Left ventricular dysfunction common after mitral valve repair

TORONTO – Early postoperative left ventricular dysfunction occurs in about 18% of patients who undergo "early" mitral valve repair for severe degenerative disease and have normal preoperative ejection fractions exceeding 60%.

In two-thirds of these patients, the left ventricular dysfunction is persistent and associated with increased mortality, reported Dr. Rakesh Suri of the Mayo Clinic in Rochester, Minn.

"These results may help redefine what we have held true for the last few decades," Dr. David H. Adams said after hearing the data presented at the annual meeting of the American Association for Thoracic Surgery.

Dr. Adams is program director of the Mitral Valve Repair Center, Mount Sinai Medical Center, New York.

Guidelines from the American College of Cardiology/American Heart Association recommend that, for patients with severe degenerative mitral regurgitation due to leaflet prolapse, mitral valve repair needs to be done before the onset of left ventricular dysfunction.

However, despite this preemptive approach, a proportion of patients experience a profound decrease in left ventricular ejection fraction (LVEF), to less than 50% in the immediate postoperative period.

Dr. Suri and his colleagues studied the incidence, predictors, and short- and long-term consequences of this phenomenon in 1,705 patients with severe degenerative mitral regurgitation but LVEF greater than 60% who underwent mitral valve repair at the Mayo Clinic from Jan. 1, 1993, to June 30, 2012.

Patients were excluded from the study if they were under age 18, had a history of significant coronary artery disease, or were undergoing concomitant cardiac procedures other than Maze, tricuspid valve repair, or closure of a patent foramen ovale, the researchers noted.

After mitral valve repair, 82% of the cohort had normal LVEF (50% or more), and 18% developed early LV dysfunction (less than 50%).

Mean preoperative LVEF was 65.8% in the group that maintained normal ejection fraction post repair and 66.3% in the group that developed LV dysfunction (P less than .001).

In the group of patients in whom an early decline in LV function was noted, the mean fall in LVEF was 36%, compared with a postrepair drop of 11% in patients whose function remained in the normal range (P less than .001).

When the researchers looked at whether or not patients went to surgery with guideline-based class I or IIa triggers for mitral valve repair, those being symptoms of LV dysfunction, atrial fibrillation, or pulmonary hypertension, they found that 37% of patients who did not develop LV dysfunction and 22% of those who did had no class I or IIa triggers.

"In other words, the guidelines were incapable of defining this population prior to the performance of mitral valve repair," Dr. Suri explained.

On multivariate analysis, predictors of early LV dysfunction were higher right ventricular systolic pressure and LV end-systolic dimension (both P less than .001).

Patients with early LV dysfunction continued to have significantly diminished LVEF at less than 5, 5-10, and less than 10 years.

"Examined in terms of the ability to recover a normal ejection fraction with time, we saw that amongst those with no LV dysfunction following mitral valve repair, two-thirds went on to complete recovery," explained Dr. Suri.

"In contrast, among those with early LV dysfunction, only one-third were capable of recovering normal LV function with time. In other words, two-thirds had persistent LV dysfunction despite undergoing ‘early’ mitral valve repair," Dr. Suri said.

Early LVEF of less than 40% was seen to increased late mortality risk by 70%.

According to these data, a "normal" preoperative ejection fraction should not provide false reassurance of the capacity for restoration of LV function late following mitral valve repair, suggesting that surgical intervention prior to the onset of excessive LV dilation or pulmonary hypertension is warranted, Dr. Suri said.

"So much of the evidence base that serves as a foundation for the ACC/AHA guidelines comes from the Mayo experience, and your new data is provocative and will have implications for future guidelines," said Dr. Adams, the invited discussant for the abstract.

Dr. Suri reported having no disclosures related to this presentation.

TORONTO – Early postoperative left ventricular dysfunction occurs in about 18% of patients who undergo "early" mitral valve repair for severe degenerative disease and have normal preoperative ejection fractions exceeding 60%.

In two-thirds of these patients, the left ventricular dysfunction is persistent and associated with increased mortality, reported Dr. Rakesh Suri of the Mayo Clinic in Rochester, Minn.

"These results may help redefine what we have held true for the last few decades," Dr. David H. Adams said after hearing the data presented at the annual meeting of the American Association for Thoracic Surgery.

Dr. Adams is program director of the Mitral Valve Repair Center, Mount Sinai Medical Center, New York.

Guidelines from the American College of Cardiology/American Heart Association recommend that, for patients with severe degenerative mitral regurgitation due to leaflet prolapse, mitral valve repair needs to be done before the onset of left ventricular dysfunction.

However, despite this preemptive approach, a proportion of patients experience a profound decrease in left ventricular ejection fraction (LVEF), to less than 50% in the immediate postoperative period.

Dr. Suri and his colleagues studied the incidence, predictors, and short- and long-term consequences of this phenomenon in 1,705 patients with severe degenerative mitral regurgitation but LVEF greater than 60% who underwent mitral valve repair at the Mayo Clinic from Jan. 1, 1993, to June 30, 2012.

Patients were excluded from the study if they were under age 18, had a history of significant coronary artery disease, or were undergoing concomitant cardiac procedures other than Maze, tricuspid valve repair, or closure of a patent foramen ovale, the researchers noted.

After mitral valve repair, 82% of the cohort had normal LVEF (50% or more), and 18% developed early LV dysfunction (less than 50%).

Mean preoperative LVEF was 65.8% in the group that maintained normal ejection fraction post repair and 66.3% in the group that developed LV dysfunction (P less than .001).

