Angiotensin-converting enzyme (ACE) inhibitors have been FDA-approved for treating refractory hypertension since 1981. Since then, clinical investigations support the benefits of ACE inhibition (ACE‑I) in pathologies like congestive heart failure, myocardial infarction, diabetes mellitus, chronic renal insufficiency, and atherosclerotic cardiovascular disease. Both, clinical trials and animal models of type I and type II diabetes have shown that hyperactivity of the angiotensin II signaling pathway contributes to the development of diabetes and its complications, and that blockade of the renin‑angiotensin system prevents new onset diabetes and reduces the risk of diabetic complications. Furthermore, ACE inhibitors are generally well tolerated and have few contraindications. This article describes ACE as a target molecule and gives an overview on the clinical evidence that supports the use of ACE inhibitors in diabetes.
{"title":"Benefits of ACE Inhibitors in Diabetes","authors":"M. Ramos-Nino, Steven R. Blumen","doi":"10.4137/CMT.S2027","DOIUrl":"https://doi.org/10.4137/CMT.S2027","url":null,"abstract":"Angiotensin-converting enzyme (ACE) inhibitors have been FDA-approved for treating refractory hypertension since 1981. Since then, clinical investigations support the benefits of ACE inhibition (ACE‑I) in pathologies like congestive heart failure, myocardial infarction, diabetes mellitus, chronic renal insufficiency, and atherosclerotic cardiovascular disease. Both, clinical trials and animal models of type I and type II diabetes have shown that hyperactivity of the angiotensin II signaling pathway contributes to the development of diabetes and its complications, and that blockade of the renin‑angiotensin system prevents new onset diabetes and reduces the risk of diabetic complications. Furthermore, ACE inhibitors are generally well tolerated and have few contraindications. This article describes ACE as a target molecule and gives an overview on the clinical evidence that supports the use of ACE inhibitors in diabetes.","PeriodicalId":10428,"journal":{"name":"Clinical Medicine and Therapeutics","volume":"1 1","pages":"1041-1051"},"PeriodicalIF":0.0,"publicationDate":"2009-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90297550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The present paper presents a review of the literature examining the efficacy of eszopiclone for treating insomnia. The purpose of the paper was to evaluate both the statistical and clinical efficacy of eszopiclone for treating insomnia. Both subjective and objective assessments of insomnia were evaluated across various sleep variables. Additionally, the efficacy of eszopiclone for treating insomnia comorbid with other conditions (sleep disordered breathing, psychiatric diagnoses, peri/post-menopause, rheumatoid arthritis), transient insomnia, and across diverse samples (adults, older adults, and samples pooled by race) was reviewed. Finally, the impact of eszopiclone use on daytime functioning was examined.
{"title":"Insomnia: A Review of the Use of eszopiclone","authors":"Natalie D Dautovich, Jacob M Williams, C. McCrae","doi":"10.4137/CMT.S1940","DOIUrl":"https://doi.org/10.4137/CMT.S1940","url":null,"abstract":"The present paper presents a review of the literature examining the efficacy of eszopiclone for treating insomnia. The purpose of the paper was to evaluate both the statistical and clinical efficacy of eszopiclone for treating insomnia. Both subjective and objective assessments of insomnia were evaluated across various sleep variables. Additionally, the efficacy of eszopiclone for treating insomnia comorbid with other conditions (sleep disordered breathing, psychiatric diagnoses, peri/post-menopause, rheumatoid arthritis), transient insomnia, and across diverse samples (adults, older adults, and samples pooled by race) was reviewed. Finally, the impact of eszopiclone use on daytime functioning was examined.","PeriodicalId":10428,"journal":{"name":"Clinical Medicine and Therapeutics","volume":"103 1","pages":"963-982"},"PeriodicalIF":0.0,"publicationDate":"2009-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80775055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gefitinib is a first generation, reversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), and EGFR TKIs, such as gefitinib and erlotinib, have yielded dramatic and durable responses in approximately 75% of of non-small cell lung cancer (NSCLC) patients whose tumor has an activating EGFR mutation. EGFR mutations are found in approximately 10%–15% of lung cancers in Caucasians, and they are more frequent in female patients, patients with adenocarcinoma, patients who are never- smokers or have a history of light-smoking, and patients with Asian ethnicity. Recent phase III trials comparing gefitinib with standard chemotherapy have demonstrated a similar survival benefit of gefitinib in patients with NSCLC and improved quality of life both in a first-line setting (IPASS; comparing gefitinib with carboplatin/paclitaxel) and a previously-treated setting (INTEREST; comparing gefitinib with docetaxel). Subset analyses of the data obtained in these studies showed that in patients with EGFR-mutant NSCLC gefitinib yielded a higher response rate, longer progression-free survival, and similar overall survival than standard cytotoxic chemotherapy did. The toxicity of EGFR TKIs is generally milder than that of standard cytotoxic chemotherapy. This review focuses on gefitinib, and issues in the management of EGFR-mutant NSCLC are discussed.
