Интересные ссылки

[Yariko]

The ACC/AHA 2013 guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular disease risk in adults: the good the bad and the uncertain:acomparison with ESC/EAS guidelines for the management of dyslipidaemias 2011

European Heart Journal
doi:10.1093/eurheartj/ehu107

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[angio]

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[Dr.Vad]

Cardiovasc Ther. 2014 Apr 23. doi: 10.1111/1755-5922.12076.
Pentoxifylline in heart failure: a meta-analysis of clinical trials.
Champion S, Lapidus N, Cherié G, Spagnoli V, Oliary J, Solal AC.

BACKGROUND: Pentoxifylline possess anti-inflammatory and rheological properties and has been tested in heart failure (HF).

METHODS: A comprehensive search was performed from 1980 until July 2013 in PubMed, to identify randomized controlled trials evaluating pentoxifylline versus placebo in HF, in order to determine impact on mortality. Search strategy: "Pentoxifylline" AND "heart" AND "trial". Study selection of 6 randomized controlled trials evaluating mortality as outcome. Then we conducted a meta-analysis of randomized controlled trials versus placebo in HF. Determination of Mantel-Haenszel fixed effect and random effect pooled odds ratios for all-cause mortality and corresponding 95% confidence intervals.

RESULTS: Data from a total of 221 patients with LVEF≤40% from six randomized controlled trials were included in this analysis. Pentoxifylline 1200 mg per day was administered during 6 months, except in one study (administered during 1 month for severe acute HF). The use of pentoxifylline was not significantly associated with a reduction of mortality in HF in individual studies. The pooled data including 221 patients showed a nearly fourfold reduction in mortality (5.4% vs 18.3%; OR 0.29; CI 0.12-0.74; p<0.01) with homogenous results (I² 0%).

CONCLUSION: A meta-analysis evaluating pentoxifylline versus placebo in HF suggested a significant nearly fourfold decrease in all-cause mortality in the pentoxifylline group.

[angio]

Хм-м. Интересно, а если так- [Ссылки доступны только зарегистрированным пользователям ]

2014 AF Treatment Guidelines: 10 Things to Like and Only One to Dislike
John MandrolaMarch 31, 2014
The "2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation" is here. I've read the entire 123 pages. Let's do this report in 10 categories (some with bulleted lists). I'll mix reporting with editorial comment. I'll try to keep it to one to two paragraphs per issue, and look for blatant editorial to be in italics. At the end, I'll offer one criticism.

The writers began strongly—with the obvious, which is often elusive.

1. Guidelines are for guidance. Let's start with this quote from the introduction (emphasis mine): "The guidelines attempt to define practices that meet the needs of most patients in most circumstances. The ultimate judgment about care of a particular patient must be made by the clinician and patient in light of all the circumstances presented by that patient." Writing committee chair Dr Craig January (University of Wisconsin, Madison) offered this nugget of self-awareness in the press release: "Because what we say in the guideline can affect how a drug is used, we were careful to be even-handed and evidence-based in presenting new drugs."

These two statements deserve emphasis because patient-centered care is threatened when guidelines morph into scripture. Good on the writers.

2. Nonvalvular AF gets a definition (sort of): From table 3: Nonvalvular AF is that which occurs in the absence of rheumatic mitral stenosis, a mechanical or bioprosthetic heart valve, or mitral-valve repair. Hmm?

3. Atrial flutter gets special emphasis: Heart-rhythm doctors are seeing more atrial flutter. The increased incidence of typical flutter, which we painfully call cavotricuspid-isthmus (CTI) dependent, parallels the rise in obesity, sleep apnea, use of AF drugs, and advancing age of the populace. Our efforts in the left atrium—with ablation catheters—have brought us enhanced knowledge of the atypical forms of flutter.

The writers urge care with the flutter/fib diagnosis, specifically calling out the fact that "coarse" AF can be mistaken as atrial flutter—a common error in the real world. Also, efforts to distinguish typical from atypical flutter are important for counseling patients on expectations of ablation. The former is easy to ablate, and the latter is not.

4. Antithrombotic-therapy recommendations: Check this out.The very first class I recommendation: "In patients with AF, antithrombotic therapy should be individualized based on shared decision-making after discussion of the absolute and [relative risks] RRs of stroke and bleeding and the patient's values and preferences. Read that again. The patient-centric nature of that statement is a remarkable and welcome stand for experts to take. Thank you.

