Using focus groups to identify characteristics of an ideal work environment for Advanced Practice Clinicians.

Advanced Practice Clinicians (APCs) in collaborative practice represent a diverse and valuable group of health care professionals, including nurse practitioners, physician assistants, nurse anesthetists, and nurse midwives. Because these healthcare professionals have been identified as part of the solution to physician shortages, it is critical for health networks to examine and address issues affecting collaborative relationships. We invited our network APCs to participate in focus group sessions to determine both attributes and barriers to an ideal work environment. Four major themes emerged: (1) compensation, (2) network representation, (3) employment structure, and (4) workplace culture. While issues relating to compensation and representation were prevalent, discussions also revealed the importance of relationships and communication. To ensure successful collaboration and, thereby, reduce clinician turnover, leaders must address gaps between the existing and ideal states in structural factors affecting job satisfaction (Themes 1-3) as well as the behavioral factors represented in workplace culture (Theme 4).

Components of the metabolic syndrome differ between young and old adults in the US population.

Prevalence of the metabolic syndrome (MetS) is high in the United States and is associated with increased risk of cardiovascular disease and diabetes. The authors examined whether the prevalence of the MetS and its components differs across age groups. Data were analyzed from 4 National Health and Nutrition Examination Surveys between the years 1999 and 2006. Prevalence of MetS as defined by the Third Report of the Adult Treatment Panel criteria and prevalence of associated cardiac risk factors were determined in 41,474 participants aged 18 years and older without a history of cardiovascular disease (CVD). All estimates were weighted. Prevalence of MetS among asymptomatic adults without CVD was 20.5% and remained stable for the total population during survey periods. Prevalence of MetS increased with age: 6.6% in young adults (age 18-29 years) and 34.6% in older adults (70 and older). Components of MetS differed between young and old adults. Young adults had lower levels of high-density lipoprotein cholesterol, less glucose intolerance, and less hypertension. This study provides an estimate of MetS prevalence in asymptomatic adults in the United States during an 8-year period revealing that MetS affects a large number of Americans. Components of MetS differ between young and old adults and may have important implications in their clinical management.

The relationship of peripheral arterial disease and metabolic syndrome prevalence in asymptomatic US adults 40 years and older: results from the National Health and Nutrition Examination Survey (1999-2004).

Peripheral arterial disease (PAD) is a subclinical marker of coronary artery disease and identifies asymptomatic individuals at high risk for cardiovascular disease (CVD) events. The metabolic syndrome (MetS) is a constellation of clinical factors that increases the risk of developing diabetes and CVD. The authors' objectives were to estimate the prevalence of MetS in patients with PAD and to determine the prevalence of PAD in the population of asymptomatic US adults 40 years and older with MetS. The authors analyzed data from 3 National Health and Nutrition Examination Surveys (NHANES, 1999-2004). Prevalence of MetS as defined by the Third Report of the Adult Treatment Panel criteria and prevalence of associated cardiac risk factors were determined in 5376 asymptomatic participants 40 years and older. Presence of PAD was defined as ankle-brachial index <0.9. Estimates were weighted with the sample weights accounting for the unequal selection probability of complex NHANES sampling and over sampling of selected population subgroups. Prevalence of PAD in asymptomatic US adults 40 years and older was 4.2%. PAD prevalence in persons with MetS was 7.0% compared with 3.3% in persons without MetS. A total of 38% of the population with PAD also had MetS. High rates of abdominal obesity, hypertension, hyperglycemia, and low high-density lipoprotein cholesterol are significant contributors to both MetS and PAD. Persons with MetS have twice the risk of having PAD. Of persons with PAD, almost 40% have MetS. The presence of either PAD or MetS should warrant screening for both conditions so that risk stratification and management of risk factors may be performed.

Overexpression of ornithine decarboxylase decreases ventricular systolic function during induction of cardiac hypertrophy.