{"title":"Management of eGFR-Mutant non-small cell Lung cancer: Focus on Gefitinib","authors":"Y. Naito, K. Goto","doi":"10.4137/CMT.S2122","DOIUrl":"https://doi.org/10.4137/CMT.S2122","url":null,"abstract":"Gefitinib is a first generation, reversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), and EGFR TKIs, such as gefitinib and erlotinib, have yielded dramatic and durable responses in approximately 75% of of non-small cell lung cancer (NSCLC) patients whose tumor has an activating EGFR mutation. EGFR mutations are found in approximately 10%–15% of lung cancers in Caucasians, and they are more frequent in female patients, patients with adenocarcinoma, patients who are never- smokers or have a history of light-smoking, and patients with Asian ethnicity. Recent phase III trials comparing gefitinib with standard chemotherapy have demonstrated a similar survival benefit of gefitinib in patients with NSCLC and improved quality of life both in a first-line setting (IPASS; comparing gefitinib with carboplatin/paclitaxel) and a previously-treated setting (INTEREST; comparing gefitinib with docetaxel). Subset analyses of the data obtained in these studies showed that in patients with EGFR-mutant NSCLC gefitinib yielded a higher response rate, longer progression-free survival, and similar overall survival than standard cytotoxic chemotherapy did. The toxicity of EGFR TKIs is generally milder than that of standard cytotoxic chemotherapy. This review focuses on gefitinib, and issues in the management of EGFR-mutant NSCLC are discussed.","PeriodicalId":10428,"journal":{"name":"Clinical Medicine and Therapeutics","volume":"14 1","pages":"1027-1040"},"PeriodicalIF":0.0,"publicationDate":"2009-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76689031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mycophenolic acid inhibits an enzyme, inosine monophosphate dehydrogenase (IMPDH), blocking purine synthesis of lymphocytes and therefore functioning as an effective immunosuppressive agent in transplantation. Currently, there are two available forms of mycophenolic acid (MPA) available; mycophenolate mofetil (MMF) and enteric-coated, delayed-release mycophenolate sodium (EC-MPS). Both products are approved for prophylaxis of organ rejection in renal transplant recipients. The use of MPA may be associated with adverse gastrointestinal effects which can lead to a reduction of the dose or discontinuation of therapy. Enteric-coated MPS was developed to reduce the upper gastrointestinal side effects due to its delayed release in the small intestines. Similar systemic MPA exposure is provided by oral administration of MMF 1000 mg daily and EC-MPS 720 mg, which contain near equimolar MPA content. Clinical trials in renal transplant recipients have demonstrated that EC-MPS is therapeutically equivalent to MMF when used at the time of transplantation and when used for conversion for gastrointestinal complications. The available literature regarding the incidence and severity of gastrointestinal adverse effects and the impact on quality of life remains controversial. Prospective, randomized trials of the available MPA formulations are warranted to further explore the gastrointestinal adverse effect profiles.