Let's do a bulleted list of other notables on stroke-prevention strategies:

Use the CHA2DS2-VASc score rather than the CHADS2 score.

Bleeding scores, such as HAS-BLED, REITE, and HEMORR2HAGES may be helpful in defining risk, but the evidence for using them for specific recommendations was not sufficient.

The non–vitamin K–antagonist anticoagulant (NOAC) drugs—dabigatran etexilate (Pradaxa, Boehringer Ingelheim), rivaroxaban (Xarelto, Bayer/Janssen Pharmaceuticals), and apixaban (Eliquis, Bristol-Myers Squibb/Pfizer)—were added to warfarin as preferred therapy.

Patients who struggle to maintain stable INRs may be considered for NOAC drugs. In my view, INR yo-yoing most often reflects deficits in patient education and/or adherence. Neither of these are necessarily good situations for the use of NOAC drugs.

Bridging strategies with unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) came with strong wording to "balance the risks of stroke and bleeding." My take on bridging is that it's no small thing. So I am glad for this language.

In patients with AF who are undergoing stent placement, bare-metal stents could be considered as well as dual antiplatelet therapy (minus aspirin).

5. Little benefit with aspirin: This quote says a lot. "No studies, with the exception of the [Stroke Prevention in Atrial Fibrillation-1] SPAF-1 trial, show benefit for aspirin alone in preventing stroke among patients with AF."

The writers then use data that I quote often in the clinic. The Birmingham Atrial Fibrillation Treatment of the Aged (BAFTA) trial compared warfarin and aspirin in high-risk subjects greater than 75 years old. Those treated with warfarin had fewer strokes and similar rates of bleeding. Most striking: the risk of extracranial bleeding was 1.4% with warfarin and 1.6% with aspirin.

We were also urged to question the common practice of using aspirin in low-risk patients. Did you know "aspirin has not been studied in a low-risk AF population?"

6. Warfarin vs NOAC drugs: What was so notable about the discussion of how and why to choose between agents was what the writers did not say. They did not use the word superior, nor did they recommend one drug over another. Rather, a reader learned the pros, cons, and expectations of each drug. Good. Doctors and patients should be able to evaluate the results of the clinical trials that enrolled more than 50 000 patients and counted easy things to count, such as strokes, bleeds, and deaths.

7. Wait and see on LAA occlusion: Percutaneous left atrial appendage occlusion devices earned a couple of paragraphs, but no formal recommendations were made. Comments regarding surgical closure at the time of concomitant cardiac surgery were interesting. "The current data regarding LAA occlusion at the time of concomitant cardiac surgery reveals a lack of clear consensus because of the inconsistency of techniques used for surgical excision, the highly variable rates of successful LAA occlusion, and the unknown impact LAA occlusion may or may not have upon future thromboembolic events." On the matter of the left atrial appendage, put me down as skeptical on the idea that a focal strategy (LAA occlusion) can treat a systemic disease (stroke).

8. Rate control: There were not many surprises in the recommendations on rate control. Here are four topics worth mentioning:

Acute rate control: Ca-channel blocker vs beta-blocker? The clinical trials of acute rate control were performed in the 1980s and 1990s. These studies had variable end points and small sample sizes and were often from single sites. It is with great pleasure that I offer this quote: "Unless immediate rate control is required or an enteral route of administration is not available, oral administration is appropriate." Regular readers know how this column feels about using IV drugs when oral ones will do.

Be cautious with digoxin. The writers reiterate the pharmacology of digoxin and give mention to recent meta-analyses that suggest a possible signal of harm. Attention to digoxin's narrow therapeutic window is laudable.

Lenient rate-control strategy (less than 110 bpm) may be reasonable: The caveat is that patients remain symptom-free with preserved LV function. Noting the limitations of the RACE-II trial, the writers expressed worry that its findings may not apply well to a broad group of AF patients.

AV-node ablation and pacing earns a class IIa indication. The writers make it clear that this irreversible procedure has both benefits and risks. They also nudge us to think about the benefits of cardiac resynchronization therapy (CRT) pacing for patients who have undergone AV node ablation and have moderate to severe LV systolic dysfunction.

9. Rhythm control: The writers were clear that rhythm-control therapy of AF must be individualized. Four topics struck me as notable.

