myxomatous mitral valve disease

Methods: We evaluated 38 patients with myxomatous mitral valve disease (mean age 57 ± 15 years; 18 females) and used standard transthoracic echocardiography for measuring the MAD. Mitral annular function, assessed by end-diastolic and end-systolic annular diameters, was compared between patients with and without MAD. We compared the incidence of arrhythmias in a subset of 21 patients studied with 24-hour Holter monitoring. Results: MAD was present in 21 (55%) patients (mean length: 7.4 ± 8.7 mm), and was more common in women (61% vs 38% in men; p = 0.047). MAD patients more frequently presented chest pain (43% vs 12% in the absence of MAD; p = 0.07). Mitral annular function was significantly impaired in patients with MAD in whom the mitral annular diameter was paradoxically larger in systole than in diastole: the diastolic-to-systolic mitral annular diameter difference was -4,6 ± 4,7 mm in these patients vs 3,4 ± 1,1 mm in those without MAD (p < 0.001). The severity of MAD significantly correlated with the occurrence of non-sustained ventricular tachycardia (NSVT) on Holter monitoring: MAD›8.5 mm was a strong predictor for (NSVT), (area under ROC curve = 0.74 (95% CI, 0.5-0.9); sensitivity 67%, specificity 83%). There were no differences between groups regarding functional class, severity of mitral regurgitation, LV volumes, and LV systolic function.

Dyspnea can also be caused by pleural effusion or ascites due to right heart failure. Right heart failure in MMVD is a sign of progressive mitral valve disease and pulmonary hypertension that can be accompanied by tricuspid valve degeneration. Clinical signs may develop gradually and progress or they may come acutely due to sudden worsening of the disease. The owner may not have noticed the gradual declining of the dog’s physical activity, or acute disease may be caused by a rupture of chordae tendinae, the onset of arrhythmia (usually atrial fibrillation) or some kind of stress that puts the animal over the edge (separation from the owner, new environment, exertion). Hearing the typical murmur over the mitral area can determine the diagnosis of MMVD, and heart failure can be confirmed by thoracic radiography (Fig 3). Echocardiography further documents the individual chamber enlargement, the magnitude of regurgitant flow, the severity of mitral degeneration, valve prolapse, chordal rupture and pulmonary hypertension (Fig 6). Systolic function is difficult to assess in MMVD due to the enhanced sympathetic tone (24).

The term heart disease is used synonymously with cardiac pathology — in this case, myxomatous degenerative changes of the mitral valve. Heart disease, depending on its nature, rate of progression, and patient age and condition may or may not lead to heart failure. The term “ heart failure ” refers to clinical signs caused by heart dysfunction. Heart failure is caused by heart disease that affects heart function such that either venous pressures increase so severely that fluid accumulates in the lungs or a body cavity (congestive heart failure [CHF], sometimes called “ back- ward heart failure because the heart fails to drain the veins adequately), or the heart's pumping ability is compromised such that it cannot meet the body's needs either during exercise or at rest, in the face of either normal or increased venous pressures (sometimes called “ forward heart failure ” ).

pimobendan mediates its favorable effect (ie, it interve- nes on the “causal pathway”) once the reduction in sys- tolic diameter is taken into account in a multivariable analysis, the association between treatment and the out- come is no longer apparent. These findings add further weight to the existing literature which suggests that, at least in part, the benefit of pimobendan treatment in canine heart disease is mediated through the reduction in heart size that it brings about. This speculation about a potential mechanism of action in dogs with MR is supported by experimental findings in dogs with induced MR which suggest that reduced heart size and enhanced contractile function are associated with a reduction in mitral regurgitant orifice area and therefore reduced MR. 21,22

Exclusion Criteria. Dogs were excluded from the study if they had any of the following: known clinically important systemic or other organ-related disease that was expected to limit the dog’s life expectancy or required chronic cardiovascular medication precluded as part of the trial (Table 1). Dogs with hypothyroidism could be included provided the investigator deemed them clinically stable on treatment. Dogs with current or previous evidence of cardiogenic pulmonary edema, pulmonary venous congestion or both, cardiac disease other than MMVD, clinically significant supraventricular, ventricular tachyarrhythmias or both (i.e, requiring antiarrhythmic treatment), or evidence of pulmonary hypertension considered to be clinically relevant (RV:RA pressure gradient > 65 mmHg) were excluded. Dogs with a history of chronic or recent administration ( > 14 days of duration or within 30 days of intended enrollment) of any medication listed in Table 1 were excluded. Dogs that were pregnant or lactating were not eligible for enrollment. In the event that before study enrollment, a dog had received short-term treat- ment ( < 14 days) with agents listed in Table 1, but was no longer receiving treatment and had not received it within 30 days of intended enrollment, then the dog was eligible for inclusion.

