The mean ejection fraction was moderately reduced, and PCWP was elevated (ie, > 15 mm Hg) in 22 patients (52%). In 11 patients (26%), the PCWP was < 10 mm Hg, and in 15 patients (36%) it was > 20 mm Hg. The PAR ranged from 0.28 to 1.15 (mean, 0.71 ± 0.23). In seven patients (17%), the pulse amplitude did not decrease during the VM (ie, PAR, > 1.0). As shown in Figure 1, the PAR predicted the invasively measured PCWP with an acceptable accuracy over a range of 2 to 32 mm Hg (R2 = 0.75; root mean square error = 4.1 mm Hg; p < 0.001). The Bland-Altman plot (Fig 2) gives the difference between the true and calculated PCWPs, demonstrating that 31 of the noninvasively assessed PCWPs (74%) did not differ by > 4 mm Hg from the invasively measured PCWPs. Although the accuracy of this correlation has its limitations, a PAR of > 0.7 predicted the presence of an elevated PCWP (ie, > 15 mm Hg) with a sensitivity of 91% and a specificity of 95% (Table 2). The positive predictive value was 95%, the negative predictive value was 91%, and the diagnostic accuracy was 93%. Despite some inaccuracy of the linear correlation, the area under the curve of the ROC was very high (0.985 ± 0.013; p < 0.001). Accordingly, cutoff values of PAR for 100% sensitivity and 100% specificity were separated by only 0.06 (ie, 0.66 and 0.72, respectively). Thus, all patients with PARs < 0.66 had a PCWP of < 15 mm Hg, while all patients with PARs > 0.72 had PCWPs > 15 mm Hg.
Medication with an antiadrenergic agent (ie, a P-blocker or amiodarone) did not influence the correlation between the PAR and the PCWP (Fig 3, 4). No patient was treated simultaneously with a P-blocker and amiodarone. Patients receiving ACE inhibitors had a slightly, but statistically not significant, better correlation (R2 = 0.81; p < 0.001) compared to patients not receiving ACE inhibitors (R2 = 0.63; p = 0.001) this mycanadianpharmacy. The area under the curve of the ROC was identical in patients receiving ACE inhibitors (0.99 ± 0.01; p < 0.001) as in patients not receiving ACE inhibitors (0.98 ± 0.03; p = 0.003).
Figure 1. Scatterplot of the PAR during the VM (phase 2 to phase 1) and the invasively measured PCWP.
Figure 2. Bland-Altman plot of the difference between the estimated pressure (ie, PAR) and the invasively measured PCWP in relation to the invasively measured PCWP. The dotted lines denote 2 SDs. Two diamonds depict identical values of two patients.
Figure 3. Scatterplot of the PAR during the VM (phase 2 to phase 1) and the invasively measured PCWP in patients receiving P-blockers or amiodarone (A, dotted line) and those not receiving P-blockers or amiodarone (♦).
Figure 4. Bland-Altman plot of the difference between the estimated (PAR) and the invasively measured PCWP in relation to the invasively measured PCWP in patients receiving P-block-ers or amiodarone (A) and those not receiving P-blockers or amiodarone ( ♦). The dotted lines denote 2 SDs. Two diamonds depict identical values of two patients.
Table 2——Relationship of PAR During the VM and the Invasively Assessed PCWP
|PAR||< 15 mm Hg||> 15 mm Hg|
|< 0.7||19 (45)||2 (5)|
|> 0.7||1(2)||20 (48)|