Nonsurgical management of left main coronary artery aneurysms: report of 2 cases and review of the literature.

Aneurysms of the left main coronary artery are exceedingly rare clinical entities, encountered incidentally in approximately 0.1% of patients who undergo routine angiography. Thrombosis within the aneurysm can lead to distal embolization and myocardial infarction. These lesions can extend into adjacent coronary branches and can occur in the presence or absence of obstructive coronary disease. Depending on the severity of coexistent coronary stenoses, patients with left main coronary artery aneurysms can be effectively managed either operatively or medically. We report the cases of 2 patients who were treated medically for large left main coronary aneurysms and concomitant right coronary artery ectasia.

A comparison of mechanical and laser transmyocardial revascularization for induction of angiogenesis and arteriogenesis in chronically ischemic myocardium.

OBJECTIVES: The purpose of the present study was to compare the use of a mechanical transmyocardial implant (TMI) device with transmyocardial laser revascularization (TMR) for induction of therapeutic angiogenesis and arteriogenesis in the chronically ischemic heart. BACKGROUND: Prior experimental studies have demonstrated evidence for neovascularization after both mechanical and laser transmyocardial revascularization, although a long-term comparison of the two techniques has not been performed. METHODS: Using an established model of chronic hibernating myocardium, mini-swine underwent 90% proximal left circumflex (LCx) coronary artery stenosis. One month later, baseline positron emission tomography (PET) and dobutamine stress echocardiography (DSE) were performed to quantitate regional myocardial blood flow (MBF) and function. Animals then underwent TMR with a holmium:yttrium-aluminum-garnet (holmium:YAG) laser (n = 5), TMI (n = 5), or sham redo-thoracotomy (n = 5). In the TMR group, the entire LCx region was treated with transmural laser channels at a density of 1/cm(2). Transmyocardial implants were placed transmurally at a similar density in the LCx region of the TMI group. Six months later, the PET and DSE studies were repeated, and the animals were euthanized. RESULTS: Six months after TMR, there was a significant increase over baseline in resting MBF to the lased LCx region (68.9 +/- 4.6% vs. 89.3 +/- 3.0% reference non-ischemic septal segments; p < 0.001). This increased MBF was accompanied by a significant improvement in LCx regional wall motion during peak dobutamine stress (p = 0.04). Compared with baseline, there was no change in LCx region MBF six months after either TMI (72.9 +/- 4.8% vs. 85.7 +/- 3.4%; p = 0.10) or sham redo-thoracotomy (75.6 +/- 4.6% vs. 80.1 +/- 5.0%; p > 0.2). Likewise, there was no significant change in rest or stress wall motion by DSE six months postoperatively in either group. Overall vascular density was increased only in the TMR-treated regions six months postoperatively. The difference between groups was most notable for a twofold increase in the number of small arterioles seen in the lased (4.4 +/- 0.3 arterioles per high power field; p < 0.001 vs. both TMI and sham) compared with TMI (2.2 +/- 0.2) and sham (1.9 +/- 0.2)-treated regions. CONCLUSIONS: Mechanical transmyocardial revascularization with a TMI device does not appear to promote physiologically significant angiogenesis or arteriogenesis in the chronically ischemic porcine heart and cannot be recommended for clinical trials at this time. Infrared laser-mediated injury mechanisms may be important for inducing therapeutic neovascularization with direct myocardial revascularization techniques.

Arterial conduits should be evaluated preoperatively in coronary artery bypass patients with pseudoxanthoma elasticum.

A 74-year-old man who had pseudoxanthoma elasticum presented with unstable angina and underwent urgent coronary artery bypass grafting. Preoperative angiography did not include the internal mammary arteries. Intraoperatively, the left internal mammary artery was found to be diseased and could not be used. This case lends support to the need for thorough preoperative evaluation, including angiography, of potential arterial conduits in patients with pseudoxanthoma elasticum.

Correlation of cell-mediated immunity against porcine reproductive and respiratory syndrome virus with protection against reproductive failure in sows during outbreaks of porcine reproductive and respiratory syndrome in commercial herds.

