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Stuart W Jamieson

Publications and source records attributed to Stuart W Jamieson.

At least 19 recordsLinked to original sources
PubMed2006

Outcomes of pulmonary endarterectomy for treatment of extreme thromboembolic pulmonary hypertension.

OBJECTIVE: Pulmonary endarterectomy is the operation of choice for thromboembolic pulmonary hypertension. As the largest referral center for thromboembolic pulmonary hypertension in the world, we are frequently asked whether patients with extreme pulmonary hypertension (pulmonary artery systolic pressure >100 mm Hg) can safely undergo this operation with therapeutic benefit. METHODS: To determine whether patients with pulmonary artery systolic pressures of greater than 100 mm Hg have favorable outcomes after pulmonary endarterectomy, we reviewed the outcomes of 743 patients who underwent this operation between 1999 and 2004. We compared hemodynamic and outcome parameters of 65 patients (group 1: 26 male and 39 female patients; mean age, 49.5 years) who had preoperative pulmonary artery systolic pressures of greater than 100 mm Hg with 678 patients (group 2: 314 male and 364 female patients; mean age, 50.3 years) with preoperative pulmonary artery systolic pressures of less than 100 mm Hg. RESULTS: Group 1 patients had a greater overall diminution in pulmonary vascular resistance (mean decrease: 926.7 +/- 511.1 vs 546.4 +/- 365.1 dynes x sec x cm(-5), P < .01) and reduction in pulmonary artery systolic pressure (mean decrease: 50.5 +/- 18.7 vs 27.2 +/- 18.6 mm Hg, P < .05), with similar improvement in cardiac output (mean increase: 1.53 +/- 1.47 vs 1.55 +/- 1.58 L/min) compared with values seen in group 2 patients. Although length of hospital stay was similar for the 2 groups, overall perioperative survival was slightly lower in group 1 patients (89.2% [58/65] for group 1 vs 96.5% [654/678] for group 2). Patients with extreme pulmonary hypertension manifest a higher rate of postoperative reperfusion edema, leading to longer days of intubation compared with group 2 patients. CONCLUSIONS: Pulmonary endarterectomy can be performed safely in patients with severe thromboembolic pulmonary hypertension. The magnitude of preoperative pulmonary artery systolic pressure or pulmonary vascular resistance is not a contraindication for surgical intervention. Indeed, patients with extreme pulmonary hypertension might benefit the most from this operation.

Adolescent↗
PubMed2006

Venovenous extracorporeal life support after pulmonary endarterectomy: indications, techniques, and outcomes.

BACKGROUND: Pulmonary endarterectomy is the accepted therapy for thromboembolic pulmonary hypertension. A recognized complication of this surgery is the postoperative development of reperfusion edema, a potentially fatal cause of respiratory failure. Because reperfusion edema can be a reversible process, temporizing support measures may be life saving. METHODS: We retrospectively reviewed our experience with venovenous extracorporeal life support (V-V ECLS) from July 1990 to February 2006, in 20 adult patients (mean age 50.5 +/- 14.5 years) presenting with potentially reversible respiratory failure after pulmonary endarterectomy. This subset of patients comprised 1.12% of our total pulmonary endarterectomy experience during that time (1,790 cases). RESULTS: Overall in-hospital survival was 30.0% for patients requiring ECLS support after pulmonary endarterectomy versus 94.2% for patients who underwent pulmonary endarterectomy alone during the same timeframe. V-V ECLS was instituted at a mean of 86.8 hours after surgery. The mean duration of V-V ECLS was 123.4 +/- 71.3 hours. The most common cause of death in ECLS patients after pulmonary endarterectomy was pulmonary hemorrhage. Survival was greater in patients cannulated within 120 hours of surgery (46.2% survival; 6 of 13 patients) compared with those cannulated after 120 hours (0 of 7 patients). Multiple logistic regression identified long duration of mechanical ventilation pre-ECLS and severity of preoperative pulmonary hypertension together as predictors of mortality. CONCLUSIONS: A small subset of patients undergoing pulmonary endarterectomy develop temporary life-threatening respiratory failure secondary to severe reperfusion edema. In those patients with satisfactory hemodynamic outcome, V-V ECLS is a therapeutic option when all other conventional strategies have been exhausted.

Adult↗
PubMed2006

Technical advances of pulmonary endarterectomy for chronic thromboembolic pulmonary hypertension.

