NCT03855540

Atrial Fibrillation in Relationship to Sleep Quality and Plasma Biomarkers

AFISBIO - Atrial Fibrillation in Relationship to Sleep Quality and Plasma Biomarkers.

• Status: Unknown
• Phase: —
• Study type: Observational
• Enrollment: 200 (estimated)
• Sponsor: Premedix Academy · Academic / Other
• Sex: All
• Age: 18 Years
• Healthy volunteers: Not accepted

Summary

A. Compare the plasmatic biomarkers between the cohort with and without AFib. B. Find sensitive and specific biomarkers that could be used for the diagnostic management of AFib. C. Compare the quality of sleep between the cohort with and without AFib by the means of sleeping quality questionnaire

Detailed description

AFib is the most common sustained arrhythmia, associated with an increased risk of stroke, heart failure, and mortality. Despite the high prevalence, AFib may be asymptomatic and consequently subclinical. Detection of subclinical AFib is highly challenging as only a minority of the patients is diagnosed during a standard examinations with a 12 - lead ECG or a 24h ECG Holter monitoring. Documented AFib causes 15% of ischemic strokes, however approximately 25% of ischemic strokes is of an unknown etiology. It is believed that undetected subclinical AFib is responsible for these strokes. There is also evidence that asymptomatic AFib is associated with a higher incidence of strokes in comparison to symptomatic AFib. Due to the fact that the standard ECG examination is not sufficient for AFib detection, various ECG screening methods have been introduced. Intermittent short ECG recording seems to be more effective than 24-hour Holter ECG in the detection of the arrhythmia however, it is not known whether it is superior to the 7 - day ECG Holter monitoring. Plasmatic biomarkers might be of a paramount importance in the diagnostic management. Several plasmatic biomarkers were tested to find an association with AFib. Perhaps the most studied ones were the natriuretic peptides that showed to be significantly increased in patients with AFib. Similarly, high sensitivity troponins are elevated in patients with the AFib. Another marker of left atrial stretching and also of ionotropic effects is apelin. Patients with lone AFib showed a significantly decreased levels of this peptide. Conflicting results were shown in studies with inflammatory biomarkers such as high sensitivity CRP Parameters reflecting thrombogenesis were also found to be associated with the arrhythmia. Fibrinogen and fibrin D-dimer were significantly increased in paroxysmal AFib. Finally, in the last years, the circulating micro RNAs emerged as a promising biomarker of AFib, having important function in suppression of messenger RNA responsible for thrombogenesis and ionotropic functions. The weakness of the mentioned studies is, that the biomarkers were usually tested in patients with a few comorbidities. So, it is not known whether these biomarkers are specific for AFib "per se" or whether they just reflect pathophysiological mechanisms like inflammation, fibrogenesis or left atrium stretching that is also present in other cardiovascular diseases. Furthermore, the AFib cohorts were often not matched with the control groups adding more uncertainty. To clarify these questions, we designed a study where plasmatic biomarkers will be studied in high risk cohort of patients with AFib having several cardiovascular comorbidities. These patients will be subsequently matched with a control group according to the age, gender and the cardiovascular comorbidities. Similarly, as the continuum of organic changes of the heart from the left ventricular diastolic dysfunction, left atrial dilatation ending with heart failure, there is also "arrhythmology continuum" in patients with arterial hypertension to supraventricular premature contractions via paroxysmal tachycardia of fibrillation up to the permanent atrial fibrillation (AFib). A common etiopathology factor of these disorders is increased sympathetic activity, which together with the catecholamine release during the stress causes arrhythmogenic substrates due to the atrial fibrogenesis. The relation between sleep disorders and the AFib is poorly understood. Micro awakenings during the night increases sympathetic activity and the arterial blood pressure. Other possible mechanism might be the decrease of plasmatic melatonin related to aging. Sleep disorders are linked to the increased heart rate, worsening of the heart rate variability, increased metabolism and body temperature, increased beta EEG activity and activation of the hypothalamic - pituitary - adrenal axis. In patients with arterial hypertension, there is an increased occurrence of premature atrial contractions that is linked to increased risk of AF incidence.

Conditions

• Atrial Fibrillation

Interventions

Type	Name	Description
DIAGNOSTIC_TEST	ECHOcardiography	ECHO parameters 1. LA diameter 2. LVEDD 3. LVEF 4. Diastolic dysfunction 5. Valvular disease
DIAGNOSTIC_TEST	Peripheral blood samples for plasmatic biomarkers	1. Coagulation * D - dimer * Fibrinogen 2. Inflammation and fibrosis * Hs - CRP * AGEs * Soluble RAGE 3. Hemodynamics (LA stretch) * Apelin * NT - proBNP * Hs - troponin 4. MiRNA * miRNA - 1 * miRNA - 133 * miRNA - 29b * miRNA - 208a * miRNA - 208b * miRNA - 499
DIAGNOSTIC_TEST	Athens insomnia scale questionnaire	Athens insomnia scale questionnaire
DIAGNOSTIC_TEST	ECG Holter monitor	Patient receives ECG Holter monitor if included to the control group
DIAGNOSTIC_TEST	ECG event recorder	Patient receives ECG event recorder for twice daily (or if symptoms), 90 seconds duration ECG monitoring if included to the control group

Timeline

• Start date: 2018-04-11
• Primary completion: 2019-12-31
• Completion: 2019-12-31
• First posted: 2019-02-26
• Last updated: 2019-03-29

Locations

4 sites across 1 country: Slovakia