{"title":"A Review of Enteric-coated Mycophenolate Sodium for Renal Transplant Immunosuppression","authors":"N. Newbold, B. Riley, K. Hardinger","doi":"10.4137/CMT.S2218","DOIUrl":"https://doi.org/10.4137/CMT.S2218","url":null,"abstract":"Mycophenolic acid inhibits an enzyme, inosine monophosphate dehydrogenase (IMPDH), blocking purine synthesis of lymphocytes and therefore functioning as an effective immunosuppressive agent in transplantation. Currently, there are two available forms of mycophenolic acid (MPA) available; mycophenolate mofetil (MMF) and enteric-coated, delayed-release mycophenolate sodium (EC-MPS). Both products are approved for prophylaxis of organ rejection in renal transplant recipients. The use of MPA may be associated with adverse gastrointestinal effects which can lead to a reduction of the dose or discontinuation of therapy. Enteric-coated MPS was developed to reduce the upper gastrointestinal side effects due to its delayed release in the small intestines. Similar systemic MPA exposure is provided by oral administration of MMF 1000 mg daily and EC-MPS 720 mg, which contain near equimolar MPA content. Clinical trials in renal transplant recipients have demonstrated that EC-MPS is therapeutically equivalent to MMF when used at the time of transplantation and when used for conversion for gastrointestinal complications. The available literature regarding the incidence and severity of gastrointestinal adverse effects and the impact on quality of life remains controversial. Prospective, randomized trials of the available MPA formulations are warranted to further explore the gastrointestinal adverse effect profiles.","PeriodicalId":10428,"journal":{"name":"Clinical Medicine and Therapeutics","volume":"4 1","pages":"927-933"},"PeriodicalIF":0.0,"publicationDate":"2009-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89699497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R. Rossini, G. Musumeci, Tamar Nijaradze, A. Gavazzi
Antiplatelet therapy is the cornerstone in the modern therapy of patients with acute coronary syndromes (ACS), because of the unique role of platelets in coronary thrombosis. Clopidogrel in combination with aspirin is the current “gold standard” for reducing cardiovascular events in such patients, providing a synergistic platelet inhibition through different platelet activation pathways. Clopidogrel is a thienopyridine which inhibits ADP-induced platelet aggregation, with no direct effects on the metabolism of arachidonic acid. Due to a better safety profile with a similar antiplatelet effectiveness, it is preferred to ticlopidine. In patients with ACS without ST segment elevation (NSTEMI), clopidogrel plus aspirin is able to reduce the relative risk of adverse cardiovascular events by 20%, compared with aspirin alone. Clopidogrel plays a key role also in patients undergoing coronary stenting, in order to prevent stent thrombosis. Pretreatment and long-term treatment with clopidogrel reduces by about one-third the risk of cardiovascular death or myocardial infarction in NSTEMI ACS patients undergoing percutaneous coronary angioplasty (PCI). However, a long-term dual antiplatelet therapy is associated with a higher rate of bleeding events. Clinical practice guidelines currently recommend long-term dual antiplatelet therapy with aspirin and clopidogrel in patients with ACS and a pre-treatment with clopidogrel in every patient scheduled for PCI. The concept of clopidogrel resistance and the need for a pretreatment in patients undergoing coronary stent implantation led to the concept that an improved antiplatelet regimen with novel drugs is desirable.
