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Current management strategies in patients with syncope due to intrinsic cardiac tachyarrhythmia are summarized in Figure 15 .

Figure 15
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Choice of therapy for patients presenting with syncope due to cardiac tachyarrhythmias as the primary cause. AA = antiarrhythmic; ICD = implantable cardioverter defibrillator; SVT = supraventricular tachycardia; VT = ventricular tachycardia.

Figure 15
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Choice of therapy for patients presenting with syncope due to cardiac tachyarrhythmias as the primary cause. AA = antiarrhythmic; ICD = implantable cardioverter defibrillator; SVT = supraventricular tachycardia; VT = ventricular tachycardia.

In patients with paroxysmal AV nodal re-entrant tachycardia, AV re-entrant tachycardia, typical atrial flutter, and ectopic tachycardia associated with syncope, catheter ablation is the first-choice treatment. In these patients, the role of drug therapy is limited to being a bridge to ablation or being used when ablation has failed. In patients with syncope associated with atrial fibrillation or atypical left atrial flutter, the decision should be individualized.

Syncope due to torsade de pointes is not uncommon and is, in its acquired form, the result of drugs that prolong the QT interval. Treatment is the immediate discontinuation of the suspected drug.

Catheter ablation or drug therapy is recommended in patients with syncope due to VT in the presence or absence of structural heart disease in order to prevent syncope recurrence ( Figure 15 ). Detailed guidelines regarding antiarrhythmic drug usage in patients with VT can be found in the 2015 ESC Guidelines for VA and the prevention of SCD. 46

An ICD is indicated in patients with syncope and depressed cardiac function, and VT or VF without correctable cause. Although ICD may not prevent syncope recurrence in these patients, 31 , 348 it is indicated to reduce the risk of SCD (refer to the 2015 ESC Guidelines for VA and the prevention of SCD 46 ). An ICD is also indicated in patients with syncope and previous myocardial infarction who have VT induced during EPS 346 (see section 4.2.6).

In patients with preserved systolic function, the indication for ICD is weaker because trials have not addressed this specific issue. However, when VT causes syncope, this Task Force believes that an ICD is warranted if catheter ablation and pharmacological therapy have failed or could not be performed ( Figure 15 ).

Treatment of syncope due to cardiac arrhythmias

AF = atrial fibrillation; AV = atrioventricular; BBB = bundle branch block; CSM = carotid sinus massage; ECG = electrocardiogram; EPS = electrophysiological study; ICD = implantable cardioverter defibrillator; ILR = implantable loop recorder; SCD = sudden cardiac death; SVT = supraventricular tachycardia; VT = ventricular tachycardia.

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Treatment of syncope due to cardiac arrhythmias

AF = atrial fibrillation; AV = atrioventricular; BBB = bundle branch block; CSM = carotid sinus massage; ECG = electrocardiogram; EPS = electrophysiological study; ICD = implantable cardioverter defibrillator; ILR = implantable loop recorder; SCD = sudden cardiac death; SVT = supraventricular tachycardia; VT = ventricular tachycardia.

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Cardiac syncope is diagnosed when syncope presents in patients with severe aortic stenosis, acute myocardial infarction/ischaemia, HCM, cardiac masses (atrial myxoma, ball thrombus, etc.), pericardial disease/tamponade, congenital anomalies of the coronary arteries, prosthetic valve dysfunction, pulmonary embolus, acute aortic dissection, and pulmonary hypertension (see section 4.1.1). Structural cardiac or cardiopulmonary disease can be present in some patients with syncope, and its incidence increases in older patients. The mere presence of heart disease does not imply that syncope is related to the underlying cardiac disorder. Some of these patients have typical reflex syncope; in others, such as those with inferior myocardial infarction or aortic stenosis, the underlying cardiac disease may play a role in triggering or potentiating a reflex mechanism, and—finally—the underlying cardiac disease may be the substrate for conduction disturbances, supraventricular arrhythmia, or VA that causes syncope.

2) Large clinical studies that test the superiority of management in a dedicated syncope facility vs. conventional management

BP recording is crucial for the majority of clinical TLOC situations and will yield important information for the treatment of syncope. Unfortunately, current long-term BP (or surrogate) recording systems are not optimal for diagnostic use in the syncope evaluation setting.

3) Development and validation of new diagnostic multiparametric devices that can record heart rhythm and BP (and possibly other physiological parameters such as cerebral saturation or EEG) at the time of a syncopal event.

Only a few small RCTs have been conducted on treatment of syncope. In addition, syncopal recurrences are unpredictable and often decrease spontaneously after medical assessment, even in the absence of a specific therapy. The consequence of the spontaneous decrease is that any therapy for syncope prevention appears to be more effective than it actually is, making the results of observational data on therapy questionable in the absence of a control group. No therapy can be effective for all patients. Any therapy should be assessed in homogeneous subgroups.

Therefore, there is strong urgent need for RCTs on the efficacy of:

4) Pharmacological therapies targeted to specific subgroups of reflex syncope.

5) Pacemaker therapy targeted to specific subgroups of cardioinhibitory reflex syncope.

6) Pharmacological therapies of OH-mediated syncope.

7) ICD therapy targeted to specific subgroups of patients with unexplained syncope at risk of SCD.