Ornithine decarboxylase (ODC), the first enzyme of polyamine metabolism, is rapidly upregulated in response to agents that induce a pathological cardiac hypertrophy. Transgenic mice overexpressing ODC in the heart (MHC-ODC mice) experience a much more dramatic left ventricular hypertrophy in response to ß-adrenergic stimulation with isoproterenol (ISO) compared to wild-type (WT) controls. ISO also induced arginase activity in transgenic hearts but not in controls. The current work studies the cooperation between the cardiac polyamines and L-arginine (L-Arg) availability in MHC-ODC mice. Although ISO-induced hypertrophy is well-compensated, MHC-ODC mice administered L-Arg along with ISO showed a rapid onset of systolic dysfunction and died within 48 h. Myocytes isolated from MHC-ODC mice administered L-Arg/ISO exhibited reduced contractility and altered calcium transients, suggesting an alteration in [Ca(2+)] homeostasis, and abbreviated action potential duration, which may contribute to arrhythmogenesis. The already elevated levels of spermidine and spermine were not further altered in MHC-ODC hearts by L-Arg/ISO treatment, suggesting alternative L-Arg utilization pathways lead to dysregulation of intracellular calcium. MHC-ODC mice administered an arginase inhibitor (Nor-NOHA) along with ISO died almost as rapidly as L-Arg/ISO-treated mice, while the iNOS inhibitor S-methyl-isothiourea (SMT) was strongly protective against L-Arg/ISO. These results point to the induction of arginase as a protective response to ß-adrenergic stimulation in the setting of high polyamines. Further, NO generated by exogenously supplied L-Arg may contribute to the lethal consequences of L-Arg/ISO treatment. Since considerable variations in human cardiac polyamine and L-Arg content are likely, it is possible that alterations in these factors may influence myocyte contractility.

Statin use is associated with improved survival in patients with advanced heart failure receiving resynchronization therapy.

It is unknown whether statin use improves survival in patients with advanced chronic heart failure (HF) receiving cardiac resynchronization therapy (CRT). The authors retrospectively assessed the effect of statin use on survival in patients with advanced chronic HF receiving CRT alone (CRT-P) or CRT with implantable cardioverter-defibrillator therapy (CRT-D) in 1520 patients with advanced chronic HF from the Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) trial database. Six hundred three patients (40%) were taking statins at baseline. All-cause mortality was 18% in the statin group and 22% in the no statin group (hazard ratio [HR] 0.85; confidence interval (CI), 0.67-1.07; P=.15). In a multivariable analysis controlling for significant baseline characteristics and use of CRT-P/CRT-D, statin use was associated with a 23% relative risk reduction in mortality (HR, 0.77; CI, 0.61-0.97; P=.03). Statin use is associated with improved survival in patients with advanced chronic HF receiving CRT. No survival benefit was seen in patients receiving statins and optimal pharmacologic therapy without CRT.

Prevalence of peripheral artery disease varies significantly depending upon the method of calculating ankle brachial index.

OBJECTIVE: Peripheral artery disease (PAD) identifies individuals at high risk for future cardiovascular disease (CVD) warranting aggressive risk reduction therapies. PAD can be diagnosed noninvasively by calculating the ankle brachial index (ABI), a ratio of ankle and arm blood pressures. We examined the existing various methods of calculating ABI and the resulting estimates of PAD prevalence. METHODS: We analyzed data from three National Health and Nutrition Examination Surveys. PAD prevalence using three different methods of calculating ABI was determined in 5,376 participants, aged > or =40 years without prior history of CVD. ABI was defined as an ankle brachial index of less than 0.9. Statistical analysis was performed using SPSS V15.0. RESULTS: PAD prevalence among asymptomatic adults without CVD increased significantly during the 6-year time period (1999-2004), regardless of the method used for determining ABI. However, across the National Health and Nutrition Examination Survey assessments, ABI method significantly affected calculated PAD prevalence. Differences in calculated PAD prevalence correspond to approximately 2.2 million persons who would be reclassified as having or not having PAD. CONCLUSION: The calculated prevalence of asymptomatic PAD varies significantly by the ABI method used. Further study is required to determine the most accurate method of performing ABI.

