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PubMed1998

[Duplex scanning of the internal thoracic artery for coronary artery surgery].

Ultrasonic duplex scanning was used to examine 77 internal thoracic arteries (ITA). The investigated vessels were classified as normal, stenosed (peak systolic velocity was faster than 150 cm/sec and doppler signals showed turbulent pattern), small (diameter measurements were smaller than 1.4 mm and mean flow velocities were slower than 20 cm/sec in distal part of the vessels), and occluded (no flow characteristics could be detected) by the doppler spectrum analysis and the two-dimensional B-mode images. The results of the duplex examination were compared with operative findings and angiograpic findings. Diameter measurements by duplex scanning compared with operative findings showed virtually no differences. One stenosed ITA, a 75% stenosis in the proximal part of the vessel, and two small ITAs were detected by duplex scanning. We performed coronary artery bypass grafting using distal part of the stenosed ITA as a free graft, and used small ITAs as individual bypass grafts. Two normal ITAs were misjudged as small, and one small ITA was misjudged as occluded. All normal ITAs of duplex examination showed normal findings of angiography. Duplex scanning is a reliable, sensitive, and noninvasive technique for the preoperative assessment of the ITA, and is a suitable screening for coronary artery surgery.

Coronary Artery Bypass↗

PubMed2004

Effects of L-NAME and inhaled nitric oxide on ventilator-induced lung injury in isolated, perfused rabbit lungs.

OBJECTIVE: To determine whether nitric oxide (NO) might modulate ventilator-induced lung injury. DESIGN: Randomized prospective animal study. SETTING: Animal research laboratory in a university hospital. SUBJECTS: Isolated, perfused rabbit heart-lung preparation. INTERVENTIONS: Thirty-six isolated, perfused rabbit lungs were randomized into six groups (n = 6) and ventilated using pressure-controlled ventilation for two consecutive periods (T1 and T2). Peak alveolar pressure during pressure-controlled ventilation was 20 cm H2O at T1 and was subsequently (T2) either reduced to 15 cm H2O in the three low-pressure control groups (Cx) or increased to 25 cm H2O in the three high-pressure groups (Px). In the control and high-pressure groups, NO concentration was increased to approximately equal to 20 ppm (inhaled NO groups: CNO, PNO), reduced by NO synthase inhibition (L-NAME groups: CL-Name, PL-Name), or not manipulated (groups CE, PE). MEASUREMENTS AND MAIN RESULTS: Changes in ultrafiltration coefficients (deltaKf [vascular permeability index: g.min(-1).cm H2O(-1).100 g(-1)]), bronchoalveolar lavage fluid 8-isoprostane, and NOx (nitrate + nitrite) concentrations were the measures examined. Neither L-NAME nor inhaled NO altered lung permeability in the setting of low peak alveolar pressure (control groups). In contrast, L-NAME virtually abolished the change in permeability (deltaKf: PL-Name (0.10 +/- 0.03) vs. PNO [1.75 +/- 1.10] and PE [0.37 +/- 0.11; p <.05]) and the increase in bronchoalveolar lavage 8-isoprostane concentration induced by high-pressure ventilation. Although inhaled NO was associated with the largest change in permeability, no significant difference between the PE and PL-NAME groups was observed. The change in permeability (deltaKf) correlated with bronchoalveolar lavage NOx (r2 =.6; p <.001). CONCLUSIONS: L-NAME may attenuate ventilator-induced microvascular leak and lipid peroxidation and NO may contribute to the development of ventilator-induced lung injury. Measurement of NO metabolites in the bronchoalveolar lavage may afford a means to monitor lung injury induced by mechanical stress.

Administration, Inhalation↗

PubMed2003

Generation of a phenotypic array of hypothalamic neuronal cell models to study complex neuroendocrine disorders.

