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A case of aortic dissection (De Bakey type I) with a fistula to the right atrium through the interatrial septum, diagnosed by transthoracic and transesophageal echocardiography is reported. The patient presented with cardiac failure and a continuous murmur in the right second and third intercostal spaces. The patient underwent successful operative repair.
Diagnostic imaging for aortic dissection has dramatically changed in recent years. Previously, imaging consisted of conventional X-ray radiography, followed by invasive catheter angiography. Now imaging of dissection is performed primarily with multidetector CT, and to a lesser extent, with ultrasound and MRI. Catheter angiography is used primarily as a means of treating complications. Which modality to choose depends on patient factors, physician preference, and differences in availability of state-of-the-art equipment. All three modalities are highly accurate in experienced hands and have revolutionized the detection and evaluation of this condition.
An experimental model of acute aortic dissection has been designed in an effort to examine myocardial contractility and systolic arterial pressure as factors influencing the progression of dissection. Thirty mongrel dogs divided into three experimental groups underwent left thoracotomy and construction of a standard intimal tear in the proximal descending aorta. Nine of ten animals in the control group showed progression of the aortic dissection a mean of 81.5 percent of the distance from the aortotomy to the celiac axis. Group II consisted of ten dogs pretreated with propranolol. The myocardial contractility (dp/dt) was significantly depressed in this group without change in systolic pressure. However, progression of dissection occurred in nine of ten animals as in the control group. In Group III, ten dogs were pretreated with trimethaphan lowering the systolic blood pressure to 90 mm. Hg and depressing the dp/dt to levels equal to those of Group II. There was no progression of aortic dissection in any of the animals in this group. The results indicate that, under these experimental conditions, depression of myocardial contractility alone has no inhibitory effect on the progression of dissection. When controlled hypotension is added to myocardial depression, aortic dissection is inhibited completely.
In five patients with aortic dissection, signs and/or symptoms of pericarditis were part of the early manifestations of the aortic disease. Signs of inflammatory pericarditis were noted clinically in four patients and were found at autopsy in one. In the three nonoperated patients who died of aortic rupture leading to fatal hemopericardium, symptoms of pericarditis preceded fatal rupture of the aorta by four to five days. A fourth patient died after surgical repair of aortic dissection 35 days after the onset of pericarditis. In the fifth patient, manifestations of chronic constrictive pericardial disease occurred over a period of seven months after which old aortic dissection was first identified. In each case, the internal tear of classic aortic dissection was located in the ascending aorta. Microscopic evidence of cystic medial necrosis of the aorta was present in each case. In each of two cases, there was a congenital bicuspid aortic valve. The phenomenon observed represents acute aortic dissection in which slow penetration of blood into the pericardial space caused inflammatory pericarditis. The interval between the onset of pericarditis and rupture of the aorta may allow sufficient time for appropriate diagnosis and potentially lifesaving treatment of the aortic disease.
Intraoperative aortic dissection is one of the complications of aortic cannulation, which is potentially lethal with an incidence of about 0.16%. Early diagnosis and treatment can lower the mortality rate effectively. We report a 68 y/o female patient sustaining an acute type A aortic dissection in consequence of aortic cannulation for mitral valve replacement surgery. Induction of general anesthesia and endotracheal intubation were performed smoothly. Transesophageal echocardiography (TEE) has proven itself as an important tool to offer definite diagnosis of aortic dissection. Iatrogenic intraoperative aortic dissection is rare but is potentially a fatal complication. Early diagnosis and prompt treatment are important for survival.
Patients after aortic dissection repair still have long-term unfavorable prognosis and need careful monitoring. The purpose of this study was to analyze the evolution of aortic dissection after surgical repair in correlation to anatomic changes emerging from systematic magnetic resonance imaging (MRI) follow-up. Between January 1992 and June 1998, 70 patients underwent surgery for type A aortic dissection. Fifty-eight patients were discharged from the hospital (17% operative mortality) and were followed by serial MRI for 12 to 90 months after surgery. In all, 436 postoperative MRI examinations were analyzed. In 13 patients (22.5%) no residual intimal flap was identified, whereas 45 patients (77.5%) presented with distal dissection, with a partial thrombosis of the false lumen in 24. The yearly aortic growth rate was maximum in the descending aortic segment (0.37 +/- 0.43 cm) and was significantly higher in the absence of thrombus in the false lumen (0.56 +/- 0.57 cm) (p <0.05). There were 4 sudden deaths, with documented aortic rupture in 2. Sixteen patients underwent reoperation for expanding aortic diameter. In all but 1 patient, a residual dissection was present (in 13 without any thrombosis of the false lumen). Close MRI follow-up in patients after dissection surgical repair can identify the progression of aortic pathology, providing effective prevention of aortic rupture and timely reoperation. Thrombosis of the false lumen appears to be a protective factor against aortic dilation.
