ABSTRACT
BACKGROUND/AIM: A possible cause of malignant heart rhythm disorders is the syndrome of sleep apnea (periodic cessation of breathing during sleep longer than 10 seconds). Recent 24 h ECG software systems have the option of determination ECG apnea index (AI) based on the change in voltage of QRS complexes. The aim of the study was to determine the significance of AI evaluation in routine 24-hour Holter ECG on a group of 12 patients. METHODS: We presented a total of 12 consecutive patients with previously documented arrhythmias and the history of breathing disorders during night. They were analyzed by 24 h ECG (Medilog AR 12 plus Darwin), that is able to determine AI. RESULTS: We presented a case series of 12 patients, 8 men and 4 women, mean age 58.75 years and the average AI 5.78. In the whole group there was a trend of increasing prevalence of complex rhythm disorders with increasing of AI and increased frequency of arrhythmias in the night phase vs. day phase. CONCLUSION: Determination of AI using routine long term (24 h) ECG analysis is important because sleep apnea can be successfully treated as an etiological or contributing factor of arrhythmias.
Subject(s)
Arrhythmias, Cardiac/physiopathology , Electrocardiography, Ambulatory , Sleep Apnea Syndromes/diagnosis , Sleep Apnea Syndromes/physiopathology , Adult , Aged , Female , Humans , Male , Middle Aged , Pilot Projects , Polysomnography , SoftwareABSTRACT
OBJECTIVE: This study on responsiveness to clopidogrel and aspirin evaluates its interaction with: (i) patient characteristics; (ii) procedure characteristics; (iii) antiplatelet dose. METHODS AND RESULTS: After elective PCI, 60 patients receiving aspirin 100 mg daily, and clopidogrel 75 mg daily were monitored with the PFA 100 test and VASP assay. Non-responsiveness to aspirin and clopidogrel was found in 23 (38%) and 18 (30%) of 60 patients, respectively. Seven (12%) patients were dual nonresponders. Non-responders to both aspirin and clopidogrel were more often smokers. Non-responders to clopidogrel, in addition had elevated inflammatory markers (P < 0.05). Dual non-responders had (i) a higher platelet count, LDL, and CRP; (ii) a lower HDL (P < 0.05). Clopidogrel non-responders were receiving 150 mg clopidogrel, with a positive response in 72%. Eighty % of non-responders to 150 mg clopidogrel were also non-responders to aspirin. CONCLUSION: Baseline patient characteristics and clopidogrel dose modify the antiplatelet response. Also, patients resistant to both aspirin and clopidogrel do no benefit from an increased clopidogrel dose.
