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Objectives: This study sought to report our experience with a routine completion angiogram after coronary artery bypass surgery (CABG) and simultaneous (1-stop) percutaneous coronary intervention (PCI) at the time of CABG performed in the hybrid catheterization laboratory/operating room. Background: The value of a routine completion angiogram after CABG and 1-stop hybrid CABG/PCI remains unresolved. Methods: Between April 2005 and July 2007, 366 consecutive patients underwent CABG surgery, with (n = 112) or without (n = 254) concomitant 1-stop PCI (hybrid), all with completion angiography before chest closure. Among the 112 1-stop hybrid CABG/PCI patients, 67 (60%) underwent a planned hybrid procedure based on pre-operative assessment, whereas 45 (40%) underwent open-chest PCI (unplanned hybrid) based on intraoperative findings. Results: Among the 796 CABG grafts (345 left internal mammary artery, 12 right internal mammary artery/radial, and 439 veins), 97 (12%) angiographic defects were identified. Defects were repaired with either a minor adjustment of the graft (n = 22, 2.8%), with intraoperative open-chest PCI (unplanned hybrid, n = 48, 6%) or with traditional surgical revision (n = 27, 3.4%). Hybrid patients had clinical outcomes similar to standard CABG patients. Conclusions: Routine completion angiography detected 12% of grafts with important angiographic defects. One-stop hybrid coronary revascularization is reasonable, safe, and feasible. Combining the tools of the catheterization laboratory and operating room greatly enhances the options available to the surgeon and cardiologist for patients with complex coronary artery disease. [ABSTRACT FROM AUTHOR]

Intrathoracic subclavian artery aneurysms (ISAAs) are infrequently seen in clinical practice. We report the repair of a left ISAA associated with a long segment dissection from the ostia extending to the axillary artery. A hybrid approach was used. Carotid-to-axillary bypass using a reversed greater saphenous vein was first performed, followed by coverage of the origin of the subclavian artery using a thoracic stent graft. Finally, percutaneous access of the radial artery with coil embolization was performed to successfully thrombose the ISAA., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Background: Increasing evidence indicates that proteotoxicity plays a pathophysiologic role in experimental and human cardiomyopathy. In organ-specific amyloidoses, soluble protein oligomers are the primary cytotoxic species in the process of protein aggregation. While isolated atrial amyloidosis can develop with aging, the presence of preamyloid oligomers (PAOs) in atrial tissue has not been previously investigated., Methods and Results: Atrial samples were collected during elective cardiac surgery in patients without a history of atrial arrhythmias, congestive heart failure, cardiomyopathy, or amyloidosis. Immunohistochemistry was performed for PAOs using a conformation-specific antibody, as well as for candidate proteins identified previously in isolated atrial amyloidosis. Using a myocardium-specific marker, the fraction of myocardium colocalizing with PAOs (PAO burden) was quantified (green/red ratio). Atrial samples were obtained from 92 patients, with a mean age of 61.7±13.8 years. Most patients (62%) were male, 23% had diabetes, 72% had hypertension, and 42% had coronary artery disease. A majority (n=62) underwent aortic valve replacement, with fewer undergoing coronary artery bypass grafting (n=34) or mitral valve replacement/repair (n=24). Immunostaining detected intracellular PAOs in a majority of atrial samples, with a heterogeneous distribution throughout the myocardium. Mean green/red ratio value for the samples was 0.11±0.1 (range 0.03 to 0.77), with a value ≥0.05 in 74 patients. Atrial natriuretic peptide colocalized with PAOs in myocardium, whereas transthyretin was located in the interstitium. Adjusting for multiple covariates, PAO burden was independently associated with the presence of hypertension., Conclusion: PAOs are frequently detected in human atrium, where their presence is associated with clinical hypertension., (© 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.)