The value of non-invasive medical imagings in diagnosis of dissecting aortic aneurysm was evaluated in 23 patients by two-dimensional transesophageal echocardiography (TEE) and in 23 patients by MRI. An intimal flap was demonstrated in all 23 cases by TEE and in 21 of 23 cases (91.3%) by MRI. DeBakey type classification could be recognized in 20 of 23 cases (87.0%) by TEE and in 21 of 23 cases (91.3%) by MRI. The entry of aortic dissection could be identified in 20 of 23 cases (87.0%) by TEE in 9 of 23 cases (39.1%) by MRI. The differentiation between true and false lumen could be performed in all 23 cases by TEE and in 21 of 23 cases (91.3%) by MRI. The capability of TEE to visualize the lesion of descending aorta was superior to any other conventional diagnostic method, however, there were difficulties in scanning the distal part of the ascending aorta and aortic arch. MRI could not detect the small lesion such as entry in almost all cases, but was superior in diagnosis of the lesion of aortic arch and in recognition of the whole imagings. Since transthoracic echocardiography has an additional value in diagnosis of dissecting aortic aneurysm, the diagnostic method of a combination of transthoracic and transesophageal echocardiography seems to be more valuable. We believe that operation could be carried out solely on the basis of diagnosis of dissecting aortic aneurysm by echocardiography in emergency cases.
BACKGROUND: Aortic dissection is the most frequent cause of premature death in Marfan's syndrome. Low-risk elective surgery of the abnormal aortic root has the potential to prevent this complication. METHODS: We examine genetic, structural, and pathophysiological mechanisms of aortic dissection and discuss the surgical methods used when dissection occurs. RESULTS: Abnormal fibrillin disturbs the functional relationship between blood flow and vascular endothelial cell response (mechanotransduction). Decreased arterial distensibility also decreases aortic wall stress, thereby predisposing to dissection in the weakened arterial wall. Radical root and wall surgery and lifelong beta-blockade are required after aortic dissection. CONCLUSIONS: Detailed lifelong medical and surgical treatment can greatly prolong life in Marfan's syndrome. Elective aortic root replacement is paramount in preventing aortic dissection and avoiding subsequent problems in the distal aorta.
A classification of dissecting aortic aneurysms is presented. It allows one to determine more accurately any given pathology in any patient. It helps the surgeon select the most appropriate operative variant and to define tactics of treatment. For example, to discuss the necessity of repeated reconstruction. Our clinical cases have confirmed it.
PURPOSE: To create an experimental model of aortic dissection with a long-lasting patent false lumen as a proper animal model for development of less-invasive treatment for aortic dissection. MATERIALS AND METHODS: Fifteen adult beagle dogs (weight, 10-12 kg) were used. The descending aorta was exposed by a left thoracotomy at the sixth intercostal space. The entry for the aortic dissection was created surgically just distal to the origin of the left innominate artery and the reentry was 5 cm distal to the entry point. Normal saline solution was injected into the aortic wall (ie, media) between these two points to create the dissection. The dogs were followed up at 1 day, 3 months, 1 year, and 2 years. RESULTS: All 12 surviving dogs had completely patent true and false lumina without any thrombi. Microscopic examination showed that the dissection was created in the tunica media layer, making it identical to aortic dissection in humans. Color Doppler imaging confirmed the patency of the true and false lumina and the relatively narrowed true lumen. CONCLUSION: In this canine model of aortic dissection, the false lumen has excellent long-term patency and the dissection plane is histologically similar to that in human aortic dissection. This model may contribute to the development of new treatments for Stanford type B aortic dissection.
Aortic dissection is an acute cardiovascular disease associated with high mortality and morbidity. Although uncommon, recent studies have shown that the incidence of this catastrophic disease is steadily increasing. Unfortunately, the disease is still not well recognized on clinical presentation due to lack of specific signs and symptoms. As early diagnosis and initial management are critical for survival, we focused on developing a biochemical diagnostic approach for this disease given its meritorious properties in use in the acute clinical situation and additional projected combined use with established imaging modalities. Studies using an assay developed against smooth muscle myosin heavy chain, a protein which is released from the aortic medial smooth muscle cells on insult to the aortic wall, showed promising results for use of this assay in the diagnosis of aortic dissection. The background of this pioneering assay in addition to its clinical use are discussed in this review.
Recently two cases of Stanford type A acute aortic dissection with stenosis of the branches of aortic arch were operated. Both of them had the intimal tear in the ascending aorta, and the stenosis caused by the dissection was present in the left subclavian artery in the first case and in the brachiocephalic and the right common carotid arteries in the second case. Repairs of the dissected ascending aorta were performed successfully with the interposition of the ringed intraluminal graft in the first case, and with the composite graft replacement of the ascending aorta and the aortic valve in the second case. Complete remission or significant relief of the branch stenoses which had not been given direct surgical repairs was observed by the postoperative angiograms.