Inclusion Criteria. Dogs were eligible for inclusion in the study provided the owner had given informed consent. To be eligible for inclusion at the time of the 1st examination, the dog must have been > 5 years of age, weighed between 5 and 20 kg, had a characteristic heart murmur of moderate to high intensity with maximal intensity over the mitral area, had echocardiographic evidence of advanced MMVD defined as characteristic valvular lesions of the mitral valve apparatus (leaflet thickening, valve prolapse), demonstrated mitral regurgitation on color Doppler echocardiography, had echocardiographic evidence of moderate to severe left atrial, left ventricular enlargement, or both (ie, left atrial to aortic root [LA/Ao] ratio > 1.5 12 and left ventricular internal diameter in diastole [LVIDd] values above normal refer- ence range 13 ), and demonstrated current or prior radiographic evidence of pulmonary edema and cardiomegaly (ie, vertebral heart scale [VHS] > 10.5). 14 Clinical signs of decompensated CHF

Surgical techniques: The general anaesthesia was provided according to the standard protocol by endotracheal intubation with both lung ventilation, peripheral femoral arterial cannulation and central jugular venous cannulation. Trans- oesophageal echocardiography (TEE) was done in all patients to assess mitral valve morphology and adequacy of repair. Median sternotomy was done. Systemic heparinization was done at the dose of 3-4 mg/kg to achieve activated clotting time (ACT)>400 Seconds. Cardio-pulmonary bypass (CPB) was established by aorto-bicaval cannulation. Myocardial protection was achieved by antegrade hyperkalemic cold blood cardioplegia solution through aortic root every 20 minutes. The temperature during CPB was maintained at 32 0 c. The left atrium was opened parallel and posterior to interatrial groove to access the mitral valve. Thorough evaluation of mitral valve apparatus was done for suitability of repair. Annuloplasty sutures with 2-0 ethibond were taken initially as it provides better assessment and exposure of mitral valve. Mitral valve repair was done according to Carpentier’s principle. Autologous pericardial patch was harvested and treated with 0.6% gluteraldehyde in patients where leaflet augmentation was needed. The details of various techniques used are described in Table 1. Commissurotomy was the most commonly performed procedure. Annuloplaty was done with different types of ring. The details of rings used are described in Table 2. Capentier classic annuloplasty ring was most commonly used. Left atriotomy was closed with 4-0 polypropylene suture. Right atriotomy was done in patients in whom tricuspid valve repair was done. Cryocoxmaze III was done in patients of persistant atrial fibrillation (AF).

We report, to the best of our knowledge, the largest number of SCD cases with MVP as lone abnormal finding, having had consistent systematic pathology analysis performed for diagnostic purposes by the same expert cardiovascular pathologist (MNS), guided by no preconceived research hypothesis. The reported findings were only retrospectively reviewed and interpreted by the authors of this paper with the aim to characterise malig- nant MVP. Our study found Barlow disease mitral valve characteristics and features of a distinct cardiomyopathy in MVP-related SCD.

enlargement and annular dilatation that impair their nor- mal functions and lead to valve prolapse and MR [3]. So far, myxomatous degeneration was mainly considered as a passive mechanism and only a few studies investi- gated the underlying physiological deregulation. How- ever, some works have highlighted interesting tracks in the understanding of the physiopathological mechanisms associated with this disease process. For example, matrix remodeling, with structural alteration of elastic fibers and collagen, could be explained by the excessive matrix met- alloproteinase proteins (MMPs) and cathepsins secre- tion by valvular interstitial cells (VICs) in myxomatous mitral valves (MMV) [4]. These VICs can differentiate into active myofibroblasts with a significant increase of

Cardiac Insufficiency is the main reason for hospitalization in the Cardiology Department at the Good Samaritan Hospital of N’Djamena in Chad. In this study, the four leading causes of CI were Rheumatic valvulopathy, congenital heart disease, dilated cardiomyopathy, and hypertensive cardiomyopathy. How- ever, Ischemic heart disease was rare. In young people, the main etiology was rheumatic valvulopathy, whereas, in the elderly it was DCM.

