ABSTRACT
Atrial fibrillation is the arrhythmia that most frequently leads to hospital admission. As prevalence of atrial fibrillation increases with age, its epidemiological relevance will increase due to the well-known changes in life expectancy. In the presence of atrial fibrillation the cardiovascular mortality and the risk for a stroke are considerably elevated. Interventional treatment, such as catheter ablation or special pacemaker algorithms, have been improved extensively in the last years as a therapeutic option. Nevertheless drug therapy is still the first choice of treating atrial fibrillation.
Subject(s)
Anti-Arrhythmia Agents/therapeutic use , Atrial Fibrillation/therapy , Atrial Fibrillation/drug therapy , Atrial Fibrillation/epidemiology , Humans , Pacemaker, Artificial , Risk , Stroke/epidemiology , Stroke/etiologyABSTRACT
RATIONALE: There is growing evidence that obstructive sleep apnea is associated with coronary artery disease. However, there are no data on the course of coronary stenosis after percutaneous coronary intervention in patients with obstructive sleep apnea. OBJECTIVES: To determine whether sleep apnea is associated with increased late lumen loss and restenosis after percutaneous coronary intervention. METHODS: 78 patients with coronary artery disease who underwent elective percutaneous coronary intervention were divided in 2 groups: 43 patients with an apnea hypopnea - Index < 10/h (group I) and 35 pt. with obstructive sleep apnea and an AHI > 10/h (group II). Late lumen loss, a marker of restenosis, was determined using quantitative coronary angiography after 6.9 +/- 3.1 months. MAIN RESULTS: Angiographic restenosis (>50% luminal diameter), was present in 6 (14%) of group I and in 9 (25%) of group II (p = 0.11). Late lumen loss was significant higher in pt. with an AHI > 10/h (0.7 +/- 0.69 mm vs. 0.38 +/- 0.37 mm, p = 0.01). Among these 35 patients, 21(60%) used their CPAP devices regularly. There was a marginally lower late lumen loss in treated patients, nevertheless, this difference did not reach statistical significance (0.57 +/- 0.47 mm vs. 0.99 +/- 0.86 mm, p = 0.08). There was no difference in late lumen loss between treated patients and the group I (p = 0.206). CONCLUSION: In summary, patients with OSA and coronary artery disease have a higher degree of late lumen loss, which is a marker of restenosis and vessel remodeling after elective percutaneous intervention.
Subject(s)
Angioplasty, Balloon, Coronary , Coronary Restenosis/etiology , Myocardial Ischemia/therapy , Sleep Apnea, Obstructive/complications , Aged , Case-Control Studies , Continuous Positive Airway Pressure , Coronary Angiography , Coronary Artery Disease/etiology , Coronary Artery Disease/therapy , Coronary Restenosis/pathology , Coronary Vessels/pathology , Female , Follow-Up Studies , Humans , Male , Middle Aged , Myocardial Ischemia/etiology , Sleep Apnea, Obstructive/therapyABSTRACT
At least half of patients with heart failure (HF) suffer from sleep apnea. Growing evidence suggests that there may be a strong pathophysiological link between chronic HF and sleep apnea due to nocturnal oxygen desaturation and sympathetic activation. It seems that sleep apnea contributes to systolic and diastolic HF, reduced left and right ventricular function, and arrhythmia (e.g. atrial fibrillation, bradycardia, or ventricular ectopy). Therefore, treatment of sleep apnea might alleviate cardiac symptoms and improve cardiac function. Nevertheless, the exact role of long-term treatment of sleep apnea in HF patients remains to be elucidated, as important clinical endpoints (e.g mortality) have been assessed in only a few studies. Heart Fail Monit 2008;5(4):106-11.
Subject(s)
Heart Failure , Sleep Apnea Syndromes , Atrial Fibrillation , Continuous Positive Airway Pressure , Humans , SystoleABSTRACT
Arterial hypertension (HTN) represents one of the major causes of atrial fibrillation, a cardiac arrhythmia with high prevalence and comorbidity. The aim of this study was to investigate whether paroxysmal atrial fibrillation can be treated by the regression of left ventricular hypertrophy achieved by antihypertensive therapy. Included in the present study were 104 patients who had had HTN for more than 1 year. None of them suffered from coronary heart disease. All patients were investigated by 24-h Holter ECG and echocardiography at baseline and after a mean of 24 months. Patients were divided into two groups: group A consisted of those (53.8%) who showed a regression of the left ventricular muscle mass index (LVMMI) during the follow-up (154.9+/-5.1 vs. 123.5+/-2.8 g/m(2)), and group B those (45.2%) who showed a progression of LVMMI (122.2+/-3.2 vs. 143.2+/-3.2 g/m(2)). In group A the prevalence of atrial fibrillation decreased from 12.5% to 1.8% (p<0.05), while it was increased in group B from 8.5% to 17.0%. The left atrial diameter was reduced following antihypertensive therapy in group A from 39.1+/-5.3 mm to 37.4+/-4.6 mm (p<0.01) and increased in group B from 37.0+/-0.7 mm to 39.0+/-0.9 mm (p<0.01). We conclude that a regression of the left ventricular muscle mass leads to a reduction of left atrial diameter and consecutively to a decrease in the prevalence of intermittent atrial fibrillation. This may be explained by a better left ventricular diastolic function following decreased vascular and extravascular resistance of the coronary arteries. This relation shows the benefits of causal antihypertensive therapy for the treatment of paroxysmal atrial fibrillation.