In the group of patients in whom an early decline in LV function was noted, the mean fall in LVEF was 36%, compared with a postrepair drop of 11% in patients whose function remained in the normal range (P less than .001).

When the researchers looked at whether or not patients went to surgery with guideline-based class I or IIa triggers for mitral valve repair, those being symptoms of LV dysfunction, atrial fibrillation, or pulmonary hypertension, they found that 37% of patients who did not develop LV dysfunction and 22% of those who did had no class I or IIa triggers.

"In other words, the guidelines were incapable of defining this population prior to the performance of mitral valve repair," Dr. Suri explained.

On multivariate analysis, predictors of early LV dysfunction were higher right ventricular systolic pressure and LV end-systolic dimension (both P less than .001).

Patients with early LV dysfunction continued to have significantly diminished LVEF at less than 5, 5-10, and less than 10 years.

"Examined in terms of the ability to recover a normal ejection fraction with time, we saw that amongst those with no LV dysfunction following mitral valve repair, two-thirds went on to complete recovery," explained Dr. Suri.

"In contrast, among those with early LV dysfunction, only one-third were capable of recovering normal LV function with time. In other words, two-thirds had persistent LV dysfunction despite undergoing ‘early’ mitral valve repair," Dr. Suri said.

Early LVEF of less than 40% was seen to increased late mortality risk by 70%.

According to these data, a "normal" preoperative ejection fraction should not provide false reassurance of the capacity for restoration of LV function late following mitral valve repair, suggesting that surgical intervention prior to the onset of excessive LV dilation or pulmonary hypertension is warranted, Dr. Suri said.

"So much of the evidence base that serves as a foundation for the ACC/AHA guidelines comes from the Mayo experience, and your new data is provocative and will have implications for future guidelines," said Dr. Adams, the invited discussant for the abstract.

Dr. Suri reported having no disclosures related to this presentation.

TORONTO – Early postoperative left ventricular dysfunction occurs in about 18% of patients who undergo "early" mitral valve repair for severe degenerative disease and have normal preoperative ejection fractions exceeding 60%.

In two-thirds of these patients, the left ventricular dysfunction is persistent and associated with increased mortality, reported Dr. Rakesh Suri of the Mayo Clinic in Rochester, Minn.

"These results may help redefine what we have held true for the last few decades," Dr. David H. Adams said after hearing the data presented at the annual meeting of the American Association for Thoracic Surgery.

Dr. Adams is program director of the Mitral Valve Repair Center, Mount Sinai Medical Center, New York.

Guidelines from the American College of Cardiology/American Heart Association recommend that, for patients with severe degenerative mitral regurgitation due to leaflet prolapse, mitral valve repair needs to be done before the onset of left ventricular dysfunction.

However, despite this preemptive approach, a proportion of patients experience a profound decrease in left ventricular ejection fraction (LVEF), to less than 50% in the immediate postoperative period.

Dr. Suri and his colleagues studied the incidence, predictors, and short- and long-term consequences of this phenomenon in 1,705 patients with severe degenerative mitral regurgitation but LVEF greater than 60% who underwent mitral valve repair at the Mayo Clinic from Jan. 1, 1993, to June 30, 2012.

Patients were excluded from the study if they were under age 18, had a history of significant coronary artery disease, or were undergoing concomitant cardiac procedures other than Maze, tricuspid valve repair, or closure of a patent foramen ovale, the researchers noted.

After mitral valve repair, 82% of the cohort had normal LVEF (50% or more), and 18% developed early LV dysfunction (less than 50%).

Mean preoperative LVEF was 65.8% in the group that maintained normal ejection fraction post repair and 66.3% in the group that developed LV dysfunction (P less than .001).

In the group of patients in whom an early decline in LV function was noted, the mean fall in LVEF was 36%, compared with a postrepair drop of 11% in patients whose function remained in the normal range (P less than .001).

When the researchers looked at whether or not patients went to surgery with guideline-based class I or IIa triggers for mitral valve repair, those being symptoms of LV dysfunction, atrial fibrillation, or pulmonary hypertension, they found that 37% of patients who did not develop LV dysfunction and 22% of those who did had no class I or IIa triggers.

"In other words, the guidelines were incapable of defining this population prior to the performance of mitral valve repair," Dr. Suri explained.

On multivariate analysis, predictors of early LV dysfunction were higher right ventricular systolic pressure and LV end-systolic dimension (both P less than .001).

Patients with early LV dysfunction continued to have significantly diminished LVEF at less than 5, 5-10, and less than 10 years.

"Examined in terms of the ability to recover a normal ejection fraction with time, we saw that amongst those with no LV dysfunction following mitral valve repair, two-thirds went on to complete recovery," explained Dr. Suri.

"In contrast, among those with early LV dysfunction, only one-third were capable of recovering normal LV function with time. In other words, two-thirds had persistent LV dysfunction despite undergoing ‘early’ mitral valve repair," Dr. Suri said.

Early LVEF of less than 40% was seen to increased late mortality risk by 70%.

According to these data, a "normal" preoperative ejection fraction should not provide false reassurance of the capacity for restoration of LV function late following mitral valve repair, suggesting that surgical intervention prior to the onset of excessive LV dilation or pulmonary hypertension is warranted, Dr. Suri said.

"So much of the evidence base that serves as a foundation for the ACC/AHA guidelines comes from the Mayo experience, and your new data is provocative and will have implications for future guidelines," said Dr. Adams, the invited discussant for the abstract.

Dr. Suri reported having no disclosures related to this presentation.