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Treatment options in adult congenital heart disease


Authors: Budts, Werner (Leuven, Belgium)
The session on treatment options in adult congenital heart disease, organized by the Working Group on Grown-up Congenital Heart Disease, focussed on clinically relevant questions.

SA Qureshi (London, GB) discussed “when are you too old for atrial septal defect closure”. Data in the literature show that atrial septal defect closure at older age (above 60 years) improves symptoms, increases quality of live, induces positive remodelling of the right ventricle and decreases pulmonary arterial pressures. Because of these findings, atrial septal defect closure might indeed be indicated at older age. However, the effect on the development of atrial fibrillation after closure is unclear and closure is preferred to be percutaneous where applicable.

P Trigo Trindade (Zurich, CH), the new chairman of the Working Group, gave an excellent overview about the treatment of Ebstein anomaly: atrial septal defect closure, tricuspid valvuloplasty or conservative? Ebstein anomaly is not a benign disease and needs careful follow-up. Natural history is not uneventful (progressive valve dysfunction, atrial arrhythmias), so that not infrequently, interventions are needed. Depending on the right ventricular function, signs of right heart failure, cyanosis through an interatrial communication, the type of structural and/or electrophysiological intervention are chosen. In case of a right to left shunt and good tricuspid valve function, only closure of the interatrial defect might be indicated; when severe valvular dysfunction is present, surgical valve repair or replacement is needed. In this way, P Trigo Trindade referred to the recently presented and published guidelines of Grown-up Congenital Heart Diseases, where the choice of therapeutic approach is more elucidated.

PJ Holm (Lund, SE) focussed on medical therapy in adult congenital heart disease. A main problem in several patients is the function of a systemic right ventricle. A substantial number of congenital heart disease patients die because of heart failure (26%). To prevent heart failure, treatment to reduce afterload, diuretics and betablockers are frequently started. Although symptomatic patients seem to improve with this therapy, no large randomized trials are conducted to answer the question of whether they would influence outcome. The effect of ACE-inhibitors or sartans on the systemic right ventricular function remains unclear, and in some patients betablockers are even contra-indicated. A case of a patient with a systemic right ventricle and successful resynchronisation therapy on top of medical treatment was presented. Unfortunately, several patients still die suddenly (19%), even when in NYHA class I, so that the issue rose for arrhythmic prophylaxis.

The last speaker, K Dimopoulos (London, GB), highlighted the importance of iron repletion, especially in patients with secondary erythrocytosis. Low iron reserves might lead to the same symptoms as those of hyperviscocity, are related to the occurrence of stroke, and by repletion, patients feel better, have better exercise capacity and increased functionality. However, the debate is still going on as to what the minimal and/or maximal iron reserves have to be, and what the dose of substitution should be. He stressed that phlebotomies in secondary erythrocytosis need to be discouraged in order to avoid the risk of iron depletion. He finally mentioned that low iron reserves might enhance hypoxic vasoconstrictor responses.

I appreciated this as an excellent session with a lot of attendees. The speakers focussed their talks on clinically relevant issues, and that was highly appreciated by the audience. Take home messages were clear, and the new guidelines will help to implement all this in daily practice. I would encourage the working group to continue with sessions such as this.

_________________
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The ebb and flow of atrial fibrillation


Authors: Casadei, Barbara (Oxford, United Kingdom)


This symposium reviewed a number of emerging mechanisms that may promote the new-onset or persistence of atrial fibrillation (AF).

Intriguing findings on cellular “structural” remodelling of left atrial myocytes in a sheep model of heart failure were presented by Dr Kathryn Dibb. Left ventricular failure and mitral valve regurgitation were associated with a loss of T-tubules and profound alterations in calcium handling in atrial myocytes, brought about by dyssynchronous intracellular EC coupling. The functional consequences of these cellular structural changes and their relevance to the AF substrate in the presence of heart failure are the focus of ongoing investigations.

It is increasingly difficult to imagine how we managed to make sense of myocardial signalling, growth and EC coupling before we knew of the importance of Calmodulin kinase and, more specifically, of CamKId. Over the last few years CamKId -signalling has been implicated in the dysregulation of EC coupling in experimental and human heart failure and AF. In a series of elegant experiments, Dr Dobrev illustrated the role of CamKId in the regulation of phospholamban and RyR phosphorylation in human atrial myocytes from patients with AF and in genetically modified mouse models. Availability of small molecules able to modulate CamKId activity will soon test the potential of this signalling pathway as a therapeutic target.

As illustrated by the new ESC guidelines on the management of AF, restoring sinus rhythm in patients with AF and atrial structural remodelling remains a significant clinical problem. Dr Schotten presented new and exciting data on the qualitative and quantitative differences in atrial fibrosis induced by AV block or long-term AF and their impact on AF organisation and reversibility. Finally, Dr Hatem illustrated a number of new mechanisms that may underlie ion currents remodelling in AF, including modulation of transcription, trafficking and post-translational modifications of ion channels.

Taken together these talks have highlighted a number of promising new targets in the “upstream” treatment of AF

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European Forum on Cardiovascular Disease Prevention: from implementation to evaluation


Authors: Ryden, Lars (Stockholm, Sweden)


During the session held by the European forum held on CVD, a variety of issues were reviewed from the outline of Guidelines via their implementation, adherence to set targets, the economy of prevention and its political impact.

Prof. Ian Graham from Ireland started by discussing what we may learn from different European projects, also discussing tools and activities initiated to improve tools. He underlined that the European stage (EU) is of vital importance but there is no legal framework created. If available, it would much help implementation not only at a European, but also a national level. The framework for such legislation is available, for instance, the European Heart Health Charter and the joint European Prevention Guidelines. There are a number of important measures to be taken, not least lifestyle oriented factors, that indeed are poorly practiced. The European Association for CVD prevention and rehabilitation has created a special group working with these questions and surveys in a simple and rapid form (E-SURF) and a more comprehensive form is under way in Euroaspire 4.

In the next presentation, H. Mc Gee from Dublin reported on an evaluation of implementation of the fourth joint Task Force Guidelines for CVD prevention. A study is performed in 13 countries based on interviews with representatives of the cardiovascular profession; governmental and non-governmental organisations. Preliminary results show that different countries are working in different ways and that some have comprehensive networks created on the topic of implementation while others still have a long way to go. A detailed presentation will be ready for the European prevent summit at the European Heart House to be held on November 30, 2010.

In the next presentation, Lieven Annemanns from Gent, BE, presented a model for evaluating the cost-effectiveness of cardiovascular prevention based on EuroAspire III data and risk prediction registries across Europe. This work will fill a big gap in the knowledge on the economical impact of prevention, highly needed. The model takes into account what would happen if set blood pressure, blood lipid etc targets are reached as regards savings of QALYs. Presently, 1 QALY is valued at 30,000 Euro and by means of such information it will be possible to relate the cost of improved prevention to saved QALYs in a way which is predicted, showing that prevention truly makes sense. Once more, detailed results will be available at the European Prevention Summit, November 30 at the European Heart House.

Simon Capewell from Liverpool, UK, reviewed various signs of how EuroHeart, an EU supported shared project between the European Heart Network ande the ESC have impacted politicians view of the need for further and improved preventive measures in Europe. Several of the working packages have been labelled as European flagships in the sector of prevention and among them, he mentioned women and CHD, and the European Heart Health Charter. The NICE guidance has just been released in the UK and is well worth reading for those interested; It has been estimated that in the UK alone, one may save up to 10 billion UK pounds by reducing salt intake, increasing fruit and vegetable consumption and eliminating saturated fat. In principle, 1.5 million life years may be saved in the UK by successful implementation of healthy choices before those who are increasing the risk of CV disease. The NICE document is available on the web.

Finally, Joep Perk summarised by talking about his view on whether we have succeeded in influencing clinical care in the sector of CV prevention. His short and pessimistic view was “no – not really”. He did however expand and said that there is a long way to go and one of the problems is that we have underestimated the need for, or not been able to establish alliances between nurses, GPs, cardiologists, health workers in society and others involved. If we can do that in a better way, we will probably succeed within a reasonable future.