We started our minimally invasive mitral valve pro- gram at University Hospital Basel in 2010, reaching a volume of 60 – 70 patients per year. From a total of 69 patients who received mitral valve repair in a min- imally invasive setting from May 2013 until June 2014, 60 patients we evaluated retrospectively. These patients underwent isolated minimally invasive mitral valve repair in Carpentier Type-II mitral disease, all of them having an annuloplasty ring implanted in combination with correction of the prolapsing leaflet using artificial chords (GoreTex CV4). Repair was performed in the first run without the need for any further correction. Thirty patients after implementa- tion of a novel automated fastener (November 2013– June 2014) were compared with 30 patients corrected with a traditional knot pusher (May 2013– October 2013). To increase homogeneity in both groups the following 9 patients were excluded: Patients, who underwent combination surgery with tricuspid valve repair or atrial septal defect closure (n = 3), Patients just receiving a ring- annuloplasty (n = 5) and one pa- tient who needed a second cross-clamp period for a suboptimal result in the first run. No significant dif- ferences regarding demographic data (age, gender, NYHA class, ejection fraction, BMI, cardiovascular

Of the 38 patients, 20 patients (53%) and 18 patients (47%) were identified as having mild MR and moderate to severe MR respectively (ERO = 45 ± 27 mm 2 vs. 5 ± 7 mm 2 , p < 0.001) (Table 1). Patients with moderate to severe MR were older (61 ± 14 years vs. 41 ± 18 years, p < 0.001) and had a slightly larger LV end diastolic diameter (49 ± 6 mm vs. 45 ± 4 mm, p = 0.03). There was no significant differ- ence between both groups regarding LV end systolic dia- meter and LV ejection fraction. With regard to mitral valve morphology, patients with ERO ≥ 20 mm 2 had a longer posterior leaflet (18.4 ± 4.2 mm vs. 13.6 ± 3.6 mm, p < 0.001) and greater prolapsing depth (8.4 ± 3.8 mm vs. 5.5 ± 2.0 mm, p = 0.007). Diastolic leaflet thickness was similar between both groups (5.5 ± 0.9 mm vs. 5.3 ± 1.0 mm, p = 0.57). Billowing area tended to be different in patients with moderate to severe MR (1.0 ± 0.6 cm 2 vs. 0.7 ± 0.4 cm 2 , p = 0.08). As expected, the non-coaptation dis- tance between leaflets was greater among those with ERO ≥ 20 mm 2 (5.0 ± 1.6 mm vs. 2.0 ± 2.5 mm, p < 0.001). Pro- portion patients with classical form of MVP (thickened leaflets ≥ 5 mm) was similar in both groups (30% vs. 33%, p = 0.82). On univariate analysis, the strongest predictors of significant MR were the non-coaptation distance (OR 6.2 per 1 mm increase; 95% CI 1.72-22.3) and the prolap- sing depth (OR 1, 4 per 1 mm increase; 95% CI 1.1-1.7) Thick mitral valve leaflet as traditionally reported ( ≥ 5

All examinations were performed at rest without pharmacological restraint. A transthoracic echocardio- graphic (TTE) examination was performed in all dogs with an Aloka 4000 (after September 2005) or SC300 PANDION (before September 2005) ultrasound ma- chines both equipped with a cardiology programs and 2.5 - 7-megahertz (mHz) sector transducers. The exami- nations were performed and interpreted by one of two doctors working in the Cardiology Service. Examinations were performed according to published norms [1,2], in some cases the examination was carried out on dogs in standing position [1,3]. Basic information from the echo- cardiographic examination allowing for a diagnosis of chronic valve disease included lesions of the mitral valve with regurgitation, lesion of the tricuspid valve with re- gurgitation, enlarged left atrium, increased left ventricu- lar end-diastolic diameter, increased left ventricular end- systolic diameter, hyperdynamic left ventricular motion, hypodynamic left ventricular motion. Electrocardiogra- phic examination (leads I,II, III, aVL, aVF and aVR) were performed with a BTL-08 MD machine. Radiological examination of the chest was performed with the G&E Prestige II X-ray machine.

