Guide Osteoporosis in Clinical Practice: A Practical Guide for Diagnosis and Treatment

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Most statin trials excluded patients with HF because it was uncertain that they would benefit. Patients with HFrEF receiving oral anticoagulation because of concurrent AF or risk of venous thromboembolism should continue anticoagulation. Detailed information is provided in Section Similarly, there is no evidence on the benefits of antiplatelet drugs including acetylsalicylic acid in patients with HF without accompanying CAD, whereas there is a substantial risk of gastrointestinal bleeding, particularly in elderly subjects, related with this treatment.

Aliskiren direct renin inhibitor failed to improve outcomes for patients hospitalized for HF at 6 months or 12 months in one study and is not presently recommended as an alternative to an ACEI or ARB. Diltiazem and verapamil have been shown to be unsafe in patients with HFrEF. There is a variety of dihydropyridine CCBs; some are known to increase sympathetic tone and they may have a negative safety profile in HFrEF. There is only evidence on safety for amlodipine and felodipine in patients with HFrEF, and they can be used only if there is a compelling indication in patients with HFrEF.

Currently, the evidence is considered insufficient to support specific guideline recommendations for other therapeutic technologies, including baroreflex activation therapy, vagal stimulation, diaphragmatic pacing , and cardiac contractility modulation; , further research is required. Implantable devices to monitor arrhythmias or haemodynamics are discussed elsewhere in these guidelines.

A high proportion of deaths among patients with HF, especially those with milder symptoms, occur suddenly and unexpectedly. Many of these are due to electrical disturbances, including ventricular arrhythmias, bradycardia and asystole, although some are due to coronary, cerebral or aortic vascular events. Treatments that improve or delay the progression of cardiovascular disease will reduce the annual rate of sudden death, but they may have little effect on lifetime risk and will not treat arrhythmic events when they occur.

Guideline Focus and Target Population

ICDs are effective in preventing bradycardia and correcting potentially lethal ventricular arrhythmias. Some antiarrhythmic drugs might reduce the rate of tachyarrhythmias and sudden death, but they do not reduce overall mortality and may increase it. Compared with amiodarone treatment, ICDs reduce mortality in survivors of cardiac arrest and in patients who have experienced sustained symptomatic ventricular arrhythmias.

Although amiodarone may have reduced mortality in older trials of HF, , contemporary studies conducted since the widespread introduction of beta-blockers suggest that it does not reduce mortality in patients with HFrEF. Accordingly, an ICD is contraindicated in this time period. A wearable defibrillator may be considered if the patient is deemed to be at high risk of ventricular fibrillation, although evidence from randomized trials is lacking.

Conservative programming with long delays between detection and the ICD delivering therapy dramatically reduces the risk of both inappropriate due to artefacts or AF and appropriate but unnecessary [due to self-terminating ventricular tachycardia VT ] shocks. See the guideline on CRT for further details Section 8. ICD therapy is not recommended in patients in NYHA Class IV with severe symptoms refractory to pharmacological therapy who are not candidates for CRT, a ventricular assist device or cardiac transplantation, because such patients have a very limited life expectancy and are likely to die from pump failure.

Patients with serious co-morbidities who are unlikely to survive substantially more than 1 year are unlikely to obtain substantial benefit from an ICD. Patients should be counselled as to the purpose of an ICD, complications related to implantation and device activation predominantly inappropriate shocks and under what circumstances it might be deactivated terminal disease or explanted infection, recovery of LV function.

If HF deteriorates, deactivation of a patient's ICD may be considered after appropriate discussion with the patient and caregiver s. If the ICD generator reaches its end of life or requires explantation, it should not automatically be replaced.

Osteoporosis in Clinical Practice

Treatment goals may have changed and the risk of fatal arrhythmia may be lower or the risk of non-arrhythmic death higher. It is a matter of some controversy whether patients whose LVEF has greatly improved and who have not required device therapy during the lifetime of the ICD should have another device implanted. Subcutaneous defibrillators may be as effective as conventional ICDs with a lower risk from the implantation procedure.