{"title":"Clopidogrel Bisulfate: A Review of its Use in the Management of Acute Coronary Syndrome","authors":"R. Rossini, G. Musumeci, Tamar Nijaradze, A. Gavazzi","doi":"10.4137/CMT.S1170","DOIUrl":"https://doi.org/10.4137/CMT.S1170","url":null,"abstract":"Antiplatelet therapy is the cornerstone in the modern therapy of patients with acute coronary syndromes (ACS), because of the unique role of platelets in coronary thrombosis. Clopidogrel in combination with aspirin is the current “gold standard” for reducing cardiovascular events in such patients, providing a synergistic platelet inhibition through different platelet activation pathways. Clopidogrel is a thienopyridine which inhibits ADP-induced platelet aggregation, with no direct effects on the metabolism of arachidonic acid. Due to a better safety profile with a similar antiplatelet effectiveness, it is preferred to ticlopidine. In patients with ACS without ST segment elevation (NSTEMI), clopidogrel plus aspirin is able to reduce the relative risk of adverse cardiovascular events by 20%, compared with aspirin alone. Clopidogrel plays a key role also in patients undergoing coronary stenting, in order to prevent stent thrombosis. Pretreatment and long-term treatment with clopidogrel reduces by about one-third the risk of cardiovascular death or myocardial infarction in NSTEMI ACS patients undergoing percutaneous coronary angioplasty (PCI). However, a long-term dual antiplatelet therapy is associated with a higher rate of bleeding events. Clinical practice guidelines currently recommend long-term dual antiplatelet therapy with aspirin and clopidogrel in patients with ACS and a pre-treatment with clopidogrel in every patient scheduled for PCI. The concept of clopidogrel resistance and the need for a pretreatment in patients undergoing coronary stent implantation led to the concept that an improved antiplatelet regimen with novel drugs is desirable.","PeriodicalId":10428,"journal":{"name":"Clinical Medicine and Therapeutics","volume":"2009 1","pages":"899-910"},"PeriodicalIF":0.0,"publicationDate":"2009-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78216870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gastroesophageal reflux disease (GERD) is very common and is a costly problem to manage. The annual direct cost for managing the disease is estimated to be more than $9 billion dollars in the USA. In western populations, 25% of people over age 30 report having heartburn at least once a month, 12% at least once per week, and 5% describe daily symptoms. However, the prevalence of the disease tends to be underestimated, with unrecognized GERD occurring in more than 50% of patients seen in general practice for unrelated conditions. GERD is defined as symptoms or mucosal damage produced by the abnormal reflux of gastric contents against the gradient of the lower esophageal sphincter (LES) pressure into the distal esophagus, leading to impaired quality of life and other complications. The disease is thought to be caused by reduced pressure of the lower esophageal sphincter (LES) and delayed gastric emptying. It is well-recognized that GERD is associated with a variety of clinical syndromes and that it is frequently a chronic condition, often requiring long-term maintenance therapy. It can be subdivided into erosive esophagitis (EE) and non-erosive reflux disease (NERD). Patients with NERD have no mucosal breaks in the esophagus, but have typical reflux symptoms. The spectrum of upper gastrointestinal complications of GERD includes erosive esophagitis, stricture and Barrett’s esophagus, which may increase the risk of esophageal adenocarcinoma. Treatment options available for GERD range from over-the-counter (OTC) antacids to proton pump inhibitors (PPIs) and anti-reflux endoscopic procedures and surgery. This article will review each of the pharmacotherapeutic options, including new developments in proton pump inhibitor isomers, potassium competitive acid blockers and endoscopic therapy for gastroesophageal reflux disease.
