Heart rate variability parameters and ventricular arrhythmia correlate with pulmonary arterial pressure in adult patients with idiopathic pulmonary arterial hypertension

Arrhythmias in pulmonary arterial hypertension

“…[13] In a cohort of patients with the congenital heart disease and the Eisenmenger reaction there was evidence of more sustained ventricular arrhythmias with 5% of patients demonstrating ventricular tachycardia although the demonstration of ventricular tachycardia was not associated with sudden cardiac death [12]. In a retrospective analysis of 3110 patients with PAH over 3 years in a multicentre study 513 patients died, and of these 17% were due to sudden and unexpected causes.…”

Advanced and traditional electrocardiographic risk factors in pulmonary arterial hypertension: the significance of ventricular late potentials

“…The impaired cardiac autonomic control as reflected by the frequency-domain HRV parameters, related to the peak oxygen uptake as a marker of the severity of the disease, had been reported in PAH previously [17]. It was also stated that higher pulmonary arterial pressure was correlated with lower time-domain and frequency HRV indices [18]. Abnormal frequency-and time-domain HRV indices remain compromised even after one year of disease-specific treatment [19].…”

Sympatho–Vagal Dysfunction in Patients with End-Stage Lung Disease Awaiting Lung Transplantation

“…For example, in PAH, sympathetic overactivity is evidenced in some studies by increased systemic vascular resistance [19] or direct measurement of muscle sympathetic nervous activity, and chronic overactivity could relate to disease severity [20,21]. However, HRV studies revealed that, regarding the autonomic modulation of the heart, both sympathetic and vagal branches are impaired in PAH patients compared to healthy controls [17,21,22]. The incoherence of increased muscle sympathetic nerve activity and decrease in both vagal-and sympathetic-mediated HRV indexes is not completely explained yet.…”

“…The respiratory rate was significantly coupled with the HF component of the RR interval, as expressed by RR-RESP HFk 2 values (> 0.5) for all groups (Tables 2 and 3); LTx patients showed higher levels of RESP HF than HC. (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27), p = 0.02), a marker of sympathetic modulation, and lower levels of 2LV% (7 (4-13) vs. 11 (8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18), p = 0.005), a marker of vagal modulation, in comparison to healthy controls ( Figure 1). These observations are consistent with the previous ones, confirming a higher sympathetic modulation and a lower vagal modulation in patients with end-stage lung disease.…”

“…Again, symbolic analysis ( Figure 3) showed a difference between the two groups: more severely affected patients had lower levels of 0V% (15 (±13) vs. 29 (±15), p = 0.006) and significantly higher levels of 2LV% (11 (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19) vs. 6 (3-11), p = 0.023) and 2UV% (26 (12-37) vs. 18 (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23), p = 0.04). These data confirmed a lower sympathetic modulation and a predominant vagal modulation in more severely affected patients.…”