Pulmonary endarterectomy is the definitive treatment for chronic pulmonary hypertension as the result of thromboembolic disease. Although significant progress has been made over the last decade in recognition, diagnostic modalities, and treatment of this disease, chronic thromboembolic pulmonary hypertension (CTEPH) continues to be severely underdiagnosed and as a consequence pulmonary endarterectomy remains an uncommon procedure. Patients with CTEPH may present with a variety of debilitating cardiopulmonary symptoms. However, once diagnosed, there is no curative role for medical management, and surgery remains the only option. Medical management in these patients is only palliative, and surgery by means of transplantation for this type of pulmonary hypertension is an inappropriate use of resources with less than satisfactory results. In this article we describe the technical advances of pulmonary endarterectomy and the current procedure as it is performed at University of California-San Diego Medical Center.

Chronic Disease↗
PubMed2006

Historical perspective: surgery for chronic thromboembolic disease.

This article provides a historical perspective for our current understanding of chronic thromboembolic pulmonary hypertension and surgery for this disease. It chronicles the developments in surgical techniques that have made pulmonary endarterectomy the procedure of choice for obstruction of pulmonary vessels by organized thromboemboli and secondary vessel wall thickening.

Chronic Disease↗
PubMed2006

Outcomes of pulmonary endarterectomy surgery.

Chronic thromboembolic pulmonary hypertension has emerged as one of the leading causes of severe pulmonary hypertension. This disease is estimated to occur in approximately 1 to 5% of all patients who have previously developed an acute pulmonary embolism, although the true prevalence is suspected to be much higher. Chronic thromboembolic pulmonary hypertension is characterized by intraluminal thrombus organization, fibrous stenosis, and vascular remodeling of pulmonary vessels. Pulmonary endarterectomy is an operation that is considered curative for thromboembolic pulmonary hypertension and is therefore superior to transplantation for this condition. This article focuses on the surgical outcomes of patients undergoing pulmonary endarterectomy for chronic thromboembolic pulmonary hypertension and discusses the currently known factors that affect survival after this operation.

Aged↗
PubMed2005

Hypoxia-inducible factor 1-alpha reduces infarction and attenuates progression of cardiac dysfunction after myocardial infarction in the mouse.

OBJECTIVES: The aim of this research was to test whether constitutive expression of hypoxia-inducible factor 1-alpha (HIF-1alpha) influences infarction size and cardiac performance after myocardial infarction. BACKGROUND: A major question in clinical medicine is whether infarction size and border zone remodeling of the heart can be influenced by the overexpression of specific genes in the peri-infarction region. METHODS: We investigated the role of constitutive HIF-1alpha expression in acute myocardial infarction using a transgenic model. Transgenic mice containing the HIF-1alpha gene under the control of the alpha-myosin heavy chain promoter were constructed. Myocardial infarction was produced by coronary ligation in HIF-1alpha transgenic mice and control animals. Extent of infarction was then quantitated by two-dimensional and M-mode echocardiography as well as by molecular and pathologic analysis of heart samples in infarct, peri-infarct, and remote heart regions at serial time points. RESULTS: Constitutive overexpression of HIF-1alpha in the murine heart resulted in attenuated infarct size and improved cardiac function 4 weeks after myocardial infarction. Significantly, we found an increase in both capillary density as well as vascular endothelial growth factor and inducible nitric oxide synthase expression in peri-infarct and infarct regions in the hearts of constitutive HIF-1alpha-expressing animals compared to control animals. CONCLUSIONS: These observations suggest the involvement of HIF-1alpha in myocardial remodeling and peri-infarct vascularization. Our results show that supranormal amounts of this peptide protect against extension of infarction and improve border zone survival in myocardial infarction.

Animals↗
PubMed2005

Gene transfer of a TIE2 receptor antagonist prevents pulmonary hypertension in rodents.