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Cardiac imaging for atrial fibrillation management

Authors: Caso, Pio (Naples, Italy)


Atrial fibrillation (AF) is the most common cardiac rhythm disorder in clinical practice. The estimated prevalence of AF is 0.4–1% in the general population, increasing with age to 8% in patients older than 80 years. The recognized risk factors for developing AF include age, hypertension, structural heart disease, diabetes mellitus and hyperthyroidism. How we can identify the characteristics of the atrium at risk of atrial fibrillation? Atrial dilatation, left atrial volume >24 ml/m², atrial deformation (strain about 20-25 %) can define the atrial risk, says Dr Leung from Liverpoool.

Dr Sitges from Barcelona presented the use of imaging in selection of the right therapeutic strategy. Whether you choose heart rhythm control or cardioversion depends on information obtained by echocardiography and MRI. A very large left atrium, low appendage velocity, and depression of deformation index can induce heart control. Otherwise good deformation index, volumes less than 32 ml/m² can justify cardioversion.

The imaging modalities can also guide antithrombotic therapy, as Dr. Paolo Colonna from Bari, Italy explained, in patients with atrial fibrillation that need cardioversion evaluating dimension and function of the atrium. The presentation by Dr. Colonna showed the utility of cardiac imaging to guide antithrombotic therapy in atrial fibrillation. At first, transoesophageal echocardiography is useful to shorten the pre-cardioversion time, as recently confirmed in the 2010 atrial fibrillation guidelines from the ESC. Moreover, cardiac imaging can be used to define the selection of patients who need anticoagulation. The presence on transoesophageal echocardiography of left atrial thrombus, complex aortic plaques, spontaneous echo-contrast and low atrial appendage velocities are independent predictors of stroke and thrombo-emboli. After cardioversion, anticoagulation is necessary for four weeks for stunned phenomena. We can reduce this time to one week if a second TEE is performed and good appendage velocities are observed.

Which imaging technique before, during and after atrial fibrillation ablation? Echocardiography is the better technique for selection and evaluation of patients during and after ablation. We can use transthoracic and transesopahgeal echo before, and intracardiac echo (ICE) during ablation to localize the ablation area and for complications, while transthoracic echo can be used after ablation to show recovery of atrial wall with new technologies such as strain and strain rate. Furthermore, MRI and CT angio are able to help in selection of patients, and after ablation for better evaluation of the pulmonary vein.

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CARE HF LTFU: Cardiac Resynchronisation in Heart Failure: Long-Term Follow-up

List of Authors: John GF Cleland, Nick Freemantle, Erland Erdmann, Daniel Gras, Lukas Kappenberger, Luigi Tavazzi, Jean-Claude Daubert

Abstract:

Introduction: The CARE-HF trial, first presented in 2005, established that cardiac resynchronisation therapy (CRT) exerted a striking reduction in mortality in patients with heart failure who had features of dyssynchrony. There are very few long-term followup data in patients with CRT. This is a report on the long-term outcome of patients in the trial.

Methods: Enrolment began at the end of 2000 and was complete by March 2003. After reporting the main study results in 2005, investigators were asked to inform patients of the results and implant a CRT device if still appropriate and subsequently asked to consent patients for long-term follow-up until 30th September 2009.

Results: Of 813 patients originally enrolled, 343 (42%) died prior to re-consent, 111 patients (14%) were not or could not be contacted, 50 (6%) were alive but declined to participate and 309 (38%) consented to long-term follow-up. Of patients originally assigned to control, most survivors had received CRT by the time of re-consent. From the time of randomization, 222 patients originally assigned to pharmacological therapy and 192 originally assigned to CRT were known to have died. The hazard ratio for mortality in patients originally assigned to CRT compared to those originally assigned to the control group was 0.768 (95% CI 0.633 to 0.931; P = 0.007). No subgroup interactions were observed.

Conclusion: The effect of CRT on mortality observed in the randomised phase of CARE-HF persisted during long-term follow-up. Implantation of CRT devices after study completion may have prevented further divergence of the survival curves. The benefit of CRT was observed in patients above and below the median age of 66 years. In patients aged <66 years with moderate to severe heart failure and evidence of cardiac dyssynchrony, CRT would be expected to increase median survival from about 5 years to >8 years. Survival might have been even greater in this group had CRT-defbrillators, rather than CRT-only devices, been used.


Discussant Breithardt, Ole A (Germany)

Report:
Introduction:
Several randomized controlled clinical trials have well established the important role of cardiac resynchronisation therapy (CRT) for selected symptomatic patients with advanced systolic heart failure with cardiac dyssynchrony identified by the presence of a widened QRS complex, typically a left bundle branch block. However, the available information of the key clinical trials is limited to a follow-up duration between one to two years. Thus, it was so far unclear whether the clinical benefit of CRT would persist for a longer period. Small single centre studies have analysed the long-term clinical outcome and patient survival for longer periods, but without a control group for comparison.

The CARE-HF study is unique among the major CRT trials as the patients in the active treatment arm received only CRT pacemakers (CRT-P) without defibrillator backup. Furthermore, the CARE-HF trial reported results from a comparatively long average follow-up of 29 months in the main trial and 37 months in the “extension trial”. After termination of the main study, the investigators initiated the CARE-HF Long-Term Follow-Up study (CARE-HF LTFU) and obtained further data on patient survival and device status with an even longer follow-up duration between 6.5 to 9 years. These results were presented by J.G.F. Cleland during the Clinical Trial Update Session.

It is important to note that CARE-HF LTFU is not a true randomized trial, but a follow-up registry of patients previously implanted within a randomized trial. After the main study demonstrated a clear survival benefit for the active treatment group (with a CRT-P device), more than 90% of patients from the initially medically treated control group crossed over and had received a CRT device at the time of re-consent for CARE-HF LTFU. Thus, the presented study results do not show the complete survival benefit of CRT in such a typical heart failure population, but rather the effect of delayed CRT implantation. This might be appreciated in the presented survival curves which clearly diverge early during the course of the randomized main study – showing the clear survival benefit for patients with a CRT device. Between 3-6 years, after termination of the main study, most control patients received a CRT device and the curves run parallel. Finally, the survival curves seem to converge again slightly towards the end of the LTFU, possible showing the beneficial effects of delayed CRT implantation. There is no information about the percentage of implanted CRT defibrillators (CRT-D) in the original control group and it can only be speculated that a significant proportion of control patients received a CRT-D device, which might provide some additional survival benefit.

Conclusion:
A clear conclusion from CARE-HF LTFU is that delayed CRT implantation is associated with a persistent reduction in overall survival. Based on this information, delaying CRT implantation in eligible patients - based on the inclusion criteria of the CARE-HF main study - can not be justified. The median survival of more than 7 years for patients with advanced heart failure, dyssynchrony and an age of less than 66 years treated with a CRT-P device without defibrillator backup is remarkable.

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REALISE-AF registry: an international, observational, cross-sectional survey describing characteristics, cardiovascular risk, and management of patients with atrial fibrillation


List of Authors:
STEG, Philippe Gabriel; ALAM, S; CHIANG, CE; GAMRA, Habib; GOETHALS, M; INOUE, H; LEWALTER, Thorsten; MURIN, Jan; O'Neill, J; PONIKOWSKI, Piotr

Abstract:
Purpose:
The epidemiology and management of atrial fibrillation (AF) vary according to geography, prevalence and type of comorbidities, physician specialties, and types of AF. Most of the data available pertain to North America and Western Europe.

Methods:
The REALISE-AF registry is an international cross sectional registry of AF: Approximately 10,000 patients with history of AF (treated or not and whatever the rhythm at inclusion) with at least one AF episode documented by standard ECG or by ECG-Holter monitoring in the last 12 months, or documented current AF, are being recruited from 859 sites in 26 countries on 4 continents. Participating physicians were randomly selected among a global list of office-based or hospital-based cardiologists and internists, on the basis of epidemiologic data regarding local practice. Patient information is collected using a centralized case report form and includes baseline characteristics, symptoms, prior tests, ECG data, medical history and risk factors, medications, history and characteristics of AF, management of AF, in term of strategy chosen (rate vs. rhythm control) , antiarrhythmic drugs,, and/or rate control agents chosen, use of antithrombotics (in relation to CHADS2 score) and consistency with international guidelines. In addition, the registry will assess health-related quality of life (QoL) (using the validated EQ-5D tool). Physician information at each site is also collected. Primary analyses include frequency of AF control (ie achieving either sinus rhythm or resting HR <80 bpm) and description of cardiovascular (CV) risk. Secondary analyses include relationship between AF control and cardiovascular risk factors, as well as assessment of other AF-related CV endpoints, and health-related QoL.

