.12556
Cady, R., Lipton, R., Buse, D., Lindstén, A., & Ettrup, A. (2022). Optimization of acute medication use following eptinezumab initiation during a migraine attack: post hoc analysis of the RELIEF study. *The Journal of Headache and Pain*, 23(1). https://doi.org/10.1186/s10194-022-01463-3
Gelfand, A., & Goadsby, P. (2012). A neurologist’s guide to acute migraine therapy in the emergency room. *The Neurohospitalist*, 2(2), 51-59. https://doi.org/10.1177/1941874412439583
Grazzi, L., Toppo, C., D’Amico, D., Leonardi, M., Martelletti, P., Raggi, A., … & Guastafierro, E. (2021). Non-pharmacological approaches to headaches: non-invasive neuromodulation, nutraceuticals, and behavioral approaches. *International Journal of Environmental Research and Public Health*, 18(4), 1503. https://doi.org/10.3390/ijerph18041503
Marmura, M., Silberstein, S., & Schwedt, T. (2015). The acute treatment of migraine in adults: the American Headache Society evidence assessment of migraine pharmacotherapies. *Headache: The Journal of Head and Face Pain*, 55(1), 3-20. https://doi.org/10.1111/head.12499
Marzoughi, S., & Spacey, S. (2023). Acute and prophylactic treatment of migraine. *Canadian Primary Care Today*. https://doi.org/10.58931/cpct.2023.1216
Mavridis, T., Breza, M., Deligianni, C., & Mitsikostas, D. (2020). Therapeutic management: when and what. *IntechOpen*. https://doi.org/10.5772/intechopen.93096
Nijjar, S., Pink, L., & Gordon, A. (2011). Examination of migraine management in emergency departments. *Pain Research and Management*, 16(3), 183-186. https://doi.org/10.1155/2011/182867
Orr, S., Kabbouche, M., O’Brien, H., Kacperski, J., Powers, S., & Hershey, A. (2018). Paediatric migraine: evidence-based management and future directions. *Nature Reviews Neurology*, 14(9), 515-527. https://doi.org/10.1038/s41582-018-0042-7
Pozo-Rosich, P. (2024). Migraine treatment: quo vadis? Real-world data study (2015–2022) in Spain. *BMC Neurology*, 24(1). https://doi.org/10.1186/s12883-024-03600-8
Taylor, F. (2010). Acute treatment of migraine headaches. *Seminars in Neurology*, 30(02), 145-153. https://doi.org/10.1055/s-0030-1249223
Valade, D., Lucas, C., Calvel, L., Plaisance, P., Derouet, N., Meric, G., … & Giroud, M. (2010). Migraine diagnosis and management in general emergency departments in France. *Cephalalgia*, 31(4), 471-480. https://doi.org/10.1177/0333102410378178
Yang, S., Orlova, Y., Lipe, A., Macy, B., Hincapie-Castillo, J., Park, H., … & Lo‐Ciganic, W. (2022). Trends in the management of headache disorders in US emergency departments: analysis of 2007–2018 national hospital ambulatory medical care survey data. *Journal of Clinical Medicine*, 11(5), 1401. https://doi.org/10.3390/jcm11051401
Yarnitsky, D., Dodick, D., Grosberg, B., Burstein, R., Ironi, A., Harris, D., … & Silberstein, S. (2019). Remote electrical neuromodulation (REN) relieves acute migraine: a randomized, double‐blind, placebo‐controlled, multicenter trial. *Headache: The Journal of Head and Face Pain*, 59(8), 1240-1252. https://doi.org/10.1111/head.13551
https://bnf.nice.org.uk/treatment-summaries/migraine/
The management of stable angina, a condition characterized by chest pain due to myocardial ischemia, is a critical aspect of cardiovascular care. The National Institute for Health and Care Excellence (NICE) guidelines provide a comprehensive framework for the pharmacological management of stable angina, emphasizing the importance of symptom relief, prevention of disease progression, and improvement of quality of life for patients. According to these guidelines, the initial pharmacotherapy typically includes beta-blockers, which are recognized as first-line agents due to their efficacy in reducing anginal symptoms and improving exercise tolerance (Rousan & Thadani, 2019; , Khera et al., 2014). Additionally, the use of long-acting nitrates and calcium channel blockers is recommended when beta-blockers are contraindicated or insufficient (Khera et al., 2014).