Knowledge of how the brain achieves its diverse central control of basic physiology is severely limited by the virtual absence of appropriate cell models. Isolation of clonal populations of unique peptidergic neurons from the hypothalamus will facilitate these studies. Herein we describe the mass immortalization of mouse primary hypothalamic cells in monolayer culture, resulting in the generation of a vast representation of hypothalamic cell types. Subcloning of the heterogeneous cell populations resulted in the establishment of 38 representative clonal neuronal cell lines, of which 16 have been further characterized by analysis of 28 neuroendocrine markers. These cell lines represent the first available models to study the regulation of neuropeptides associated with the control of feeding behavior, including neuropeptide Y, ghrelin, urocortin, proopiomelanocortin, melanin-concentrating hormone, neurotensin, proglucagon, and GHRH. Importantly, a representative cell line responds appropriately to leptin stimulation and results in the repression of neuropeptide Y gene expression. These cell models can be used for detailed molecular analysis of neuropeptide gene regulation and signal transduction events involved in the direct hormonal control of unique hypothalamic neurons, not yet possible in the whole brain. Such studies may contribute information necessary for the strategic design of therapeutic interventions for complex neuroendocrine disorders, such as obesity.

Animals↗

PubMed2002

Vertebral height, disc height, posteroanterior displacement and dens-atlas gap in the cervical spine: precision measurement protocol and normal data.

OBJECTIVE: (1) Precise measurement of vertebral height, disc height, posteroanterior displacement and dens-atlas gap from lateral radiographic views of the cervical spine. (2) Compilation of a normative database for these parameters, specifying dependence on gender and age. DESIGN: Descriptive study, based on measurements from lateral radiographic views of the cervical spine of healthy subjects. BACKGROUND: Normal data of vertebral height, disc height, posteroanterior displacement and size of the dens-atlas gap as well as their biological range of variation and potential dependence on gender and age are not available. METHODS: Based on computer-aided measurements from lateral radiographic views of the cervical spine, a new protocol determines these parameters. RESULTS: are compensated for radiographic magnification, variation in stature and the individually adopted posture of the cervical spine; they are virtually uninfluenced by radiographic distortion and patient alignment errors. A specimen study as well as inter- and intra-observer studies quantify measurement errors.Results. Employing the new protocol, vertebral height C3-C7 and disc height C2/C3-C6/C7 are measured with relative errors of 3.9% and 5.7% respectively. Posteroanterior displacement C1/C2 to C6/C7 is measured with an error of 2.8% of mean vertebral depth and the dens-atlas gap is measured with an error of <1.8% of the depth of C2. A normal database for the dimensions of cervical vertebrae and discs as well as of the sagittal plane alignment of the vertebrae within the cervical spine is compiled from 135 lateral views of healthy adults. CONCLUSIONS: Vertebral height, disc height, posteroanterior displacement and size of the dens-atlas gap are measured with high precision. Normal data are presented for the first time. RELEVANCE: The new protocol in conjunction with the normal database enables future studies detecting or monitoring morphological effects of, for example, trauma, long-term high mechanical loading, disc degeneration, rheumatoid arthritis, fusion or other surgical interventions.

Adult↗

PubMed1999

Neuropsychiatric aspects of carbon monoxide poisoning: a review and single case report suggesting a role for amphetamines.

Sublethal exposure to carbon monoxide (CO) can result in severe neurologic and psychiatric complications. Once in the body, CO can wreak havoc on virtually every organ system, with the brain being the most vulnerable to the damaging effects. Neuropathological injury is frequently widespread, and while white matter injury is most common, both gray and white matter injury occurs. Consequently, no neurologic or psychiatric syndrome is pathognomonic for CO poisoning. There are currently no effective treatments for the delayed neuropsychiatric sequelae of CO poisoning, and medical management focuses on correcting immediate symptoms through the use of oxygen, hyperbaric oxygen therapy, and supportive measures. Preliminary data suggest, however, that dopaminergic agents may be useful for the treatment of some of the delayed sequelae of CO neurotoxicity. To our knowledge, ours is the first case report in which dextroamphetamine (DAMP), a potent dopaminergic agent, has been used for treating the neuropsychiatric symptoms of CO poisoning. Our data demonstrate that it is effective in shortening cognitive and motor recovery time, that psychostimulant actions occur slightly sooner than locomotor effects, and that theraputic benefit is most dramatic within the first ten days of use. Therefore, DAMP appears to be a pharmacological agent that can be combined with supportive interventions to reverse, attenuate, or symptomatically improve the delayed sequelae that occur in these patients.