Results:
Data collection ends in March 2010 and results will be available for presentation in late August. This presentation will be the first disclosure of the results worldwide.

Conclusion:
RealiseAF is the 1st global, observational, cross-sectional registry to provide information on all AF types, associated CV risk and subsequent therapeutic decisions.

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KYOTO HEART: Effect of valsartan on cardiovascular outcomes in patients with high-risk hypertension: updated analyses of the KYOTO HEART Study

List of Authors:
Hiroaki Matsubara, Takahisa Sawada, Hiroyuki Yamada, Shinzo Kimura, Jun Shiraishi

Abstract:
Purpose:
The KYOTO HEART Study showed an additional beyond BP lowering benefit of Valsartan on cardio- and cerebrovascular (CV) events in high-risk hypertensive patients (Eur Heart J 2009;30:2461). We here report the ancillary analysis regarding primary & secondary prevention, combination therapy with calcium channel blockers (CCB), and CV event prevention.

Methods and results:
The KYOTO HEART Study is a multicenter, two-arm parallel treatment group comparison study with response-dependent dose titration scheme. High-risk Japanese patients with uncontrolled hypertension (n=3031) were randomized to receive either additional Valsartan or conventional non-ARB therapies. The primary endpoint was a composite of defined CV events such as stroke, myocardial infarction, heart failure, and angina pectoris (AP). Updated analyses were as follows; 1) 915 had previous CV event history and 2116 without CV events. Compared with non-ARB, Valsartan was effective for both primary prevention (3.0% vs 6.7%, HR 0.44, 95%CI:0.29-0.68) in which stroke is significantly inhibited, and secondary prevention (11.5% vs 18.1%, HR 0.63, 95%CI:0.44-0.89) in which AP is significantly inhibited. 2) primary endpoint events in Valsartan plus CCB group (n=773), Valsartan plus non-CCB (744), non-ARB plus CCB (1034), non-ARB plus non-CCB (480) were 5.0%, 6.0%, 9.8% and 11.0%, respectively. Valsartan plus CCB combination showed lower primary events than non-ARB plus CCB (p=0.0003, HR 0.50, 95%CI:0.35-0.73), and Valsartan plus non-CCB vs. non-ARB plus non-CCB (p=0.002, HR 0.55, 95%CI:0.37-0.80). The patient background and BP during follow-up showed no significant differences. 3) AP events were separated into unstable AP and effort AP using clinical information and coronary angiographic findings. Valsartan was significantly effective for effort AP prevention (1.1% vs 2.3%, p=0.01), but was not effective for unstable AP (0.20% vs 0.59%, p=0.10). 4) stroke prevention was mainly due to inhibition in cerebral infarction (18 vs 36 events) but not bleeding (2 vs 5).

Conclusions:
Valsartan is effective for primary stroke and secondary AP prevention in high-risk hypertensive patients, and Valsartan plus CCB combination therapy provides a more efficient prevention against CV events. Beneficial effects of Valsartan on cardiovascular outcomes were due to prevention of cerebral infarction and effort AP.

Discussant Laurent, Stephane (France)


Report:
In these ancillary analyses of the KYOTO HEART Study, presented at the ESC Congress 2010, Matsubara H. et coll. investigated (a) the effects of valsartan on primary and secondary prevention, (b) the effects of combination therapy with calcium channel blockers (CCB), and (c) performed additional analyses on angina and stroke events.

In the main study (Sawada T. et al. Eur Heart J 2009), they previously showed that a valsartan add-on treatment was more effective than a non-ARB regimen for preventing CV events in uncontrolled hypertensive patients with high CV risk. The new finding is that these results are confirmed both for secondary prevention (i.e. in patients with previous CV events, HR=0.63 [0.44-0.89], p=0.0088) and primary prevention (HR=0.44 [0.29-0.68], p=0.0002). Here, the primary end-point is the same as in the main study, i.e. a composite of CV events such as stroke/TIA, MI, worsening HF, angina, dissecting aortic aneurysm, lower limb arterial obstruction, transition to dialysis or doubling of serum creatinin levels. In both secondary and primary prevention, the benefit can be attributed to valsartan, because both “valsartan add-on” and “non-ARB” arms displayed a similar reduction in brachial BP, a similar level of CV risk at baseline, and similar baseline medications.
The results concerning primary prevention are particularly important not only for the Japanese/Asian population, but also because in most countries, 1/2 to 2/3 of hypertensives (i.e. no previous CV disease) are at high CV risk; and 2/3 of treated hypertensive patients are currently not controlled. Thus, in those patients, adding valsartan to previous treatment is more effective than a non-ARB regimen for preventing CV events.

This ancillary analysis benefits from several strengths: a prespecified analysis, a large number of patients in both primary (n=2116) and secondary (n=915) prevention groups; a similar number of patients in both arms (“valsartan add-on” and “non-ARB”) for primary (1065/1051) and secondary (452/463) prevention; and an incidence of primary end-points close to that expected (10.2% vs 12% in 3 yrs FU), and high enough both in primary (n=102 in 3 yrs FU) and secondary prevention groups (n=146) to correctly size the statistical power.
However, a limitation concerns the secondary prevention group: ACE inhibitors were given to 29% of patients at baseline (CHD, CHF), and were continued during FU. Thus, about one third of ARB patients had an AR+ACEI combination, which may have increased the benefit of valsartan. Some remaining issues are: (a) whether the benefit (i.e. prevention of CV events) can be attributed to valsartan, or the ARB pharmacological class, or the RAS blockade (ACE inhibitors were not allowed during the trial); (b) whether these results can be extrapolated to Western populations; and (c) whether valsartan may exert its protective effect, at least in part, through a higher reduction in central BP, for a given fall in brachial BP.

An additional ancillary analysis concerned the combination of valsartan with a CCB. The authors’ conclusion that “combination therapy with valsartan+CCB showed lower primary events than non-ARB+CCB” should not be taken in a restrictive way, since the benefit of valsartan over non-ARB has also been shown in patients receiving no CCB. It would be more balanced to state that valsartan add-on treatment lowered the incidence of CV events whether patients received in addition CCB or not.

Finally, the authors’ conclusions that “valsartan was significantly effective for prevention of effort angina but not unstable angina” should be taken with caution since only a small number of unstable angina occurred, which may have undersized the statistical power. Thus, it would be more balanced to state that angina prevention by valsartan was rather due to inhibition of effort angina than unstable angina.

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JIKEI HEART: Effect of valsartan in Japanese subjects with coronary heart disease: Sub-analysis of results of JIKEI HEART Study

List of Authors: Mitsuyuki Shimizu, Hiroshi Yoshida, Katsunori Ikewaki, Ikuo Taniguchi, Michihiro Yoshimura, Björn Dahlöf, Seibu Mochizuki, for Jikei Heart Study group

Abstract:
Aim:
The risk of cardiac events in hypertensive patients with coronary artery disease (CAD) was higher than in those without CAD. We here report the result of a sub-analysis of a large-scale trial [JIKEI HEART Study (JHS)] which demonstrated that the addition of the angiotensin II receptor blocker (ARB) valsartan to standard cardiovascular treatments significantly reduced the primary composite endpoint of cardiovascular complications as compared with conventional treatments without ARB in Japanese patients.

Methods:
One thousand thirty six CAD patients in the JHS were subjected to this study. We assessed the following endpoints such as myocardial infarction, angina pectoris and congestive heart failure between valsartan group and non-ARB group. Electrocardiography and echocardiography were performed at baseline, 1, 2 and 3 years after randomization.