{"title":"Current and Prospective Pharmacotherapies in Gastroesophageal Reflux Disease","authors":"L. Nguyen, J. Birk","doi":"10.4137/CMT.S2744","DOIUrl":"https://doi.org/10.4137/CMT.S2744","url":null,"abstract":"Gastroesophageal reflux disease (GERD) is very common and is a costly problem to manage. The annual direct cost for managing the disease is estimated to be more than $9 billion dollars in the USA. In western populations, 25% of people over age 30 report having heartburn at least once a month, 12% at least once per week, and 5% describe daily symptoms. However, the prevalence of the disease tends to be underestimated, with unrecognized GERD occurring in more than 50% of patients seen in general practice for unrelated conditions. GERD is defined as symptoms or mucosal damage produced by the abnormal reflux of gastric contents against the gradient of the lower esophageal sphincter (LES) pressure into the distal esophagus, leading to impaired quality of life and other complications. The disease is thought to be caused by reduced pressure of the lower esophageal sphincter (LES) and delayed gastric emptying. It is well-recognized that GERD is associated with a variety of clinical syndromes and that it is frequently a chronic condition, often requiring long-term maintenance therapy. It can be subdivided into erosive esophagitis (EE) and non-erosive reflux disease (NERD). Patients with NERD have no mucosal breaks in the esophagus, but have typical reflux symptoms. The spectrum of upper gastrointestinal complications of GERD includes erosive esophagitis, stricture and Barrett’s esophagus, which may increase the risk of esophageal adenocarcinoma. Treatment options available for GERD range from over-the-counter (OTC) antacids to proton pump inhibitors (PPIs) and anti-reflux endoscopic procedures and surgery. This article will review each of the pharmacotherapeutic options, including new developments in proton pump inhibitor isomers, potassium competitive acid blockers and endoscopic therapy for gastroesophageal reflux disease.","PeriodicalId":10428,"journal":{"name":"Clinical Medicine and Therapeutics","volume":"8 1","pages":"983-997"},"PeriodicalIF":0.0,"publicationDate":"2009-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82069506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Levetiracetam is a second-generation antiepileptic drug which first came to the United States market in 1999. It has a mechanism of action that is not well elucidated. However, it is a very favorable antiepileptic drug due to its reliable pharmacokinetics, minimal drug interactions, seizure efficacy and good tolerability. It is an agent that has established efficacy as an adjunct therapy agent for partial and refractory seizures. As a monotherapy agent, levetiracetam also appears to be an attractive agent with observed efficacy and tolerability. Since levetiracetam has recently become available intravenously, it is also being reviewed as an agent for acute status epilepticus. In pediatrics, levetiracetam is widely used with efficacy seen in small clinical trials for a variety of seizure types. Levetiracetam is well tolerated: the most common adverse effect being somnolence and behavioral effects. Overall, levetiracetam is a notable antiepileptic drug that has added significantly to the current antiepileptic armamentarium.
{"title":"Pharmacotherapy of Epilepsy: Focus on Levetiracetam","authors":"M. E. Adams, A. Chung, Lea S. Eiland","doi":"10.4137/CMT.S1096","DOIUrl":"https://doi.org/10.4137/CMT.S1096","url":null,"abstract":"Levetiracetam is a second-generation antiepileptic drug which first came to the United States market in 1999. It has a mechanism of action that is not well elucidated. However, it is a very favorable antiepileptic drug due to its reliable pharmacokinetics, minimal drug interactions, seizure efficacy and good tolerability. It is an agent that has established efficacy as an adjunct therapy agent for partial and refractory seizures. As a monotherapy agent, levetiracetam also appears to be an attractive agent with observed efficacy and tolerability. Since levetiracetam has recently become available intravenously, it is also being reviewed as an agent for acute status epilepticus. In pediatrics, levetiracetam is widely used with efficacy seen in small clinical trials for a variety of seizure types. Levetiracetam is well tolerated: the most common adverse effect being somnolence and behavioral effects. Overall, levetiracetam is a notable antiepileptic drug that has added significantly to the current antiepileptic armamentarium.","PeriodicalId":10428,"journal":{"name":"Clinical Medicine and Therapeutics","volume":"95 1","pages":"935-952"},"PeriodicalIF":0.0,"publicationDate":"2009-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75273181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Espinel-Ingroff, E. Cantón, E. Martín-Mazuelos, J. Pemán
The classic recommended antifungal agents for the treatment of invasive Candida infections were amphotericin B, a lipid formulation of amphotericin B and fluconazole in both neutropenic or nonneutropenic patients as either primary or alternative therapies. Voriconazole has been recommended when additional coverage for filamentous fungi is needed (e.g. neutropenic patients). More recently and based on well designed comparative clinical trials, the three echinocandins, caspofungin, anidulafungin and micafungin have been added as primary or alternative therapies especially for critically ill or neutropenic patients. In general, the echinocandins are most useful when patients have previously been exposed to an azole or are unstable.