Amphetamines↗

PubMed1997

Common cancers--genetics, origin, prevention, screening: Parts I and II.

Carcinogenesis is a stepwise process that occurs through mutations of cancer-related genes. Five or more genes must be mutated before malignant transformation occurs in most adult cancers; in some childhood cancers as few as two mutated genes may be sufficient. A rare inherited mutation of a critical gene may predestine cancer to occur in one or more sites. This germline mutation is present in virtually every cell in the body, except half of the germ cells, which do not contain the mutated gene in their haploid chromosome set. These and other genes have been used to piece together a puzzle of regulatory systems that govern cell division and proliferation, as well as apoptosis or programmed cell death. Mutations of these genes result not only in increased cell proliferation but also in diminished cell death. Most genetic changes that occur during carcinogenesis are not inherited or germline. They are acquired after birth and are called somatic mutations. A somatic mutation affects only the mutated cell and its progeny. Each time a cell divides, there is a chance of somatic mutation, and therefore there always is a low, background risk for cancer and other malignant lesions. A far more prevalent cause of cancer-related death in the United States is environmental exposure. Such exposure causes somatic mutations of cancer-related genes through direct damage to DNA or through alteration of proliferation or cell death, which enhances the baseline risk for mutation. As carcinogenesis becomes understood, interventions may be designed that selectively interfere in important steps. Screening for cancer is based on the premise that one can treat a patient for a cancer that has not spread from its primary site. Nevertheless, cancer screening is controversial and often confusing. Issues of costs, risks versus benefits, physical time and effort, and patient compliance all affect the clinician's view of screening, often to the extent that the true value of this approach to cancer control is underappreciated and underutilized. A clinician should consider the following questions when assessing the priority, scope, and intensity of cancer screening. Is the cancer an important public health problem? Can preclinical stages be detected and cured? Are effective screening tests available? Are the tests feasible and acceptable? Have screening programs reduced cancer-specific mortality? Is the screening program cost effective? Is screening generally recommended? There is clear-cut evidence of benefit from screening for cancer of the cervix, breast, colon and rectum, and skin and some specific genetic syndromes. Evidence of survival benefit from screening for prostate cancer is lacking, although prostate specific antigen screening is widely used. Screening for lung and ovarian cancer is ineffective.

Adult↗

PubMed2004

Autoantibodies as predictors of disease.

CONTEXT: Many human diseases are the result of autoimmune attack, presumably related to a loss of tolerance to self. Autoimmune disease can be divided into either organ-specific illnesses, such as thyroid disease, type 1 diabetes, and mysasthenia gravis, or systemic illnesses, such as rheumatoid arthritis and systemic lupus erythematosus. The pathogenesis of autoimmune damage also segregates autoimmune disease in that some diseases or manifestations are mainly induced by autoantibodies. Pathogenesis may be mainly mediated by autoimmune T lymphocytes. Notwithstanding the underlying mechanism of disease, virtually all autoimmune diseases are associated with circulating autoantibodies, which bind self-protein. Furthermore, for many diseases these autoantibodies are found in serum samples many years before disease onset. STARTING POINT: In the past several years a new autoantibody specificity has been identified in the sera of patients with rheumatoid arthritis. These autoantibodies bind citrulline, a post-translational modification of arginine. Markus Nielen and colleagues recently studied the presence of these autoantibodies and rheumatoid factor in blood donors who later developed rheumatoid arthritis (Arthritis Rheum 2004; 50: 380-86). About half the patients were positive for at least autoantibody at a median of 4.5 years before the onset of disease. The negative predictive value of these tests was high, while the positive predictive value was very high. WHERE NEXT? Autoantibodies might not be directly responsible for many of the manifestations of autoimmune disease, but they are markers of future disease in presently healthy individuals. Long-term large studies of outcome are needed to assess the use of assaying autoantibodies for prediction of disease. Such data could lead to intervention trials to prevent autoimmune disease, as are already underway in type 1 diabetes.

