Syncope Publications (18145)

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Syncope Publications

2017Jan
Ann Pharmacother
Ann Pharmacother 2017 Jan 1:1060028016689264. Epub 2017 Jan 1.
2 VA Ann Arbor Healthcare System, Ann Arbor, MI, USA.

To review the efficacy and safety of pharmacological and nonpharmacological strategies used to treat primary orthostatic hypotension (OH).
A literature review using PubMed and MEDLINE databases searching hypotension, non-pharmacological therapy, midodrine, droxidopa, pyridostigmine, fludrocortisone, atomoxetine, pseudoephedrine, and octreotide was performed.
Randomized or observational studies, cohorts, case series, or case reports written in English between January 1970 and November 2016 that assessed primary OH treatment in adult patients were evaluated. Read More


Based on the chosen criteria, it was found that OH patients make up approximately 15% of all syncope patients, predominantly as a result of cardiovascular or neurological insults, or offending medication. Nonpharmacological strategies are the primary treatment, such as discontinuing offending medications, switching medication administration to bedtime, avoiding large carbohydrate-rich meals, limiting alcohol, maintaining adequate hydration, adding salt to diet, and so on. If these fail, pharmacotherapy can help ameliorate symptoms, including midodrine, droxidopa, fludrocortisone, pyridostigmine, atomoxetine, sympathomimetic agents, and octreotide.
Midodrine and droxidopa possess the most evidence with respect to increasing blood pressure and alleviating symptoms. Pyridostigmine and fludrocortisone can be used in patients who fail to respond to these agents. Emerging evidence with low-dose atomoxetine is promising, especially in those with central autonomic failure, and may prove to be a viable alternative treatment option. Data surrounding other therapies such as sympathomimetic agents or octreotide are minimal. Medication management of primary OH should be guided by patient-specific factors, such as tolerability, adverse effects, and drug-drug and drug-disease interactions.

2017Feb
J Clin Med Res
J Clin Med Res 2017 Feb 31;9(2):163-169. Epub 2016 Dec 31.
Department of Cardiology, LPS Institute of Cardiology, G.S.V.M. Medical College, Kanpur, Uttar Pradesh 208002, India.

Thrombolysis in acute submassive pulmonary embolism (PE) remains controversial. So we studied impact of thrombolytic therapy in acute submassive PE in terms of mortality, hemodynamic status, improvement in right ventricular function, and safety in terms of major and minor bleeding.
A single-center, prospective, randomized study of 86 patients was conducted at LPS Institute of Cardiology, G. Read More

S.V.M. Medical College, Kanpur, India. Patients received thrombolysis (single bolus of tenecteplase) with unfractionated heparin (UFH, group I) or placebo with UFH (group II).
Mean age of patients was 54.35 ± 12.8 years with male dominance (M:F = 70%:30%). Smoking was the most common risk factor seen in 29% of all patients, followed by recent history of immobilization (25%), history of surgery or major trauma within past 1 month (15%), dyslipidemia (10%) and diabetes mellitus (10%). Dyspnea was the most common symptom in 80% of all patients, followed by chest pain in 55% and syncope in 6%. Primary efficacy outcome occurred significantly better in group I vs. group II (4.5% vs. 20%; P = 0.04), and significant difference was also found in hemodynamic decompensation (4.5% vs. 20%; P = 0.04), the fall in mean pulmonary artery systolic pressure (PASP) (28.8% vs. 22.5%; P = 0.03), improvement in right ventricular (RV) function (70% vs. 40%; P = 0.001) and mean hospital stay (8.1 ± 2.5 vs. 11.1 ± 2.14 days; P = 0.001). There was no difference in mortality and major bleeding as safety outcome but increased minor bleeding occurred in group I patients (16% vs. 12%; P = 0.04).
Patients with acute submassive PE do not derive overall mortality benefit, recurrent PE and rehospitalization with thrombolytic therapy but had improved clinical outcome in form of decrease in hemodynamic decompensation, mean hospital stay, PASP and improvement of RV function with similar risk of major bleed but at cost of increased minor bleeding.