The guidelines also underscore the significance of risk factor modification, including the use of antiplatelet agents like aspirin and lipid-lowering medications such as statins, which play a vital role in reducing cardiovascular events and improving patient outcomes (Rousan & Thadani, 2019; , Rousan et al., 2017). Recent advancements in pharmacotherapy have introduced agents like ranolazine and ivabradine, which offer alternative mechanisms of action for patients who do not achieve adequate symptom control with traditional therapies (Luca et al., 2018; , Giavarini & Silva, 2016). These newer agents can be particularly beneficial in managing heart rate and anginal frequency, thereby enhancing the overall treatment strategy for stable angina (Giavarini & Silva, 2016).
Moreover, the NICE guidelines advocate for a patient-centered approach, where treatment regimens are tailored to individual needs based on the severity of symptoms, comorbid conditions, and patient preferences (Tarkin & Kaski, 2013). This personalized approach is crucial, as many patients with stable angina continue to experience symptoms despite optimal medical therapy, necessitating a careful evaluation of treatment effectiveness and adherence (Farmakis et al., 2019). The integration of lifestyle modifications, such as smoking cessation and increased physical activity, alongside pharmacological interventions, is essential for achieving optimal management of stable angina (Nabati et al., 2016).
Step | Medication | Mechanism of Action/Explanation |
---|---|---|
Step 1 | Short-acting nitrate (e.g., glyceryl trinitrate) | Nitrates cause vasodilation, especially of the coronary arteries, increasing blood flow to the heart muscle and relieving angina pain. These are used immediately before exertion or during angina episodes to prevent or treat symptoms. |
Step 2 | Aspirin 75 mg daily (Secondary prevention) | Aspirin is an antiplatelet agent, preventing clot formation by inhibiting platelet aggregation, reducing the risk of heart attacks or strokes in people with cardiovascular disease. |
Step 3 | ACE inhibitors (e.g., ramipril) for patients with diabetes or hypertension | ACE inhibitors reduce blood pressure by inhibiting the angiotensin-converting enzyme, which helps relax blood vessels, reducing the workload on the heart and lowering the risk of cardiovascular events. |
Step 4 | Statins (e.g., atorvastatin) (Secondary prevention) | Statins lower cholesterol levels by inhibiting HMG-CoA reductase, helping reduce atherosclerosis progression, improving blood flow to the heart, and reducing the risk of heart attack and stroke. |
Step 5 | First-line anti-anginal treatment: Beta-blockers (e.g., atenolol) or calcium channel blockers (e.g., amlodipine) | - Beta-blockers reduce heart rate and the force of contraction, reducing oxygen demand and preventing angina symptoms. - Calcium channel blockers relax the coronary arteries and reduce the heart's workload, easing angina. |
Step 6 | Second-line anti-anginal treatment: Long-acting nitrates (e.g., isosorbide mononitrate), Ivabradine, Nicorandil, or Ranolazine | - Long-acting nitrates maintain vasodilation, preventing angina. - Ivabradine reduces heart rate by inhibiting the If current in the sinoatrial node, lowering oxygen demand. - Nicorandil acts as a vasodilator, improving blood flow and reducing angina symptoms. - Ranolazine helps the heart work more efficiently by inhibiting late sodium current, reducing oxygen demand. |
Step 7 | Combination Therapy (Beta-blocker + Calcium channel blocker) | If symptoms are not controlled with a single agent, a combination of a beta-blocker and a dihydropyridine calcium channel blocker (e.g., amlodipine or nifedipine) may be used to provide enhanced relief of angina symptoms by affecting both heart rate and vasodilation. |
Step 8 | Additional drug if both beta-blockers and calcium channel blockers are contraindicated | Monotherapy with a long-acting nitrate, ivabradine, nicorandil, or ranolazine can be considered if beta-blockers or calcium channel blockers are contraindicated or not tolerated. |
Step 9 | Consider adding a third anti-anginal drug | This is only considered if symptoms are not controlled with two anti-anginal drugs and revascularization is not appropriate. The choice of drug depends on comorbidities, patient preference, and drug cost. |
In conclusion, the NICE guidelines for the management of stable angina provide a robust framework that encompasses both pharmacological and non-pharmacological strategies aimed at alleviating symptoms, preventing disease progression, and enhancing the quality of life for patients. The ongoing evolution of treatment options and the emphasis on individualized care highlight the dynamic nature of stable angina management in contemporary clinical practice.