Abnormalities in atrial myocardium increase the likelihood of arrhythmias, including atrial fibrillation (AF). The deposition of misfolded protein, or amyloidosis, plays an important role in the pathophysiology of many diseases, including human cardiomyopathies. We have shown that genes implicated in amyloidosis are activated in a cellular model of AF, with the development of preamyloid oligomers (PAOs). PAOs are intermediates in the formation of amyloid fibrils, and they are now recognized to be the cytotoxic species during amyloidosis. To investigate the presence of PAOs in human atrium, we developed a microscopic imaging-based protocol to enable robust and reproducible quantitative analysis of PAO burden in atrial samples harvested at the time of elective cardiac surgery. Using PAO- and myocardial-specific antibodies, we found that PAO distribution was typically heterogeneous within a myocardial sample. Rigorous imaging and analysis protocols were developed to quantify the relative area of myocardium containing PAOs, termed the Green/Red ratio (G/R), for a given sample. Using these methods, reproducible G/R values were obtained when different sections of a sample were independently processed, imaged, and analyzed by different investigators. This robust technique will enable studies to investigate the role of this novel structural abnormality in the pathophysiology of and arrhythmia generation in human atrial tissue., (© The Author(s) 2014.)

Objectives: We propose a simplified anatomic classification for pulmonary emboli that algorithmically differentiates those who might be best treated with surgical pulmonary embolectomy (type A) from those best treated medically (type B). We hypothesized that patients with type A pulmonary emboli treated with immediate surgical embolectomy demonstrate superior long-term survival compared with patients with type A pulmonary emboli treated medically., Methods: Patients admitted between 2002 and 2008 with a diagnosis of pulmonary emboli made based on computed tomographic angiographic imaging (n = 779) were analyzed. Computed tomographic angiographic images were reviewed in a blind fashion, and anatomic classification of emboli was made. Patients with central thrombus, defined by location medial to the lateral mediastinal boundaries (ie, involving the main, primary, or both branch pulmonary arteries), were classified as having type A pulmonary emboli (n = 107), whereas those with peripheral pulmonary emboli located beyond these boundaries were classified as having type B pulmonary emboli (n = 672). Four patients with type A pulmonary emboli treated with catheter embolectomy were excluded from the analysis., Results: Of the 103 patients with type A pulmonary emboli, 15 (14%) were treated with immediate surgical pulmonary embolectomy, and 88 (85%) were treated medically. Patients with type A pulmonary emboli treated surgically had similar 30-day mortality compared with those treated medically (13% vs 17%, P = .532). At a mean of 24 ± 18 months' follow-up (range, 1-82 months), survival at 1, 3, and 5 years for patients with type A pulmonary emboli treated surgically was significantly better than that in the patients with type A pulmonary emboli treated medically (P = .0001)., Conclusions: For patients with type A pulmonary emboli, immediate surgical intervention appears to offer superior midterm survival compared with medical treatment alone. Although the medical and surgical groups were substantially different and the differences might have affected survival, this simplified classification for pulmonary emboli might help direct optimal treatment strategies., (Copyright © 2011. Published by Mosby, Inc.)

Background: The benefits of a minimally invasive approach to off-pump coronary artery bypass remain controversial. The value of completion arteriography in validating this technique has not been investigated., Methods: From April 2007 to October 2009, fifty-six patients underwent isolated minimally invasive coronary artery bypass grafting through a left thoracotomy without cardiopulmonary bypass. Forty-three of these patients underwent completion arteriography., Results: Sixty-five grafts were performed in these 56 patients, (average, 1.2 grafts per patient; range, 1 to 3). Forty-eight grafts were studied in the 43 patients undergoing completion arteriography. There were 4 findings on arteriogram leading to further immediate intervention (8.3%). These included 3 grafts with anastomotic stenoses or spasm requiring stent placement, and 1 patient who had limited dissection in the left internal mammary artery graft and underwent placement of an additional vein graft. These findings were independent of electrocardiographic changes or hemodynamic instability. The remainder of the studies showed no significant abnormalities. There were no deaths. One patient who did not have a completion arteriogram suffered a postoperative myocardial infarction requiring stent placement for anastomotic stenosis. Patients were discharged home an average of 6.8 days postoperatively. There were no instances of renal dysfunction postoperatively attributable to catheterization., Conclusions: Minimally invasive coronary artery bypass is safe and effective. Findings of completion arteriography occasionally reveal previously under-recognized findings that, if corrected in a timely fashion, could potentially impact graft patency and clinical outcomes. Our experience validates this minimally invasive technique., (Copyright © 2011 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

Carney's complex is an autosomal dominant syndrome characterized by recurrent atrial myxomas with concurrent endocrinopathies and characteristic dermatologic features. We present the case of a woman who presented with a recurrent atrial myxoma after two previous resections for myxomas through median sternotomies. As a consequence, we utilized a minimally invasive right thoracotomy approach. We discuss the clinical and pathologic features of Carney complex and the importance of identifying individuals and families with this condition for treatment and counseling., (© 2010 Wiley Periodicals, Inc.)