2017Jan

Syncope is a common problem among the elderly and a permanent pacemaker is a therapeutic option when a bradycardic etiology is revealed. However, the benefit of pacing when no association of symptoms to bradycardia has been shown is not clear, especially in the elderly OBJECTIVES: Aim of this study was to evaluate the effect of pacing on syncope-free mortality in patients ≥80 years old, with unexplained syncope and positive invasive electrophysiologic testing (EPS).
This was an observational study. Read More

A "positive" EPS for the purposes of this study was defined by at least one of the following: corrected sinus node recovery time >525 ms, basic HV interval >55 ms, detection of infra-Hisian block or appearance of 2(nd) degree atrioventricular block on atrial decremental pacing at a paced cycle length of >400 ms.
Among 2435 screened patients, 228 eligible patients were identified, 145 of whom were implanted with a pacemaker. Kaplan-Meier-determined time-to-event (syncope or death) was 50.1 (95% confidence interval 45.4-54.8) months with a pacemaker versus 37.8 (95% confidence interval 31.3-44.4) months without one (log rank p=0.001). The 4-year time-dependent-estimate of the rate of syncope was 12% versus 44% (p<0.001) and that of any-cause death was 41% versus 56% (p=0.023), respectively. The multivariable odds ratio was 0.25 (95% confidence interval 0.15-0.40), after adjustment for potential confounders.
In patients with unexplained syncope and signs of sinus node dysfunction or impaired atrioventricular conduction on invasive EPS, pacemaker implantation was independently associated with longer syncope-free survival. Significant differences were also shown in the individual components of the primary outcome measure (syncope and death from any cause).

2017Jan
Cardiol Young
Cardiol Young 2017 Jan;27(S1):S110-S114
Division of Cardiology,Children's Hospital Los Angeles,Keck School of Medicine,University of Southern California,Los Angeles,California,United States of America.

Improved public awareness and advances in medical diagnostics have resulted in the development of criteria to determine eligibility or disqualification for the athlete with cardiovascular abnormalities. Simultaneously, protocols have been developed for athletes with concussion or orthopaedic injuries to guide team physicians and consultants in return-to-play decisions. However, there are currently inadequate data to allow the development of such protocols for athletes with cardiovascular abnormalities who have undergone treatment. Read More

Further complicating the decision process is the designation of the team physician as the ultimate authority in making return-to-play decisions - where the team physician often is an employee of the team and supports the team's goal and players as well as the individual athlete. This review will discuss the ethical dilemma of the team physician and the role of the cardiovascular consultant. Following this, current data and practices regarding return to play will be discussed for the following conditions or diagnoses: following catheter ablation for supraventricular tachycardia; following pacemaker or implantable cardioverter-defibrillator implantation; unexplained syncope; and the athlete with a genetic mutation in the absence of any phenotype of associated disease. These recommendations will undoubtedly continue to evolve and improve and should be considered at this time as a point of departure.

2017Jan
Clin. Auton. Res.
Clin Auton Res 2017 Jan 12. Epub 2017 Jan 12.
The Irish Longitudinal Study on Ageing (TILDA), Department of Medical Gerontology, Trinity College, Dublin, Ireland.

To assess the test-retest reliability of orthostatic beat-to-beat blood pressure responses to active standing and related clinical definitions of orthostatic hypotension.
A random sample of community-dwelling older adults from the pan-European Survey of Health, Ageing and Retirement in Europe, Ireland underwent a health assessment that mimicked that of the Irish Longitudinal Study on Ageing. An active stand test was performed using continuous blood pressure measurements. Read More

Participants attended a repeat assessment 4-12 weeks after the initial measurement. A mixed-effects regression model estimated the reliability and minimum detectable change while controlling for fixed observer and time of day effects.
A total of 125 individuals underwent repeat assessment (mean age 66.2 ± 7.5 years; 55.6% female). Mean time between visits was 84.3 ± 23.3 days. There was no significant mean difference in heart rate or blood pressure recovery variables between the first and repeat assessments. Minimum detectable change was noted for changes from resting values in systolic blood pressure (26.4 mmHg) and diastolic blood pressure (13.7 mmHg) at 110 s and for changes in heart rate (10.9 bpm) from resting values at 30 s after standing. Intra-class correlation values ranged from 0.47 for nadir values to 0.80 for heart rate and systolic blood pressure values measured 110 s after standing.
Continuous orthostatic beat-to-beat blood pressure and related clinical definitions show low to moderate reliability and substantial natural variation over a 4-12-week period. Understanding variation in measures is essential for study design or estimating the effects of orthostatic hypotension, while clinically it can be used when evaluating longer term treatment effects.