1. Farmakis, D., Andrikopoulos, G., Giamouzis, G., Giannakoulas, G., Poulimenos, L., Skalidis, E., & Parissis, J. (2019). Practical recommendations for the diagnosis and medical management of stable angina: an expert panel consensus. *Journal of Cardiovascular Pharmacology*, 74(4), 308-314. https://doi.org/10.1097/fjc.0000000000000716
2. Giavarini, A., & Silva, R. (2016). The role of ivabradine in the management of angina pectoris. *Cardiovascular Drugs and Therapy*, 30(4), 407-417. https://doi.org/10.1007/s10557-016-6678-x
3. Khera, S., Kolte, D., & Aronow, W. (2014). Use of ranolazine in patients with stable angina pectoris. *Cardiology*, 128(3), 251-258. https://doi.org/10.1159/000358871
4. Luca, L., Temporelli, P., Lucci, D., Colivicchi, F., Calabrò, P., Riccio, C., & Gulizia, M. (2018). Characteristics, treatment and quality of life of stable coronary artery disease patients with or without angina: insights from the START study. *Plos One*, 13(7), e0199770. https://doi.org/10.1371/journal.pone.0199770
5. Nabati, M., Vazirian, E., Ghaemian, A., Yazdani, J., & Hosseinzadeh, M. (2016). Comparison between revascularization and optimal medical therapy in patients with stable angina pectoris. *Iranian Journal of Health Sciences*, 4(2), 71-80. https://doi.org/10.18869/acadpub.jhs.4.2.71
6. Rousan, T., & Thadani, U. (2019). Stable angina medical therapy management guidelines: a critical review of guidelines from the European Society of Cardiology and National Institute for Health and Care Excellence. *European Cardiology Review*, 14(1), 18-22. https://doi.org/10.15420/ecr.2018.26.1
7. Rousan, T., Mathew, S., & Thadani, U. (2017). Drug therapy for stable angina pectoris. *Drugs*, 77(3), 265-284. https://doi.org/10.1007/s40265-017-0691-7
8. Tarkin, J., & Kaski, J. (2013). Pharmacological treatment of chronic stable angina pectoris. *Clinical Medicine*, 13(1), 63-70. https://doi.org/10.7861/clinmedicine.13-1-63
Stable angina is characterized by chest pain or discomfort, typically triggered by physical exertion or emotional stress, which may radiate to the neck, jaw, shoulders, or arms. It is the result of myocardial ischemia, usually caused by atherosclerotic coronary artery disease, restricting blood flow to the heart. While chest pain is the hallmark symptom, some individuals may experience atypical presentations such as breathlessness, gastrointestinal discomfort, or nausea.
Angina affects a significant portion of the population, with an estimated 2 million people in England currently diagnosed or having a history of the condition. The prevalence increases with age, with men more commonly affected than women. Managing stable angina aims to minimize symptoms, improve quality of life, and reduce the risk of acute coronary events or death through lifestyle modifications, pharmacological treatments, and revascularization techniques.
The diagnosis and testing recommendations for stable angina, as outlined by NICE, are based on a comprehensive evaluation of available treatments, balancing the benefits of medical management with revascularization approaches such as coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI). Advances in both drug therapies and revascularization techniques, including the use of drug-eluting stents, have refined the approach to managing stable angina, improving outcomes for patients. NICE guidelines also highlight the importance of individualizing treatment plans, considering both traditional and off-label use of medications when supported by evidence.
This introduction provides a framework for understanding the role of diagnostic testing in the management of stable angina, as outlined by NICE, to ensure optimal patient care.