OBJECTIVES: Overexpression of angiopoietin 1 in the lung has been associated with human pulmonary hypertension. We hypothesized that inhibiting angiopoietin 1 signaling in the lung by administration of a receptor antagonist would block the development of pulmonary hypertensive vasculopathy in rodent models. METHODS: We injected 2 and 4 x 10(10) genomic particles of adeno-associated virus containing an extracellular fragment of the TIE2 receptor (AAV-sTIE2) into the pulmonary artery of 60 rats by using adeno-associated virus-lacZ and carrier-injected rats as control animals. Pulmonary hypertension was then induced by each of the following methods: (1) monocrotaline (group 1); (2) angiopoietin 1 expression in pulmonary vascular smooth muscle by adeno-associated virus gene transfer (group 2); or (3) oxygen deprivation (group 3). Animals were sacrificed at serial time points. At each time point, pulmonary artery pressures were measured, and pulmonary angiography was performed. Lungs were harvested for pathologic-molecular analysis. RESULTS: Each rodent pulmonary hypertension model demonstrated a significant increase in pulmonary artery pressures compared with that seen in control animals (P < .01). Administration of AAV-sTIE2 prevented pulmonary hypertension in the monocrotaline and angiopoietin 1 groups (from 44.6 +/- 2.1 to 18.8 +/- 1.9 mm Hg in the monocrotaline group and from 31.2 +/- 3.7 to 18.2 +/- 1.8 mm Hg in the angiopoietin 1 group, P < .001) but did not affect pulmonary hypertension in the hypoxia group. Pathologic analysis of group 1 and 2 lungs treated with AAV-sTIE2 demonstrated absence of smooth muscle cell proliferation within arterioles. Pulmonary angiography confirmed a lack of small pulmonary vessel occlusion in group 1 and 2 animals treated with AAV-sTIE2. CONCLUSIONS: Molecular blocking of the interaction between angiopoietin 1 and its endothelial receptor, TIE2, in the lung prevents pulmonary hypertension in 2 animal models of the disease. These experiments suggest a new strategy for understanding pulmonary hypertension based on the molecular biology of the pulmonary vascular wall.

Angiopoietin-1↗
PubMed2005

Chronic thromboembolic pulmonary hypertension and pulmonary thromboendarterectomy.

Chronic thromboembolic pulmonary hypertension results from incomplete resolution of a pulmonary embolus or from recurrent pulmonary emboli. Its incidence is underappreciated, and it is currently an undertreated phenomenon. Pulmonary thromboendarterectomy is currently the safest and most effective treatment for this condition. The surgery involves midline sternotomy, profound hypothermic circulatory arrest, and complete endarterectomy of the pulmonary vascular tree. Success depends on effective coordination of multiple medical teams, including pulmonary medicine, anesthesiology, and surgery. This review, based on the past 30 years of experience at University of California San Diego Medical Center, includes information about the clinical history, diagnostic workup, anesthesia, surgical approach, and postoperative care. Outcome data are discussed, as are avenues for future research.

Anesthesia↗
PubMed2004

Does lowering pulmonary arterial pressure eliminate severe functional tricuspid regurgitation? Insights from pulmonary thromboendarterectomy.

OBJECTIVES: Because pulmonary thromboendarterectomy (PTE) can result in an immediate reduction in pulmonary artery (PA) pressure, we sought to evaluate the effect of PTE on severe tricuspid regurgitation (TR) without tricuspid annuloplasty. BACKGROUND: Few data exist regarding the frequency and magnitude of functional TR improvement after reduction in PA pressure. METHODS: We identified 27 patients with severe TR, defined by a regurgitant index (RI) >33%, who underwent PTE. The RI, tricuspid annular diameter (TAD), apical displacement of leaflet coaptation, and estimated PA systolic pressure were determined on pre- and post-PTE echocardiograms. Patients were stratified based on resolution (RI < or =33%) or persistence (RI >33%) of severe TR. RESULTS: Comparing pre- and post-PTE echocardiography results, severe TR resolved in 19 of 27 (70%) patients. This group had a more effective PA systolic pressure reduction after PTE (49 +/- 20 mm Hg vs. 32 +/- 16 mm Hg by echocardiography, p = 0.075, and 37 +/- 16 mm Hg vs. 16 +/- 13 mm Hg by catheter measurement, p = 0.004). No difference was observed in TAD, apical displacement of the tricuspid valve, or other features compared with the group with persistent severe TR. There was a trend toward longer hospital stays in the group with persistent severe TR (19 +/- 15 days vs. 14 +/- 9 days; p = 0.55). CONCLUSIONS: After significant PA pressure reduction by PTE, severe functional TR with a dilated annulus may improve without annuloplasty despite dilated tricuspid annulus diameters.

Adult↗
PubMed2004

Interventional and surgical modalities of treatment for pulmonary arterial hypertension.

Beyond medical therapy, different interventional and surgical approaches exist for treatment of pulmonary arterial hypertension (PAH). Atrial septostomy has been applied in patients with lack of response to medical therapy in the absence of other surgical treatment options. With growing experience, procedure-related death rates have been reduced to 5.4%, and the most suitable patient group has been identified among patients with a mean right atrial pressure between 10 and 20 mm Hg. Pulmonary endarterectomy is the accepted form of treatment for patients with chronic thromboembolic pulmonary hypertension. Establishing the diagnosis and the classification of the type of lesions by pulmonary angiography is crucial for optimal patient selection. Perioperative mortality rates have been reduced to <10% in experienced centers, and the hemodynamic improvement is dramatic and sustained. Lung and heart-lung transplantation remains the procedure of choice for patients unsuitable for other treatment modalities. Timing of the procedure is difficult because waiting times vary between centers and usually are in a high range. Early referral of patients unresponsive to other treatment forms is therefore of importance to avoid transplantation of patients with established significant comorbidity. The survival rate during the first five years after transplantation for PAH is intermediate among the lung diseases, lower than chronic obstructive pulmonary disease but higher than idiopathic pulmonary fibrosis.