Results:
The addition of the ARB valsartan to standard cardiovascular therapy reduced angina pectoris (HR: 0.28: 0.12-0.53: p<0.00008) and heart failure (HR: 0.32: 0.15-0.86: p<0.02402) as compared with non-ARB treatment in patients with CAD. However, there was no significant difference in the incidence of myocardial infarction. The blood pressures and heart rate were not different between these two treatment groups throughout the trial. The significant reduction in left ventricular mass index (LVMI), evaluated by echocardiography, was observed in the valsartan group (p<0.001)

Conclusion:
The present study provided convincing evidence that ARB valsartan significantly reduced the incidence of angina pectoris and congestive heart failure particularly in the high risk patients with CAD which may be attributed in part to the improvements of myocardial remodeling.

Discussant Maggioni, Aldo Pietro (Italy)

Report:
The original trial
The JIKEI trial had the aim to investigate the effect of control of blood pressure (to a target of less than 130/80 mm Hg) with an added angiotensin receptor blocker, valsartan, compared with conventional treatment in a large Japanese population (3081 patients), aged 20–79 years, (mean 65 [SD 10] years), who were undergoing conventional treatment for hypertension, coronary heart disease, heart failure, or a combination of these disorders. The hypothesis was that treatment with valsartan would yield additional protective benefits, compared with conventional treatment, beyond those attributable to control of blood pressure. The trial concluded that the addition of valsartan to conventional treatment prevented more cardiovascular events than supplementary conventional treatment and that these benefits could not be entirely explained by a difference in blood pressure control.

The specific subanalysis
The data presented today are a post-hoc subgroup analysis of the JIKEI randomized clinical trial.
Rationale: The risk of cardiac events in hypertensive patients with CAD is higher than in those without CAD.
Aim: This subanalysis of the database of the JIKEI trial has the aim to demonstrate that valsartan can decrease the occurrence of major CV events, with respect to standard treatment, in the subgroup of patients with a story of CAD in a greater extent than in patients without CAD.
Main results: Valsartan significantly reduced the incidence of the primary end-point in the high risk patients with CAD which may be attributed in part to the improvements of myocardial remodeling. The primary endpoint was a composite of CV mortality and morbidity. The components of the endpoint included the following

hospital admissions for stroke or TIA
myocardial infarction
admission for congestive heart failure
admission because of angina pectoris
dissecting aneurysm of the aorta
doubling of serum creatinine; or transition to dialysis
The first of these events to arise in any specific patient was noted as the primary event: the reduction of this primary end-point in patients with CAD was quantifiable in more than 50%.
Some strenghts

Randomized trial conducted in Japan
More than 3,000 patients, 1,036 of whom with a documented CAD, object of this subanalysis
Low mean dose of valsartan (76 mg daily) but in the range for Japanise people (40-80 mg daily)
Electrocardiography and echocardiography performed in all patients at baseline,1 and 3 years after randomization
Relevant weaknesses
Prospective randomised open-blinded-label endpoint (PROBE) design with a long list of hard and soft end-points
No effects on all hard end-points (stroke, AMI, death)
Favorable effect just on softer end-points (hospitalization for angina or HF)
Post-hoc subgroup analysis
No p-value for interaction available

Conclusions
The JIKEI investigators are to be congratulated for this trial conducted in more than 3000 Japanise patients, 1036 of whon with a documented story of CAD, However, the data presented here cannot fully support the conclusions of the authors. For this reason, the results of this post-hoc subgroup analysis cannot be extrapolated to general practice.

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PACE: Pacing to Avoid Cardiac Enlargement (PACE) study

List of Authors:


Cheuk-Man Yu, MD, FRCP; Joseph Yat-Sun Chan, FHKAM(Medicine); Fang Fang, PhD; Qing Zhang, MM, PhD; Omar Razali, MD; Gabriel Wai-Kwok Yip, MD, FACC; Hussin Azlan, MD; Hamish Chi-Kin Chan, FRCP; Jeffrey Wing-Hong Fung, MD, FRCP

Abstract:
Background: The recently published Pacing to Avoid Cardiac Enlargement (PACE) study is a prospective, double-blinded, randomized, multicenter study that has confirmed the superiority of biventricular (BiV) pacing to right ventricular apical (RVA) pacing in prevention of left ventricular (LV) remodeling at 12 months follow up, in patients with bradycardia and preserved LV systolic function [ejection fraction (EF) ≥45%]. However, it is unclear whether this is related to pacing-induced systolic dyssynchrony. We hypothesized that patients who developed dyssynchrony at early stage is a major determinant of medium-term remodeling and deterioration of LV systolic function.

Methods: In the whole PACE study population (n=177) which included 89 patients randomized to BiV pacing and 88 to RVA pacing, serial echocardiography was performed at baseline, 1 month and 12 months. Systolic dyssynchrony was measured by tissue Doppler imaging using the LV 6-basal, 6-mid segmental model (i.e., Ts-SD >33ms) at 1-month follow up. Significant deterioration of LV systolic function was defined as reduction of EF ≥5% at 12 months.

Result: At 1 month, systolic dyssynchrony was present in 52% (n=46) of patients in RVA pacing group and 15% (n=13) in the BiV pacing group (2=28.25, p<0.001). At 12 months, increase in LV volume and decrease in EF was only observed in patients who developed systolic dyssynchrony at 1 month (Table). Reduction of EF ≥5% occurred in 67% (n=39) of patients who had dyssynchrony at 1 month, but only in 18% (n=21) who did not (χ2=40.83, p<0.001); and is more prevalent in the RVA than BiV pacing group (50% vs. 20%, χ2=17.71, p<0.001). By multivariate analysis, both systolic dyssynchrony at 1 month [odds ratios (OR): 7.081, 95% CI: 3.164-15.848, p<0.001) and RVA pacing mode (OR: 2.373, 95% CI: 1.070-5.264, p=0.033) were the two independent predictors for reduction of EF at 12 months. Furthermore, RVA pacing mode had incremental predictive value on top of pacing-induced systolic dyssynchrony at 1 month (χ2=4.324, p=0.037).

Conclusion: The PACE study shows that in patients received RVA pacing, medium-term LV remodeling and deterioration of EF occurred in those who developed early systolic dyssynchrony. These adverse consequences could be prevented effectively by BiV pacing.


Discussant Abraham, William (United States of America)

Report:
This pre-specified analysis evaluated the potential mechanism of deterioration in left ventricular ejection fraction (LVEF) and increases in left ventricular volumes seen in response to right ventricular versus biventricular pacing in the PACE study. The main results of this study have been published (Yu CM et al., N Engl J Med 2009; 361:2123-2134). In 177 patients with a bradycardia pacing indication and normal LV systolic function randomized to receive right ventricular apical pacing or biventricular pacing, LV ejection fraction was significantly lower in the right ventricular pacing group than in the biventricular pacing group (54.8±9.1% vs. 62.2±7.0%, P<0.001) and LV end-systolic volume was significantly higher in the right ventricular pacing group than in the biventricular pacing group (35.7±16.3 ml vs. 27.6±10.4 ml, P<0.001), following 12 months of follow-up.
Clinical outcomes were not different between the two groups; however, the study was not powered to detect such differences. The findings suggest that conventional right ventricular apical pacing results in adverse LV remodeling and that biventricular pacing prevents these deleterious effects. The implication is that perhaps all patients with a bradypacing indication and normal LV systolic function should receive biventricular rather than right ventricular apical pacing.

The present PACE analysis was undertaken to explore the mechanism of pathological remodeling associated with pacing. Specifically, the investigators set out to determine whether pacing-induced systolic dysynchrony was the major determinant of deterioration of LV ejection fraction and increases in LV volumes. Systolic dysynchrony at one month (Dysynchrony Group) occurred in 52% of patients with right ventricular apical pacing, but only 15% with biventricular pacing (p<0 0.001).
The Dysynchrony Group had significantly lower LV ejection fraction with an absolute difference of 7.1% (p<0.001). LV end-systolic volume increased significantly in the Dysynchrony Group with a relative difference of 30.7% (p<0.001). Reduction of ejection fraction ≥5% occurred in 67% of patients in the Dysynchrony Group, but only in 18% in the No Dysynchrony Group (p<0 0.001). By univariate and multivariate analyses, right ventricular pacing mode was only weakly predictive of the fall in LVEF, while dysynchrony at 1 month was most strongly predictive (odds ratio [95% confidence interval] 7.081 [3.164 3.164-15.848], <0.001). No clinical characteristic at baseline was predictive of the decline in LVEF.