OBJECTIVE: To determine whether cell-mediated immunity against porcine reproductive and respiratory syndrome (PRRS) virus is correlated with protection against reproductive failure in sows during clinical outbreaks of PRRS in commercial herds. DESIGN: Outbreak investigation in 4 swine breeding herds. ANIMALS: 97 sows. PROCEDURES: On each farm, blood samples were collected from sows with clinical signs (abortion or increased fetal death; case sows) and from clinically normal sows (control sows). The intensity of the cell-mediated immune (CMI) response was determined by use of an interferon-gamma enzyme-linked immunospot (ELISPOT) assay. Multiple logistic regression analyses and t tests were used to compare ELISPOT assay values between case and control sows. Multiple linear regression was used to investigate associations between cell-mediated immunity and the magnitude of clinical signs. RESULTS: In 2 farms, case sows had lower ELISPOT assay values than control sows. A negative association between the intensity of the CMI response and the number of pigs born dead per litter was detected on 1 farm. In 1 farm, no association was detected between the intensity of the CMI response and protection against reproductive failure. CONCLUSIONS AND CLINICAL RELEVANCE: Evidence that a strong CMI response was correlated with protection against clinical PRRS was detected in 3 of 4 farms. However, farms and sows within farms varied considerably in their immune responsiveness and in the degree to which they were protected clinically. Increasing cell-mediated immunity within infected herds has the potential to decrease clinical reproductive disease, but only if the sources of intra- and interfarm variation in the intensity of cell-mediated immunity to PRRS virus can be identified.

Intramyocardial and intracoronary basic fibroblast growth factor in porcine hibernating myocardium: a comparative study.

OBJECTIVE: Therapeutic angiogenesis is an alternative method of revascularization for end-stage coronary artery disease. We determined the effects of intramyocardial and intracoronary basic fibroblast growth factor 2 on myocardial blood flow and function in a porcine model of hibernating myocardium. METHODS: Twenty-four mini-swine with 90% left circumflex artery stenosis and documented hibernating myocardium by positron emission tomography and dobutamine stress echocardiography were randomized to intramyocardial basic fibroblast growth factor 2 at 0.6 microg/kg (mid-dose, n = 6, 30 injections/animal), 6 microg/kg (high-dose, n = 6, 30 injections/animal), or intramyocardial vehicle control (n = 6). The intracoronary group received 6 microg/kg basic fibroblast growth factor 2 (n = 6) into the right and left circumflex artery coronary arteries. Positron emission tomography and dobutamine stress echocardiography were repeated at 1 and 3 months. RESULTS: In the vehicle group, normalized left circumflex artery myocardial blood flow was 0.74 +/- 0.04 at 1 month and 0.75 +/- 0.07 at 3 months compared with 0.68 +/- 0.03 at baseline. In the intracoronary group, myocardial blood flow was 0.71 +/- 0.03 at 1 month and 0.72 +/- 0.04 at 3 months compared with 0.67 +/- 0.04 at baseline. In the mid group, myocardial blood flow was 0.73 +/- 0.06 at 1 month and 0.85 +/- 0.05 at 3 months (P <.001) compared with 0.67 +/- 0.04 at baseline. In the high group, myocardial blood flow was 0.81 +/- 0.06 at 1 month and 0.83 +/-.04 at 3 months (P =.03) compared with 0.71 +/- 0.02 at baseline. No significant improvements in ischemia were demonstrated in any of the groups by dobutamine stress echocardiography at 1 or 3 months. CONCLUSIONS: In porcine hibernating myocardium, intramyocardial basic fibroblast growth factor 2 significantly improved regional myocardial blood flow 3 months after treatment. There was no significant change in function in any of the 4 groups. These data suggest that intramyocardial dosing of basic fibroblast growth factor 2 (0.6 microg/kg) may be an optimal dose for improving perfusion in the treatment of end-stage coronary artery disease.

Thoracic surgery workforce: snapshot at the end of the twentieth century and implications for the new millennium.