Arthritis, Rheumatoid↗

PubMed2003

The potential role of flow cytometry in the diagnosis of small cell carcinoma.

CONTEXT: Virtually no information exists in the medical literature on the immunophenotyping of small cell carcinoma by flow cytometry. CD56, or neural cell adhesion molecule, is widely expressed by small cell carcinoma and easily measured by flow cytometry. OBJECTIVE: To determine the potential usefulness of flow cytometry in the diagnosis of small cell carcinoma. DESIGN AND SETTING: Retrospective data and archival material on 27 patients were obtained from community hospitals. Specimens (needle aspirations and tissue biopsies) from all patients demonstrated cytomorphologic and flow cytometric features consistent with small cell carcinoma. All measurements were performed at a large reference laboratory. Routine 3- and 4-color flow cytometry using a lymphoma antibody panel, including anti-CD56, was performed. Anti-cytokeratin antibody was also used in the last 12 cases. Immunohistochemical staining with a panel of conventional markers for neuroendocrine neoplasms was performed on available tissue for purposes of confirmation of small cell carcinoma. PATIENTS: Twenty-seven patients whose tissue specimens showed a clearly defined population of CD45-CD56+ cells by flow cytometry and cytomorphologic features consistent with small cell carcinoma. INTERVENTIONS: Needle aspiration (n = 3) and tissue biopsy (n = 24) from a variety of sites. RESULTS: CD56 positivity by flow cytometry was 100 to 1000 times that of the matched isotype control in 25 cases and 10 to 100 times that of the control in 2 cases. Cytokeratin positivity by flow cytometry was found in 12 of 12 cases. Immunohistochemical staining showed positivity for at least 1 cytokeratin and 1 or more neuroendocrine markers in 26 of 27 cases and confirmed the diagnosis of small cell carcinoma. CONCLUSIONS: Routine flow cytometry can identify a neuroendocrine phenotype that shows a strong correlation with confirmatory immunohistochemical markers in cases exhibiting cytomorphologic features of small cell carcinoma. Flow cytometry appears to complement and may possibly be a satisfactory alternative to immunohistochemical staining when small cell carcinoma is suspected.

Biomarkers, Tumor↗

PubMed1990

Platelet-neutrophil interactions. 12S,20- and 5S,12S-dihydroxyeicosapentaenoic acids: two novel neutrophil metabolites from platelet-derived 12S-hydroxyeicosapentaenoic acid.

Dietary marine n-3 polyunsaturated fatty acids have demonstrated an antiinflammatory potential in epidemiologic and intervention studies in humans. Proposed mechanisms, involving only leukocytes, fall short of explaining this potential completely. Enriched by dietary means with eicosapentaenoic acid (EPA), stimulated human platelets release substantial amounts of eicosapentaenoic acid and 12S-hydroxyeicosapentaenoic acid (12S-HEPE) in addition to 12S-hydroxyeicosatetraenoic acid (12S-HETE) derived from arachidonic acid. Human neutrophils metabolize 12S-HETE to 5S,12S-DiHETE when stimulated, whereas unstimulated neutrophils produce 12S,20-DiHETE. This study was undertaken to characterize metabolism of 12S-HEPE in human neutrophils. We demonstrate herein for the first time that 12S-HEPE is metabolized by human neutrophils. In unstimulated neutrophils 20-hydroxylation to 12S,20-DiHEPE occurs, whereas in stimulated neurtrophils 5-lipoxygenation to 5S,12S-DiHEPE takes place. The structures of these metabolites were characterized by their relative retention times on reversed-phase high pressure liquid chromatography, by their UV absorbance spectra, and by gas-liquid chromatography-mass spectrometry. With increasing amounts of 12S-HEPE, stimulated neutrophils produced increasing amounts of 5S,12S-DiHEPE, which is virtually inactive biologically. Concomitantly, production of the potent chemokinetic and chemoattractant arachidonic acid derivative leukotriene B4 decreased. Thus, 12S-HEPE can compete with endogenous arachidonic acid for 5-lipoxygenation in stimulated human neutrophils. 12,20-DiHEPE, LTB5, and 5S,12S-DiHEPE were detectable after coincubating EPA-enriched platelets with unenriched neutrophils, and arachidonic acid-derived 5-lipoxygenase products were decreased. We conclude that 12S-HEPE can participate in platelet-neutrophil interactions in a manner similar to 12S-HETE. By providing competing substrates for neutrophil 5-lipoxygenase, platelets might contribute to the antiinflammatory potential of dietary n-3 fatty acids through platelet-neutrophil interaction.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2006

