Faculty Bibliography

BACKGROUND: Abdominal aortic aneurysm (AAA) is associated with atherosclerosis elsewhere. Thoracic aortic atheromas (ATHs) seen on transesophageal echocardiography (TEE) are an important cause of stroke and peripheral embolization. The purposes of this study were to determine whether an association exists between AAA and ATHs and to assess the importance of screening patients with ATHs for AAA. METHODS: For the retrospective analysis, 109 patients with AAA and 109 matched controls were compared for the prevalence of ATHs on TEE and for historical variables. For the prospective analysis, screening for AAA on ultrasonography was performed in 364 patients at the time of TEE. RESULTS: Results of the retrospective analysis showed that ATHs were present in 52% of patients with AAA and in 25% of controls (odds ratio [OR] = 3.3; P =.00003). There was a significantly higher prevalence of hypertension, myocardial infarction, heart failure, smoking, and carotid or peripheral arterial disease in patients with AAA. However, only ATHs were independently associated with AAA on multivariate analysis (P =.001). Results of the prospective analysis showed that screening at the time of TEE in 364 patients revealed AAA in 13.9% of those with ATHs and in 1.4% of those without ATHs (P <.0001; OR = 11.4). CONCLUSIONS: (1) There is a strong, highly significant association between abdominal aneurysm and thoracic atheromas. (2) Patients with AAA may be at high risk for stroke because of the concomitance of thoracic aortic atheromas. (3) The high prevalence of abdominal aneurysm in patients with thoracic atheromas suggests that screening for abdominal aneurysm should be carried out in all patients with thoracic atheromas identified by TEE

The pulmonary artery is typically seen on transthoracic echocardiography in its longitudinal axis. Therefore, short axis views of the pulmonic valve leaflets are not generally obtained, and the distinction between tricuspid and bicuspid pulmonic valves is difficult or impossible. Bicuspid pulmonic valve is one cause of pulmonic stenosis, which is especially common in tetralogy of Fallot. Presented here are 2 patients in whom the orientation of the pulmonary artery was unusual, and the pulmonic valve was seen en face. The first patient had tetralogy of Fallot and a bicuspid pulmonic valve. The severe obstruction to right ventricular outflow was infundibular. The second patient had severe stenosis of a tricuspid pulmonic valve, which was treated with balloon valvuloplasty. These unusual views of the pulmonic valve leaflets were obtained because of anterior displacement of the pulmonary artery, and precise anatomic delineation of the problem in each case was possible with transthoracic echocardiography

BACKGROUND: The pulmonary venous flow velocity pattern (PVFVP) in atrial septal defect (ASD) has not been previously studied in detail. Normally, PVFVP is primarily determined by the left heart performance. We hypothesized that the impact of left-sided heart dynamics on PVFVP is diminished in patients with ASD because of the presence of a left-to-right shunt into the low-resistance right side of the heart. METHODS AND RESULTS: Transesophageal echocardiography was performed in 19 adults and 3 children with a large, uncomplicated secundum ASD (maximum diameter 0.6 to 3.0 cm). All patients were in normal sinus rhythm with an average heart rate of 78 bpm in adults and 116 bpm in children. In 21 subjects the antegrade PVFVP lacked distinct systolic (S) and diastolic (D) waves. Instead, we observed a single continuous antegrade wave extending from the beginning of systole to the onset of atrial contraction. Furthermore, the amplitude of the atrial reversal (AR) wave was smaller than in historical controls. In 3 patients in whom ASD was surgically repaired, we observed an immediate return of distinct S and D waves postoperatively. This confirmed that PVFVP abnormality was indeed the result of the ASD. Also a large increase in the AR wave amplitude (46 + 15 cm/s) was noted postoperatively. CONCLUSIONS: This previously unrecognized PVFVP comprising a single continuous antegrade wave and a diminished AR wave sheds new light on the hemodynamics of ASDs. Its presence may also alert the echocardiographer to the possibility of an ASD when the septal defect cannot be visualized directly

The left atrial appendage of patients with mitral valve disease is commonly a source of thromboembolus and is often ligated during mitral valve surgery to diminish this risk. However, ligation is often incomplete. We describe a patient with a stroke whose only source of embolus was an incompletely ligated left atrial appendage. Attempts to exclude the left atrial appendage from the arterial circulation by suture ligation may not decrease the risk of thromboemboli and instead may increase such risk

OBJECTIVES: This study sought to determine the incidence of incomplete ligation of the left atrial appendage (LAA) during mitral valve surgery. BACKGROUND: Ligation of the LAA to prevent future thromboembolic events is commonly performed during mitral surgery. However, success in completely exduding the appendage from the circulation has never been systematically assessed. METHODS: Using transesophageal Doppler echocardiography, we studied 50 patients who underwent mitral valve surgery and ligation of the LAA. Thirty patients were studied immediately postoperative, and 20 patients were studied 6 days to 13 years after surgery. Incomplete ligation was detected by demonstrating a color jet traversing the separation between the left atrial body and appendage. RESULTS: Transesophageal echocardiography detected incomplete LAA ligation in 18 of 50 (36%) patients. The incidence of incomplete ligation was not significantly different between patients studied immediately postoperative and patients studied at various times after surgery. Type of mitral surgery (repair vs. replacement), operative approach (sternotomy vs. port access), left atrial size or degree of mitral regurgias unrelated to type of surgery, surgical approach, left atrial size or degree of mitral regurgitation. Residual communication between the incompletely ligated appendage and the left atrial body may produce a milieu of stagnant blood flow within the appendage and be a potential mechanism for embolic events