Catheterization↗
PubMed2004

Pulmonary thromboendarterectomy surgery.

Considerable progress has been made over the past decade in understanding the etiology, prevalence, natural history, and therapeutic approach to chronic thromboembolic pulmonary hypertension. Pulmonary endarterectomy is now widely recognized as the definitive treatment for chronic pulmonary hypertension resulting from thromboembolic disease. This article focuses on the surgical treatment of chronic thromboembolic pulmonary hypertension.

Chronic Disease↗
PubMed2004

Late recurrence of cardiac sarcoma presenting as giant pulmonary artery aneurysm.

We report the case of a 46-year-old woman who had undergone cardiac transplantation for a malignant, right ventricular sarcoma. Five years later, she experienced pulmonary hypertension and a pulmonary artery aneurysm. Medical management of the pulmonary hypertension being unsuccessful, she underwent surgical exploration of the pulmonary artery aneurysm and bilateral pulmonary endarterectomy. Intra-operative findings revealed pulmonary artery sarcoma and an unresectable pulmonary artery aneurysm.

Aneurysm↗
PubMed2004

Differential myocardial gene delivery by recombinant serotype-specific adeno-associated viral vectors.

Recombinant cross-packaging of adeno-associated virus (AAV) genome of one serotype into other AAV serotypes has the potential to optimize tissue-specific gene transduction and expression in the heart. To evaluate the role of AAV1 to 5 virion shells on AAV2 transgene transduction, we constructed hybrid vectors in which each serotype capsid coding domain was cloned into a common vector backbone containing AAV2 replication genes. Constructs were tested for expression in: (1) adult murine heart in vivo using direct injection of virus, (2) neonatal and adult murine ventricular cardiomyocytes in vitro, and (3) adult human ventricular cardiomyocytes in vitro, using green fluorescent protein (GFP) as the measurable transgene. Serotype 1 virus demonstrated the highest transduction efficiency in adult murine cardiomyocytes both in vitro and in vivo, while serotype 2 virus had the greater transduction efficiency in neonatal cardiomyocytes in vitro. Prolonged in vivo myocardial GFP expression was observed for up to 12 months using serotype 1 and 2 vectors only. In human cardiomyocytes, serotype 1 vector was superior in transduction efficiency, followed by types 2, 5, 4, and 3. These data establish a hierarchy for efficient serotype-specific vector transduction in myocardial tissue. AAV1 serotype packaging results in more efficient transduction of genes in the murine and human adult heart, compared to other AAV serotypes. Our results suggest that adult human cardiac gene therapy may be enhanced by the use of serotype 1-specific AAV vectors.

Animals↗
PubMed2004

A new animal model for pulmonary hypertension based on the overexpression of a single gene, angiopoietin-1.

BACKGROUND: Angiopoietin-1 gene expression in human pulmonary hypertensive lungs is directly proportional to increasing pulmonary vascular resistance. We hypothesized that targeted overexpresssion of angiopoietin-1 in the lung would cause persistent pulmonary hypertension in an animal model. METHODS: We injected 2 x 10(10) genomic particles of adeno-associated virus-angiopoietin-1 (AAV-Ang-1) into the right ventricular outflow tract of 30 Fischer rats while using adeno-associated virus-lacZ (AAV-lacZ) injected rats and carrier-injected rats as our control groups. All animals underwent survival surgery and were sacrificed at serial timepoints postgene delivery. At each timepoint, pulmonary artery pressures were measured and pulmonary angiography using the Microfil polymer perfusion technique was performed. The lungs were harvested for pathologic analysis, mRNA analysis, Western blot assays, and in situ RNA hybridization to localize gene expression. RESULTS: Pulmonary artery pressures of AAV-Ang-1 injected rats were significantly increased compared with the control groups (p < 0.01) at all timepoints. Pathologic analysis of AAV-Ang-1 lung specimens demonstrated increased smooth muscle cell proliferation within the medial layer of arterioles with obliteration of small vessels similar to that seen in human pulmonary hypertension. Angiograms of AAV-Ang-1 injected lungs showed blunting of small peripheral arterioles consistent with advanced pulmonary hypertension. In situ RNA hybridization localized angiopoietin-1 expression to the vascular wall of small-caliber pulmonary vessels. Protein and mRNA assays confirmed persistent angiopoietin-1 expression in the lung for up to 60 days postgene delivery. CONCLUSIONS: Overexpression of angiopoietin-1 using an adeno-associated virus vector causes pulmonary hypertension in rats. These data provide a novel physiologic animal model for pulmonary hypertension.