Imaging vulnerable plaque by ultrasound.

Diagnostic techniques to identify vulnerable plaques are rapidly evolving. Intravascular ultrasound (IVUS) has the ability to detect and localize plaque as well as quantitate plaque burden. Recent IVUS studies have suggested that patients presenting with acute coronary syndromes have an approximate 25% incidence of additional ruptured plaques in arteries other than the culprit lesion. The ability of IVUS to detect vulnerable plaques before rupture is currently being evaluated by novel techniques. Initially, IVUS was shown to be able to characterize plaque broadly as calcified or fibrofatty but was limited in its ability to more precisely detect lipid-rich plaques, necrotic cores, and thrombus. Recent advances in new applications of IVUS, such as integrated backscatter, wavelet analysis, and virtual histology, have focused on evaluating and mathematically transforming the radiofrequency signal from ultrasound waves into a color-coded representation of plaque characteristics such as lipid, fibrous tissue, calcification, and necrotic core. In addition, targeted contrast agents, applicable to both intravascular and transthoracic studies, are being evaluated in experimental models and aim to highlight specific plaque components, such as endothelial adhesion molecules and other plaque components that might be useful in targeting vulnerable plaques. These advances pave the way for future clinical trials in assessing the ability of such techniques to diagnose vulnerable plaques and to assess the effects of both pharmacologic and mechanical therapies on plaque characteristics.

Atherosclerosis↗

PubMed2003

[Sudden infant death--prevention programs in Austria].

In the current study, design and success of intervention programmes to prevent sudden infant death syndrome (SIDS) in Austria are described and major future challenges indicated. Various prevention programmes are being carried out in the federal states of Austria and they focus on the detailed information of parents about modifiable SIDS risk factors. Relevant topics such as guidelines for home monitoring are carefully addressed in the Austrian consensus statements. With the introduction of the first campaigns SIDS incidence rates have gradually dropped from 1.69 (1988) to 0.51 per 1000 life births (2000). In line, there was a decline in the prevalence of risk behaviour, especially of the prone sleeping position (federal state of the Tyrol: 53.7% before the campaign (1984-1994) vs. 4.7% thereafter (1995-2001), p < 0.001). Because of this latter trend smoking during pregnancy became the most prevalent SIDS risk factor and the prevalence of the side sleeping position substantially increased. To maintain the current success in lowering SIDS frequency, prevention programmes ought to continue and changes in the weight of risk factors should be considered. Further efforts are required to achieve a thorough post-mortem examination in virtually all sudden unexpected deaths, to establish a country-wide SIDS data base and to continuously update SIDS risk profiles in Austria.

Austria↗

PubMed1998

In vivo knee joint loading and kinematics before and after ACL transection in an animal model.