What's a reversible cause of AF? The writers say this: "Class I: Before initiating antiarrhythmic drug therapy, treatment of precipitating or reversible causes of AF is recommended."

Here we have a real dilemma. In past guidelines, this sort of wording implied underlying causes like ectopic atrial tachycardia, hyperthyroidism, acute alcohol ingestion, infection, chronic obstructive pulmonary disease (COPD) exacerbation, or trauma. Okay. I get that. Fix those problems and AF might resolve itself. The interesting caveat now is that we know obesity, sleep apnea, hypertension, and metabolic syndrome are both precipitating and reversible causes of AF.

So, do the writers mean we should treat these problems before initiating rhythm control? Because if they do, there will be a lot fewer AF patients treated with AF drugs and ablation. It's provocative to even think that patients help themselves. But you see where failing in this regard got us with hypertension therapy—eg, drugs (and kidney ablation almost) get used as substitutes for lifestyle changes.

Big changes in AF ablation recommendations: AF ablation has been moved to first-line status for both paroxysmal and persistent AF patients. This welcome change aligns these guidelines with those from Europe. My previous post discusses many of the issues surrounding the decision-making in the initial approach to rhythm control.

Class III harm distinction added for two false beliefs . AF ablation should not be performed in patients who cannot be treated with anticoagulants, and AF ablation should not be done with the sole intent of avoiding anticoagulation. This might seem obvious to electrophysiologists but it is not well-known in the real world. A good add.

Don't forget about the surgical maze option: Both stand-alone and concomitant procedures are mentioned as options. This is a worthy addition because AF surgery offers selected patients reasonable options.

[angio]

"Cardiology's Biggest Lie: No MRI for Your Device Patient"
Melissa Walton-Shirley, MD Cardiologist, Cardiology Associates, Glasgow, Kentucky

Pooling their data with published papers, the German authors found that 1043 patients with devices (including ICDs) had undergone MRI safely. "No life-threatening complications have been observed," they concluded. In addition, "in just 11 cases (1%), electrical resetting of the device was necessary, and a significant increase in pacing threshold (>1.0 mV) was seen in 16 cases (1.5%)." While they acknowledge that the study conditions varied widely, including differences in localization, field strength of the scanner, device, sensors, etc, their review provides a good estimation of how frequently complications can be expected.

In March of 2011, Russo received approval from the CMS for payment for MRI scans if a facility agreed to participate in the MagnaSafe trial. Previously reported by heartwire , the trial was originally set to enroll 1500 participants and excluded pacer-dependent patients who have ICDs, abandoned leads, and abdominal implants. It also excluded those patients with any device with an FDA MRI-friendly label. According to Clinicaltrials.gov, there are 21 facilities in 14 states that are participating. The study is ongoing but not recruiting.

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другое мнение:

In fact, shortly after this, the author reports the reported rates of adverse events from the study, with 1.5% of participants seeing a post-MRI "significant increase in pacing threshold." One of the leading theories of the cause of the need of the pacer to send greater voltage to the heart in order to effectively pace it after an MRI exam is because of lead heating damaging or destroying cells in direct contact with the lead tips. This essentially creates an electrically-insulating barrier between the lead tip and the cardiac tissues, requiring the pulse generator to expend more energy to accomplish the job.

The American College of Radiology, in their 2013 Guidance Document on MR Safety Practices, offers the following list of potential risks associated with imaging pacing devices not specifically approved for use in MRI:

"Potential Complications: Unexpected programming changes, inhibition of pacemaker output, failure to pace, transient asynchronous pacing, rapid cardiac pacing, the induction of ventricular fibrillation, heating of the tissue adjacent to the pacing or ICD system and especially cardiac tissue near the lead tip, early battery depletion, and outright device failure requiring replacement may occur during MRI of patients with pacemakers or ICDs (18,29–31). Multiple deaths have been documented to occur under poorly and incompletely characterized circumstances when CIED patients underwent MRI (32–34). These deaths may have occurred as a result of pacemaker inhibition, failure to capture or device failure (resulting in prolonged asystole) and or rapid cardiac pacing or asynchronous pacing (resulting in the initiation of ventricular tachycardia or fibrillation)." -- [Ссылки доступны только зарегистрированным пользователям ]

[Chevychelov]