{"title":"pharmacotherapy of Candida Infections with echinocandins","authors":"A. Espinel-Ingroff, E. Cantón, E. Martín-Mazuelos, J. Pemán","doi":"10.4137/CMT.S2311","DOIUrl":"https://doi.org/10.4137/CMT.S2311","url":null,"abstract":"The classic recommended antifungal agents for the treatment of invasive Candida infections were amphotericin B, a lipid formulation of amphotericin B and fluconazole in both neutropenic or nonneutropenic patients as either primary or alternative therapies. Voriconazole has been recommended when additional coverage for filamentous fungi is needed (e.g. neutropenic patients). More recently and based on well designed comparative clinical trials, the three echinocandins, caspofungin, anidulafungin and micafungin have been added as primary or alternative therapies especially for critically ill or neutropenic patients. In general, the echinocandins are most useful when patients have previously been exposed to an azole or are unstable.","PeriodicalId":10428,"journal":{"name":"Clinical Medicine and Therapeutics","volume":"92 1","pages":"889-897"},"PeriodicalIF":0.0,"publicationDate":"2009-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80503550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chronic stable angina pectoris results from a fixed coronary arterial obstruction causing an imbalance between myocardial oxygen supply and demand. Current therapy aims to reduce cardiovascular events (vasculoprotective) thereby improving survival, and/or relieve ischemic symptoms (antianginal) thereby improving the quality of life. Vasculoprotective therapy consists of lifestyle modification, antiplatelet agents, lipid lowering therapy and angiotensin-converting enzyme (ACE) inhibitors. Conventional antianginal therapy for patients with chronic stable angina consists of beta-blockers, calcium channel blockers and nitrates, with surgical or percutaneous revascularization serving an adjunctive role. Despite the investigation of multiple novel therapies and medications over the past 25 years, arguably the most significant contribution to antianginal therapy during that time involved the recent introduction of ranolazine. Ranolazine acts via a distinctive pathway, inhibiting the late sodium current of the action potential in ischemic myocytes. Multiple studies have demonstrated that ranolazine significantly reduces anginal symptoms and improves exercise performance in patients with chronic stable angina but does not reduce mortality. Ranolazine does not affect either heart rate or blood pressure, a unique property among the current antianginal agents. Despite its QT prolongation, ranolazine has a proven safety profile and is not proarrhythmic. In fact, in a recent large randomized trial, ranolazine reduced the incidence of supraventricular tachycardia, ventricular tachycardia, new-onset atrial fibrillation and bradycardic events. Ranolazine may confer some additional benefits such as a reduction in HbA1c levels and improved left ventricular diastolic function. Ranolazine is now approved for use in chronic stable angina. Current guidelines recommend beta-blockers as the first line antianginal agent due to the proven mortality reduction. However, for patients with bradycardia or hypotension, ranolazine may be considered as initial antianginal therapy.