Nonobese, insulin-deficient Ins2Akita mice develop type 2 diabetes phenotypes including insulin resistance and cardiac remodeling.

Although insulin resistance has been traditionally associated with type 2 diabetes, recent evidence in humans and animal models indicates that insulin resistance may also develop in type 1 diabetes. A point mutation of insulin 2 gene in Ins2(Akita) mice leads to pancreatic beta-cell apoptosis and hyperglycemia, and these mice are commonly used to investigate type 1 diabetes and complications. Since insulin resistance plays an important role in diabetic complications, we performed hyperinsulinemic-euglycemic clamps in awake Ins2(Akita) and wild-type mice to measure insulin action and glucose metabolism in vivo. Nonobese Ins2(Akita) mice developed insulin resistance, as indicated by an approximately 80% reduction in glucose infusion rate during clamps. Insulin resistance was due to approximately 50% decreases in glucose uptake in skeletal muscle and brown adipose tissue as well as hepatic insulin action. Skeletal muscle insulin resistance was associated with a 40% reduction in total GLUT4 and a threefold increase in PKCepsilon levels in Ins2(Akita) mice. Chronic phloridzin treatment lowered systemic glucose levels and normalized muscle insulin action, GLUT4 and PKCepsilon levels in Ins2(Akita) mice, indicating that hyperglycemia plays a role in insulin resistance. Echocardiography showed significant cardiac remodeling with ventricular hypertrophy that was ameliorated following chronic phloridzin treatment in Ins2(Akita) mice. Overall, we report for the first time that nonobese, insulin-deficient Ins2(Akita) mice develop type 2 diabetes phenotypes including peripheral and hepatic insulin resistance and cardiac remodeling. Our findings provide important insights into the pathogenesis of metabolic abnormalities and complications affecting type 1 diabetes and lean type 2 diabetes subjects.

M(1) and M(2) muscarinic acetylcholine receptor subtypes mediate Ca(2+) channel current inhibition in rat sympathetic stellate ganglion neurons.

Muscarinic acetylcholine receptors (mAChRs) are known to mediate the acetylcholine inhibition of Ca(2+) channels in central and peripheral neurons. Stellate ganglion (SG) neurons provide the main sympathetic input to the heart and contribute to the regulation of heart rate and myocardial contractility. Little information is available regarding mAChR regulation of Ca(2+) channels in SG neurons. The purpose of this study was to identify the mAChR subtypes that modulate Ca(2+) channel currents in rat SG neurons innervating heart muscle. Accordingly, the modulation of Ca(2+) channel currents by the muscarinic cholinergic agonist, oxotremorine-methiodide (Oxo-M), and mAChR blockers was examined. Oxo-M-mediated mAChR stimulation led to inhibition of Ca(2+) currents through voltage-dependent (VD) and voltage-independent (VI) pathways. Pre-exposure of SG neurons to the M(1) receptor blocker, M(1)-toxin, resulted in VD inhibition of Ca(2+) currents after Oxo-M application. On the other hand, VI modulation of Ca(2+) currents was observed after pretreatment of cells with methoctramine (M(2) mAChR blocker). The Oxo-M-mediated inhibition was nearly eliminated in the presence of both M(1) and M(2) mAChR blockers but was unaltered when SG neurons were exposed to the M(4) mAChR toxin, M(4)-toxin. Finally, the results from single-cell RT-PCR and immunofluorescence assays indicated that M(1) and M(2) receptors are expressed and located on the surface of SG neurons. Overall, the results indicate that SG neurons that innervate cardiac muscle express M(1) and M(2) mAChR, and activation of these receptors leads to inhibition of Ca(2+) channel currents through VI and VD pathways, respectively.

Modulation of Ca2+ channels by opioid receptor-like 1 receptors natively expressed in rat stellate ganglion neurons innervating cardiac muscle.