Ну очень любопытная эта панель 8 по АГ

[Ссылки доступны только зарегистрированным пользователям ]
Evidence-Based Guideline for the Management of High Blood Pressure in Adults: Report From the Panel Members Appointed to the Eighth Joint National Committee (JNC 8)

1. Классификация и риски уже не нужны, в любом случае, не важны.
2. Целевое АД для лиц равно старше 60 лет меньше 150/90, меньше 60 лет - меньше 140/90, для СД и болезни почек старше 18 лет - меньше 140/90.
3. При АД больше целевого сразу медикаментозное лечение.
4. Титрование до 3 препаратов только 4 группами: иАПФ, БРА (вместе нельзя), тиазиды, БКК. Если нужен четвертый препарат - любой из ББ или альфа-блокаторов и других групп (ББ никак не выделяются)

[Yariko]

свеженькая инфо

Based on our findings, β blockers should not be used preferentially over other rate-control medications and not regarded as standard therapy to improve prognosis in patients with concomitant heart failure and atrial fibrillation.

Efficacy of β blockers in patients with heart failure plus atrial fibrillation: an individual-patient data meta-analysis

Background

Atrial fibrillation and heart failure often coexist, causing substantial cardiovascular morbidity and mortality. β blockers are indicated in patients with symptomatic heart failure with reduced ejection fraction; however, the efficacy of these drugs in patients with concomitant atrial fibrillation is uncertain. We therefore meta-analysed individual-patient data to assess the efficacy of β blockers in patients with heart failure and sinus rhythm compared with atrial fibrillation.


Methods

We extracted individual-patient data from ten randomised controlled trials of the comparison of β blockers versus placebo in heart failure. The presence of sinus rhythm or atrial fibrillation was ascertained from the baseline electrocardiograph. The primary outcome was all-cause mortality. Analysis was by intention to treat. Outcome data were meta-analysed with an adjusted Cox proportional hazards regression. The study is registered with Clinicaltrials.gov, number NCT0083244, and PROSPERO, number CRD42014010012.


Findings

18 254 patients were assessed, and of these 13 946 (76%) had sinus rhythm and 3066 (17%) had atrial fibrillation at baseline. Crude death rates over a mean follow-up of 1·5 years (SD 1·1) were 16% (2237 of 13 945) in patients with sinus rhythm and 21% (633 of 3064) in patients with atrial fibrillation. β-blocker therapy led to a significant reduction in all-cause mortality in patients with sinus rhythm (hazard ratio 0·73, 0·67—0·80; p<0·001), but not in patients with atrial fibrillation (0·97, 0·83—1·14; p=0·73), with a significant p value for interaction of baseline rhythm (p=0·002). The lack of efficacy for the primary outcome was noted in all subgroups of atrial fibrillation, including age, sex, left ventricular ejection fraction, New York Heart Association class, heart rate, and baseline medical therapy.


Interpretation

Based on our findings, β blockers should not be used preferentially over other rate-control medications and not regarded as standard therapy to improve prognosis in patients with concomitant heart failure and atrial fibrillation.

[Ссылки доступны только зарегистрированным пользователям ]

[angio]

Treatment with alirocumab (Sanofi/Regeneron Pharmaceuticals), an investigational proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor, resulted in significant reductions in LDL cholesterol in various groups of patients who received the drug, including individuals at high risk for cardiovascular events currently taking a maximally tolerated statin dose.

In one analysis of the ODYSSEY Long-Term Study , a study consisting of 2341 patients at high risk for cardiovascular events, investigators conducted a post hoc analysis to investigate the effect of alirocumab on major cardiovascular events, the same end point being tested in the major morbidity and mortality ODYSSEY OUTCOMES study. After 65 weeks of treatment, the results suggested alirocumab significantly reduced the risk of major events compared with those who received placebo and a maximally tolerated statin.

ODYSSEY COMBO II : Testing the efficacy and safety of alirocumab in 720 patients at high risk for cardiovascular events despite treatment with a maximally tolerated statin. Patients received a 75-mg injection of alirocumab every two weeks, and the dose was increased to 150 mg every two weeks if their LDL-cholesterol levels remained >70 mg/dL at week 8. Patients in the control arm received a maximally tolerated statin, ezetimibe 10 mg/day, and a placebo injection.