{"title":"Management Options in Chronic Stable Angina Pectoris: Focus on Ranolazine","authors":"D. Vadnais, N. Wenger","doi":"10.4137/CMT.S2214","DOIUrl":"https://doi.org/10.4137/CMT.S2214","url":null,"abstract":"Chronic stable angina pectoris results from a fixed coronary arterial obstruction causing an imbalance between myocardial oxygen supply and demand. Current therapy aims to reduce cardiovascular events (vasculoprotective) thereby improving survival, and/or relieve ischemic symptoms (antianginal) thereby improving the quality of life. Vasculoprotective therapy consists of lifestyle modification, antiplatelet agents, lipid lowering therapy and angiotensin-converting enzyme (ACE) inhibitors. Conventional antianginal therapy for patients with chronic stable angina consists of beta-blockers, calcium channel blockers and nitrates, with surgical or percutaneous revascularization serving an adjunctive role. Despite the investigation of multiple novel therapies and medications over the past 25 years, arguably the most significant contribution to antianginal therapy during that time involved the recent introduction of ranolazine. Ranolazine acts via a distinctive pathway, inhibiting the late sodium current of the action potential in ischemic myocytes. Multiple studies have demonstrated that ranolazine significantly reduces anginal symptoms and improves exercise performance in patients with chronic stable angina but does not reduce mortality. Ranolazine does not affect either heart rate or blood pressure, a unique property among the current antianginal agents. Despite its QT prolongation, ranolazine has a proven safety profile and is not proarrhythmic. In fact, in a recent large randomized trial, ranolazine reduced the incidence of supraventricular tachycardia, ventricular tachycardia, new-onset atrial fibrillation and bradycardic events. Ranolazine may confer some additional benefits such as a reduction in HbA1c levels and improved left ventricular diastolic function. Ranolazine is now approved for use in chronic stable angina. Current guidelines recommend beta-blockers as the first line antianginal agent due to the proven mortality reduction. However, for patients with bradycardia or hypotension, ranolazine may be considered as initial antianginal therapy.","PeriodicalId":10428,"journal":{"name":"Clinical Medicine and Therapeutics","volume":"4 1","pages":"871-887"},"PeriodicalIF":0.0,"publicationDate":"2009-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87867194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
High bone turnover disorders are characterized by excessive osteoclastic activity resulting in loss of bone mass and quality, fractures, deformities, debilitating pain, loss of mobility and hypercalcemia. These complications have a major impact in quality of life, and control of osteoclast activity is critical to reduce or prevent these skeletal events. Over the last 2 decades bisphosphonates became an integral part of the management of these disorders. Bisphosphonates, analogues of pyrophosphate, bind to hydroxyapatite crystals and have a very high affinity for bone mineral. Their retention in bone and rapid clearance from the circulation make them safe and effective agents for inhibition of osteoclast activity. Pamidronate is one such bisphosphonate that has been effective in treating Paget’s disease, myeloma bone disease and osteolytic bone metastases from breast cancer. This review will focus on the effects of pamidronate in these disorders.
{"title":"pharmacotherapy with pamidronate Disodium of Osteolytic Bone Metastases of Breast cancer, Osteolytic Lesions of Multiple Myeloma, and paget's Disease","authors":"A. Hoff, Y. Novis","doi":"10.4137/CMT.S2166","DOIUrl":"https://doi.org/10.4137/CMT.S2166","url":null,"abstract":"High bone turnover disorders are characterized by excessive osteoclastic activity resulting in loss of bone mass and quality, fractures, deformities, debilitating pain, loss of mobility and hypercalcemia. These complications have a major impact in quality of life, and control of osteoclast activity is critical to reduce or prevent these skeletal events. Over the last 2 decades bisphosphonates became an integral part of the management of these disorders. Bisphosphonates, analogues of pyrophosphate, bind to hydroxyapatite crystals and have a very high affinity for bone mineral. Their retention in bone and rapid clearance from the circulation make them safe and effective agents for inhibition of osteoclast activity. Pamidronate is one such bisphosphonate that has been effective in treating Paget’s disease, myeloma bone disease and osteolytic bone metastases from breast cancer. This review will focus on the effects of pamidronate in these disorders.","PeriodicalId":10428,"journal":{"name":"Clinical Medicine and Therapeutics","volume":"19 1","pages":"953-962"},"PeriodicalIF":0.0,"publicationDate":"2009-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79189466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：