Background and Aim of the Study: The study aim was to determine the safety and benefits of minimally invasive mitral valve surgery without aortic cross-clamping for mitral valve surgery after previous cardiac surgery., Methods: Between January 2006 and August 2008, a total of 90 consecutive patients (38 females, 52 males; mean age 66 +/- 9 years) underwent minimally invasive mitral valve surgery after having undergone previous cardiac surgery. Of these patients, 80 (89%) underwent mitral valve replacement and 10 (11%) mitral valve repair utilizing a small (5 cm) right lateral thoracotomy along the 4th or 5th intercostal space under fibrillatory arrest (mean temperature 28 +/- 2 degrees C). The predicted mortality, calculated using the Society of Thoracic Surgeons (STS) algorithm, was compared to the observed mortality., Results: The mean ejection fraction was 45 +/- 13%, mean NYHA class 3 +/- 1, while 66 patients (73%) had previous coronary artery bypass grafting and 37 (41%) had previous valve surgery. Twenty-six patients (29%) underwent non-elective surgery. Cardiopulmonary bypass was instituted through axillary (n = 19), femoral (n = 70) or direct use aortic (n = 1) cannulation. Operative mortality was 2% (2/90), lower than the STS-predicted mortality of 7%. Three patients (3%) developed acute renal failure postoperatively, one patient (1%) required new-onset hemodialysis, and one (1%) developed postoperative stroke. No patients developed postoperative myocardial infarction. The mean postoperative packed red blood cell transfusion requirement at 48 h was 2 +/- 3 units., Conclusion: Minimally invasive right thoracotomy without aortic cross-clamping is an excellent alternative to conventional redo-sternotomy for reoperative mitral valve surgery. The present study confirmed that this technique is safe and effective in reducing operative mortality in high-risk patients undergoing reoperative cardiac surgery.

A 33-year-old, previously healthy male presented with respiratory distress and underwent intubation. A physical examination revealed a holosystolic murmur and pupillary abnormalities. Echocardiography revealed a flail anterior mitral valve leaflet with ruptured chordae and severe mitral regurgitation. The patient underwent urgent mitral valve replacement and tolerated the procedure well. The mitral valve leaflet was myxomatous and calcified -- an unusual find in such a patient. An ophthalmology consultation was obtained and the patient diagnosed with Axenfeld-Rieger syndrome, a disorder of the anterior ocular chamber that has been associated with cardiac malformations. The present case report adds to the body of literature which suggests a correlation between Axenfeld-Rieger syndrome and valvular abnormalities. Hence, it is believed prudent that patients with Axenfeld-Rieger syndrome should undergo echocardiographic screenings for valvular abnormalities.

Heparin-induced thrombocytopenia paradoxically is a transient pro-thrombotic disorder triggered by heparin exposure. If not treated appropriately, it can be life threatening because of its related thromboembolic complications. In particular, it presents a unique challenge in patients needing extracorporeal life support, because anticoagulation is essential for safe management. This case report describes the safe, efficacious use of Argatroban during short-term support of a patient with a percutaneously inserted left ventricular assist TandemHeart device.

Background: We developed a technique for open heart surgery through a small (5 cm) right-anterolateral thoracotomy without aortic cross-clamp., Methods: One hundred and ninety-five consecutive patients (103 male and 92 female), age 69 +/- 8 years, underwent surgery between January 2006 and July 2007. Mean preoperative New York Heart Association function class was 2.2 +/- 0.7. Thirty-five patients (18%) had an ejection fraction 0.35 or less. Cardiopulmonary bypass was instituted through femoral (176 of 195, 90%), axillary (18 of 195, 9%), or direct aortic (1 of 195, 0.5%) cannulation. Under cold fibrillatory arrest (mean temperature 28.2 degrees C) without aortic cross-clamp, mitral valve repair (72 of 195, 37%), mitral valve replacement (117 of 195, 60%), or other (6 of 195, 3%) procedures were performed. Concomitant procedures included maze (45 of 195, 23%), patent foramen ovale closure (42 of 195, 22%) and tricuspid valve repair (16 of 195, 8%), or replacement (4 of 195, 2%)., Results: Thirty-day mortality was 3% (6 of 195). Duration of fibrillatory arrest, cardiopulmonary bypass, and "skin to skin" surgery were 88 +/- 32, 118 +/- 52, and 280 +/- 78 minutes, respectively. Ten patients (5%) underwent reexploration for bleeding and 44% did not receive any blood transfusions. Six patients (3%) sustained a postoperative stroke, eight (4%) developed low cardiac output syndrome, and two (1%) developed renal failure requiring hemodialysis. Mean length of hospital stay was 7 +/- 4.8 days., Conclusions: This simplified technique of minimally invasive open heart surgery is safe and easily reproducible. Fibrillatory arrest without aortic cross-clamping, with coronary perfusion against an intact aortic valve, does not increase the risk of stroke or low cardiac output. It may be particularly useful in higher risk patients in whom sternotomy with aortic clamping is less desirable.