Patients must be carefully selected, as they have limited capacity to treat serious bradyarrhythmia and can deliver neither antitachycardia pacing nor CRT. Substantial RCTs with these devices and more data on safety and efficacy are awaited. Recommendations for cardiac resynchronization therapy implantation in patients with heart failure. CRT improves cardiac performance in appropriately selected patients and improves symptoms and well-being and reduces morbidity and mortality. The prevention of lethal bradycardia might be an important mechanism of benefit shared by all pacing devices.

Not all patients respond favourably to CRT. Patients with ischaemic aetiology will have less improvement in LV function due to myocardial scar tissue, which is less likely to undergo favourable remodelling. Several studies have shown that patients with left bundle branch block LBBB morphology are more likely to respond favourably to CRT, whereas there is less certainty about patients with non-LBBB morphology. Evidence from two IPD meta-analyses indicates that after accounting for QRS duration, there is little evidence to suggest that QRS morphology or aetiology of disease influence the effect of CRT on morbidity or mortality.

Clinical practice varies widely among countries. It is unclear whether CRT reduces the need for an ICD by reducing the arrhythmia burden or increases the benefit from an ICD by reducing mortality rates from worsening HF, leading to longer exposure to the risk of arrhythmia.

This can be prevented by CRT, which might improve patient outcomes. Only two small trials have compared pharmacological therapy alone vs.

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CRT in patients with AF, with conflicting results. This observation has not been confirmed in a randomized trial. Imaging tests for dyssynchrony have not yet been shown to be of value in selecting patients for CRT.

1. Preamble

The reader is directed to guidelines on pacing and CRT for recommendations on device implantation procedures. The value of trying to optimize AV or VV intervals after implantation using echo- or electrocardiographic criteria or blood pressure response is uncertain, but may be considered for patients who have had a disappointing response to CRT. For patients with HFrEF who remain symptomatic despite OMT and do not have an indication for CRT, new device therapies have been proposed and in some cases are approved for clinical use in several European Union EU countries but remain under trial evaluation.

Cardiac contractility modulation CCM is similar in its mode of insertion to CRT, but it involves non-excitatory electrical stimulation of the ventricle during the absolute refractory period to enhance contractile performance without activating extra systolic contractions. Most other devices under evaluation involve some modification of the activity of the autonomic nervous system ANS by targeted electrical stimulation.

As new data and analyses become available, it might be possible to make recommendations for each phenotype separately. The pathophysiology underlying HFpEF and HFmrEF is heterogeneous, and they are associated with different phenotypes including diverse concomitant cardiovascular diseases e. However, since these patients are often elderly and highly symptomatic, and often have a poor quality of life, an important aim of therapy may be to alleviate symptoms and improve well-being.

Diuretics will usually improve congestion, if present, thereby improving symptoms and signs of HF.

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The evidence that diuretics improve symptoms is similar across the spectrum of LVEF. Evidence that beta-blockers and MRAs improve symptoms in these patients is lacking. For patients in sinus rhythm, there is some evidence that nebivolol, , , digoxin, spironolactone and candesartan might reduce HF hospitalizations. For patients in AF, beta-blockers do not appear to be effective and digoxin has not been studied.

Patients in AF should receive an anticoagulant to reduce the risk of thromboembolic events for details, see the ESC guidelines of AF ]. Antiplatelet agents are ineffective for this purpose. Renal dysfunction, which is common in this population, may contraindicate or increase the risk of haemorrhage with NOACs.

Whether digoxin, beta-blockers or rate-limiting CCBs, or a combination of these, should be preferred is unknown. Verapamil or diltiazem should not be combined with a beta-blocker. Recently, a trial of empagliflozin showed a reduction in blood pressure and body weight, probably by inducing glycosuria and osmotic diuresis. Its use was associated with a reduction in hospitalization for HF and in cardiovascular mortality. Myocardial ischaemia may contribute to symptoms, morbidity and mortality and should be considered when assessing patients. However, there is only anecdotal evidence that revascularization improves symptoms or outcome.