Postganglionic sympathetic nerve terminals innervate cardiac muscle and express opioid receptor-like 1 (ORL1) receptors, the most recently described member of the opioid receptor subclass. ORL1 receptors are stimulated by the endogenous heptadecapeptide nociceptin (Noc). To better understand how the signaling events by Noc regulate sympathetic neuron excitability, the goal of the present study was to determine whether sympathetic stellate ganglion (SG) neurons, innervating the heart, natively express ORL1 opioid receptors and couple to Ca(2+) channels. SG neurons in adult male rats were retrograde-labeled with a fluorescent tracer via injection of the ventricular muscle employing ultrasound imaging. Thereafter, N-type Ca(2+) channel modulation was investigated using the whole-cell variant of the patch-clamp technique. Exposure of labeled SG neurons to Noc resulted in a concentration-dependent inhibition of Ca(2+) currents (with an estimated EC(50) of 193 +/- 14 nM). Pre-exposure of SG neurons to the ORL1 receptor blocker, [Nphe(1),Arg(14),Lys(15)]N/OFQ-NH(2) (UFP-101), significantly decreased the Noc-mediated Ca(2+) current inhibition. The Ca(2+) current inhibition was also blocked by pertussis toxin pretreatment, indicating that signaling occurs via Galpha(i/o) G proteins. Finally, the full-length ORL1 receptor cDNA in SG neurons was cloned and sequenced. Of the two known alternatively spliced variants in rats, sequencing analysis showed that the ORL1 receptor expressed in SG neurons is the short form. Overall, these results suggest that stimulation of postsynaptic ORL1 receptors by Noc in SG neurons regulate cardiac sympathetic activity.

A novel approach employing ultrasound guidance for percutaneous cardiac muscle injection to retrograde label rat stellate ganglion neurons.

Stellate ganglion (SG) neurons provide the main sympathetic innervation to the heart and help to regulate cardiac function. The purpose of this study was to determine if ultrasound imaging could be employed to retrograde label rat SG neurons innervating the heart without employing thoracotomy. In addition, electrophysiological experiments were performed to characterize the modulation of Ca(2+) channels by neurotransmitters in unlabeled and dye-labeled SG neurons. Fluorescence imaging of actutely isolated cells revealed that dye uptake was successful within five days following injection of dye in the cardiac muscle. Whole-cell voltage-clamp recordings revealed that the majority of the Ca(2+) current was carried by N-type Ca(2+) channels. Finally, fluorescence dye uptake did not appear to affect the modulation of Ca(2+) currents following exposure of SG neurons to norepinephrine, adenosine and neurokinin A. These results demonstrate that ultrasound imaging-guided percutaneous injection can be effectively employed to retrograde label neurons innervating the heart.

A case of paradoxical embolism "in situ" associated with massive pulmonary embolism: role of echocardiography.

A 49-year-old man was admitted in transfer for further management of a pulmonary embolism (PE) and possible mitral valve vegetation. Transthoracic echocardiography performed at our institution showed evidence of right ventricular (RV) enlargement and dysfunction. Within the right atrium was a serpentine mobile thrombus which traversed the interatrial septum at the level of the fossa ovalis and extended into the left atrium to the level of the anterior mitral valve leaflet. Because of the patient's dyspnea, RV dysfunction, and large clot burden, thrombolytic therapy was considered and would have been administered had the thrombus in situ not been identified. In light of the thrombus in situ and the concern about possible systemic embolization with thrombolytic therapy, the patient underwent successful surgical thrombectomy. This case highlights the importance of echocardiography in the management of patients with PE. We believe that all patients should undergo echocardiography prior to receiving thrombolytic therapy for pulmonary emboli. Careful interrogation of the interatrial septum for the presence of a thrombus in situ is warranted. Thrombectomy should be considered in individuals with PE who have a thrombus in situ.

Traumatic aortic transection with intraluminal aortic fat: transesophageal echocardiographic characteristics and implications.

Aortic transection can be a catastrophic complication of blunt chest trauma. Transesophageal echocardiography is a useful tool for assessing aortic pathology. Presented is a case of traumatic aortic transection in which periaortic fat was found within the aortic lumen. Transesophageal echocardiographic characteristics are reviewed and clinical implications discussed.