We describe two cases where postinfarction ventricular septal defect (VSD) was treated with a new technique. Application of direct ultrasonography to the right ventricular (RV) wall enables the surgeon to visualize the region and perform appropriate incision into the right ventricle and trabecula resection. The VSD is sealed with gelatin-resorcin-formal (GRF) glue between two patches, one placed on the left ventricular side and the other on the right ventricular side. RV incision provides easy bleeding control and the "sandwich technique" using two patches and GRF sealing provides geometric preservation of the left ventricular shape and prevents residual shunt.
Background: Sleep apnea syndrome (SAS) is an independent risk factor for hypertension which is a major risk factor for acute aortic dissection. The purposes of this study were to assess the prevalence of SAS in patients with acute aortic dissection, delineate the characteristics of patients who have acute aortic dissection with SAS. Methods: Of 95 consecutive patients with acute aortic dissection, 13 had episodes of sleep apnea and nocturnal hypoxemia. A portable sleep monitoring system was used to assess sleep status in the 13 patients. Results: The SAS-positive group consisted of 12 patients (12.6%), 8 with type A dissection and 4 with type B dissection. Age was significantly lower in the SASpositive group (47.2 ± 8.5 years) than in the SAS-negative group (64.9 ± 10.3 years) (p <0.001). The male:female ratio was significantly higher in the SAS-positive group than in the SAS-negative group (p <0.001). The body mass index was significantly greater in the SAS-positive group than in the SAS-negative group (p <0.001). All 12 patients in the SAS-positive group had hypertension. Conclusions: Patients who have acute aortic dissection with SAS are characterized by being tall, fat, and relatively young men with hypertension. Sleep apnea syndrome may be a risk factor for acute aortic dissection in middle-aged men.Keywords: aortic dissection, sleep apnea syndrome, hypertension, obesity, middle-aged men
IntroductionSleep apnea syndrome (SAS) was first described by investigators at Stanford University in 1976. Sleep apnea syndrome is defined as 30 or more episodes of apnea (cessation of airflow for at least 10 seconds) during 7 hours of sleep in a single night or 5 or more episodes of apnea per hour of sleep (apnea index = ≥5).1� Sleep apnea syndrome is classified into obstructive SAS caused by upper-airway obstruction, central SAS caused by abnormal respiratory control by the central nervous system, and mixed SAS. Obstructive SAS accounts for most cases.
1�Two large multicenter, observational studies performed in the United States, the Sleep Heart Health Study 2� and Wisconsin Sleep Cohort Study, 3� found that respiratory disturbances during sleep are an independent risk factor for hypertension. Other studies have shown that the severity of SAS is related to the incidence of cardiovascular disease, including angina pectoris, myocardial infarction, arrhythmias, and cerebrovascular disease.
4�Acute aortic dissection is a serious, life-threatening condition requiring emergent treatment.5� 6� Hypertension is also a major risk factor for aortic dissection.
Original ArticleAnn Thorac Cardiovasc Surg 2013; 19: 456-460 Original Article
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