Patients with angina should follow the same management route as patients with HFrEF. Patients with HFpEF and HFmrEF have impaired exercise tolerance, commonly accompanied by an augmented blood pressure response to exercise and chronotropic incompetence. Recommendations for treatment of patients with heart failure with preserved ejection fraction and heart failure with mid-range ejection fraction. Ambulatory electrocardiographic monitoring can be used to investigate symptoms that may be due to arrhythmias, — but evidence is lacking to support routine, systematic monitoring for all patients with HF to identify tachy- and bradyarrhythmias.

There is no evidence that clinical decisions based on routine ambulatory electrocardiographic monitoring improve outcomes for patients with HF.

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Ambulatory electrocardiographic recording detects premature ventricular complexes in virtually all patients with HF. Episodes of asymptomatic, non-sustained VT are common, increasing in frequency with the severity of HF and ventricular dysfunction and indicating a poor prognosis in patients with HF, but provide little discrimination between sudden death or death due to progressive HF. AF is the most common arrhythmia in HF irrespective of concomitant LVEF; it increases the risk of thromboembolic complications particularly stroke and may impair cardiac function, leading to worsening symptoms of HF.

Amiodarone will reduce the incidence of AF, induce pharmacological cardioversion, maintain more patients in sinus rhythm after cardioversion and may be used to control symptoms in patients with paroxysmal AF if beta-blockers fail to do so. Dronedarone is contraindicated in patients with HF and AF.

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  6. If the patient has no distressing symptoms of HF, then treatment with oral beta-blockers may be initiated to provide ventricular rate control. For patients with marked congestion who nonetheless have few symptoms at rest, initial treatment with oral or intravenous i. For patients in haemodynamic instability, an i. Longer-term infusion of amiodarone should be given only by central or long-line venous access to avoid peripheral vein phlebitis. In patients with haemodynamic collapse, emergency electrical cardioversion is recommended see also Section A resting ventricular rate in the range of 60— bpm may be considered based on the current opinion of this Task Force, , although one trial suggested that a resting ventricular rate of up to bpm might still be acceptable, and this is currently recommended by the ESC guidelines on AF.

    Assessment of ventricular rate control from the radial pulse is not ideal, especially in patients with HF, as ventricular activation may not always generate a palpable pulse. Rate control should be documented electrocardiographically.

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    A wearable device enables ventricular rate to be assessed during rest, exercise and sleep, but the value of routine monitoring has not yet been established. The optimal resting ventricular rate in patients with AF and HF is uncertain but may be between 60— bpm. Beta-blockers reduce ventricular rate during periods of activity, while digoxin exerts a greater effect at night.

    Rarely, ventricular rate cannot be reduced below — bpm by pharmacological means alone and AV node ablation with ventricular pacing may be considered; in this situation, for patients with HFrEF, CRT should be considered instead of conventional RV pacing. Also, if the patient is indicated for an ICD, AV node ablation with implantation of CRT-D may be a preferred option, especially if the patient has moderate to severe symptoms. In patients with chronic HF, a rhythm control strategy including pharmacological or electrical cardioversion has not been shown to be superior to a rate control strategy in reducing mortality or morbidity.

    A rhythm control strategy is probably best reserved for patients with a reversible secondary cause of AF e. The use of class I antiarrhythmic agents and dronedarone increases morbidity and mortality in patients with HF and AF and should be avoided. The safety and efficacy of catheter ablation in the atria and pulmonary veins PV as a rhythm control strategy in HF is at present uncertain except for tachycardia induced cardiomyopathy. Two small studies of AF ablation compared with rate control met with mixed success in terms of procedural complications and success in improving symptoms.

    Recommendations for a rhythm control management strategy in patients with atrial fibrillation, symptomatic heart failure NYHA Class II—IV and left ventricular systolic dysfunction and no evidence of acute decompensation. NOACs are preferred for patients with HF with non-valvular AF, as NOACs compared with vitamin K antagonists seem to be at least similarly effective and even safer less intracranial haemorrhage in patients with HF than in subjects without HF, , , although concerns exist about their safety in older patients with HF and poor renal function , [for a detailed description of the interaction between NOAC and renal function, see Heidbuchel et al.

    In patients with HF and AF who have mechanical heart valves or at least moderate mitral stenosis, only oral vitamin K antagonists should be used for prevention of thromboembolic stroke.