En cardiologia, en medicina siempre hay noticias, resultados de estudios clinicos que son de importancia en la practica clinica diaria Tratare de concentrar aqui otro blog que tenia en otra parte. Tratara de abstracts de articulos que seran herramientas en nuestro accionar como medicos. Salud y suerte.
Comparison of effects of rosuvastatin (10 mg) versus atorvastatin (40 mg) on rho kinase activity in caucasian men with a previous atherosclerotic event.
Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA.
In addition to inhibiting cholesterol biosynthesis, statins also inhibit the formation of isoprenoid intermediates, which are required for the activation of the Rho/Rho kinase (ROCK) pathway. Increased ROCK activity has been implicated in causing endothelial dysfunction and atherosclerosis. However, it is not known whether statins, at doses used to lower cholesterol levels, inhibit ROCK activity in humans with atherosclerosis. Furthermore, it is not known whether lipophilic and hydrophilic statins differ in their ability to inhibit ROCK activity. Accordingly, we enrolled 30 men with stable atherosclerosis (low-density lipoprotein [LDL] > or =100 mg/dL) in a randomized, double-blind study comparing equivalent LDL-lowering doses of a hydrophilic statin (rosuvastatin 10 mg once a day) with a lipophilic statin (atorvastatin 40 mg once a day) for 28 days. We assessed the change in lipids, ROCK activity, and flow-mediated dilation (FMD) of the brachial artery before and after statin therapy. Both treatment groups exhibited comparable 30% to 32% and 42% to 45% reductions in total and LDL cholesterol, respectively. Only atorvastatin reduced triglycerides, and neither statin altered high-density lipoprotein cholesterol. Whereas both statins inhibited ROCK activity (p <0.0001), the extent of inhibition was greater with rosuvastatin (18 +/- 2% vs 8 +/- 2%, p = 0.0006). Statins also improved FMD from 7.4 +/- 0.6 to 9.3 +/- 0.4 (p = 0.003) with rosuvastatin being slightly better than atorvastatin. The inhibition of ROCK activity by statins did not correlate with reductions in LDL (p = 0.57) but was associated with improvement in FMD. In conclusion, these findings provide direct clinical evidence that statins, at clinically relevant doses, could differentially inhibit ROCK activity and improve endothelial function by cholesterol-independent mechanism.
PMID: 19195498 [PubMed – indexed for MEDLINE]
Efficacy of alternate day versus daily dosing of rosuvastatin.
Division of Cardiology, University of Western Ontario, London, Ontario.
BACKGROUND: Compared with other statins, rosuvastatin has a relatively long half-life, which may allow for the administration of this medication on an alternate day basis. OBJECTIVE: To compare the efficacy of administering rosuvastatin on a daily basis versus on an alternate day basis for the treatment of dyslipidemia. METHODS: In the present crossover study, 45 patients with documented hypercholesterolemia requiring pharmacotherapy were administered either 20 mg of rosuvastatin on alternate days or 10 mg of rosuvastatin daily for six weeks. After a four-week washout period, patients were then switched to the other regimen for another six weeks. The primary end point was the percentage reduction of low-density lipoprotein cholesterol (LDL-C). RESULTS: LDL-C decreased by 48.5% versus 40.9% with daily and alternate day dosing, respectively. This represented an additional absolute reduction of LDL-C of 7.6% (95% CI 1.8% to 13.4%, P=0.012) with the daily dosing regimen. Both dosing regimens provided similar improvements in high-density lipoprotein cholesterol and triglycerides. CONCLUSiONS: Compared with alternate day dosing, daily dosing of rosuvastatin provides a statistically significant advantage in LDL-C reduction. However, the alternate day regimen may be a viable option for those patients in whom cost is a limitation to compliance.
PMID: 19214297 [PubMed – indexed for MEDLINE
Antidepressants for the treatment of insomnia : a suitable approach?
