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I K : Subendocardial Purkinje myocytes from the 48 h infarcted heart have a significantly increased density of E4031 sensitive currents (a gain in function) compared to those of normal Purkinje myocytes [9] ( Fig. 5 ). E4031 sensitive Purkinje myocyte currents differ from those of the normal or infarcted ventricular myocyte ( I Kr ) and their molecular identity is unknown at this time. However, these data do suggest that Purkinje myocytes surviving in the infarcted heart would show an increased responsiveness to this class of antiarrhythmic drugs (methanesulfonanilide).

Fig. 5
View large HÖGL Women’s 410 4232 0100 ClosedToe Pumps Black Black for sale 2014 qWBtn

Typical recordings of currents elicited using protocol shown in Purkinje myocytes from (A) a normal heart (NZPC) and (B) from a 48-h infarcted heart (IZPC) before and after superfusion with E-4031 (5 μM). Typical E-4031-sensitive currents are shown on the right sides of (A) and (B) (35°C, 4 mM K and nisoldipine Tyrode’s). Note that for small steps, E-4031-sensitive currents are instantaneous with time dependence at larger step depolarizations. (C) Average E-4031-sensitive currents for NZPCs (=13) and IZPCs (=10). E-4031-sensitive currents () were larger at all steps in IZPCs. Note the lack of strong rectification of E-4031-sensitive currents in both cell types; reproduced from [9] .

Fig. 5
View large Download slide

Typical recordings of currents elicited using protocol shown in Purkinje myocytes from (A) a normal heart (NZPC) and (B) from a 48-h infarcted heart (IZPC) before and after superfusion with E-4031 (5 μM). Typical E-4031-sensitive currents are shown on the right sides of (A) and (B) (35°C, 4 mM K and nisoldipine Tyrode’s). Note that for small steps, E-4031-sensitive currents are instantaneous with time dependence at larger step depolarizations. (C) Average E-4031-sensitive currents for NZPCs (=13) and IZPCs (=10). E-4031-sensitive currents () were larger at all steps in IZPCs. Note the lack of strong rectification of E-4031-sensitive currents in both cell types; reproduced from [9] .

I to : Action potentials recorded from the epicardial border zone cells usually show no phase 1 or reduced phase 1 of repolarization suggesting a loss in the voltage dependent transient outward current I to [10] . In contrast and as predicted, APs recorded from all cells dispersed from the normal noninfarcted epicardium show a large and prominent spike and dome morphology. Voltage clamp studies confirm that the density and kinetics of the voltage dependent, non-Ca i -dependent, transient outward current ( I to ) in the cells demonstrating the loss in the notch are reduced [10] .

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Although many hospitals have implemented an antibiotic stewardship program (ASP), it is important to sustain the program with the required resources. The benefits of ASP include improved patient outcomes, reduced adverse events (including CDI), improvement in rates of antibiotic susceptibilities, and optimization of resource utilization [ 289 ].

Although there is an epidemiologic association between PPI use and CDI, and unnecessary PPIs should always be discontinued, there is insufficient evidence for discontinuation of PPIs as a measure for preventing CDI (no recommendation).

There is a clinical association between PPI use and CDI [ 290–293 ]. Three recent meta-analyses assessed the association between PPI use and the risk for CDI using data from >47 studies containing >300000 patients. All studies demonstrated significant heterogeneity in the dataset, and 2 of 3 noted publication bias (the third did not perform this analysis due to underlying heterogeneity of data). Kwok et al assessed 42 total studies (30 case-control; 12 cohort) totaling 313000 patients [ 290 ]. Summary odds ratios (ORs) were presented for incident cases of CDI (OR, 1.74; 95% CI, 1.47–2.85) as well as recurrent CDI (OR, 2.51; 95% CI, 1.16–5.44). Concomitant use of non– C. difficile antibiotics increased the risk of CDI with PPI usage (OR, 1.96; 95% CI, 1.03–3.70). Histamine type 2 receptor antagonists had decreased risk of CDI compared to PPI use. Janarthan et al assessed 23 total studies (17 case-control and 6 cohort) totaling 288620 patients [ 293 ]. Incidence of CDI increased with exposure to PPIs (OR, 1.69; 95% CI, 1.34–1.97). There was no difference in the summary OR if the analysis was limited to cohort (OR, 1.66; 95% CI, 1.23–2.24) or case-control studies (OR, 1.65; 95% CI, 1.38–1.98). Finally, Tleyjeh assessed 47 total studies (37 case control and 14 cohort) [ 291 ]. Incidence of CDI increased with exposure to PPIs (OR, 1.69; 95% CI, 1.34–1.97). Two studies assessed the number of cases likely to occur with the addition of PPI therapy. Number needed to harm was higher for the general population (range, 899–3925) compared with hospitalized patients not on concomitant antibiotics (range, 202–367), or hospitalized patients receiving concomitant antibiotics (range, 28–50). Despite clinical data showing consistently increased risk, heterogeneity of the data, role of unknown confounders, lack of dose–response relationships, and other methodologic considerations are considerable limitations to the practical application of these data.