The results of this analysis speak to the mechanism of pathological remodeling with pacing; specifically, these results support the notion that pacing-induced dysynchrony causes the pathological LV remodeling seen. However, the practical application of these observations is unclear, since there was no clear baseline predictor of the decline in LVEF or the development of mechanical dyssynchrony that could be determined prior to device implantation and pacing. Moreover, only half of the right ventricular apical pacing patients demonstrated dysynchrony at 1 month, the strongest predictor of LV ejection fraction change, and 15% of the biventricular pacing group developed such dysynchrony.
This leaves us with a clinical dilemma: Should all patients with a bradypacing indication and normal LV systolic function receive a biventricular pacing device or should they receive a right ventricular pacing device and be upgraded later if dysynchrony is demonstrated at 1 month or later when the LVEF falls? The former approach may result in half of these patients receiving biventricular pacing unnecessarily. The latter approach potentially subjects half of the patients to a second implant procedure 1 month following the first.

In the future, the clinical decision will be guided by the results of large randomized controlled outcomes trials comparing right ventricular versus biventricular pacing, particularly by the BIOPACE and BLOCK-HF studies.
The first of these is evaluating right ventricular versus biventricular pacing in 1,800 patients enrolled regardless of ejection fraction. Many enrolled patients will likely be similar to those studied by Yu and colleagues, i.e. have normal LV systolic function.
The second will randomize approximately 1,600 patients with baseline LVEF less than or equal to 50% to right ventricular versus biventricular pacing. Taken together, these trials should inform clinical practice and expand upon Yu’s fine work.

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Unresolved issues in the surgical treatment of chronic heart failure


Authors: Sousa Uva, Miguel (Lisbon, Portugal)
An extremely interesting session gathered top experts in the field of surgical therapies for heart failure.

Mitral regurgitation (MR) was addressed by O Alfieri from Milan, a worldwide recognized expert in valvular heart repair. MR has an adverse impact on survival but the question that arises is which patients benefit from surgical repair. There are conflicting data on the advantage of mitral valve repair over optimal medical treatment in patients with advanced heart failure and poor left ventricular function and therefore patient selection is critical. Definite contraindications to mitral valve surgery are right ventricular dysfunction, absence of contractile reserve and heavy co-morbidities.

Although a survival benefit was observed in the more recent era with the use of strictly undersized rigid complete mitral rings, recurrent mitral regurgitation and absence of reverse remodeling is observed in patients with end systolic diameter > 51mm and those with increased duration of heart failure. In these patients, the incidence of residual or recurrent MR is up to 30% and is related to decreased survival.

Although undersized annuloplasty with new types of rings may be effective, mitral valve replacement with preservation of the subvalvular apparatus is indicated in case of complex multiple jets, absence of annular dilatation, severe tethering (tented area>4cm²), posterior leaflet-annular plane>45 degrees and advanced LV remodeling. Other procedures have been used in small patient series such as papillary muscle repositioning, leaflet extension, section of secondary chordae and sling around the papillary muscles. Finally, resynchronization, atrial fibrillation ablation and correction of associated tricuspid insufficiency need to be considered.

The benefit in survival of an external myocardial constraint (Cor Cap TM) placed around the left ventricle remains to be demonstrated, although it has been shown to effectively decrease ventricular volumes and improve functional capacity(R Bonifazi, Bari).

What about surgical ventricular remodeling, an operation developed by V. Dor and evaluated in the STICH trial ? Timothy Gardner (Newark, USA) reviewed the methodology and results of this large randomized trial (1000 patients) comparing CABG alone vs CABG+ventricular remodeling (SVR) that has shown no survival benefit of associating a ventricular reduction and myocardial revascularisation in patients with anterior LV akinesia and reduced EF. A sub-analysis of this study tried to find out if there was a benefit in patients with larger LV volumes, but found no difference in mortality. Gardner stressed the various flaws of this study (LV volume criteria for inclusion not always met, LV volumes inadequately measured, viability not assessed, only 50% of patients in NYHA III/IV, more than half of SVR patients did not achieve adequate volume reduction) and concluded that it may be premature to consider that SVR has no value. However the only patients that could benefit from a SVR added to CABG are those with large hearts, anterior wall akinesia without viability.

Regarding ventricular assist devices (VAD), we learned from M Stueber (Hannover, Germany) that reduction in the size and changes in the technology have occurred in recent years with non pulsatile devices having proven clear superiority in terms of survival compared with pulsatile devices. Based on improved survival and reduced rate of complications, consideration for implantation of a centrifugal non pulsatile LVAD should now be considered on a predictive probability of survival (Seattle Heart failure model) around 25%, although better models of prediction are needed. The reliability of these support systems allow long term support to an eventual heart transplantation, providing satisfactory exercise capacity, and can therefore be considered more than a simple bridge to transplant.

One of the unsolved issues in these patients is bleeding, namely gastro-intestinal bleeding. Bleeding might be related to acquired Von Willebrand Factor syndrome due to cleavage of parts of this protein, because of high shear stress, leading to a functionally inactivated protein, a condition that is only diagnosed through electrophoresis techniques.

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Я вас всех люблю, но порядок должен быть!


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Non-obstructive coronary artery disease

Authors: Crea, Filippo (Roma, Italy)


In this interesting Focus session, Prof. Maseri presented the case of a 53 year old woman with repeated episodes of epigastric pain without radiation occurring at rest, while effort tolerance was preserved. Coronary angiography showed normal coronary arteries. She was discharged on aspirin, calcium-antagonists, and beta-blockers. She remained symptom free for about a month. Then, during a very stressful period of her life, she began to present with angina during effort, sometimes on emotion. She insisted that the features of this new pain were completely different from those of the attacks leading to the previous hospital admission; indeed, this pain was located behind her upper sternum and radiated to the neck and ulnar side of the left arm.

Thus, this patient presented characteristic features of angina consistent with two distinct coronary ischemic mechanisms involving two separate regions of the ventricular wall. This conclusion was supported by the response to the provocative stressors dipyridamole and methylergometrine: microvascular dysfunction causing anterior wall ischemia in the absence of wall motional abnormalities (associated with upper sternal chest pain radiating to the left arm) revealed by dypiridamole and inferior wall ischemia caused by coronary spasm (associated with regional contractile dysfunction and the epigastric pain typically occurring spontaneously at rest) revealed by methylergometrine.

Prof. Kaski presented the case of a 66 year old woman with episodes of typical chest pain mainly during effort, which occasionally did not subsided promptly with the termination of exercise but lasted 5 to 15 minutes, with a poor response to nitroglycerine. Exercise stress test showed ST segment depression associated with her usual chest pain. Echo-dypiridamole stress test precipitated ST segment depression associated with chest pain, in the absence of regional wall motion abnormalities. Coronary angiography showed normal coronary arteries. Intracoronary injection of acetyl-choline caused diffuse coronary vasoconstriction, mainly of distal vessels, associated to ST segment depression associated with her usual chest pain.

Thus, the diagnosis was microvascular angina. Indeed, in this patient, myocardial ischemia was caused by coronary microvascular dysfunction. The patchy distribution and the limited transmural extension of the perfusion defects, determined by dysfunction of small resistance coronary artery vessels (<500 micron), may explain the absence of regional wall motion abnormalities in the presence of angina and ST segment depression caused by dypiridamole through the “steal” phenomenon. The patient was discharged on statins, ACE-inhibitors and calcium-antagonists with progressive improvement of her symptoms. A stress test carried out after few months was negative for symptoms and ECG changes.

Prof. Sechtem presented the case of a 26 year old man who presented to the hospital because of a prolonged episode of chest pain. On admission he was pain free, the ECG showed mild diffuse ST segment elevation, Troponin T was slightly elevated. Contrast-enhanced cardiac magnetic resonance was compatible with the diagnosis of myocarditis, suggested by subepicardial delayed enhancement. Coronary angiography carried out after a second episode of chest pain associated to T wave inversion, showed normal coronary arteries.