2016Jan
Front Physiol
Front Physiol 2016 27;7:650. Epub 2016 Dec 27.
Department of Cardiology, General Hospital of People's Liberation Army Beijing, China.

Mutations in hERG cause long QT syndrome type 2 which is characterized by a prolonged QT interval on electrocardiogram and predisposition to life-threatening ventricular tachyarrhythmia, syncope, and sudden death. hERG-G572S induces trafficking defects of hERG channel protein from Golgi to the plasma membrane and results in a dominant negative suppression of hERG current density. As an accessory β subunit, KCNE2 promotes hERG migration from Golgi to cellular membrane. Read More

In this study, we investigated the rescue effect of KCNE2 in a G572S mutation of hERG. Transfection was performed into HEK293 cells. Patch clamp technique, western blotting analyses and confocal microscopic examination were used. Results showed that KCNE2 had a significantly enhanced effect on G572S mutation current. The increase of current was largest at KCNH2:KCNE2 of 1:3. Confocal images showed co-expressing G572S and KCNE2 could cause a substantial up-regulated membrane protein (155 kDa) expression. Expression of membrane protein accumulated markedly with increasing ratio of KCNH2:KCNE2. G572S defective mutant could be restored by both KCNE2 and lower temperature (27°C), which suggested that the lower temperature could be the favorable circumstances for the rescue function of KCNE2. In this study, we successfully set up "the action potential" on the HEK 293 cells by genetically engineered to express Kir2.1, Nav1.5, and Kv11.1, wherein on reaching over an excitation threshold by current injection. The results suggested that KCNE2 could shorten action potential duration which was prolonged by G572S. These findings described electrophysiological characteristics of the LQT2 syndrome mutation KCNH2-G572S and regulation by accessory protein KCNE2, and provided a clue about LQT2 and relative rescue mechanism.

2016Dec
Int. J. Cardiol.
Int J Cardiol 2016 Dec 27. Epub 2016 Dec 27.
Center of Microbiology and Parasitology, Public Health Institute Niš, Serbia, Blvd Zorana Djindjica 81, 18000 Niš, Serbia; Department of Microbiology and Immunology, Faculty of Medicine, University of Niš, Serbia, Blvd Zorana Djindjica 81, 18000 Niš, Serbia.
2017Jan
Nat Rev Cardiol
Nat Rev Cardiol 2017 Jan 12. Epub 2017 Jan 12.
The Heart Institute, Le Bonheur Children's Hospital, University of Tennessee Health Science Center, and St. Jude Children's Research Hospital, 51 N Dunlap Street #100, Memphis, Tennessee 38105, USA.

Left ventricular hypertrabeculation (LVHT) or noncompaction is a myocardial abnormality of unknown aetiology, frequently associated with monogenic disorders, particularly neuromuscular disorders, or with chromosomal defects. LVHT is diagnosed usually by echocardiography by the presence of a bilayered myocardium consisting of a thick, spongy, noncompacted endocardial layer and a thin, compacted, epicardial layer. The pathogenesis of LVHT is unsolved, and the diagnostic criteria, prognosis, and optimal treatment of patients with LVHT are under debate. Read More

LVHT is categorized as distinct primary genetic cardiomyopathy by the AHA and as unclassified cardiomyopathy by the ESC. LVHT is usually asymptomatic, but can be complicated by heart failure, thromboembolism, or ventricular arrhythmias, including sudden cardiac death. Mortality of patients with LVHT ranges from 5% to 47%. Anticoagulation is indicated if atrial fibrillation, severe heart failure, previous embolism, or intracardiac thrombus formation are present. In patients with LVHT with late gadolinium enhancement, an implantable cardioverter-defibrillator might be considered if systolic dysfunction, a family history of sudden cardiac death, nonsustained ventricular tachycardia, or previous syncope is additionally present. In this Review, we discuss the current findings on the aetiology and pathophysiology of LVHT, and provide an overview of the diagnosis, available treatment, and prognosis of this cardiomyopathy.