Osteoarthritis (OA) is typically diagnosed in humans in its final stage when joint movement becomes painful. Clinical information about the onset and the mechanisms triggering the degenerative responses are virtually non-existent. However, research on animal models of experimental OA shows that joint adaptations associated with the onset of OA can be detected as early as two to four weeks following disruption of the normal joint mechanics. Transection of the anterior cruciate ligament (ACL) has been shown to cause OA-like symptoms in various animal models including the cat. However. the changes in joint loading responsible for the early tissue responses have not been quantified in vivo. Consequently, the relationship between abnormal joint loading and the onset of OA remains unknown. The purpose of this study was to quantify knee loading before and early after ACL transection in the cat. Knee mechanics were assessed by measuring patellar tendon forces, gastrocnemius forces, knee flexor and extensor EMGs, and hindlimb kinematics before and 5, 7, and 9 days following ACL transection in six experimental and two sham-operated animals. The knee mechanics were not affected by sham-surgery but the muscular forces. knee extensor EMGs, and knee range of motion were reduced following ACL transection compared to corresponding pre-intervention values. These results suggest that ACL transection causes a general unloading and changed kinematics of the knee. We speculate that the decrease in loading and the altered kinematics are responsible for the onset of biologic adaptations of the knee. Precise data about the local joint contact mechanics before and after ACL transection are now required to further relate the detailed changes in the knee mechanics to the early joint changes.

Animals↗

PubMed1993

Association between gastric intramucosal pH and splanchnic endotoxin, antibody to endotoxin, and tumor necrosis factor-alpha concentrations in patients undergoing cardiopulmonary bypass.

OBJECTIVES: To determine the association between gastric intramucosal pH, a minimally invasive marker reflecting the adequacy of oxygen delivery to the gastrointestinal tract, and splanchnic endotoxin, antibody to endotoxin, and tumor necrosis factor (TNF)-alpha concentrations in patients undergoing cardiopulmonary bypass. DESIGN: Single-arm, prospective study. SETTING: University hospital. PATIENTS: Adults (n = 10) free of hepatic, pulmonary, and renal disease undergoing nonemergent coronary artery bypass surgery. INTERVENTIONS: After induction of general anesthesia and endotracheal intubation, a tonometer nasogastric tube was positioned in the stomach, and triple-lumen fiberoptic catheters were inserted into the hepatic vein and pulmonary artery. Hepatic venous and mixed venous blood samples were analyzed for endotoxin, antibody to endotoxin, and TNF-alpha at six times: 30 mins after induction of anesthesia (time 1); during vena caval cannulation (time 2); after 15 mins of hypothermic cardiopulmonary bypass (time 3); during spontaneous left ventricular ejection after release of the aortic cross-clamp, but before termination of cardiopulmonary bypass (time 4); 15 mins after termination of cardiopulmonary bypass (time 5); and 1 hr after termination of cardiopulmonary bypass (time 6). Gastric intramucosal pH, systemic oxygen delivery (DO2), mixed venous oxygen saturation, hepatic venous oxygen saturation, and hepatic venous lactate concentrations were recorded at these same times. Data for each variable were compared with baseline values (time 1) for statistical significance. MEASUREMENTS AND MAIN RESULTS: Cardiopulmonary bypass was associated with an increase (p < .05) in systemic endotoxin concentrations from ventricular ejection until the end of the study. Virtually identical changes in the splanchnic circulation at this time approached, but did not reach, statistical significance, because hepatic venous endotoxin concentrations were higher than the mixed venous endotoxin concentrations at baseline (41.6 +/- 11.2 vs. 16.9 +/- 4.9 pg/mL). Gastric intramucosal pH was abnormal (< 7.35) at 15 mins (p > .05) and at 1 hr after termination of cardiopulmonary bypass (p > .05). The relationship between endotoxin and gastric intramucosal pH was not statistically significant (p = .15). The decrease in endotoxin antibody was small and statistically insignificant. TNF-alpha was not detected in any patient. Systemic DO2 decreased (p < .05) after 15 mins of hypothermic cardiopulmonary bypass, but returned to baseline values thereafter. There were no significant changes in mixed venous and hepatic venous oxygen saturation values. Splanchnic lactate concentrations increased at cannulation (p < .05), after 15 mins of hypothermic cardiopulmonary bypass (p < .05), and 15 mins after termination of cardiopulmonary bypass (p < .05). CONCLUSIONS: These observations are consistent with the hypothesis that impaired gut-barrier function is responsible for endotoxemia occurring during cardiopulmonary bypass. It is unclear whether increased mucosal permeability and mucosal acidosis are causally related phenomena or simply independent markers of damage to gut epithelium.

Adult↗

PubMed1994

Laser ablation of the prostate: experience with an ultrasound guided technique and a procedure under direct vision.