In this case also, intracoronary injection of acetyl-choline caused diffuse coronary vasoconstriction mainly of distal vessels, associated to ST segment depression associated with chest pain. A myocardial biopsy confirmed the diagnosis of myocarditis associated to the presence of parvovirus. Histology showed prearteriolar wall thickening. In this case, coronary microvascular dysfunction, probably caused by the endothelial localization of parvovirus, might be responsible for the anginal episodes complained of by the patient. He had an uneventful recovery in the absence of treatment.

The common denominator of the three clinical cases is angina with normal coronary arteries. This condition is not unusual. Indeed, about 10-20% of patients presenting with acute coronary syndrome and about 20-30% of patients presenting with stable angina and inducible myocardial ischemia, exhibit angiographically normal coronary arteries or non obstructive coronary atherosclerosis.

This Focus session clearly shows that before excluding a coronary origin of symptoms it is important to establish that symptoms are not caused by coronary spasm, microvascular angina or myocarditis. The choice of the most appropriate test depends on clinical reasoning: ergometrine test if coronary spasm is suspected; echo-dypiridamole stress test if microvascular angina is suspected; cardiac magnetic resonance if myocarditis is suspected.

_________________
Я вас всех люблю, но порядок должен быть!


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Tight glycaemic control - how low should you go?

Authors: Hagerman, I (Stockholm, Sweden)
More than 75% of the seats were filled in the Berlin room during the Clinical Seminar discussing the complicated issue of blood sugar control and the increasing risk for cardiovascular complications in patients with elevated fasting glucose, impaired glucose tolerance and diabetes mellitus. To go too low activates the autonomic nervous system, with a 10-50 fold increase in adrenalin and nor-adrenalin, prolongs QT-interval, induces hypokalemia and platelet activation.

Treatment strategies of the intensive care patient were overviewed by Professor Antonio Ceriello, Barcelona. Recent studies have revealed a significant association between hyperglycaemia and morbidity and mortality rates in adult patients both diabetic and non-diabetic. Conversely, the Nice Sugar Study (2009) randomized patients to intensive blood sugar control or “standard treatment” and could show a higher mortality in the intensive treated group. Glucose variability, especially with deep and frequent hypoglycaemia is associated with mortality in the ICUs, but the definition of blood sugar variability needs to be clarified. High glucose variability together with high mean glucose is associated with the highest mortality rate. Despite conflicting results in studies of intensive care patients, it was concluded that treatment should aim at “cutting the tops” and avoid hypoglycaemias.

Professor Lars Ryden, Stockholm discussed specifically the patients with coronary artery disease and the increasing burden of multiple risk factors in this group. Blood sugar level at admission has important prognostic information and 67% of patients with AMI have impaired glucose tolerance at discharge from the hospital, as showed by Norhammar et al (2002). The DIGAMI I study clearly showed that intensive treatment reduced the absolute risk of death by 11%. Mean blood sugar level at the start of treatment was 15.4 mmol/L compared to that in DIGAMI II, which was 7.1 mmol/l.

This difference may in part explain the neutral result in DIGAMI II. Occasional hypoglycaemia in the CAD-patient is not associated with increased mortality but is related to other co-morbidities. An increase in blood sugar level of 3 mmol/L results in a significant increased risk for mortality with HR 1.20. Blood glucose should be measured in all patients with acute coronary syndrome. Consider intensive treatment in levels > 10 mmol/L, aim towards 5-7.7 mmol/L. Intravenous insulin is currently the most effective method for controlling blood glucose. High dose GIK has no role in the treatment of ST-elevation AMI!

Professor Roden, Dusseldorf focused on the evidence of benefit for low HbA1c targets as elevated HbA1c is an important risk marker for CVD in line with the final speaker, Professor Stefano del Prato, Pisa, who stressed the potential risks of intensive treatment with HbA1c values below 6.5%. The ACCORD, ADVANCE and VADT studies all showed significant numbers of serious hypoglycaemias but HbA1c values below 7% were not associated with any increase in cardiovascular deaths. Overall, an 0.9% reduction in HbA1c was associated with a significant reduction of 17% in non-fatal MI and 15% reduction in CAD.

Long diabetes duration, high BMI and hypoglycaemia increases the risk of CV death with intensive treatment and the higher the HbA1c, the higher the risk of hypoglycaemia! The risk of weight gain should also be considered in patients with intensive treatment and future guidelines for HbA1c levels may be more differentiated with respect to duration of disease, body weight, age etc. Guidelines are valuables tools but should be used with clinical judgement in the treatment of the individual patient.

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Я вас всех люблю, но порядок должен быть!


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Perioperative management of antithrombotic drugs

Authors: Siegbahn, Agneta (Uppsala, Sweden)
The lecture room was filled to 100% with cardiologists that listened to and discussed the perioperative management of antithrombotic drugs.

Dr Noll first pointed out that aspirin as secondary prevention reduces the risk of CV events by 20%. Aspirin induces a small but significant risk of bleeding with OR between 1.2-2.0 and with increased risk at higher doses, i.e. 250 mg or more. Also the risk factors for bleeding and thrombotic events are very similar. Few randomized clinical studies are today available concerning aspirin treatment, bleeding propensity and surgery. Summarizing these studies the risk of bleeding on aspirin is small and can be handled. However Dr. Noll concluded that aspirin should be stopped at intracranial surgery.

Concerning platelet P2Y12 receptor inhibitors, Dr Storey discussed the importance of balancing the perioperative risks for bleeding and thrombosis. He showed data from animal studies demonstrating that the levels of P2Y12 receptor blockage clearly correlate with bleeding time. In the onset/offset study clopidogrel high responders had significantly higher inhibition of platelet aggregation in comparison to patients on ticagrelor at three days. Ticagrelor has a half-life of 12 hours and the platelets were fully recovered after three days. The variable response to clopidogrel gives variable time to recovery of the platelet function. The point of care instrument VerifyNow may be helpful for the clinical decision. The reversible binding of ticagrelor is associated with more predictable offset of effect and allows cessation of treatment closer to surgery compared to clopidogrel. However, the optimal strategy for perioperative P2Y12 inhibition remains to be defined.

Dr Husted, presenting the new anticoagulants, discussed how to evaluate the risk of perioperative bleeding and thromboembolism. Patient characteristics, type and intensity of antithrombotic treatment and the type of surgery are important factors for the evaluation of perioperative bleeding risk. Low bleeding risk surgery includes diagnostic endoscopy, oral surgery/dental extraction while high-risk includes major abdominal and orthopedic surgery and very high-risk neurosurgical procedures. He stated that individual perioperative treatment in patients using the direct oral FXa inhibitors, apixaban and rivaroxaban or direct thrombin inhibitors should be based on the evaluation of high/low risk of thrombosis in combination with high/low risk of bleeding. There are no antidotes to the new oral direct FXa and thrombin inhibitors. Reversal of anticoagulant activity at short notice in case of bleeding, overdose or urgent invasive procedures can be achieved by plasma, prothrombin complex concentrates or rFVIIa (Novoseven).

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Я вас всех люблю, но порядок должен быть!


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Представляем вашему вниманию результаты 5 исследований, вызвавших наибольший интерес (по версии ESC News Team) на прошедшем в Стокгольме Европейском Конгрессе Кардиологов 2010.
SHIFT: ВЛИЯНИЕ ИВАБРАДИНА НА ЧАСТОТУ СЕРДЕЧНО-СОСУДИСТЫХ СОБЫТИЙ У ПАЦИЕНТОВ С УМЕРЕННОЙ И ТЯЖЕЛОЙ ХРОНИЧЕСКОЙ СЕРДЕЧНОЙ НЕДОСТАТОЧНОСТЬЮ И СИСТОЛИЧЕСКОЙ ДИСФУНКЦИЕЙ ЛЕВОГО ЖЕЛУДОЧКА.

