Methods

Data were collected prospectively for 926 patients who had undergone PMV at the Massachusetts General Hospital (Boston, Massachusetts). The study subjects were divided into 2 groups: patients with PVR ≥4 WU (320 dyne·s/cm ⁵ ) and those with PVR <4 WU. We also performed an extra analysis, dividing the population according a mean pulmonary artery pressure of ≥25 mm Hg at rest, as assessed by right heart catheterization. All participants provided informed consent, and the institutional review board approved the study protocol.

PMV was performed using a transseptal antegrade technique, as previously described. Both double-balloon and Inoue techniques were used. PVR was calculated as follows: (mean pulmonary artery pressure−mean pulmonary capillary wedge pressure)/cardiac index. The cardiac output was determined by thermodilution in all cases, when feasible. If evidence of left-to-right shunting was found or significant tricuspid regurgitation (TR) was present, the cardiac output was calculated according to the assumed Fick principle (oxygen consumption was estimated as 125 ml oxygen/min/m ² ). The mitral valve area was calculated using the Gorlin formula and 2-dimensional echocardiographic planimetry.

The demographic and clinical variables, including age, gender, body surface area, New York Heart Association functional class at presentation, presence of atrial fibrillation, and previous surgical commissurotomy or PMV, were recorded. Additional variables collected included the echocardiographic score, pre- and post-PMV degree of mitral regurgitation, and the presence of fluoroscopically visible mitral valve calcification (score 0 to 4). TR before PMV was qualitatively assessed from none to severe using echocardiography. The echocardiographic studies were performed in the standard manner, and the TR grade was estimated by integrating the continuous wave Doppler signal and color flow mapping. The procedural variables included the interventional technique (double balloon vs Inoue), effective balloon dilating area to body surface area, and pre- and post-PMV hemodynamic values (mean pulmonary artery and left atrial pressures, mean mitral valve pressure gradient, mean pulmonary artery pressure, PVR, cardiac output, and calculated mitral valve area). Procedure-related complications included death, mitral valve surgery, pericardial tamponade, stroke, and post-PMV mitral regurgitation ≥3. Procedure-related death was defined as in-hospital mortality directly related to PMV. Successful PMV was defined as a post-PMV mitral valve area of ≥1.5 cm ² or a 50% increase in valve area with post-PMV mitral regurgitation <3.

The prespecified outcomes, including mortality, mitral valve surgery (mitral valve replacement), and redo PMV, were recorded at follow-up. A combine end point, including mortality, mitral valve replacement, and redo PMV, was defined, and each component of the combine end point was analyzed separately.

Continuous and categorical variables are expressed as the mean ± SD and percentages, respectively. The follow-up time is reported as the median and interquartile range. Student’ t test and the chi-square test, or Fisher exact test when necessary, were used to compare the continuous and categorical variables, respectively. Multivariate logistic regression analyses were performed to determine whether an elevated PVR and mean pulmonary pressure were independently associated with PMV success (including the covariates gender, age, echocardiographic score, mitral valve area before PMV, mitral regurgitation before PMV, and previous comissurotomy ). Kaplan-Meier estimates were used to determine the total survival and event-free survival (survival with freedom from death, mitral valve replacement, or redo-PMV) for both groups and were compared using the log-rank test. Cox proportional hazards regression models were used to test the association between an elevated PVR and long-term outcomes (including the covariates age, echocardiographic score, mitral regurgitation after PMV of ≥3, mitral regurgitation before PMV of ≥2, and previous comissurotomy ). TR was also tested as an independent predictor of adverse long-term outcomes using the same covariates. All analyses were performed using the Statistical Package for Social Sciences, version 17.0, for Windows (SPSS, Chicago, Illinois). p Values <0.05 were considered statistically significant for all tests.

Results

The study population consisted of 926 consecutive patients who had undergone PMV at our institution. Of those, 663 (71.6%) had PVR <4 WU and 263 (28.4%) had PVR ≥4 WU. The baseline characteristics of the study groups are listed in Table 1 . The hemodynamic findings in both groups before and after PMV are listed in Table 2 . The hemodynamic parameters differed significantly between the 2 groups. The procedural success rate in patients with PVR ≥4 WU was significantly lower than in those with PVR <4 WU. However, on multivariate analysis, PVR ≥4 WU was not an independent predictor of PMV success (odds ratio 1.018, 95% confidence interval 0.70 to 1.48, p = 0.925). Also, a mean pulmonary artery pressure of ≥25 mm Hg was not an independent predictor of PMV success (data shown in Supplementary Materials ).

The incidence of adverse events is listed in Table 3 . The incidence of in-hospital adverse events did not differ significantly between the 2 groups, with the exception of higher nonprocedure-related deaths in patients with PVR ≥4 WU. Long-term clinical outcomes were available for 92% of the patients at a median follow-up of 3.2 years (interquartile range 1.0 to 5.9). A lower mortality for patients with PVR <4 WU compared with patients with PVR ≥4 during follow-up (log-rank test, p = 0.003) was recorded. No differences were found in the need for mitral valve replacement or redo-PMV between patients with PVR ≥4 WU and PVR <4 WU (log-rank test, p = 0.39 and p = 0.89, respectively). Patients with PVR ≥4 WU experienced lower event-free survival (death, mitral valve replacement, redo PMV) than those with PVR <4 WU (p = 0.003). However, in the Cox regression analysis, PVR ≥4 WU was no longer an independent predictor of event-free survival (hazards ratio 1.05, 95% confidence interval 0.84 to 1.32, p = 0.61; Table 4 ). Also, a mean pulmonary artery pressure of ≥25 mm Hg was not an independent predictor of event-free survival (data shown in Supplementary Materials ).

Table 3

In-hospital complications grouped by pulmonary vascular resistance (PVR) severity

Variable	PVR (WU)		p Value
	<4	≥4
Death (in hospital)
Not procedure related	3 (0.5)	7 (2.7)	0.003
Procedure related	3 (0.5)	3 (1)	0.241
Total	6 (0.9)	10 (3.8)	0.002
Tamponade	3 (0.5)	3 (1)	0.241
Mitral valve replacement
In-hospital (total)	21 (3.2)	8 (3)	0.91
Emergent	8 (1.2)	4 (1.5)	0.70
Atrioventricular block	4 (0.6)	1 (0.4)	0.67
Stroke	11 (1.7)	3 (1.1)	0.55

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