Twenty-four patients with benign prostatic hyperplasia were treated with the Nd:YAG laser. We review our experience with two different techniques: the ultrasound-guided transurethral laser-induced prostatectomy (TULIP) and the visual laser ablation of the prostate (VLAP). Our experience with these two different laser systems shows that the treatment is relatively simple, speedy and performed with virtually no blood loss. The results, of both the TULIP and VLAP procedures, are excellent. The symptom scores decrease from 43 to 19 (TULIP) and 48 to 9 (VLAP). Furthermore, there is a marked increase in average uroflow from 7.9 to 18.6 ml/s (TULIP) and from 8.1 to 18.0 ml/s (VLAP). The patients with the TULIP procedure, however had more pronounced posttreatment complaints. These patients more often received antibiotics. Laser therapy of the prostate, although still in its infancy, gives excellent results and has substantial advantages over conventional transurethral resection of the prostate (TURP). Laser therapy may replace TURP within several years.

Humans↗

PubMed2000

Catheter mapping of spontaneous and induced atrial fibrillation in man.

The clinical electrophysiologic study of atrial fibrillation [AF] has recently progressed from static characterization of the substrate to the dynamic investigation of both induced and spontaneous AF in man. Prior studies have demonstrated inhomogeneity and greater dispersion of atrial refractoriness in patients with AF, but recently atrial electrical remodeling with consequent abbreviation of atrial refractory periods has also been reported. Yet further experimental observations have suggested the existence of additional arrhythmogenic mechanisms for certain AF subsets. These include studies that have demonstrated a stable atrial flutter circuit in one atrium with fibrillatory conduction or a focal atrial tachyarrhythmia arising commonly in the left atrium. Efforts at catheter mapping of AF are now in progress. New mapping techniques and novel devices are currently being employed. We have performed catheter mapping simultaneously in right and left atrial sites at onset and during sustained pacing-induced and spontaneous AF in patients with ischemic and/or hypertensive heart disease. Atrial premature complexes that initiated spontaneous AF typically had coupling intervals ranging from 260 to 400 ms and most frequently arose in the crista terminalis, right atrioventricular junction or superior left atrium. AF at onset showed discrete electrograms at virtually all right and left atrial regions mapped and the region of earliest atrial activation during AF was in close proximity to the premature complexes in over 90% of patients. The regional atrial activation sequence for the first 10 AF beats demonstrated stable or unstable patterns in individual patients. In contrast to spontaneous AF, the initial arrhythmia of induced AF was seen to have a significantly different site of earliest atrial activation but similar discrete electrograms in different atrial regions. However, as with spontaneous AF, the site of extrastimulus delivery was in close proximity to the first induced beat. We conclude that regional catheter mapping of AF is feasible and safe in man and organized electrical activity is frequently observed at AF onset in patients with heart disease. Both right and left atrial regions can be the source of atrial premature complexes and at the onset of spontaneous AF. Induced AF may have differing activation patterns than spontaneous AF but both demonstrate earliest activation in proximity to the initiating atrial premature complex. These findings may help explain therapeutic benefits of right and left atrial interventions and pacing therapies in AF.

Atrial Fibrillation↗

PubMed2003

Preliminary research on the efficacy of virtual reality exposure therapy to treat driving phobia.

This article presents a review of preliminary research of two studies of the efficacy of virtual reality exposure therapy (VRET) to treat driving phobia. Study 1 describes a case study of a patient who completed a 7-day baseline followed by three sessions of VRET. Her peak anxiety decreased within and across sessions. At the post-treatment assessment, her phobic-related symptoms had diminished and she no longer met diagnostic criteria for driving phobia. Clinical improvement was maintained at 1-, 3-, and 7-month follow-up. In study 2, a multiple baseline across-subjects design was used to treat five patients over eight weekly VRET sessions. Visual and statistical analyses showed clear improvement in driving anxiety and avoidance in three patients between pre- and post-treatment assessments, and they no longer met criteria for driving phobia. There was marginal improvement in one patient, and the remaining individual showed no treatment gains. There was negligible change in actual driving frequency for any of the patients. Some gains were lost at the follow-up, particularly for the two individuals with poorer treatment responses. The results from these preliminary studies suggest that VRET may be a promising intervention for treating driving phobia. Avenues for improving treatment outcome are discussed.