Авторы: Michel Komajda ; Karl Swedberg ; Michael Boehm ; Jeffrey S. Borer ; Ian Ford ; Ariane Dubost-Brama ; Guy Lerebours ; Luigi Tavazzi.
Актуальность: Хроническая сердечная недостаточность (ХСН) – заболевание, связанное с высоким уровнем заболеваемости и смертности. Повышение частоты сердечных сокращений в покое является фактором риска неблагоприятных исходов. Мы предположили, что снижение частоты сердечных сокращений с помощью селективного ингибитора рецепторов синусового узла ивабрадина можно улучшить исходы при ХСН.
Методы: В данное международное рандомизированное двойное слепое плацебо-контролируемое исследование были отобраны пациенты с симптоматической ХСН и фракцией выброса левого желудочка ≤ 35%, с синусовым ритмом и ЧСС ≥ 70 уд / мин, госпитализацией по поводу декомпенсации ХСН в течение предыдущих 12 месяцев и стабильной терапией, включающей при переносимости бета-адреноблокатор. В целом было рандомизировано 6505 пациентов, из них в группу ивабрадина 3241 (титровался до максимальной дозы 7,5 мг дважды в день), в группу плацебо - 3264. Первичная конечная точка была комбинированной и включала сердечно-сосудистую смерть или госпитализацию по поводу декомпенсации ХСН.

Результаты: Средний период наблюдения составил 22,9 месяцев. В общей сложности, 793 (24,5%) больных в группе ивабрадина и 937 (28,7%) больных в группе плацебо достигли первичной конечной точки (отношение рисков (ОР) 0,82, 95% доверительный интервал (ДИ)ДИ 0.75-0.9, р <0,0001). Основное влияние ивабрадина заключалось в снижении частоты госпитализации по поводу декомпенсации ХСН с 20,6% до 15,9% (ОР, 0,74, 95% ДИ 0.66-0.83, р <0,0001) и смертности от ХСН (ОР, 0,74, 95% ДИ 0.58-0.94, р = 0,014). Выявлено снижение частоты сердечно-сосудистой смерти (ОР, 0,91, 95% ДИ 0.80-1.03), и смерти по всем причинам (ОР, 0,90, 95% ДИ 0.80-1.02) в группе ивабрадина. Применение ивабрадина привело к снижению частоты госпитализации по всем причинам (ОР, 0,89, 95% ДИ 0.82-0.96, р = 0,003), отмечалась хорошая переносимость. Полученные в различных заданных группах результаты были сопоставимы, хотя у пациентов группы ивабрадина с наибольшей ЧСС достигнуто наибольшее снижение риска наступления первичной конечной точки.
Выводы: Полученные результаты подтверждают важность снижение ЧСС с помощью ивабрадина для улучшения клинических исходов у больных с ХСН и подтверждают важную роль ЧСС в патофизиологии ХСН.


AVERROES: СРАВНИТЕЛЬНОЕ ИССЛЕДОВАНИЕ АПИКСАБАНА И АЦЕТИЛСАЛИЦИЛОВОЙ КИСЛОТЫ (АСК) В ПРЕДОТВРАЩЕНИИ ИНСУЛЬТА

Авторы: Connolly, Stuart; Eikelboom, John; Flaker, Greg; Kaatz, Scott; Avezum, Alvara; Piegas, Leopoldo; Hermosillo, Antonio; Hohnloser, Stefan; Golitsyn, Sergey; Yusuf, Salim.
Актуальность: У пациентов с мерцательной аритмией (МА) повышен риск развития инсульта. Применение антагонистов витамина К (ВКА), таких как варфарин, приводит к снижению риска развития инсульта, но связано с повышенным риском кровотечений. Кроме того, ведение пациента на ВКА сложно, требует частого мониторирования МНО из-за генетических особенностей, взаимодействия с лекарственными препаратами и продуктами питания. Многих пациентов с фибрилляцией предсердий невозможно адекватно вести на ВКА, у некоторых развились осложнения, а некоторые отказываются принимать данные препараты. Для пациентов, которые не могут принимать ВКА, единственной альтернативой является лечение аспирином, который недостаточно эффективен. Апиксабан является исследуемым пероральным антикоагулянтом, избирательно ингибирующим фактор Ха. Исследования по профилактике венозной тромбоэмболии показали, что апиксабан является эффективным препаратом, обладающим благоприятным профилем риск-польза по сравнению с низкомолекулярными гепаринами.
Цель. Целью исследования AVERROES была оценка эффективности апиксабана для профилактики инсульта и системной эмболии у пациентов с фибрилляцией предсердий и риском развития инсульта, не подходящих для терапии ВКА. Апиксабан сравнивали со стандартной терапией - аспирином.
Методы: AVERROES - двойное слепое, рандомизированное, контролируемое исследование по сравнению апиксабана и аспирина. Пациенты с документированной фибрилляцией предсердий и по крайней мере одним фактором риска развития инсульта, которые также не подходят для терапии ВКА, были рандомизированы в 2 группы - апиксабана 5 мг два раза в сутки (2,5 мг два раза для отдельных пациентов) или аспирина (81-324 мг / в день). Исследование проведено в 520 центрах во всем мире и включило 5600 пациентов, завершено в декабре 2009 года. Комитет по мониторированию данных - Data Monitoring Committee (DMC) провел свой первый официальный промежуточный анализ эффективности после наступления 50% заданных первичных конечных точек и повторно рассмотрели эффективность три месяца спустя, 28 мая 2010, в соответствии с уставом DMC. На основе неоспоримых фактов, подтверждающих эффективность апиксабана в профилактике инсульта и системной эмболии, наряду с высокой безопасностью, они рекомендовали окончить исследование, чтобы все пациенты могли получать препарат в открытой фазе. Эта рекомендация была принята в Steering Committee (Руководящий комитет) и спонсорами исследования.
Результаты: Кратко описаны предварительные результаты. Лечение пациентов значимо не различались между 2 группами. Средний возраст составил 70 лет. Средний балл по шкале CHADS2 составил 2,0. 75% больных получали аспирин, на момент начала исследования, а 15% получали пероральные антикоагулянты. 40% из них ранее получали ВКА. Частота инсульта или системной эмболии (первичная конечная точка) составила 4,0% в год в группе аспирина и 1,7% в год в группе апиксабана (отношение рисков 0,43, 95% ДИ 0.30-0.62, р = 0,000004). Частота больших кровотечений составила 1,2% в год в группе аспирина и 1,5% в год - апиксабана (ОР 1,26, 95% ДИ, 0.79-2.00, р = 0,33). Частота геморрагического инсульта - 0,2% в год в обеих группах (ОР 1,15, 95% ДИ, 0.42-3.17, р = 0,79). Не выявлено признаков гепатотоксичности или других побочных эффектов.
Выводы: У пациентов с фибрилляцией предсердий и риском инсульта, не подходящим для терапии ВКА, апиксабан снижает риск инсульта и системной эмболии на 57% без значительного увеличения риска крупных кровотечений. Апиксабан обладает рядом важных преимуществ по сравнению с аспирином в профилактике инсульта у данной группы больных.


