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.