Implementation of Institutional Discharge Protocols and Transition of Care Following Acute Coronary Syndrome.

Despite improvements in acute care and survival following acute coronary syndrome (ACS) hospitalization, readmission remains common. In response, individual institutions have begun to develop their own protocols to reduce variability of care and readmission rates. This review provides approaches for developing and implementing institutional discharge protocols for continuity of care for ACS patients and describes key components of the discharge protocol. Furthermore, specific objectives of the protocol, including medication adherence, patient education, enabling access to cardiac rehabilitation, and clinical follow-up, as well as consideration of patient-specific needs, are discussed with the aim of providing successful continuity of care. TABLE OF CONTENTS SUMMARY: This review discusses approaches for developing and implementing institutional discharge protocols for continuity of care for patients with acute coronary syndrome. The discussion revolves around key components and objectives of a discharge protocol for facilitating successful transition of care.

Clinical significance of intermediate left ventricular trabeculations in cardiac magnetic resonance.

OBJECTIVE: Although the clinical importance of left ventricular noncompaction cardiomyopathy (LVNC) is known, few data exist that describe the prognosis associated with intermediate levels of LV trabeculations that do not meet criteria for LVNC. METHODS: Trabeculation/possible LVNC by CMR was retrospectively observed among 122 consecutive cases. We assessed the end-systolic noncompacted-to-compacted ratios (ESNCCR) along with deaths, embolic events, congestive heart failure (CHF) readmissions, ventricular arrhythmias, myocardial thickening (MT), and ejection fraction (EF). ESNCCRs were categorized as follows: <1, 1<1.5, 1.5<2, ≥2. General linear models were used to compare combined events (death, CHF readmission, embolism, ventricular arrhythmia) between categories of ESNCCR. There were 3 models used: model 1: unadjusted; model 2: adjusted for age, race, gender, body surface area, LV ejection fraction, and trabeculated segments; model 3: model 2+adjustment for myocardial thickening. RESULTS: In model 1, those with an ESNCCR<1 had a lower association with composite clinical events than those with a ratio between 1.5<2 and those≥2 (P<0.002 and P<0.001, respectively). In model 2, the lower association continued, (P=0.009 and P<0.001, respectively), but in model 3, those with a ratio from 1.5-2 only had a trend towards a higher association with composite clinical events than those with a ratio<1 (P=-0.09). Those with a ratio≥2 continued to have a higher association (P=-0.001). CONCLUSION: Patients with intermediate trabeculations not meeting criteria for LVNC had a higher association with composite clinical events, but it was mediated by decreased myocardial thickening in the associated compacted layer.

Coupling of a single nitrogen-vacancy center in diamond to a fiber-based microcavity.

We report on the coupling of a single nitrogen-vacancy (NV) center in a nanodiamond to a fiber-based microcavity at room temperature. Investigating the very same NV center inside the cavity and in free space allows us to systematically explore a regime of phonon-assisted cavity feeding. Making use of the NV center's strongly broadened emission, we realize a widely tunable, narrow band single photon source. A master equation model well reproduces our experimental results and predicts a transition into a Purcell-enhanced emission regime at low temperatures.

Single ion coupled to an optical fiber cavity.

We present the realization of a combined trapped-ion and optical cavity system, in which a single Yb(+) ion is confined by a micron-scale ion trap inside a 230 µm-long optical fiber cavity. We characterize the spatial ion-cavity coupling and measure the ion-cavity coupling strength using a cavity-stimulated Λ transition. Owing to the small mode volume of the fiber resonator, the coherent coupling strength between the ion and a single photon exceeds the natural decay rate of the dipole moment. This system can be integrated into ion-photon quantum networks and is a step towards cavity quantum electrodynamics based quantum information processing with trapped ions.

Spin waves and collisional frequency shifts of a trapped-atom clock.

We excite spin waves with spatially inhomogeneous Ramsey pulses and study the resulting frequency shifts of a chip-scale atomic clock of trapped 87Rb. The density-dependent frequency shifts of the hyperfine transition simulate the s-wave collisional frequency shifts of fermions, including those of optical lattice clocks. As the spin polarizations oscillate in the trap, the frequency shift reverses and it depends on the area of the second Ramsey pulse, exhibiting a predicted beyond mean-field frequency shift. Numerical and analytic models illustrate these observed behaviors.

Tempol, a superoxide dismutase mimetic, prevents cerebral vessel remodeling in hypertensive rats.