BACKGROUND: An appropriately sized physician workforce is an essential component for healthcare planning. Contemporary economic forces and the impact of managed care have stimulated renewed interest in understanding and monitoring workforce issues. METHODS: Between August and December of 1999, the Workforce Committee of the American Association for Thoracic Surgery and The Society of Thoracic Surgeons conducted a survey detailing demographic, geographic, and socioeconomic practice characteristics of the membership. RESULTS: The 2,515 returned surveys represented a 62.6% return rate (+/- 1.6% margin of error), providing a highly statistically valid sample. Active thoracic surgeons are a mean of 50 years old, 98% men, with a high level of career satisfaction. Length of training and educational debt has been escalating. Adult cardiac surgical case volumes have increased (mean, 225 cases) and 52% of adult cardiac surgeons perform general thoracic procedures. Surgeons work 67 hours/week and 47 weeks/year. Most are organized in single specialty groups (50%) in urban areas (59%) as for-profit corporations (77%). Half of the respondents will be retired a mean of 13 years from now corresponding to a median calendar year of 2011. CONCLUSIONS: This survey highlights significant workforce retirement during the next 10 to 15 years. Currently, the workforce in thoracic surgery appears "right sized." These valuable data provide a profile of the specialty. The information enhances our ability to strategically plan.

Mitral surgery after prior cardiac operation: port-access versus sternotomy or thoracotomy.

BACKGROUND: In reoperation for mitral valve disease, minimally invasive Port-Access (PORT) is a new alternative to standard median sternotomy (STER) or right thoracotomy (THOR); yet, the results of PORT in this setting have not been defined. The aim of this study was to evaluate the results of minimally invasive thoracotomy in reoperation for mitral valve disease. METHODS: Retrospective results are reported for three consecutive series of patients undergoing reoperation for mitral disease using either PORT (n = 60, 1996 to 2001), THOR (n = 37, 1985 to 1997), or STER (n = 155, 1985 to 1997). RESULTS: Red cell transfusion was 3 +/- 4, 14 +/- 13, and 12 +/- 12 units for PORT, THOR, and STER, respectively. Chest tube output was 352 +/- 361, 2048 +/- 3166, and 1683 +/- 3939 mL, respectively. Cardiopulmonary bypass times for these groups were 208 +/- 76 vs. 158 +/- 56 vs. 157 +/- 53 minutes. Thirty-day mortality was 0/60 (0%), 8/37 (22%), and 21/155 (14%), respectively. CONCLUSIONS: This early clinical experience suggests that PORT is an acceptable alternative to THOR or STERN in reoperation for mitral valve disease, with potential advantages of avoiding redo sternotomy and reducing the surgical incision. However, these benefits may come at the expense of longer cardiopulmonary bypass times.

Therapeutic angiogenesis in chronically ischemic porcine myocardium: comparative effects of bFGF and VEGF.

BACKGROUND: Both vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) have been used in preclinical studies to induce new blood vessel growth in ischemic cardiac muscle with promising results. However, clinical trials have been much less convincing and further work is needed. This study expands on prior work by comparing the long-term proangiogenic effects of direct intramyocardial (IM) injection of bFGF, as well as IM and intravenous (IV) VEGF in a porcine model of chronic hibernating myocardium. METHODS: Mini-swine with proximal 90% left circumflex (LCx) coronary stenosis subtending chronically ischemic, viable (hibernating) myocardium by positron emission tomography (PET) and dobutamine stress echocardiography (DSE) were randomized to IM bFGF (n = 5), IM VEGF(165) (n = 5), IV VEGF(165) (n = 5), IM vehicle (n = 5), or sham redo-thoracotomy (n = 4). The bFGF protein was administered in a total dose of 1.35 microg divided into 30 IM injections. IM VEGF(165) protein was administered in a total dose of 15 microg/kg divided into 30 injections; IV VEGF(165) was given at a dose of 50 ng. kg(-1). min(-1) for 200 minutes at three 72-hour intervals (30 microg/kg total dose). After 3 and 6 months the PET and DSE studies were repeated, and the animals were sacrificed for tissue vascular density and angiogenic protein analysis. RESULTS: Myocardial blood flow (MBF) by PET was significantly improved 3 months posttreatment in the IM bFGF and IM VEGF(165) groups, differences that were sustained at 6 months. There was no significant increase in MBF 3-months posttreatment in the IV VEGF(165) group; however, at 6 months MBF was significantly improved. No change in MBF was seen in the IM vehicle or sham groups. Regional wall motion at rest and peak stress in the LCx region demonstrated small but statistically significant improvements by 6 months in the IM bFGF and IV VEGF(165) groups only; no improvement was seen in the IM VEGF(165), IM vehicle, or sham groups. Quantitative vascular density was significantly increased in the LCx regions of all treatment groups (IM bFGF, IM VEGF(165), IV VEGF(165)) 6-months postoperatively. No significant increase in LCx region myocardial bFGF or VEGF protein levels was seen in the treated animals at 6 months. CONCLUSIONS: The IM bFGF, IM VEGF(165), and IV VEGF(165) all improve regional perfusion and vascular density 6-months posttherapy in the animal model utilized. Functional improvements were less consistent. Both bFGF and VEGF(165) may be useful therapies for improving regional perfusion in chronically ischemic myocardium, although combination therapy with additional growth factors or cellular therapies may be necessary if concomitant improvements in function are to be seen.