A number of further observational studies have investigated the association between PPI use and CDI after publication of these meta-analyses [ 27 , 294–297 ]. A large, population surveillance study of 984 patients with community-associated CDI showed that 31% of patients with CDI who did not receive antibiotics did receive a PPI [ 27 ]. Three studies investigated the association between PPI usage and recurrent CDI in 1627 patients [ 294 , 295 , 297 ]. Two of the 3 studies did not show an association between PPI use and recurrent CDI. Finally, a study of 483 patients colonized with C. difficile showed that exposure to PPI increased the risk of developing CDI [ 296 ]. Thus, there appears to be a clinical association between PPI use and CDI, but the true causal relationship is unclear. No RCTs or quasi-experimental studies have studied the relationship between discontinuing or avoiding PPI use and risk of CDI. Thus, a recommendation to globally discontinue PPIs in patients at high risk for CDI or recurrent CDI regardless of need for PPI will require further causal proof. However, stewardship activities to discontinue unneeded PPIs are warranted.

Table 12

Structure of the syncope unit

a
Table 13

Test and assessments available in a syncope unit

BP = blood pressure; CSM = carotid sinus massage; ECG = electrocardiogram; EEG = electroencephalogram.

a

Postural orthostatic tachycardia may require longer period of standing.

Table 13

Test and assessments available in a syncope unit

BP = blood pressure; CSM = carotid sinus massage; ECG = electrocardiogram; EEG = electroencephalogram.

a

Referral can be direct from family practitioners, EDs, in-hospital and out-hospital services, or self-referral from the patient. Fast-track access with a separate waiting list and scheduled follow-up visits is recommended. In particular, patients at low/intermediate risk admitted to the ED should benefit from such fast-track facilities (so-called protected discharge or advanced access with an appointment for early assessment) to reduce hospitalization rates, directly from the ED or after a short stay in the short observation unit of the ED (see section 4.1.2).

The EHRA Task Force 63 has developed the following preliminary quality indicators, based on consensus, as a rough guide for practitioners:

Absolute rate of undiagnosed TLOC should be reduced by 20%;

Less than 20% of low-/intermediate-risk TLOC patients should be admitted from the ED;

The syncope unit should have a 20% reduction in costs relative to usual practice and improved outcomes (i.e. <5% readmissions for syncope and <20% of paced patients with recurrence at 1 year).

The syncope unit clinical nurse specialist is defined as an experienced practitioner who has sufficient knowledge of history features and physical findings to recognize all major forms of TLOC, as well as syndromes of orthostatic intolerance. The clinical nurse specialist should work in close collaboration with the syncope specialist. The core competencies of the clinical nurse specialist include a specialized clinical focus, patient advocacy, education and training, auditing, research, and inter- and intradisciplinary consultations.

The clinical nurse specialist should be skilled in the performance and interpretation of structured history taking, 12-lead ECG and routine blood test results, tilt testing, active stand tests, autonomic function tests, ECG monitoring (Holter and/or external loop recorder), ABPM, ILR monitoring, and subsequent triaging of patients and monitoring responses to therapy. Other skills will depend on the service model, e.g. pacemaker interrogation. The clinical nurse specialist may have responsibility for follow-up clinics for cardiovascular risk factor management, autonomic function testing and monitoring, management (including education in PCM) of VVS and OH, and follow-up of external and internal loop and Holter monitors and ABPM 63 ( Table 14 ).