Department of Psychiatry and Psychotherapy, Sleep Disorders Center, Technical University of Munich, Munich, Germany. firstname.lastname@example.org
The popularity of antidepressants in the treatment of insomnia is not supported by a large amount of convincing data, but rather by opinions and beliefs of the prescribing physicians on the advantages of these agents compared with drugs acting on the benzodiazepine receptor or other drugs used for the treatment of insomnia. The existing data do not allow for clear-cut, evidence-based recommendations concerning the use of antidepressants in insomnia. Our conclusions result from a few short-term studies on single agents, clinical experience and inferences from knowledge on the effect of antidepressants in other indications. At present, prescribing antidepressants for short-term treatment of insomnia can be useful if there is some amount of concomitant depressive symptomology or a history of depression, raising the impression that the present insomnia may be a prodromal sign for a new depressive episode. In all other cases, benzodiazepine receptor agonists, especially the nonbenzodiazepines among them (the so-called ‘z drugs’) should be the drugs of choice. For long-term treatment, antidepressants are among the pharmacological options, in addition to other groups of psychotropics. Off-label use of antidepressants may be considered for chronic insomnia if there is a concomitant depressive symptomalogy (which is not so pronounced that an antidepressant treatment with adequate higher doses would be required) and if there is no specific indication for one of the other groups of psychotropics (e.g. dementia-related nocturnal agitation, in which case an antipsychotic would be preferred, or circadian problems, in which case melatonin or a melatonin agonist would be favoured). If antidepressants are used to treat insomnia, sedating ones should be preferred over activating agents such as serotonin reuptake inhibitors. In general, drugs lacking strong cholinergic activity should be preferred. Drugs blocking serotonin 5-HT2A or 5-HT2C receptors should be preferred over those whose sedative property is caused by histamine receptor blockade only. The dose should be as low as possible (e.g. as an initial dose: doxepin 25 mg, mirtazapine 15 mg, trazodone 50 mg, trimipramine 25 mg). Regarding the lack of substantial data allowing for evidence-based recommendations, we are facing a clear need for well designed, long-term, comparative studies to further define the role of antidepressants versus other agents in the management of insomnia.
Distinct vascular and metabolic effects of different classes of anti-hypertensive drugs.
Cardiology, Gil Medical Center, Gachon University, Incheon, Republic of Korea.
BACKGROUND: ASCOT-BPLA study demonstrates that in hypertensive subjects, atenolol+bendroflumethiazide therapy is associated with higher incidence of adverse cardiovascular outcomes and developing diabetes than an amlodipine+perindopril regimen. This is not explained by changes in blood pressure alone. We hypothesized that distinct vascular and metabolic effects of anti-hypertensive drugs may explain these differential effects. METHODS: Either placebo or one class of anti-hypertensive drug (atenolol 100 mg, amlodipine 10 mg, hydrochlorothiazide 50 mg, ramipril 10 mg, or candesartan 16 mg) was given daily during 8 weeks to 31 patients in each of 6 arms of a randomized, single-blind, placebo-controlled, parallel study. RESULTS: Atenolol, amlodipine, and candesartan therapies significantly reduced systolic blood pressure when compared with ramipril (P<0.05 by ANOVA). Atenolol and thiazide therapies increased triglycerides levels greater than ramipril or candesartan (P=0.005 by ANOVA). Amlodipine significantly increased HDL cholesterol levels greater than atenolol (P=0.011 by ANOVA). Ramipril and candesartan therapies improved FMD and increased adiponectin levels and insulin sensitivity to a greater extent than atenolol or thiazide therapies (P<0.001 and P<0.015 by ANOVA). Amlodipine therapy increased adiponectin levels greater than atenolol therapy (P<0.05 by ANOVA). Ramipril, candesartan, and amlodipine therapies significantly decreased leptin levels to a greater extent when compared with atenolol or thiazide therapies (P<0.001 by ANOVA). Amlodipine therapies significantly decreased resistin levels greater than ramipril or candesartan therapies (P=0.001 by ANOVA). CONCLUSIONS: We observed differential effects of anti-hypertensive drugs on endothelial dysfunction and plasma adipocytokines.
Certain PPIs Increase Risk of Heart Attacks for Patients on Clopidogrel
OTTAWA, Ontario — January 28, 2009 — Patients taking clopidogrel following a myocardial infarction (MI) are at a significantly higher risk of a recurrence if they are also taking proton pump inhibitors (PPIs), according to a study published early online and appearing in the March issue of the Canadian Medical Association Journal.
The study, conducted over 6 years in thousands of MI patients aged 66 years and older, found a significantly increased risk of readmission for MIs if patients were taking 1 of several PPIs, including omeprazole, lansoprazole, or rabeprazole. The investigators found no such association with pantoprazole or with other H2 receptor antagonists.
Previous research indicates that PPIs other than pantoprazole can block the liver’s ability to convert clopidogrel to its active form — a critical step required for clopidogrel’s anti-platelet effect.