Principle | Summary |
---|---|
Revascularisation for Uncontrolled Symptoms | Consider revascularisation (CABG or PCI) for people whose symptoms are not controlled with optimal medical treatment. |
Coronary Angiography | Offer coronary angiography to guide treatment strategy for people with uncontrolled symptoms. Non-invasive or invasive functional testing may be needed. |
CABG Indication | Offer CABG to people with suitable coronary anatomy if PCI is not appropriate, and symptoms are not controlled with medical treatment. |
PCI Indication | Offer PCI to people with suitable coronary anatomy if CABG is not appropriate, and symptoms are not controlled with medical treatment. |
Choosing Between CABG and PCI | When both CABG and PCI are options, explain the risks/benefits of each. If no preference is expressed, PCI may be more cost-effective for less complex disease. |
CABG Survival Advantage | Take into account the survival advantage of CABG over PCI for people with multivessel disease, especially if they have diabetes, are over 65, or have anatomically complex three-vessel disease. |
Multidisciplinary Team (MDT) Involvement | Ensure regular MDT meetings (including cardiac surgeons and interventional cardiologists) to discuss the best treatment strategy for people with complex coronary disease or those requiring revascularisation. |
Informed Patient Decision-Making | Provide balanced information on the benefits, limitations, and risks of drug treatment, CABG, and PCI. Emphasize that the primary aim of revascularisation is to relieve angina symptoms, with CABG offering a potential survival benefit in some cases. |
Practical Aspects of Revascularisation | Inform patients about the practical aspects of CABG and PCI, including vein/artery harvesting, hospital stay, recovery time, and post-procedural medications. |
Controlled Symptoms with Optimal Medical Treatment | For those with controlled symptoms, discuss prognosis, potential coronary disease risks, and the benefits/risks of CABG. Consider further testing or coronary angiography in specific high-risk cases. |
CABG for Prognosis | Consider CABG for patients with controlled symptoms but evidence of left main stem or proximal three-vessel disease based on coronary angiography results. |
Here is a list of key terminology related to revascularization that clinicians in primary care need to be familiar with, as used in the NICE guidance for stable angina:
1. **Revascularization**: A procedure to restore blood flow to the heart muscle by bypassing or opening blocked coronary arteries.
2. **Coronary Artery Bypass Graft (CABG)**: A surgical procedure where a blood vessel (vein or artery) from another part of the body is used to bypass a blocked coronary artery, restoring blood flow to the heart.
3. **Percutaneous Coronary Intervention (PCI)**: A minimally invasive procedure that involves the insertion of a catheter and balloon to open up blocked coronary arteries, often followed by placing a stent to keep the artery open.
4. **Coronary Angiography**: An imaging test that uses X-rays to visualize the coronary arteries and assess blockages. It is typically used to guide treatment decisions, including revascularization.
5. **Functional Testing**: Non-invasive tests (e.g., stress tests) used to assess how well blood flows to the heart muscle during exertion, helping to evaluate the severity of ischemia and guide treatment.
6. **Non-Invasive Anatomical Testing**: Imaging techniques such as CT coronary angiography that provide detailed pictures of the coronary arteries without the need for invasive procedures, to assess the presence of blockages.
7. **Drug-Eluting Stents**: A type of stent used during PCI that slowly releases medication to prevent restenosis (re-narrowing) of the artery.
8. **Bare Metal Stents**: An older type of stent used in PCI that does not release any medication, with a higher risk of restenosis compared to drug-eluting stents.
9. **Multivessel Disease**: A condition where multiple coronary arteries are narrowed or blocked, often requiring more complex revascularization strategies such as CABG.
10. **Left Main Stem Disease**: A condition where the left main coronary artery, which supplies a large portion of the heart, is narrowed or blocked. This is a high-risk condition often requiring CABG.
11. **Three-Vessel Disease**: A form of coronary artery disease affecting all three major coronary arteries, typically associated with a more complex revascularization approach like CABG.
12. **Anatomically Complex Disease**: Coronary artery disease involving intricate or extensive blockages that may complicate treatment decisions, often requiring consultation between cardiologists and surgeons.
13. **Multidisciplinary Team (MDT)**: A group of healthcare professionals, including cardiologists and cardiac surgeons, who collaborate to determine the best treatment strategy for complex cases of coronary artery disease.
14. **Myocardial Ischemia**: A condition where reduced blood flow to the heart muscle causes angina symptoms due to insufficient oxygen delivery.
15. **Secondary Prevention**: Measures taken after the diagnosis of coronary artery disease to prevent further events, which include lifestyle changes, medications like statins, and sometimes revascularization.
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