Adult↗

PubMed1998

Comparative hemodynamic effects of three different parenterally administered lipid emulsions in conscious dogs.

OBJECTIVE: To compare the hemodynamic side effects of three structurally different lipid emulsions. DESIGN: Randomized, controlled, prospective animal study. SETTING: University research laboratory. SUBJECTS: Six chronically instrumented mongrel dogs. INTERVENTIONS: On separate days, all animals were submitted to three different treatments, in a randomized order. After baseline measurements, either a long-chain triglyceride emulsion (treatment 1), a mixed medium-chain triglyceride/long-chain triglyceride emulsion (treatment 2), or an omega3 polyunsaturated fatty acid long-chain triglyceride (PUFA) emulsion (treatment 3) was administered intravenously over 30 mins. MEASUREMENTS AND MAIN RESULTS: Global and regional hemodynamics (sonomicrometry) were recorded for 2 hrs after baseline measurements. Arterial blood gases and plasma concentrations of hemoglobin, triglycerides, total protein, and glucose were recorded for 2 hrs. Long-chain triglycerides did not affect the cardiovascular performance in awake animals. However, medium-chain triglycerides/long-chain triglycerides and omega3 PUFA caused marked increases in systemic vascular resistance (from 1833 +/- 154 to 3277 +/- 163 mm Hg/dynexsec5, p < .05), heart rate (from 89 +/- 6 to 158 +/- 10 beats/min, p < .05), and depressed ventricular performance (wall-thickening fraction [as percentage from baseline] decreased to 53 +/- 9%, p < .05). CONCLUSIONS: Commercially available lipid emulsions can cause profound cardiovascular side effects at high doses, depending on their composition. Whereas long-chain triglyceride emulsions have virtually no effects on hemodynamics in normal dogs, medium-chain triglyceride/long-chain triglyceride, and omega3 PUFA emulsions should be used with caution in critically ill patients with compromised cardiovascular function.

Acidosis↗

PubMed2000

[Second and Third Annual Report of the German Society of Coronary Angiography and Interventions in Private Practice (BNK) concerning quality assurance in invasive cardiology].

Since 1995, the German Society for Cardiac Angiography and Interventions in Private Practice (BNK) has been intensely involved in quality assurance; since 1996, it has registered relevant data for diagnostic left heart catheterization (DIAG) and coronary interventions (PTCA). The following data are based on a total of 72,777 cardiac catheters, of which 54,513 were DIAG and 18,264 were PTCA (DIAG in 1996: 10,316; in 1997: 15,692 and in 1998: 28,505. PTCA in 1996: 2,597; in 1997: 5,600 and in 1998: 10,067). The mean patient age was 61.9 years for males and 65.3 years for females (31%). DIAG was performed on an out-patient basis in 60% of the cases. The proportion of self-referrals is circa one-third and has not increased over time. A s/p PTCA was present in 21% of the DIAG patients; those after coronary bypass surgery showed a steadily increasing trend towards a follow-up DIAG (8% of the patients). There was a distinctive decrease in the use of contrast medium from an average of 164 ml (1996) to 138 ml (1998). The symptoms leading to DIAG did not substantially change in the years from 1996 to 1998; the angiographic range of the coronary disease and the degree of an impaired myocardial function have remained virtually unchanged. The treatment recommendations appear to tend towards medical therapy with decreasing indications for PTCA (20%) and open heart surgery (16%). The mean duration of a PTCA procedure decreased from 57 +/- 8 (1996) to 44.6 +/- 25 (1998) minutes. The success rates remained unchanged for coronary stenoses as well as for recanalization of chronic total occlusions. PTCA complications: the incidence of abrupt coronary occlusions was 2% and of emergency bypass surgery 0.4%; mortality was 0.1%.

Aged↗