Recent guidelines from the American Heart Association, the American College of Gastroenterology, and the American College of Cardiology recommend PPI therapy for many patients following an MI to prevent bleeding from the stomach, including all patients aged 60 years or older receiving acetylsalicylic acid (ASA). Because clopidogrel and ASA are often prescribed together following an MI, it is probable that millions of patients worldwide will take a PPI with clopidogrel.
“Depending on the exposure to these drugs following a heart attack, we estimate that 5% to 15% of early readmissions for myocardial infarction among patients taking clopidogrel could be the result of this drug interaction,” writes Dr. David Juurlink, Head of the Division of Clinical Pharmacology and Toxicology, Sunnybrook Health Sciences Centre, Toronto, Ontario, and lead author of the study, which was conducted at the Institute for Clinical Evaluative Sciences, Toronto, Ontario. “These findings highlight a widely unappreciated, extremely common, and completely avoidable drug interaction in a population of patients at very high risk of reinfarction.”
“Our findings suggest that indiscriminate treatment with a proton pump inhibitor could result in thousands of additional cases of recurrent myocardial infarction each year, all of which could be avoided simply by selectively prescribing pantoprazole in patients receiving clopidogrel who require treatment with a proton pump inhibitor,” wrote the authors.
SOURCE: Canadian Medical Association Journal
Management of painful diabetic neuropathy.
University of Iowa Hospital and Clinics, Department of Pharmaceutical Care, Iowa City, Iowa, USA. email@example.com
Type 2 diabetes mellitus is a prevalent disease in the US which affects more than 15 million people. As the disease progresses over time, neuropathic pain can become a common complication; it is present in more than 50% of individuals with diabetes mellitus aged >60 years. The pathogenesis of diabetic neuropathy is theorized to be multifactorial. Numerous medications, some with different mechanisms of action, have been examined regarding their effects on the symptoms associated with diabetic neuropathy such as pain, paraesthesia and numbness. However, the majority of the studies have included small patient populations. Tricyclic antidepressants, amitriptyline and desipramine in particular, have been relatively well studied and shown to be effective. However, anticholinergic adverse effects may limit their usefulness and may preclude use in the elderly. Studies have also shown gabapentin to be effective and well tolerated in the treatment of diabetic neuropathy. Capsaicin cream provides another treatment option with a favourable adverse effect profile. Many other medications have been evaluated in diabetic neuropathy; however, more placebo-controlled studies with adequate patient populations need to be performed to solidify their role in treatment.
PMID: 11735621 [PubMed – indexed for MEDLINE]
Expert Opin Pharmacother. 2007 Jun;8(9):1399-402.
Clopidogrel use with stenting.
Doggrell Biomedical Communications, 14 Quandong Crescent, Nightcliff, NT0810, Australia.
Previous clinical trials have established that clopidogrel is beneficial when used with coronary artery stenting. However, questions remain as to when the clopidogrel treatment should be started and how long treatment should be continued for. In a Clopidogrel Registry, it was shown that when subjects received a loading dose of clopidogrel 300 mg, 6-24 h before the intervention and clopidogrel maintenance for 1 month, the primary end point at 30 days (acute myocardial infarction, all cause death and revascularisation) was lower than in subjects who were just given clopidogrel maintenance. An observational study has shown that there are no additional benefits from continuing to use clopidogrel after 6 months from bare-metal stenting. In contrast, long-term treatment with clopidogrel is beneficial in subjects given drug-eluting stents, when long-term stent thrombosis can be a rare complication. Thus, in subjects given drug-eluting stents, there was an incidence of death and non-fatal myocardial infarction (6-24 months after stenting) of 8.4% without clopidogrel and 2.1% with clopidogrel. These results suggest that clopidogrel pretreatment should be used with stenting, and that with drug-eluting stents, clopidogrel treatment should be continued for at least 24 months
Diabetes Res Clin Pract. 2009 Jan;83(1):50-3. Epub 2008 Dec 12
Comparison of effects of amlodipine and angiotensin receptor blockers on the intima-media thickness of carotid arterial wall (AAA study: amlodipine vs. ARB in atherosclerosis study).
Center for Diabetes & Endocrinology, The Tazuke Kofukai Foundation Medical Research Institute Kitano Hospital, Osaka 530-8480, Japan.
