Study flow chart.

<p>Study flow chart.</p

Original X-ray showing CS cannulation in LAO 30° view.

<p>1. <b>A.1-3.</b> Standard cannulation technique using preformed sheets and hydrophilic wire. <b>B.1-3.</b> Steerable EP catheter with exact cannulation. <b>C.1-2.</b> CS angiogram and coronary wire guided LV-lead positioning.</p

Effect of the time until thrombolysis onset on outcome.

<p>(A) Time dependent ROSC, (B) time dependent successful hospital discharge.</p

Adverse events associated with resuscitation and thrombolysis.

<p>14 of 104 patients could be discharged with good neurological outcome.</p

Time-outcome relation.

<p>Time of thrombolysis onset, CPR time after thrombolysis and total CPR duration in patients with and without successful CPR (A), in patients with hospital discharge vs. those who died (B), and in patients with hospital discharge versus those with secondary lethality after initially successful CPR.</p

Study flowchart in accordance to the STARD criteria.

<p>In phase 0 diagnostic criteria were evaluated in 164 patients undergoing DE and RHC. In phase 1 the calculated cut-off value for mPAP was validated in a cohort of patients with the suspicion of PH.</p

DE versus RHC correlations.

<p>DE mPAP (B) was better correlated with RHC than sPAP (A). Dotted lines mark virtual best correlation of 1 and solid lines mark the real correlation. r indicates the correlation coefficient, sPAP indicates systolic pulmonary artery pressure.</p

Characteristics of 164 patients and indications for RHC.

<p>BMI indicates body mass index (kg/m²), RHC indicates right heart catheterization.</p

Analysis of relative differences and ROC analysis of mPAP for diagnosis of PH.

<p>A, the relative positive and negative deviation between DE and RHC were larger for sPAP than mPAP. B, ROC analysis reveal an excellent diagnostic accuracy of mPAP for the diagnosis of PH with an area under the curve (AUC) of 0.95.</p

Effect of KCR1 and KCR1^siRNA on single native I_f channel gating in one-channel patches.

<p>(A) Comparison between single native I_f channels of control neonatal ventriculocytes (left), KCR1-infected (middle) and KCR1^siRNA-infected cells (right). Recording technique as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0001511#pone-0001511-g003" target="_blank">Figure 3</a>. Scale bars, 50 ms, 3 pA for unitary current traces, and 1 s, 20 fA for ensemble average current. (B) Enhanced expression and knock-down of KCR1 significantly shifted the half-maximal activation of I_f to more negative and more positive potentials, respectively. Channel activation was measured by the parameter availability, plotted against the test potential and then determined by using the Boltzmann function. For data see text. (C) Open-time histograms: KCR1 exhibited no effect on the number of native I_f open states, whereas KCR1^siRNA induced an increase of the number of open states. Number of open events (square root) were plotted against the logarithmically binned open time durations for I_f alone and with exogenous KCR1 or KCR1^siRNA (pooled one- and multi [n≤3]-channel experiments). (D) Closed-time histograms: KCR1 did not affect the number of native I_f closed states, while KCR1 knock-down resulted in a loss of one closed state. Number of closed events (square root) were plotted against the logarithmically binned closed time durations for I_f alone and with exogenous KCR1 or KCR1^siRNA (pooled one-channel experiments only).</p