Intracoronary delivery of endothelial progenitor cells (EPCs) is an emerging concept for the treatment of cardiovascular disease. Enhancement of EPC adhesion to vascular endothelium could improve cell retention within targeted organs. Because extracellular adenosine is elevated at sites of ischemia and stimulates neovascularization, we examined the potential role of adenosine in augmenting EPC retention to cardiac microvascular endothelium. Stimulation of adenosine receptors in murine embryonic EPCs (eEPCs) and cardiac endothelial cells (cECs) rapidly, within minutes, increased eEPC adhesion to cECs under static and flow conditions. Similarly, adhesion of human adult culture-expanded EPCs to human cECs was increased by stimulation of adenosine receptors. Furthermore, adenosine increased eEPC retention in isolated mouse hearts perfused with eEPCs. We determined that eEPCs and cECs preferentially express functional A1 and A2B adenosine receptor subtypes, respectively, and that both subtypes are involved in the regulation of eEPC adhesion to cECs. We documented that the interaction between P-selectin and its ligand (P-selectin glycoprotein ligand-1) plays a role in adenosine-dependent eEPC adhesion to cECs and that stimulation of adenosine receptors in cECs induces rapid cell surface expression of P-selectin. Our results suggest a role for adenosine in vasculogenesis and its potential use to stimulate engraftment in cell-based therapies.

Developing new strategies to improve patient safety and risk reduction is fundamental to hospital and patient success. Currently, there is a tendency in hospital safety management to focus solely on human error rather than organizational and educational causes that contribute to medical accidents. Although health care providers are the primary safety systems in medical facilities, there must be a more global, perhaps automated, approach using modern technology to prevent or reduce medical mishaps. Herein, we present an oxygenation failure with root cause analysis that prompted a new oxygenation safety algorithm and multi-service training initiative.

Objective: We began minimally invasive mitral valve surgery in August, 1996, to reduce hospital costs, to improve patient recovery, cosmetic appearance, and to decrease trauma, yet maintain the same quality of surgery. To validate this approach we reviewed our entire experience through May 2002., Methods: From August 1996 to May 2002, we performed 413 minimally invasive mitral valve operations including 51 mitral valve replacements and 362 mitral valve repairs. Excluding 4 robotically assisted repairs, we evaluated 358 patients, using the mitral valve repairs as the basis for this retrospective survey. These operations were performed through a 6- to 8-cm minimally invasive incision, beginning with parasternal and, most recently, lower ministernotomy (181 patients). The mitral valve reparative techniques include repair of 94 prolapsed anterior leaflets, posterior leaflet resection, leaflet advancement, commissuroplasty, Polytetrafluoroethylene (PTFE; Gore-Tex, W. L. Gore & Associates, Inc, Flagstaff, Ariz) chordal placement, and ring annuloplasty. Cannulation sites varied but primarily utilized a miniaturized system of 24F catheters in both the inferior and superior venae cavae with assisted venous suction. The Cosgrove ring was used in 95% of the patients undergoing this procedure., Results: The operative mortality was 0/358. Perioperative morbidity included a 26% incidence of new atrial fibrillation, 2% incidence of pacemaker implantation, 0.5% incidence of deep sternal wound infection, and 1.9% incidence of stroke after an operation. There were 10 arterial and 3 venous complications. The mean length of stay was 6 days and 208 patients stayed < or =5 days. Only 25% of the patients underwent homologous blood transfusion. The mean follow-up was 36 months with 1.4% lost to follow-up. There were 12 late deaths and a survival at 5 years of 95%. There were 21 valves requiring reoperation for structural valve failure of 5.8%. The probability of freedom from reoperation at 5 years was 92%., Conclusion: This study documents the safety of minimally invasive mitral valve repair surgery in 358 patients. It also documents a low incidence of homologous blood use, requirement for post-hospital rehabilitation, and general morbidity.

