OBJECTIVE
To study the structure and nature of ventricular arrhythmias (VA) in patients with sleep apnea syndromes (SAS), arterial hypertension and coronary artery disease (CAD) without chronic heart failure (CHF), as well as the most effective and safe treatment approaches.
MATERIAL AND METHODS
WE examined 167 men and women aged 41—72 years with suspected SAS considering clinical symptoms (snoring at night, severe daytime sleepiness, excess weight with body mass index (BMI) > 30 kg/m2, short and thick neck) or diagnostic data on blood pressure and heart rhythm disturbances (daily monitoring of blood pressure and ECG). Exclusion and non-inclusion criteria were age <40 or >74 years, any severe comorbidity, any form of paroxysmal supraventricular arrhythmia, permanent atrial fibrillation with CHF, intake of class IC and III antiarrhythmic drugs, electrolyte disturbances, thyroid dysfunction, previous radiofrequency ablation and/or device implantation. Cardiorespiratory monitoring (CRM) with standard registration of parameters (snoring; breathing; oxygen saturation; respiratory movements of the chest and abdominal wall; body position) was used to verify SAS. Obstructive sleep apnea syndromes were not detected in 32 out of 167 individuals. All patients included in the study had obstructive SAS (n=135), and 3 groups were formed depending on the underlying pathology: group 1 — patients with obstructive SAS and hypertension (n=58); group 2 — patients with obstructive SAS and CAD (n=31); group 3 — patients with obstructive SAS, CAD and hypertension (n=46). Considering the results of 24-hour ECG monitoring, we analyzed ventricular arrhythmias and their dynamics under drug and CPAP therapy.
RESULTS
There were no cases of central SAS. In all patients with ventricular arrhythmias, severe obstructive SAS was verified after CRM (n=135). Single premature ventricular contractions (PVC) were detected in all patients. However, patients with CAD (n=77), regardless of hypertension, demonstrated significantly (p<0.001) higher number of single PVCs compared to patients with hypertension. Also, patients with CAD regardless of hypertension were significantly more likely (p<0.001) to have potentially malignant ventricular arrhythmias (paired PVCs and paroxysms of non-sustained ventricular tachycardia). The number of single PVCs in patients with CAD significantly correlated with apnea-hypopnea index (AHI), regardless of hypertension (ρ=0.57; p=0.001). Comparison of paroxysms of non-sustained ventricular tachycardia with age, BMI, AHI and mean saturation in patients with obstructive SAS and CAD revealed a significant correlation with AHI (ρ=0.481; p=0.006).
CONCLUSION
In patients with CAD without CHF, central SAS is not recorded in severe apnea. CPAP therapy and drug therapy in patients with ventricular tachycardia and controlled hypertension significantly reduce the number of single and paired PVCs in patients with CAD regardless of hypertension (p=0.028 and p=0.001, respectively). In patients with severe obstructive SAS, CAD and hypertension, combined therapy significantly reduces the number of paroxysms of non-sustained ventricular tachycardia (p=0.01). There were no cases of sudden cardiac death throughout 6 months.
