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Underlying damage tied to mitral valve repair may lead to decline in LV function after surgery
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In certain patients with moderate to severe mitral valve regurgitation, surgical repair may confer the most benefit when performed in earlier, asymptomatic stages, according to recent findings.
Researchers determined that in patients with well-preserved preoperative left ventricular ejection fraction who undergo mitral valve repair, chronic cardiomyocyte oxidative stress and disruption of the desmin cytoskeletal structure may account for postoperative left ventricular functional decline.
Lou Dell’Italia
These findings suggest that “When people are asymptomatic, they don’t go to the doctor regularly,” Lou Dell’Italia, MD, a professor in the University of Alabama at Birmingham department of medicine and division of cardiovascular disease and associate chief of staff for research at the Birmingham VA Medical Center, said in a press release. “The results of our study demonstrate severe underlying cardiac muscle damage in patients having moderate to severe [mitral regurgitation] in the absence of symptoms and in the presence of well-preserved cardiac function by echocardiography.”
In the study, researchers evaluated LV myocardium from 22 patients (mean age, 57 years) with severe, isolated mitral regurgitation who underwent mitral valve surgery at the UAB Cardiovascular Surgical Center. The myocardial tissue, which was taken at surgery from the endocardium of the LV lateral posterior wall in all patients, was evaluated by fluorescence microscopy for the following: desmin, the voltage-dependent anion channel, alpha-B crystalline, and alpha, beta-unsaturated aldehyde 4-hydroxynonenal. This tissue was compared with control LV myocardial tissue specimens acquired at the time of autopsy from six patients with no evidence of myocardial or valvular disease.
In a second analysis, the patients with mitral regurgitation underwent MRI with tissue tagging before and 6 months after mitral valve repair. MRI also was performed in 55 control volunteers (mean age, 45 years) with no history of CVD or smoking and taking no CV medication.
Structure and function outcomes
The researchers found that in patients with mitral regurgitation, the LV end-diastolic (LVED) volume was increased more than 50% vs. controls (195 mL vs. 127 mL; P < .0001) and showed a postoperative reduction (152 mL; P = .0002). A significant difference was seen in LVED sphericity index (LVED length/LVED inner diameter) of the patients with mitral regurgitation before and after surgery (1.49 and 1.58, respectively) vs. normal controls (1.77; P < .0001 and P = .001, respectively), but this measure improved after surgery. A significant difference in LVED mass-to-volume ratio was seen between patients with mitral regurgitation (0.65 g/mL) and normal controls (0.75 g/mL; P = .042), but this measure improved and was not different after surgery from that of normal patients (0.75 g/mL; P = .0013).
A decrease in LVEF was seen after surgery, from 65% to 52% (P < .0001). Patients with mitral regurgitation had higher LV end systolic (LVES) volume vs. controls (67 mL vs. 45 mL; P < .0001), and this measure did not change significantly after surgery. LV circumferential systolic shortening strains showed a reduction after mitral valve repair vs. before surgery (P < .001) and vs. the normal controls (P < .0001). LV longitudinal systolic shortening strains showed no difference from normal controls before surgery, but showed a decrease after surgery vs, controls (P = .002) and vs. before surgery in patients with mitral regurgitation (P = .0013).
A 53% reduction in desmin was seen in mitral regurgitation hearts vs. normal hearts (P < .0001) and a 2.6-fold increase in desmin aggregates (P < .0001) vs. normal hearts. Moreover, mitral regurgitation hearts showed substantial, intense perinuclear staining of alpha, beta-unsaturated aldehyde 4-hydoxynonenal in areas of mitochondrial breakdown and clustering. Numerous electron-dense deposits, myofibrillar loss, Z-disc abnormalities and significant granulofilamentous debris identified as desmin-positive were revealed through transmission electron microscopy.
Prompt correction necessary
In a related editorial, Jordan D. Miller, PhD, from the department of surgery and the department of physiology and biomedical engineering, Mayo Clinic, and Rakesh M. Suri, MD, from the department of thoracic and cardiovascular surgery, Cleveland Clinic Foundation, Cleveland, wrote that like any good study, the one by Ahmed and colleagues “raises more questions than it answers.”
Rakesh M. Suri
“While the search for a viable diagnostic means of assessing molecular changes and targets amenable to drug therapy proceeds, prompt correction of degenerative [mitral regurgitation], with 99% certainty and less than 0.3% risk, remains the best means of preserving myocardial function, allowing patients to return to a normal life, free of symptoms and with normal life expectancy,” Miller and Suri wrote. – by Jennifer Byrne
Disclosure: The researchers, Miller and Suri report no relevant financial disclosures.
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