Patients with pulmonary metastases were previously relegated to palliative medical management. Since the first metastasectomies in the nineteenth century, general acceptance of this technique has occurred. Although, initially, indications for resection of pulmonary metastases were limited to patients with solitary nodules, over time, indications have broadened to include multiple lesions, recurrent disease, and nearly all histologies. With appropriate patient selection and the absence of extrathoracic disease, survival may be improved. For patients with disseminated and symptomatic disease, surgical therapy may also provide some relief.

Limb-girdle muscular dystrophies 2C-F represent a family of autosomal recessive diseases caused by defects in sarcoglycan genes. The cardiomyopathic hamster is a naturally occurring model for limb-girdle muscular dystrophy caused by a primary deficiency in delta-sarcoglycan. We show here that acute sarcolemmal disruption occurs in this animal model during forceful muscle contraction. A recombinant adeno-associated virus vector encoding human delta-sarcoglycan conferred efficient and stable genetic reconstitution in the adult cardiomyopathic hamster when injected directly into muscle. A quantitative assay demonstrated that vector-transduced muscle fibers are stably protected from sarcolemmal disruption; there was no associated inflammation or immunologic response to the vector-encoded protein. Efficient gene transduction with rescue of the sarcoglycan complex in muscle fibers of the distal hindlimb was also obtained after infusion of recombinant adeno-associated virus into the femoral artery in conjunction with histamine-induced endothelial permeabilization. This study provides a strong rationale for the development of gene therapy for limb-girdle muscular dystrophy.

Background: It has been reported that A1 adenosine receptor antagonists are highly effective for the prevention and early treatment of ischemia-reperfusion injury of isolated perfused cat lung, which suggests that activation of A1 adenosine receptors is important in ischemia-reperfusion injury of the lung. In addition, preconditioning ischemia reduces ischemia-reperfusion injury of the lung and heart. Moreover, activation of A1 adenosine receptors by adenosine and selective A1 adenosine receptor agonists mimics the protective effects of preconditioning ischemia in the heart. It has been reported that prior treatment with selective A1 adenosine receptor agonists results in a rapid uncoupling of A1 adenosine receptors from signal transduction mechanisms. In the heart, these effects of A1 adenosine receptor agonists have not been reported. However, if prior treatment of ischemia of the heart with adenosine or A1 adenosine receptor agonists results in uncoupling of A1 adenosine receptors from signal transduction mechanisms that produce injury after prolonged ischemia and reperfusion, A1 adenosine receptor antagonists should provide a protective effect similar to these treatments for ischemia-reperfusion injury of the heart. Therefore, it was the purpose of these experiments to investigate the effect of selective A1 adenosine receptor antagonists on ischemia-reperfusion injury of the heart., Methods and Results: With the use of a regional infarct model in open-chest cats, the left anterior descending artery or first diagonal branch was occluded for 1 hour followed by 2 hours of reperfusion. Infarct size (area of necrosis/area at risk; AN/AR) was estimated with the use of nitroblue tetrazolium staining. The selective A1 adenosine receptor antagonists xanthine amine congener (XAC; 0.1 mg.kg-1.h-1), bamifylline (BAM; 10 mg.kg-1.h-1), 1,3-dipropyl-8-cyclopentylxanthine (DPCPX; 10 micrograms.kg-1.min-1) administered as continous intravenous infusions for 1 hour before ischemia [DPCPX (I)], or DPCPX 30 micrograms.kg-1.min-1 administered intravenously during 30 minutes of ischemia and 30 minutes of reperfusion [DPCPX (I/R)] significantly (P < .05) reduced AN/AR from 52.2 +/- 3.8% (control, n = 5) to 23.4 +/- 6.6% (XAC, n = 5), 34.9 +/- 3.6% (BAM, n = 5), 15.9 +/- 2.9% [DPCPX(I), n = 5], or 13 +/- 3.2% [DPCPX (I/R), n = 5]., Conclusions: A1 adenosine receptor antagonists significantly reduce ischemia-reperfusion injury of the heart. A1 adenosine receptor antagonists may be useful for the prevention or early treatment of ischemia-reperfusion injury of the heart after coronary artery bypass graft surgery or cardiac transplant surgery and during or after angioplasty or thrombolytic therapy of the heart.

