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      Aortic Dysfunction in Mitral Regurgitation Due to Floppy Mitral Valve/Mitral Valve Prolapse

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          Abstract

          Background  Floppy mitral valve/mitral valve prolapse (FMV/MVP), a heritable disorder of connective tissue, often leads to mitral regurgitation (MR) and is the most common cause for mitral valve surgery in developed countries. Connective tissue disorders may affect aortic function, and a stiff aorta may increase the severity of MR. Aortic function, however, has not been studied in FMV/MVP with MR.

          Methods  A total of 17 patients (11 men, 6 women) with FMV/MVP and significant MR were compared with 20 controls matched for age and gender. Aortic diameters (AoD) were measured from left ventriculograms at 2 and 4 cm above the aortic valve. Aortic pressures were measured directly using fluid-filled catheters. Aortic distensibility was calculated using the formula: 2(systolic AoD—diastolic AoD)/(diastolic AoD x pulse pressure).

          Results  Aortic distensibility was significantly lower in FMV/MVP compared with control at 2 cm above the aortic valve (1.00 ± 0.19 versus 3.78 ± 1.10 10 −3 mm Hg −1 , respectively; p  = 0.027) and 4 cm above the aortic valve (0.89 ± 0.16 versus 3.22 ± 0.19 10 −3 mm Hg −1 , respectively; p  = 0.007). FMV/MVP patients had greater left ventricular (LV) end-systolic (88 ± 72 mL versus 35 ± 15 mL, p  = 0.002) and end-diastolic (165 ± 89 mL versus 100 ± 41 mL, p  = 0.005) volumes, and lower LV ejection fraction, compared with control (50 ± 12% versus 57 ± 6%, p  = 0.034).

          Conclusion  Aortic distensibility is decreased (consistent with a stiff aorta) in patients with FMV/MVP and MR. A stiff aorta may increase the severity of MR. Thus, abnormal aortic function, which also deteriorates with age, may play an important role in the natural history of MR due to FMV/MVP.

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          Most cited references28

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          Alterations with age in the viscoelastic properties of human arterial walls.

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            Effect of vasa vasorum flow on structure and function of the aorta in experimental animals.

            It is known that vasa vasorum flow contributes substantially to the nutrition of the outer layers of the thoracic aorta. This investigation was undertaken to test the hypothesis that impairment of vasa vasorum flow would alter the structure of the aortic wall and change the elastic properties of the aorta. The periaortic fat that contain the vasa vasorum for the ascending aorta was removed in seven anesthetized dogs, and the results were compared with those obtained from six weight-matched sham-operated control dogs. Aortic pressures, aortic diameters, and aortic distensibility were obtained before and 30 minutes and 15 days after removal of the periaortic vasa vasorum network. Aortic pressures were measured directly with a fluid-filled catheter. Aortic diameters were measured simultaneously with aortic pressures with an elastic, air-filled ring connected to a transducer. Aortic distensibility was calculated by the formula 2 x pulsatile change in aortic diameter/(diastolic aortic diameter x pulse pressure). Histology was performed in transverse blocks of aortic wall at the end of the experiment in both groups. The efficacy of the technique for the interruption of vasa vasorum blood supply to the aortic wall was demonstrated by histology in four additional animals that were killed without removal of vasa vasorum (two animals) and immediately after vasa vasorum removal (two animals). At baseline, heart rate, aortic pressures, aortic diameters, and aortic distensibility were similar in the two groups. A significant decrease in aortic distensibility was observed 30 minutes and 15 days after removal of the vasa vasorum in the experimental group (baseline, 3.453 +/- 1.023; 30 minutes, 2.521 +/- 0.760; 15 days, 1.586 +/- 0.488 10(-6).cm2.dyn-1; F = 9.532, P < .001). No changes were observed in aortic distensibility in the control group during the experiment. Histology of the aorta revealed medial necrosis, alterations of the elastin fibers, and a trend (P = .055) for altered collagen-to-elastin ratio in a region occupying more than the one (outer) half of the media of the experimental group animals. No changes were observed in the control group. The findings of the present study demonstrated that interruption of vasa vasorum flow led to an acute decrease in the distensibility of the ascending aorta. Moreover, structural changes of the aortic wall and further deterioration of the elastic properties of the aorta occurred 15 days after vasa vasorum removal.
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              Aortic distensibility abnormalities in coronary artery disease.

              Vasodilatory capacity of nonstenotic arteries in experimental animals with atherosclerosis is decreased. It was postulated that aortic distensibility may be abnormal in patients with coronary artery disease (CAD). Aortic distensibility was determined in 24 normotensive patients with CAD and an angiographically normal aorta and values were compared with those in 18 age-matched normal subjects. Aortic diameters were measured at 3 levels--2, 4 and 6 cm above the aortic valve--by angiographic techniques. The area of the first 6 cm of the aorta above the aortic valve was planimetered and mean aortic diameters were calculated. Distensibility was calculated using the formula: [2 X (changes of the aortic diameter)/(diastolic aortic diameter) X (changes of the aortic pressure)]. CAD patients had similar aortic pressures but markedly lower distensibility than normal subjects: 0.7 +/- 0.2 vs 1.7 +/- 0.3 (p less than 0.02); 1.5 +/- 0.3 vs 4.0 +/- 0.6 (p less than 0.02); and 1.2 +/- 0.2 vs 5.3 +/- 0.6 (p less than 0.001) at 2, 4 and 6 cm above the aortic valve, respectively. Distensibility was also calculated from the mean aortic diameters and was greater in normal subjects than in CAD patients (3.4 +/- 0.4 vs 1.6 +/- 0.1, p less than 0.001). Decreased aortic distensibility in CAD may be related to the common atherosclerotic process or to reduced ascending aorta vasa vasorum flow from coronary arteries.
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                Author and article information

                Journal
                Aorta (Stamford)
                Aorta (Stamford)
                10.1055/s-00039245
                AORTA Journal
                Thieme Medical Publishers (333 Seventh Avenue, New York, NY 10001, USA. )
                2325-4637
                June 2018
                12 September 2018
                : 6
                : 3
                : 75-80
                Affiliations
                [1 ]Division of Cardiovascular Medicine, Department of Medicine, The Ohio State University, Columbus, Ohio
                [2 ]Critical Care Department, Faculty of Medicine, Cairo University, Cairo, Egypt
                [3 ]Division of Cardiac Surgery, Department of Surgery, The Ohio State University, Columbus, Ohio
                Author notes
                Address for correspondence Konstantinos Dean Boudoulas, MD Division of Cardiovascular Medicine, The Ohio State University 473 W. 12th Avenue, Suite 200, Columbus, OH 43210 kdboudoulas@ 123456osumc.edu
                Article
                170048
                10.1055/s-0038-1669417
                6386641
                30208492
                bc28de6e-11d2-40de-b457-f0121fd296de

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 16 April 2017
                : 12 June 2018
                Funding
                Funding None.
                Categories
                Original Article

                floppy mitral valve,mitral valve prolapse,aorta,distensibility

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