An anchor consisting of a CV-2 ePTFE (Gore-Tex) suture with pledget (Gore-Tex; W.L. Gore & Associates, Flagstaff, AZ, USA) was attached to the top of papillary muscle. A CV-5 Gore-Tex suture was then passed through the anc- hor (anchoring technique). Next, the CV-5 Gore-Tex suture was passed through a cut 12 Frazier suction tube (Nipro Corporation, Osaka, Japan) and attached to the edge of the prolapsed mitral valve leaflet. The length of the cut tube was de- termined by measuring the length of near healthy native chordae as a reference. This method constitutes the measured tube technique [6]. With the aid of the cut tube, the proper length of the chordae was fixed when the suture was tied. Finally, the tube was carefully removed. In this technique, if additional artificial chordae are required, they can be easily attached using the CV-2 anchor.

Cox regression analysis was performed using all patients with the variables; procedure performed, sex, mitral valve pathology, aortic valve pathology and redo procedure. Using a forward selection process, only the variable age was significant (p < 0.001), with all the other variables exceeding p = 0.05. However, these results should be treated with caution given the relatively small sample size. Age significantly affects survival with a hazard ratio of 1.93 (CI 1.47–2.45) per decade.

Methods: Sixteen patients with American Society of Anesthesiologists status (ASA) II-III, age ≤ 70 yr, male or female, preoperatively NYHA II-III and EF ≥ 45%, scheduled for mitral valve replacement (MVR) were studied. Complete intravenous general anesthesia was used for induction and anesthesia maintenance. After anesthesia induction we put the TEE probe into the esophagus. The cardiac index was determined at three periods following MVR: T1 30 minutes later following cessation of bypass, T2 60 minutes after cessation of bypass, T3 90 minutes after cessation of bypass. Statistical analysis was made with the Bland and Altman method. Results: Ninety-six measurements were compared. The cardiac index values at the level of prosthesis mitral valve (CI MV ) ranged from 1.3 to 5.5 L·min −1 ·m −2 (mean 2.6 ±

annulus. The rings and bands can restore valve compe- tence, but they restrict most annular motion. In addition, because the annulus is fixed to the ring or band in a flat plane, it loses the commissural hinge work and three-dimensional saddle shape [2, 3]. Such normal annular geometry may be preserved by an annuloplasty strip that spares the anterior annulus and commissures. We retrospectively evaluated in a cohort of patients underwent posterior mitral annulo- plasty (PMA) using a novel strip designed for placement in the posterior annulus.

shown excellent outcomes for posterior leaflet prolapse. The concept of leaflet preservation has become increas- ingly appreciated. In mitral valve repair, the greater the mi- tral valve coaptation area is, the lighter the mitral regurgitation is. Falk et al. found that chordal placement with minimal or no leaflet resection may contribute to better durability of MVR compared with leaflet resection, because of a longer zone of coaptation [4]. Post-repair coaptation length (CL) has been shown to be related to durability of MVR in patients with ischemic MR. [5] How- ever, the association between post-repair CL and durability of MVR in degenerative MR has not been investigated. However, the exact value of the mitral valve coaptation area is not easy to obtain.

Several studies reported the inaccuracy of PHT tech- nique for MVA measurement, and the reasons such as geometric change of MV structures and net atrioven- tricular compliance when immediately after CPB ended in MVR [14-16]. And some studies suggested that other parameter such as pressure gradient was more useful for immediate postoperative MV evaluation to detect MS [17,18]. However, Maslow A et al. reported the impor- tance of optimizing haemodynamics during assessment of MVA, and suggested that the PHT technique for MVA evaluation after MVR was still useful if haemo- dynamic optimization could be made [19,20]. In the present study, according to our institutional standard Table 2 Mitral valve areas at intra- & post-operative different techniques

Forchheim, Germany). Chest CT examinations were performed during inspiratory breath-hold not using contrast and without electrocardiographic gating. Scans were recon- structed with an effective section thickness of 0.6 mm and an increment of 0.4 mm. The field of view was individu- ally adapted to the patient’s body habitus. All multidetec- tor CT scans were reviewed on an external workstation (Wizard Medical Solutions, Mount Waverley, Australia) by a radiologist with expertise in chest CT. Mitral valve calci- fications were subjectively characterized by the following criteria: presence, location (annulus or leaflet), Agatston score, and length in millimeters. 13,14 For measuring the length