There is a need to move towards personalized medicine. Improving our knowledge of the biochemical mechanisms underlying specific forms of reflex syncope will allow the development of new therapies in such specific settings. For example, a low adenosine phenotype and a low norepinephrine phenotype have been recently identified.

8) Randomized clinical trials on the efficacy of theophylline (and other xantine antagonists) for low adenosine syncope and norepinephrine transport inhibitors for low epinephrine syncope.

Syncope is a transient phenomenon. The ideal therapy should be one that is administered only when needed.

9) Randomized clinical trials of on-demand administration of specific therapy based on specific sensors similar to adrenalin injectors in asthma or nasal spray for paroxysmal SVT.

AF = atrial fibrillation; AV = atrioventricular; BBB = bundle branch block; BP = blood pressure; b.p.m. = beats per minute; CSM = carotid sinus massage; CSS = carotid sinus syndrome; ECG = electrocardiogram; ED = emergency department; EPS = electrophysiological study; ESC = European Society of Cardiology; HR = heart rate; ICD = implantable cardioverter defibrillator; ILR = implantable loop recorder; LVEF = left ventricular ejection fraction; NYHA = New York Heart Association; OH = orthostatic hypotension; SCD = sudden cardiac death; SVT = supraventricular tachycardia; VA = ventricular arrhythmia; VT = ventricular tachycardia; VVS = vasovagal syncope.

AF = atrial fibrillation; AV = atrioventricular; BBB = bundle branch block; BP = blood pressure; b.p.m. = beats per minute; CSM = carotid sinus massage; CSS = carotid sinus syndrome; ECG = electrocardiogram; ED = emergency department; EPS = electrophysiological study; ESC = European Society of Cardiology; HR = heart rate; ICD = implantable cardioverter defibrillator; ILR = implantable loop recorder; LVEF = left ventricular ejection fraction; NYHA = New York Heart Association; OH = orthostatic hypotension; SCD = sudden cardiac death; SVT = supraventricular tachycardia; VA = ventricular arrhythmia; VT = ventricular tachycardia; VVS = vasovagal syncope.

Supplementary Data with additional Web Tables complementing the full text, and an additional Web Practical Instructions document—with a glossary containing definitions of syncope and related concepts with tracings, videos, flow charts, and checklists—are available on the European Heart Journal website and via the ESC Website at www.escardio.org/guidelines .

Plasma vitamin B-12 concentrations plateaued at intakes >10 μ g/d in the Framingham Offspring Study. This is consistent with earlier observations by Chanarin (19) who summarized studies that measured vitamin B-12 absorption from radioactively labeled aqueous solutions and foods. Although >70% of the vitamin is absorbed when intake is in the range of 0.1–0.5 μ g, the ileal receptors for the vitamin B-12–intrinsic factor complex become saturated with higher intakes such that absorption falls to ≈50% of a 1- μ g dose, 15% of a 10- μ g dose, and 3% of a 25–50- μ g dose ( Figure 1 ). The maximum amount that can be absorbed from a 5–50- μ g single dose is 1.5 μ g. Above 25 μ g, only 1% of a dose is absorbed, by passive diffusion, which explains why the relative increase in serum vitamin B-12 is related to the log of the dose. In healthy Danish women, serum vitamin B-12 and other vitamin B-12 status indicators appeared to plateau at an intake (from food + supplements) >6 μ g/d ( 20 ), but in part this is expected because of the lower efficiency of absorption of the vitamin at higher intakes.

FIGURE 1
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The efficiency of absorption of a single oral dose of vitamin B-12 across a range of intakes. Based on data from reference 19 .

FIGURE 1
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The efficiency of absorption of a single oral dose of vitamin B-12 across a range of intakes. Based on data from reference 19 .

Malabsorption of vitamin B-12 from food is the main cause of deficiency in the elderly and explains why depletion occurs with aging. The condition is caused by atrophy of the gastric mucosa and the gradual loss of gastric acid, which releases the vitamin from food. In its early stages, gastric inflammation and elevated serum gastrin concentrations are common. In elderly persons in the Framingham Offspring Study, 24% of those aged 60–69 y and 37% of those aged ≥80 y had elevated serum gastrin ( 21 ). Likewise, in the SALSA Study, serum gastrin was elevated in 48% of the elderly participants with deficient plasma vitamin B-12 values, in 23% of those with marginal concentrations, and in 21% of those with normal status; overall, these concentrations were inversely correlated with plasma vitamin B-12 ( 6 ).

Food-bound cobalamin malabsorption is diagnosed when an individual has normal absorption of crystalline vitamin B-12 using a Schilling test, no antibodies to intrinsic factor or other tests positive for pernicious anemia (which is defined as vitamin B-12 malabsorption due to loss of gastric intrinsic factor secretion), and no acid-suppressing medications or gastric surgery but impaired absorption of the vitamin when administered bound to egg or chicken serum ( 22 ). Because a normal Schilling test also means that intrinsic factor secretion and function are normal, reabsorption of biliary vitamin B-12 is maintained and depletion of the vitamin will progress slowly, over years. Importantly, however, a longitudinal study revealed that serum vitamin B-12 declined between ages 70–81 y in elderly Swedish men, and for reasons not understood, the decline was most evident in those with lower serum values initially ( 23 ). It seems reasonable to assume that entering later life with low stores of the vitamin for whatever reason, including low dietary intake, would increase the risk that deficiency would result from chronic food cobalamin malabsorption.

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