Although there have been increasing reports, which suggest that angiotensin receptor blockers (ARBs) may have anti-atherogenic actions, most of them are performed in vitro and there are a few reports about anti-atherogenic action in vivo. Especially, in humans, there have been no reports about effect of ARBs on atheroslocerosis. On the other hand, there have been several reports, including ours, which indicate that amlodipine, a calcium channel blocker, has a unique property to cause a reduction in the intima-media thickness (IMT) of common carotid artery, which is established to be an indicator of early atherosclerotic lesion, in humans. The present study investigated which of amlodipine and/or ARBs might have more profound effect on IMT progression. The study included 104 hypertensive patients with type 2 diabetes. They were divided into the two groups: the amlodipine group (n=58), who received amlodipine (2.5-5mg/day) and the ARB group (n=46), who received losartan (25-50mg/day), candesartan (4-8 mg/day), valsaratan (40-80 mg/day) or telmisartan (20-40 mg/day). IMT changes were examined during an average of 56.9 weeks. The amlodipine group showed a significant decrease in IMT compared to the ARB group (-0.046 [S.E. 0.161] mm vs. 0.080 [S.E. 0.255] mm, P<0.05). These results suggest that amlodipine has an inhibitory effect on early atherosclerotic process, and that ARBs do not have any effect on it in hypertensive patients with type 2 diabetes.
Vitamin D: How much is too much?
Is it possible to take too much vitamin D? I know vitamin D is important, but I wonder if too much is dangerous?
Vitamin D is an essential nutrient for your entire body. Still, it’s possible to have too much of a good thing.
Vitamin D has long been known to promote healthy bones. Some research suggests that vitamin D may also help prevent certain cancers, as well as diabetes, high blood pressure, multiple sclerosis and various other conditions.
Vitamin D is naturally present in some foods and is added to others. It is also available as a dietary supplement. The best food sources of vitamin D include salmon, mackerel, sardines, tuna and fortified milk. Cod liver oil also contains large amounts of vitamin D. Vitamin D is also produced by the body, triggered by sunlight on the skin.
Recent research suggests that many people may not be getting enough vitamin D. More exposure to sunlight can help, but this increases the risk of skin cancer and other skin problems. The National Academy of Sciences currently recommends 200 international units (IU) of vitamin D a day for children and adults up to age 50. This is about the amount of vitamin D in 3 ounces of tuna or 16 ounces of fortified milk. For adults older than age 50, the recommendation increases to 400 to 600 IU a day. If you’re not getting enough vitamin D, your doctor may recommend vitamin D supplements. Still, moderation is important.
You’re unlikely to get too much vitamin D from the food you eat, and prolonged sun exposure doesn’t seem to cause vitamin D toxicity. Over time, however, megadoses of vitamin D supplements can cause nausea, vomiting, poor appetite, constipation, weakness and weight loss. More seriously, excessive doses of vitamin D can raise the level of calcium in your blood — which can cause confusion and changes in heart rhythm. Generally, the upper limit for vitamin D is 2,000 IU a day.
If you’re concerned that you’re getting too little — or too much — vitamin D, contact your doctor. He or she may recommend a blood test to check the level of vitamin D in your blood.
Calcium supplements: Do they interfere with blood pressure drugs?
Is it true that calcium supplements may interfere with blood pressure medications?
Yes. In large amounts, calcium supplements may interfere with some blood pressure medications. Interactions may occur with the following blood pressure medications:
- Thiazide diuretics. Ingesting large amounts of calcium with thiazide diuretics — such as chlorothiazide, hydrochlorothiazide and indapamide — can result in milk-alkali syndrome, a serious condition characterized by excessively high levels of calcium and a shift in the body’s acid-base balance to alkaline. In general, avoid consuming more than 1,500 milligrams of calcium (supplements and food sources combined) a day if you’re taking a thiazide diuretic. If you do take calcium supplements while taking a thiazide diuretic, talk to your doctor about the appropriate dose and have your blood pressure and calcium levels monitored.
- Calcium channel blockers. When taken intravenously, calcium may decrease the effects of calcium channel blockers such as nifedipine, verapamil, diltiazem and others. In fact, intravenous calcium is used to help reverse calcium channel blocker overdose. However, there’s no evidence that standard calcium supplements interfere with calcium channel blockers. To be safe, check your blood pressure regularly if taking calcium channel blockers and calcium supplements concurrently.
Calcium supplements don’t appear to interact with other commonly prescribed blood pressure medications, such as beta blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers or renin inhibitors. Talk to your doctor if you take high blood pressure medications and calcium supplements and are concerned about interactions.