ANTIPAF: АНТАГОНИСТЫ РЕЦЕПТОРОВ АНГИОТЕНЗИНА II ПРИ ПАРОКСИЗМАЛЬНОЙ ФОРМЕ МЕРЦАТЕЛЬНОЙ АРИТМИИ

Авторы: Andreas Goette, Norbert Schön Paulus Kirchhof, Günter Breithardt, Thomas Fetsch, Helmut U. Klein, Gerhard Steinbeck, Karl Wegscheider, Thomas Meinertz.
Актуальность: В отличие от антиаритмических препаратов, безопасность и положительный эффект антагонистов рецепторов ангиотензина II (АРА) у пациентов с органической патологией сердца широко известны. Клиническая эффективность АРА для предотвращения фибрилляции предсердий (ФП) изучена до сих пор только у пациентов, имеющих органическую патологию сердца. Здесь приводятся основные результаты исследования ANTIPAF, в котором изучалось влияние олмесартана медоксомила в сравнении с плацебо у пациентов с пароксизмальной ФП без органических заболеваний сердца.
Методы: ANTIPAF - проспективное рандомизированное плацебо-контролируемое, многоцентровое исследование. В качестве первичной конечной точки принимался процент дней с документированными эпизодами пароксизмальной ФП. Период наблюдения составил 12 месяцев. 430 пациентов с документированной пароксизмальной ФП без органических заболеваний сердца были рандомизированы в группу плацебо или 40 мг олмесартана 1 раз в сутки. Сопутствующая терапия АРА, ингибиторами АПФ и антиаритмическими препаратами запрещалсь. Пациентам ежедневно выполнялась ЭКГ, передаваемая через телефон, вне зависимости от симптомов.
Результаты: В соответствии с анализом «intension-to-treat» (ITT) исследуемая популяция составила 425 пациентов (211 группы плацебо и 214 группы олмесартана). В общей сложности было проанализировано 87 818 телефонных ЭКГ (тЭКГ) (44 888 ЭКГ в группе плацебо и 42 930 ЭКГ в группы олмесартана). Таким образом, в среднем, на одного пациента было зарегистрировано 207 тЭКГ, в среднем по 1,12 тЭКГ на одного пациента в день. Число первичных конечных точек не различалось между группами (р = 0,7702), как и число вторичных конечных точек (качество жизни). В частности, время до первого пароксизма ФП, время до персистирования ФП и число госпитализаций были одинаковыми в обеих группах. Время до назначения антиаритмика, восстанавливающего ритм (амиодарон) является единственным параметром, по которому достигнуто достоверное различие с более ранним назначением амиодарона в группе плацебо (р = 0,0365).
Выводы: Терапия АРА сама по себе не уменьшила количество эпизодов ФП у пациентов с пароксизмальной ФП без органических заболеваний сердца. Таким образом, АРА не могут быть рекомендованы в качестве первой линии лечения пароксизмальной ФП при отсутствии других показаний.


CARE HF LTFU: РЕСИНХРОНИЗАЦИОННАЯ ТЕРАПИЯ ПРИ СЕРДЕЧНОЙ НЕДОСТАТОЧНОСТИ: ОТДАЛЕННЫЕ РЕЗУЛЬТАТЫ

Авторы: John GF Cleland, Nick Freemantle, Erland Erdmann, Daniel Gras, Lukas Kappenberger, Luigi Tavazzi, Jean-Claude Daubert.
Актуальность: Исследование CARE-HF впервые было представлено в 2005 году и показало, что ресинхронизационная терапия (РТ) значительно снижает смертность у пациентов с сердечной недостаточностью с признаками десинхронизации. Существует очень мало длительных исследований среди больных с РТ.
Методы: Набор пациентов начался в конце 2000 года и был завершен к марту 2003 года. После доклада основных результатов в 2005 году, исследователей попросили информировать пациентов о результатах и имплантировать устройство для РТ при сохранении показаний, а затем попросить согласия пациентов для отдаленного наблюдения - до 30 сентября 2009.
Результаты: Из 813 пациентов, первоначально включенных в исследование, 343 (42%) умерли до повторного согласия, 111 пациентов (14%) не были доступны для контакта, 50 (6%) были живы, но отказались от дальнейшего участия и 309 (38% ) дали согласие на дальнейшее наблюдение. Из пациентов, изначально взятых под наблюдение, большинство выживших уже получили РТ к моменту повторного согласия. С момента рандомизации умерло 222 пациентов, изначально получавших фармакотерапию, и 192 - изначально получивших РТ. Отношение рисков по смертности среди пациентов, изначально получивших РТ по сравнению с контрольной группой, составило 0,768 (95% ДИ от 0,633 до 0,931, P = 0,007). Взаимодействий между подгруппами не наблюдалось.
Выводы: Влияние РТ на смертность, выявленное в фазе рандомизации CARE-HF сохраняется при длительном отдаленном наблюдении. Имплантация устройства для РТ после завершения исследования, возможно, может предотвратить дальнейшее расхождение кривых выживаемости. Преимущество РТ наблюдается у пациентов, старше и младше среднего возраста 66 лет. У пациентов в возрасте до 66 лет с умеренной и тяжелой сердечной недостаточностью и признаками сердечной десинхронизации, от РТ можно ожидать увеличения медианы выживаемости примерно с 5 лет до > 8 лет. Выживание должно быть еще больше в группе пациентов с РТ-дефибрилляторами, а не только с устройствами для РТ.

EINSTEIN DVT: СРАВНИТЕЛЬНОЕ ИССЛЕДОВАНИЕ ПЕРОРАЛЬНОГО ПРИЕМА РИВАРОКСАБАНА И СТАНДАРТНОЙ ТЕРАПИИ ДЛЯ СТАРТОВОГО ЛЕЧЕНИЯ СИМПТОМАТИЧЕСКОГО ТРОМБОЗА ГЛУБОКИХ ВЕН И ДОЛГОСРОЧНОЙ ПРОФИЛАКТИКИ РЕЦИДИВОВ ВЕНОЗНОЙ ТРОМБОЭМБОЛИИ

Авторы: Buller, Harry - Darius, Harald
Актуальность: В схему стандартного лечения венозной тромбоэмболии входят низкомолекулярный гепарин, а затем антагонист витамина K. В 2 исследованиях по изучению дозировок среди пациентов с симптомами тромбоза глубоких вен, ривароксабан, прямой пероральный ингибитор фактора Ха, показал свою эффективность и безопасность, сходные со стандартной терапией. Мы исследовали возможность использования ривароксабана в качестве альтернативы стандартной терапии в крупной и репрезентативной выборке пациентов с тромбозом глубоких вен.
Методы: эффективность ривароксабана в сравнении со стандартной терапией изучалась в рандомизированном, открытом, слепом исследовании с участием более 3400 пациентов с острым симптоматическим проксимальным тромбозом глубоких вен, но без сопутствующей симптоматической тромбоэмболии легочной артерии.
Пациенты получили перорально ривароксабан (интенсивный курс в течение первых 3 недель - 15 мг два раза в день, затем 20 мг однократно) или рассчитанную по весу дозу эноксапарина (1 мг/кг), а затем антагонист витамина К (варфарин или аценокумарол) в дозе, необходимой для поддержания МНО в пределах 2,0-3,0 (целевое значение 2,5) в течение 3, 6 или 12 месяцев, на основе клинической оценки врачом состояния пациента на исходном визите. Все пациенты, рандомизированные в группу ривароксабана, получали фиксированные дозы, в том числе пациенты с умеренным нарушением функции почек (клиренс креатинина 30-50 мл/мин) и большой или низкой массой тела. Первичной конечной точкой по эффективности была общая заболеваемость симптоматической повторной тромбоэмболией вен (без смертельного исхода или со смертельным исходом). Главным исходом по безопасности стала комбинированная точка, включающая крупное или некрупное, но клинически значимое кровотечение. Для подтверждения того, что ривароксабан не уступает стандартной терапии, требовалось наступление как минимум 88 повторных событий. Все результаты оценивались независимой комиссией, ослепленной к назначаемому лечению.
Целью исследования стало последовательное включение ряда пациентов, для оптимизации обобщения и возможности проведения и контроля за стандартной терапии в локальных условиях. Были предприняты некоторые меры, чтобы гарантировать аналогичный контроль во время периода отсроченного наблюдения и оценки результатов.
Результаты: Всего было рандомизировано более 3400 пациентов в период с февраля 2007 года по август 2009 в 253 центрах в 32 странах. Максимальная длительность лечения составила 6 месяцев для последних рандомизированных пациентов. Целевой показатель в 88 событий был достигнут, в связи с чем ожидается закрытие базы данных в июне 2010 года. Характеристика пациентов сходна с таковой типичных пациентов с тромбозом глубоких вен и сопоставима с современными исследованиями. Ожидается представление окончательных результатов.
Выводы: Если исследование Einstein-DVT достигнет своей цели – продемонстрирует, что ривароксабан не уступает стандартной схеме лечения, монотерапия данным препаратом обеспечит клиницистам и пациентам привлекательный простой альтернативный режим стартового лечения тромбоза глубоких вен, а также долгосрочной вторичной профилактики повторных венозных тромбоэмболий.

Материал подготовлен Лианой Оганезовой.

Источник http://medic.ossn.ru/news/11/1512/

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