Laser-assisted extraction of pacemaker and defibrillator leads: the role of the cardiac surgeon.

BACKGROUND: The development of laser-assisted extraction techniques for chronically implanted pacemaker and defibrillator leads has reduced the need for open surgical removal. Reports of the mortality from laser-assisted extraction range from 1.9% to 3.4%. The purpose of this study was to determine the rate of major cardiovascular injury and emphasize the need for cardiothoracic surgical participation in this procedure. METHODS: A retrospective cohort study was performed of 112 consecutive laser-assisted lead extractions at a single university medical center during a 6-year period. Patient and lead characteristics were analyzed as well as indications, outcomes, and major complications. RESULTS: Successful lead extraction was accomplished in 103 (92%) of the 112 patients. Elective sternotomy after failure of laser-assisted lead removal was successfully performed in 4 patients. Emergent surgical intervention was required in 4 patients for caval perforation (n = 2), subclavian vein injury (n = 1), or right atrial injury (n = 1). Three of the 4 patients requiring emergent intervention died, for an overall series mortality of 2.6%. In July of 2006, a policy of cardiothoracic surgeon presence during the laser-assisted extraction was instituted. Since that time, there has been one emergent sternotomy and one elective sternotomy for lead removal with no procedure-related deaths. CONCLUSIONS: Despite recent advances in laser technology for the removal of pacemaker and defibrillator leads, the potential for major cardiovascular injury and death remains. Involvement of the cardiothoracic surgeon in both the preoperative decision-making process as well as the laser-assisted lead extraction is critical to prevent or emergently treat any major complications.

Unusual cause of superior vena cava syndrome diagnosed with transesophageal echocardiography.

PURPOSE: An unusual case of superior vena cava (SVC) syndrome caused by an infected right atrial-SVC junction thrombus may be diagnosed using transesophageal echocardiography. CLINICAL FEATURES: A 59-yr-old male with end-stage renal disease requiring hemodialysis presented with fungemia and later developed facial and bilateral upper extremity edema. Transesophageal echocardiography revealed subtotal occlusion of the SVC at its junction with the right atrium. The mass was surgically removed with cardiopulmonary bypass support. Pathological examination of the mass confirmed the presence of a large fungal colony of Candida species mixed in the thrombus. The patient's signs and symptoms of SVC obstruction resolved, and he was discharged from the hospital four weeks later in stable condition. CONCLUSION: Although usually caused by extrinsic tumour compression, SVC syndrome can result from intravascular caval obstruction. This etiology should also be considered in the differential diagnosis, particularly in patients with intravascular devices. Transesophageal echocardiography is a valuable diagnostic tool in these cases.

Selective activation of human atrial Galpha12 and Galpha13 by Galphaq-coupled angiotensin and endothelin receptors.

Galphaq-coupled receptors such as alpha1-adrenergic, angiotensin, and endothelin receptors, play key roles in cardiac physiology. These receptors have also been shown to couple to G proteins of the G12 family, including Galpha12 and Galpha13. In this report, we determined whether these G proteins interact with endothelin, angiotensin, and alpha1-adrenergic receptors in the human heart. We find that these receptors activate cardiac Galpha12 and Galpha13 differentially; endothelin receptors activate only Galpha12 (to 218 +/- 22% of unstimulated levels), angiotensin receptors activate only Galpha13 (to 236 +/- 49% of unstimulated levels), and alpha1-adrenergic receptors activate neither Galpha12 (123 +/- 18% of unstimulated levels) nor Galpha13 (113 +/- 12% of unstimulated levels). Consistent with these data, translocation of guanine nucleotide exchange factor p115RhoGEF, which responds to Galpha13, occurs only after stimulation of angiotensin receptors (shifting from 73 +/- 12% to 41 +/- 10% cytosolic). These differences in the activation of Galpha12 and Galpha13 by Galphaq-coupled receptors may underlie reported differences in the functions of these receptors.