ORIGINAL INVESTIGATION: Sugar-Sweetened Beverages and Incidence of Type 2 Diabetes Mellitus in African American Women
Background Type 2 diabetes mellitus is an increasingly serious health problem among African American women. Consumption of sugar-sweetened drinks was associated with an increased risk of diabetes in 2 studies but not in a third; however, to our knowledge, no data are available on African Americans regarding this issue. Our objective was to examine the association between consumption of sugar-sweetened beverages, weight gain, and incidence of type 2 diabetes mellitus in African American women.
Methods A prospective follow-up study of 59 000 African American women has been in progress since 1995. Participants reported on food and beverage consumption in 1995 and 2001. Biennial follow-up questionnaires ascertained new diagnoses of type 2 diabetes. The present analyses included 43 960 women who gave complete dietary and weight information and were free from diabetes at baseline. We identified 2713 incident cases of type 2 diabetes mellitus during 338 884 person-years of follow-up. The main outcome measure was the incidence of type 2 diabetes mellitus.
Results The incidence of type 2 diabetes mellitus was higher with higher intake of both sugar-sweetened soft drinks and fruit drinks. After adjustment for confounding variables including other dietary factors, the incidence rate ratio for 2 or more soft drinks per day was 1.24 (95% confidence interval, 1.06-1.45). For fruit drinks, the comparable incidence rate ratio was 1.31 (95% confidence interval, 1.13-1.52). The association of diabetes with soft drink consumption was almost entirely mediated by body mass index, whereas the association with fruit drink consumption was independent of body mass index.
Conclusions Regular consumption of sugar-sweetened soft drinks and fruit drinks is associated with an increased risk of type 2 diabetes mellitus in African American women. While there has been increasing public awareness of the adverse health effects of soft drinks, little attention has been given to fruit drinks, which are often marketed as a healthier alternative to soft drinks.
Effects of graduated compression stockings with different pressure profiles on lower-limb venous structures and haemodynamics
- Rong Liu, North Carolina State University College of Textiles Raleigh, NC USA
- Terence T. Lao, Faculty of Medicine, University of Hong Kong Department of Obstetrics and Gynaecology Hong Kong Hong Kong
- Yi Lin Kwok, The Hong Kong Polytechnic University Institute of Textiles and Clothing Hong Kong Hong Kong
- Yi Li, The Hong Kong Polytechnic University Institute of Textiles and Clothing Hong Kong Hong Kong
- Michael Tin-Cheung Ying, The Hong Kong Polytechnic University Department of Health Technology and Informatics Hong Kong Hong Kong
J Am Coll Cardiol. 2008 Jan 22;51(3):261-3.
Influence of omeprazole on the antiplatelet action of clopidogrel associated with aspirin: the randomized, double-blind OCLA (Omeprazole CLopidogrel Aspirin) study.
Department of Cardiology, Brest University Hospital, Brest, France. firstname.lastname@example.org
OBJECTIVES: This trial sought to assess the influence of omeprazole on clopidogrel efficacy. BACKGROUND: Clopidogrel has proved its benefit in the treatment of atherothrombotic diseases. In a previous observational study, we found clopidogrel activity on platelets, tested by vasodilator-stimulated phosphoprotein (VASP) phosphorylation, to be diminished in patients receiving proton pump inhibitor (PPI) treatment. METHODS: In this double-blind placebo-controlled trial, all consecutive patients undergoing coronary artery stent implantation received aspirin (75 mg/day) and clopidogrel (loading dose, followed by 75 mg/day) and were randomized to receive either associated omeprazole (20 mg/day) or placebo for 7 days. Clopidogrel effect was tested on days 1 and 7 in both groups by measuring platelet phosphorylated-VASP expressed as a platelet reactivity index (PRI). Our main end point compared PRI value at the 7-day treatment period in the 2 groups. RESULTS: Data for 124 patients were analyzed. On day 1, mean PRI was 83.2% (standard deviation [SD] 5.6) and 83.9% (SD 4.6), respectively, in the placebo and omeprazole groups (p = NS), and on day 7, 39.8% (SD 15.4) and 51.4% (SD 16.4), respectively (p < 0.0001). RESULTS: Omeprazole significantly decreased clopidogrel inhibitory effect on platelet P2Y12 as assessed by VASP phosphorylation test. Aspirin-clopidogrel antiplatelet dual therapy is widely prescribed worldwide, with PPIs frequently associated to prevent gastrointestinal bleeding. The clinical impact of these results remains uncertain but merits further investigation.