Increased reactive oxygen species (ROS) production is involved in the pathogenesis of hypertension and stroke. The effects of ROS on cerebral vessels from hypertensive rats have not been studied. We hypothesized that tempol, a superoxide dismutase mimetic, would prevent middle cerebral artery (MCA) remodeling in stroke-prone spontaneously hypertensive rats (SHRSP). Six-week-old male SHRSP were treated with tempol (1mM) for 6weeks. The MCA was then removed and mounted in a pressure myograph to study tone generation, vessel reactivity, and passive vessel structure. Data are shown as mean±SEM, tempol vs. control. Plasma thiobarbituric acid reactive substances (TBARS) were decreased by tempol treatment (14.15±1.46 vs. 20.55±1.25nM of malondialdehyde [MDA]/ml, p=0.008). Maximum serotonin-induced constriction was increased by tempol treatment, without changes in dilation to adenosine diphosphate or tone generation. At an intralumenal pressure of 80mmHg, tempol caused a dramatic increase in the MCA lumen diameter (246±5 vs. 207±3µm, p<0.001), outer diameter (281±5 vs. 241±3µm, p<0.001), lumen cross-sectional area, and vessel cross-sectional area. Collagen IV mRNA expressions were increased by 2.4-fold after tempol treatment. These results suggest that ROS are involved in the remodeling of the cerebral vasculature of SHRSP and that ROS scavenging can attenuate this process.

Effect of high soy diet on the cerebrovasculature and endothelial nitric oxide synthase in the ovariectomized rat.

High soy (HS) diets are neuroprotective and promote vascular dilatation in the periphery. We hypothesized that an HS diet would promote vascular dilatation in the cerebrovasculature by mimicking estradiol's actions on the endothelial nitric oxide synthase (eNOS) system including increasing eNOS expression and decreasing caveolin-1 expression to increase nitric oxide (NO) production. Ovariectomized rats were fed HS or a soy-free diet (SF)+/-low physiological estradiol (E2) for 4weeks. Neither E2 nor HS altered middle cerebral artery (MCA) structure or vascular responses to acetylcholine, serotonin, or phenylephrine. Estradiol enhanced bradykinin-induced relaxation in an eNOS-dependent manner. Although E2 and HS increased eNOS mRNA expression in the brain and cerebrovasculature, they had no effect on eNOS protein expression or phosphorylation in the MCA. However, E2 decreased caveolin-1 protein in the MCA. In MCAs neither E2 nor HS altered estrogen receptor (ER) alpha expression, but E2 did reduce ER beta levels. These data suggest that HS diets have no effect on vascular NO production, and that E2 may modulate basal NO production by reducing the expression of caveolin-1, an allosteric inhibitor of NOS activity. However, the effects of E2 and HS on the cerebrovasculature are small and may not underlie their protective actions in pathological states.

Preliminary results of the trapped atom clock on a chip.

We present an atomic clock based on the interrogation of magnetically trapped (87)Rb atoms. Two photons, in the microwave and radiofrequency domain, excite the clock transition. At a magnetic field of 3.23 G the clock transition from |F = 1, m(F) = -1> to |F = 2, m(F) = 1> is 1st-order insensitive to magnetic field variations. Ramsey interrogation times longer than 2 s can be achieved, leading to a projected clock stability in the low 10(-13) at 1 s for a cloud of 10(5) atoms. We use an atom chip to cool and trap the atoms. A coplanar waveguide is integrated to the chip to carry the Ramsey interrogation signal, making the physics package as small as (5 cm)(3). We describe the experimental setup and show preliminary Ramsey fringes of line width 1.25 Hz.

Diet-induced obesity causes cerebral vessel remodeling and increases the damage caused by ischemic stroke.

Hypertension, elevated fasting blood glucose and plasma insulin develop in rats fed a high fat (HF) diet. Our goal was to assess the effects of obesity, beginning in childhood, on the adult cardiovascular system. We hypothesized that rats fed a HF diet would have larger ischemic cerebral infarcts and middle cerebral artery (MCA) remodeling. Three-week-old male Sprague Dawley rats were fed a HF (obese) or control diet for 10 weeks. Cerebral ischemia was induced by MCA occlusion (MCAO). MCA structure was assessed by pressure myography and cerebral vessel matrix metalloproteinase (MMP) activity and expression and collagen levels were measured in vessels from rats that did not undergo MCAO. The cerebral infarct was greater in the obese rats than the control (46.0+/-2.1 vs 28.0+/-7.5% of the hemisphere infarcted, obese vs control p<0.05). The MCAs from obese rats had smaller lumens (232+/-7.2 vs 254+/-7.8 microm obese vs control p<0.05) and thicker walls (19.6+/-0.8 vs 17.8+/-0.9 microm obese vs control p<0.05) and were less compliant than MCAs from control rats. MMP-2 activity and collagen I expression were increased in vessels from obese rats and MMP-13 expression was reduced. These results suggest that obesity, beginning in childhood, causes inward vessel remodeling with a concomitant increase in vessel stiffness due to increased collagen deposition. These changes in MCA structure may be responsible for the increase in the ischemic damage after MCAO.