Angiopoietin-1↗
PubMed2004

Deep hypothermic circulatory arrest and the femoral-to-radial arterial pressure gradient.

OBJECTIVES: To determine the femoral-to-radial arterial pressure gradient, as well as the factors associated with them, in patients receiving cardiopulmonary bypass (CPB) with profound hypothermia and circulatory arrest. DESIGN: Retrospective automated hemodynamic record review. SETTING: University hospital. PARTICIPANTS: Patients undergoing pulmonary thromboendarterectomy with deep hypothermic circulatory arrest. MEASUREMENTS AND MAIN RESULTS: The automated hemodynamic records of 54 consecutive patients undergoing pulmonary thromboendarterectomy with deep hypothermic circulatory arrest were reviewed, comparing the femoral and radial arterial pressures throughout the intraoperative period. In 20 of the patients, the hemodynamic data from the first 16 postoperative hours were also studied. Forty-one of 54 (76%) of the patients exhibited a mean arterial gradient of at least 10 mmHg either during or after CPB, femoral being higher. Clinically significant gradients were noted throughout the CPB period and the post-CPB period in these patients. In the 54 patients studied, the systolic blood pressure (SBP) gradient was 32 +/- 19 mmHg after CPB (95% confidence limits 28.2 mmHg, 39.0 mmHg), and the mean arterial pressure (MAP) gradient was 6.3 +/- 4.9 mmHg (95% confidence limits 5.5 mmHg, 8.6 mmHg). The duration of clinically significant SBP (>10 mmHg) and MAP (>5 mmHg) gradients in the postoperative period were 5.2 +/- 5.7 hours and 5.8 +/- 7.2 hours, respectively. Advanced age correlated with high post-CPB pressure gradients in this population and was associated with prolonged postoperative resolution of the gradients. CONCLUSIONS: The femoral-to-radial arterial pressure gradients, particularly systolic, after CPB, were greater and of longer duration in these patients undergoing deep hypothermic circulatory arrest than gradients previously reported for routine CPB. Central arterial pressure monitoring is recommended for patients undergoing deep hypothermic circulatory arrest, being valuable both for intraoperative and postoperative care.

Age Factors↗
PubMed2004

Hemodynamic observations on a yogic breathing technique claimed to help eliminate and prevent heart attacks: a pilot study.

OBJECTIVE: This pilot study investigated the hemodynamics of a yogic breathing technique claimed "to help eliminate and prevent heart attacks due to abnormal electrical events to the heart," and to generally "enhance performance of the central nervous system (CNS) and to help eliminate the effects of traumatic shock and stress to the CNS." DESIGN: Parameters for (4) subjects were recorded during a preexercise resting period, a 31-minute exercise period, and a postexercise resting period. SETTINGS/LOCATION: Parameters for subjects were recorded in a laboratory at the University of California, San Diego. SUBJECTS: Parameters for 3 males (ages 44, 45, 67) and 1 female (age 41) were recorded. One (1) subject (male age 45) had extensive training in this technique. INTERVENTIONS: This yogic technique is a 1 breath per minute (BPM) respiratory exercise with slow inspiration for 20 seconds, breath retention for 20 seconds, and slow expiration for 20 seconds, for 31 consecutive minutes. OUTCOME MEASURES: Fourteen beat-to-beat parameters were measured noninvasively and calculated for body surface area to yield: stroke index (SI), heart rate (HR), cardiac index, end diastolic index, peak flow, ejection fraction, thoracic fluid index, index of contractility, ejection ratio, systolic time ratio, acceleration index, and systolic, diastolic, and mean arterial pressures (MAPs). Left stroke work index (LSWI) and stroke systemic vascular resistance index (SSVRI) were calculated. RESULTS: We report on SI, HR, MAP, LSWI, and SSVRI and how they can help to describe hemodynamicstate changes. This technique induces dramatic shifts in all hemodynamic variables during the 1 BPM exercise and can produce unique changes in the postexercise resting period after long-term practice that appears to have a unique effect on the brain stem cardiorespiratory center regulating the Mayer wave (0.1-0.01 Hz) patterns of the cardiovascular system. CONCLUSIONS: Preclinical studies are warranted to examine the possible long-term effects of this technique that appear to reset a cardiorespiratory brain-stem pacemaker. We postulate that this effect may be the basis for the purported yogic health claim.

Adult↗