ODYSSEY FH I and I: In total, 735 heterozygous familial hypercholesterolemia (FH) patients treated with a maximally tolerated statin who were not at the recommended LDL-cholesterol goal of <70 mg/dL (history of cardiovascular disease) or <100 mg/dL (no history of cardiovascular disease) were randomized to alirocumab 75 mg every two weeks or to placebo. Like the COMBO study, the dose was increased to 150 mg every two weeks if the patient's LDL-cholesterol level remained above 70 mg/dL at week eight.

ODYSSEY Long-Term: Evaluated the safety and efficacy of alirocumab in 2341 patients with heterozygous FH or at high risk for cardiovascular events who were receiving a maximally tolerated dose of statin but who had an LDL-cholesterol level >70 mg/dL. Patients were randomized to alirocumab 150 mg every two weeks or to placebo. The primary efficacy end point was the reduction in LDL-cholesterol levels at 24 weeks, but the study will continue to evaluate patients beyond one year.

As noted, the long-term study also evaluated major cardiovascular events at 65 weeks. Using the same end point as that used in the alirocumab outcomes study, which was the time to first coronary heart disease death, nonfatal MI, fatal and nonfatal ischemic stroke, or unstable angina requiring hospitalization, there was a benefit to treatment with the PCSK9 inhibitor. The absolute event rate of major cardiovascular events was 1.4% in the alirocumab arm and 3.0% in the placebo arm, a difference that translated into a relative risk reduction of 54%.

Asked about repeating history with another version of ezetimibe, that being the approval of alirocumab, evolocumab, or bococizumab (Pfizer) based on surrogate end points without any idea if the drugs reduce hard clinical end points, Ballantyne said the two scenarios are very different. When ezetimibe was approved based on LDL lowering, an outcomes study wasn't even in the works (the IMPROVE-IT study will finally be presented this November at the American Heart Association meeting, 12 years after the drug was approved by the FDA). With the PCSK9 inhibitors, the sponsors have all initiated outcomes studies, and enrollment has already begun in these large morbidity and mortality trials, he said

ищите на Medscape: Huge Decreases in LDL Cholesterol With Alirocumab: ODYSSEY.

Интересно сколько это будет стоить лет хотя бы через десять (не в абсолютных цифрах, а в отношении к стоимости максимальной дозы статинов)????

[Korzun]

Наконец-то появился мощный негатив по сервьешному Ивабрадину:

[Ссылки доступны только зарегистрированным пользователям ]
The European Medicines Agency (EMA), following a review by the Pharmacovigilance Risk Assessment Committee (PRAC), is making new recommendations on the use ivabradine (Corlentor/Procoralan, Servier) for the treatment of patients with symptoms of angina or heart failure[1].

The review is based on "surprising" data that came to light from the Study Assessing the Morbidity-Mortality Benefits of the If Inhibitor Ivabradine in Patients with Coronary Artery Disease (SIGNIFY).

As reported by heartwire , a prespecified analysis showed ivabradine to be associated with an increase in the combined end point of death or nonfatal MI in a subgroup of more than 12 000 patients with symptomatic angina (Canadian Cardiovascular Society class 2–4), one of the approved indications for the drug in Europe.

SIGNIFY was published in the New England Journal of Medicine this past August and presented at the European Society of Cardiology 2014 Congress in Barcelona, Spain. The results showed that adding ivabradine to standard therapy had no effect, overall, on cardiovascular events in the placebo-controlled trial of more than 19 000 patients with stable coronary artery disease. Treatment with the drug did produce an average 10-beat-per-minute reduction in heart rate compared with placebo when measured after the trial's third month.

The EMA's PRAC review noted that patients in SIGNIFY were treated with as much as 20 mg of ivabradine daily (10 mg twice per day), a dose that is higher than the currently authorized maximum daily dose (7.5 mg twice a day). While the PRAC does not believe the higher dose fully explains the findings, "the committee reiterated that the starting dose for angina should not exceed 5 mg twice a day and that the maximum dose should not exceed 7.5 mg twice a day."

The PRAC reminds physicians that when ivabradine is prescribed for angina, "it should be used only to alleviate symptoms, as the available data do not indicate that the medicine provides benefits on outcomes such as reducing heart attack or cardiovascular death."

In its evaluation, thhe PRAC also concluded that patients treated with ivabradine are at an increased risk of developing atrial fibrillation compared with control-treated patients. Although the increased risk appears modest (4.86% vs 4.08%), the committee recommends that physicians monitor patients for the arrhythmia.