BACKGROUND: The outcome of aortic valve replacement for severe aortic stenosis is worse in patients with impaired left ventricular function. Such dysfunction in aortic stenosis may be reversible if caused by afterload mismatch, but not if it is caused by superimposed myocardial infarction. METHODS: From our echocardiography database, 55 patients with severe aortic stenosis (valve area < or =0.75 cm2) and ejection fractions of 30% or lower who subsequently underwent aortic valve replacement were included. The operative mortality and clinical follow-up were detailed. RESULTS: There were 10 perioperative deaths (operative mortality, 18%). Twenty (36%) of the 55 patients had a prior myocardial infarction. In the 35 patients without prior myocardial infarction, there was only 1 death (3%). In contrast, 9 of 20 patients with prior myocardial infarction died (mortality rate, 45%; P< or =.001). The factors significantly associated with perioperative death on univariate analysis (functional class, mean aortic gradient, and prior myocardial infarction) were entered into a model for stepwise logistic regression. This multivariate analysis showed that only prior myocardial infarction was independently associated with perioperative death (odds ratio, 14.9; 95% confidence interval, 2.4-92.1; P = .004). CONCLUSIONS: The risk of aortic valve replacement in patients with severe aortic stenosis and severely reduced left ventricular systolic function is extremely high if the patients have had a prior myocardial infarction. This information should be factored into the risk-benefit analysis that is done preoperatively for these patients, and it may preclude operation for some

Echocardiography demonstrated an 8-cm mass adjacent to the right side of the heart in a 79-year-old man with a history of hypertension and a repaired abdominal aortic aneurysm. The results of Doppler echocardiography and magnetic resonance imaging suggested the diagnosis of an unusually large coronary artery aneurysm, and this was confirmed with coronary angiography. At surgery, the 8- to 10-cm coronary aneurysm was resected, and the patient made an uneventful recovery

BACKGROUND: The intraaortic balloon pump has been shown to improve cardiac output and diastolic coronary flow. Animal studies with balloon counterpulsation have shown variable effects on carotid and cerebral blood flow. We investigated the effects of counterpulsation with the intraaortic balloon pump on blood flow in the common carotid artery in human beings. METHODS AND RESULTS: We studied 14 patients who had an intraaortic balloon pump placed for clinical indications; 9 were hypotensive (4 in the setting of an acute myocardial infarction and 5 immediately after cardiac surgery). Five patients required counterpulsation after undergoing complicated coronary angioplasty. Common carotid artery blood flow was assessed with carotid Duplex scanning both with and without 1:1 balloon augmentation. We found no net increase in the total blood flow in the common carotid artery with intraaortic balloon counterpulsation. This result occurred despite a significant mean increase in both the peak flow velocity and flow velocity integral of the augmented diastolic flows by 160% and 78%, respectively. Total flow did not change because an early systolic reversal of blood flow was seen only with balloon augmentation, which negated the augmented diastolic flow. CONCLUSION: Despite a significant augmentation in diastolic blood flow with balloon counterpulsation, no increase occurred in total carotid artery blood flow. This appeared to be caused by improper timing of balloon deflation. This could result in no improvement in cerebral blood flow with intraaortic balloon pump counterpulsation in critically ill patients

The purpose of this study was to evaluate the effect of sequential external counterpulsation (SECP) on cerebral and renal blood flow. The effect of SECP on carotid and renal artery blood flow was studied in 35 and 18 patients, respectively. With a portable unit, cuffs were applied to the calves and thighs, sequentially inflated with air at the onset of diastole, and deflated at the onset of systole. Carotid and renal artery Duplex studies were performed during intermittent SECP. Flow velocity and flow velocity integral were measured at baseline and during SECP. Diastolic augmentation of carotid and renal artery flow velocity was observed in all patients. The mean carotid flow velocity integral increased by 22% from 27.7 +/- 1.8 cm to 33.1 +/- 2.3 cm (P = 0.001). The mean renal artery flow velocity integral increased by 19% from 21 +/- 1 cm to 25 +/- 1 cm (P = 0.0001). With SECP, a new diastolic Doppler flow velocity wave was observed, with an average peak carotid diastolic flow velocity of 56 +/- 4 cm/sec and an average peak renal artery diastolic flow velocity of 40 +/- 2.5 cm/sec. This diastolic wave was 75% (carotid) and 68% (renal) as high as the systolic wave during SECP. In addition, with SECP the systolic wave increased by 6% and 8% in the carotid and renal artery, respectively (P = 0.02 and 0.006, respectively). In conclusion, SECP significantly increases carotid and renal blood flow. This noninvasive, harmless treatment may be useful to support patients with decreased cerebral and renal perfusion