Adenoviral vectors have been shown to effect efficient somatic gene transfer in skeletal muscle and thus offer potential for the development of therapy for Duchenne muscular dystrophy (DMD). Efficient transfer of recombinant genes has been demonstrated in skeletal muscle using recombinant adenoviruses deleted of E1. Application of this vector system to the treatment of DMD is limited by the vector immunogenicity, as well as by size constraints for insertion of recombinant genes, precluding the incorporation of a full-length dystrophin minigene construct. We describe in this study the use of helper adenovirus to generate a recombinant vector deleted of all viral open reading frames and containing a full-length dystrophin minigene. We show that this deleted vector (delta vector) is capable of efficiently transducing dystrophin in mdx mice, in myotubes in vitro and muscle fibers in vivo. Our modification of adenoviral vector technology may be useful for the development of gene therapies for DMD and other diseases.

Atrial natriuretic factor (ANF) is a hormone that regulates fluid and electrolyte homeostasis. Increased intra-atrial pressure or atrial distention, which might occur secondary to intravascular volume expansion, stimulate the secretion of ANF by human atrial myocytes. During normal human pregnancy, there is a progressive increase in total intravascular fluid volume. Thus, we asked the following question: Does this physiologic adaptation to pregnancy result in an increase in ANF concentrations? Concentrations of alpha-human ANF (alpha-hANF) were measured by a specific radioimmunoassay in venous blood samples obtained longitudinally in the first, second, and third trimesters of pregnancy, during the intrapartum period, in the early postpartum period, and 6 to 8 weeks postpartum from 11 normal women who had no antepartum, intrapartum, or postpartum complications. Maternal circulating alpha-hANF levels were not different from those seen in the nonpregnant state. However, higher alpha-hANF concentrations were noted in the early postpartum period. Although the hypervolemia of normal pregnancy is not associated with higher alpha-hANF concentrations, other possibilities (such as increased ANF clearance, dilutional effects) need to be investigated. Finally, the etiology for the transient increase in alpha-hANF levels in the early postpartum period remains to be elucidated.

The secretion of atrial natriuretic factor by human atrial myocytes is stimulated by increased intraatrial pressure or atrial distention. To determine whether acute intravascular volume expansion affects atrial natriuretic factor concentrations during pregnancy, circulating atrial natriuretic factor levels were measured in pregnant women at term (before elective cesarean section) and nonpregnant control subjects before and during intravenous infusion of lactated Ringer's solution (approximately 30 ml/kg). Venous plasma concentrations of alpha-human atrial natriuretic factor were determined by a specific radioimmunoassay. A significant increase in alpha-human atrial natriuretic factor levels in nonpregnant subjects was seen. Pregnant women did not show a significant response to a similar stimulus. Finally, basal alpha-human atrial natriuretic factor levels in pregnant and nonpregnant women were not different. Volume expansion (long-term or short-term) in normal human pregnancy may not be sensed by atrial volume sensors, possibly because it is accommodated by an enlarged maternal vascular compartment.

There is a reduction in intravascular volume in patients with preeclampsia. Since the secretion of atrial natriuretic factor by human atrial myocytes is stimulated by increased intraatrial pressure or atrial distention, we sought to determine whether circulating maternal plasma atrial natriuretic factor concentrations were lower in patients with preeclampsia compared to normal pregnant women. The level of alpha-human atrial natriuretic factor was measured by a specific radioimmunoassay. Maternal venous concentrations of a alpha-human atrial natriuretic factor were higher in patients with severe preeclampsia (116.12 +/- 13.37 pg/ml) than in normal pregnant women (80.30 +/- 4.02 pg/ml). Umbilical artery alpha-human atrial natriuretic factor concentrations were higher in fetuses born to patients with severe preeclampsia (197.68 +/- 29.10 pg/ml) than normal control subjects (118.00 +/- 12.52 pg/ml). Umbilical artery alpha-human atrial natriuretic factor concentrations were higher than umbilical or maternal venous concentrations. In cases of severe preeclampsia, despite the presumed volume changes, maternal atrial natriuretic factor concentrations are higher than in normal pregnant women. The fetus appears to produce its own atrial natriuretic factor. Umbilical artery atrial natriuretic factor concentrations in fetuses born to preeclamptic mothers are higher than those seen in normal control subjects.