Finally, the committee notes that bradycardia risk is significantly elevated with ivabradine. Given the increased risk—in SIGNIFY, 17.9% developed bradycardia compared with 2.1% of the placebo-treated patients—the PRAC recommends physicians check baseline heart rate before starting treatment or when the dose is adjusted.

Ivabradine is approved in the European Union but is not available in the US.

Не назначал и не буду

[Dr.Vad]

Результаты DAPT:

Twelve or 30 Months of Dual Antiplatelet Therapy after Drug-Eluting Stents
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ред.коммент [Ссылки доступны только зарегистрированным пользователям ]

[angio]

[Ссылки доступны только зарегистрированным пользователям ]

[Dr.Vad]

Аспиринка перед сном у пациентов с ИБС не влияет на АД, но снижает утреннюю реактивность тромбоцитов:

Hypertension. 2015 Feb 17.
Time-Dependent Effects of Aspirin on Blood Pressure and Morning Platelet Reactivity: A Randomized Cross-Over Trial.
Bonten TN и соавт.
Aspirin is used for cardiovascular disease (CVD) prevention by millions of patients on a daily basis. Previous studies suggested that aspirin intake at bedtime reduces blood pressure compared with intake on awakening. This has never been studied in patients with CVD. Moreover, platelet reactivity and CVD incidence is highest during morning hours. Bedtime aspirin intake may attenuate morning platelet reactivity. This clinical trial examined the effect of bedtime aspirin intake compared with intake on awakening on 24-hour ambulatory blood pressure measurement and morning platelet reactivity in patients using aspirin for CVD prevention. In this randomized open-label crossover trial, 290 patients were randomized to take 100 mg aspirin on awakening or at bedtime during 2 periods of 3 months. At the end of each period, 24-hour blood pressure and morning platelet reactivity were measured. The primary analysis population comprised 263 (blood pressure) and 133 (platelet reactivity) patients. Aspirin intake at bedtime did not reduce blood pressure compared with intake on awakening (difference systolic/diastolic: -0.1 [95% confidence interval, -1.0, 0.9]/-0.6 [95% confidence interval, -1.2, 0.0] mm Hg). Platelet reactivity during morning hours was reduced with bedtime aspirin intake (difference: -22 aspirin reaction units [95% confidence interval, -35, -9]). The intake of low-dose aspirin at bedtime compared with intake on awakening did not reduce blood pressure of patients with CVD. However, bedtime aspirin reduced morning platelet reactivity.
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[Dr.Vad]

Наличие анемии повышает в полтора раза риск смертности и возникновения др. тромботических осложнений у пациентов с ФП на фоне назначения антикоагулянтов и в 2 раза риск больших кровотечений - данные из RE-LY:

[Ссылки доступны только зарегистрированным пользователям ]

[Yariko]

В Schein's common sense 'Prevention and management of Surgical complications' обнаружила забавную заметку
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[Dr.Vad]

Как празолы или Н2-блокеры и у кого предотвращают ЖКК на фоне приема дабигатрана:

Among the 5041 patients newly prescribed dabigatran, 124 (2.5%) developed GIB during follow-up (4.2/100 patient-years). The risk of GIB in this population increased among patients 75 y old or older (IRR, 2.47; 95% confidence interval [CI], 1.66-3.68), patients with a history of peptic ulcers or GIB (IRR, 2.31; 95% CI, 1.54-3.46), and patients who used aspirin (IRR, 1.52; 95% CI, 1.03-2.24). Concomitant use of GPAs was associated with a reduced risk of GIB (IRR, 0.52; 95% CI, 0.35-0.77). Subcategory analysis showed that use of proton-pump inhibitors (IRR, 0.53; 95% CI, 0.31-0.91) or histamine type-2 receptor antagonists (IRR, 0.61; 95% CI, 0.40-0.94) were associated with lower risk of GIB. Further analysis revealed that the risk reduction by GPAs was significant for only upper GIB (IRR, 0.29; 95% CI, 0.15-0.54) and only for patients with prior history of peptic ulcers or GIB (IRR, 0.14; 95% CI, 0.06-0.30).
---
Gastroenterology. 2015 May 7.
Prevention of Dabigatran-related Gastrointestinal Bleeding With Gastroprotective Agents: A Population-Based Study.
Chan EW, и соавт.
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