A 37-year-old male who was on chronic dialysis regimen for IgA nephropathy developed acute Stanford A type aortic dissection. Replacement of the ascending aorta was performed with the aid of extracorporeal circulation, selective cerebral perfusion, and open distal anastomosis technique. The site of the intimal tear in the ascending aorta was resected and the gelatin-resorcin-formaldehyde (GRF) glue was applied to both stumps. The outside of dissecting aortic wall was reinforced with Teflon-felt strips. Two months after the operation, the patient required an urgent operation due to threatening spindle evolution of a persisting dissection in the descending aorta. Replacement of the total arch and the descending aorta was carried out via the median sternotomy with the left anterior thoracotomy, and a subclavian incision. Continuous veno-venous hemofiltration was initiated immediately after both operations and the water balance was maintained well. The patient was discharged 1 month postoperatively. It was suggested that the inside of the dissected aortic wall should be also reinforced even when the GRF glue was used in patients who have a fragile intimal flap and a wide tear.
BACKGROUND: Patients with acute type A aortic dissection are associated with a high mortality rate and postoperative complications. This study was designed to explore perioperative risk factors for death in patients with acute type A aortic dissection. METHODS AND RESULTS: One hundred nine consecutive surgical patients with acute type A aortic dissection were included in the present study. Thirty-five perioperative risk factors were used in the statistical analysis for mortality prediction. The 30-day mortality rate for all patients was 30% (33 of 109). Univariate analysis revealed 5 preoperative and intraoperative risk factors that were found to be statistically significant predictors for death: older age, renal failure, preoperative hemodynamic instability, preoperative cardiopulmonary resuscitation, and lack of retrograde cerebral perfusion (P < 0.05). Rupture of aneurysm, hypothermic circulatory arrest time, and operation date were not found to be risk factors for death. Stepwise multiple logistic regression confirmed that older age and lack of retrograde cerebral perfusion were statistically significant independent risk factors for death (P < 0.05). Four postoperative complications were found to be statistically significant prognostic indicators for death: liver failure, stroke, sepsis, and reoperation after the initial surgery (P < 0.05). CONCLUSIONS: Perioperative risk factors for death after the operation for acute type A aortic dissection were identified. This will allow physicians and surgeons to better assess the patient's risk, which will lead to better outcome.
Intraoperative dissection and late ascending aortic dissection and aneurysm formation infrequently complicate cardiac operations but remain a significant source of morbidity and mortality. A review of 11,145 consecutive cardiac operations at Emory University from January, 1982 through December, 1988 yielded 27 patients with an intraoperative ascending aortic dissection (incidence 0.24%) occurring at the time of the original procedure, with a hospital mortality of 14.8%. Nine additional patients with ascending aortic dissection or aneurysm, presenting late after a previous cardiac operation, were treated during this same period with three deaths. The technical aspects and decision making for application of closed aortic plication, open aortic reconstruction, and ascending aortic replacement based directly on the extent of the intraoperative dissection is detailed. An individualized technical approach tailored to the pathology encountered is outlined for the reoperative group of patients. Etiology, risk factors, principles of prevention, and indications for operation are also discussed.
Aortic dissection rarely occurs in 2 or more family members without Marfan's syndrome. This report describes two aged siblings who underwent emergency operations for aortic dissection. Case 1: A 71-year-old female (sister), who had Stanford type B aortic dissection, underwent replacement of the descending aorta with a Hemashield graft. Case 2: A 72-year-old male (brother of case 1), who had Stanford type A aortic dissection, underwent replacement of the ascending aorta with a UBE graft following the closure of the entry located in the proximal arch. Neither of 2 siblings nor other family members had any features of the Marfan's syndrome. It is proposed that two aortic dissections occurred coincidentally in one family without Marfan's syndrome.
Acute aortic dissection may have variable presentations, making the diagnosis clinically challenging. Acute neurologic syndromes secondary to dissection of the aorta are uncommon. However, including aortic dissection in the differential diagnosis is imperative. This report describes the first reported case of an acute thoracic aortic dissection presenting with the chief complaint of unilateral lower extremity numbness. Peripheral ischemic neuropathy as the result of vascular occlusion is uncommon. The pathophysiology and clinical manifestations of ischemic neuropathies in the setting of acute aortic dissection are discussed.
Until recently, the diagnosis of aortic dissection rested on aortography. The purpose of this study was to evaluate the diagnostic value of echocardiography in that disease and its ability to inform on the extent of the dissection and on the presence of associated lesions. Twenty-six patients (mean age 64 +/- 10 years) admitted for suspected aortic dissection were explored by echocardiography and the results were compared with those of angiography and/or anatomical findings. Echocardiography provided the diagnosis in 14 of the 16 patients with aortic dissection and excluded it in the remaining 10 patients. The sensitivity and specificity of the method were 87.5 p. 100 and 100 p. 100 respectively. The type of dissection was correctly determined in 90 p. 100 of the patients whose aorta had been totally explored by echocardiography. Aortic regurgitation and pericardial effusion were detected in 81 p. 100 and 50 p. 100 respectively of patients with aortic dissection. These results confirm the diagnostic value of echocardiography in dissection of the aorta. The extent of the lesion can only be evaluated when the whole of the aorta is visualized. The echocardiographic diagnosis is easier when the ascending aorta is involved (type I), while in type III aortic dissection there is a risk of missing a retrograde lesion of the aorta and confusing this type with type I. In this study two kinds of intimal flap motion were observed: in the first one the motion was independent of that of the aorta, while the second one resembled a division of the aortic, wall the motion of which is parallel to that of the aorta.