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Cardiovascular Disease in Women
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Stephen T. Sinatra, Sara Gottfried
MVP is relatively benign condition of the mitral valve. Sometimes, the mitral valve leaflets become thickened, stretched or even voluminous, which may cause a slight to even a profound leakage of the valve. Many times on physical evaluation, a mid- to late systolic click may be heard followed by a late systolic murmur in most cases or a mid-systolic murmur in some. While most patients may not even know they have MVP, a few are particularly bothered by symptoms of atypical chest discomfort, shortness of breath, irregular heartbeats or even fatigue. In rare cases, spontaneous rupture of the chordae tendineae may occur resulting in symptoms of severe shortness of breath, significant mitral regurgitation and even left ventricular dysfunction or failure.
Complications of Septal Myectomy
Published in Srilakshmi M. Adhyapak, V. Rao Parachuri, Hypertrophic Cardiomyopathy, 2020
Lawrence M. Wei, Charlotte Spear, Vinay Badhwar
In the majority of cases, performing an adequate septal myectomy requires extending the resection apically at least to the mid-papillary muscle level. The chordae tendineae of the mitral valve are at risk of injury because of limited visibility deep in the ventricle. The surgeon must be careful to visualize and avoid injuring the chordae during septal resection. Use of a malleable “ribbon” retractor to retract the mitral structures in a posterior direction can be helpful. If a primary chord is injured, MV regurgitation may ensue. The damage may be repaired by transferring a secondary chord, implanting an artificial chord, or performing edge-to-edge leaflet repair. Absent surgical injury, residual MV regurgitation following discontinuation of cardiopulmonary bypass most commonly occurs because insufficient left ventricular muscle has been resected from the septum. Resuming cardiopulmonary bypass and completing the resection will resolve the problem in the vast majority of cases. If significant persistent MV regurgitation remains following re-resection, the valve must be repaired or replaced. Mortality for MV repair is significantly lower than for MV replacement when performed in conjunction with septal myectomy [6, 8]. Standard techniques of MV repair that involve posterior leaflet height reduction are applicable, but unusual mitral pathology including abnormal papillary muscles may be present and must be addressed.
Functions of the Cardiovascular System
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Cardiac valves ensure unidirectional flow of blood within the cardiac chambers, movement of the valve flaps being passive. The tricuspid (right) and mitral (left) atrioventricular (AV) valves lie between the atria and the ventricles and prevent reflux of blood into the atria during ventricular contraction. Chordae tendineae connect the edges of the AV valves to papillary muscles within the ventricles. When atrial pressure exceeds ventricular pressure, the AV valves open and ventricular filling takes place. When the ventricles contract, ventricular pressure exceeds atrial pressure and the AV valves close. The papillary muscles and the chordae tendineae limit any eversion or bulging of the AV valves into the atria during ventricular contraction. Semilunar valves lie between the right ventricle and pulmonary artery (pulmonary valve) and the left ventricle and aorta (aortic valve). They open during ventricular contraction, when ventricular pressure exceeds pulmonary arterial and aortic pressure, and close passively, when ventricular pressure falls during diastole, preventing reflux of blood into the ventricles.
Papillary muscle rupture of the mitral valve following blunt thoracic trauma
Published in Baylor University Medical Center Proceedings, 2023
Zaheer Faizi, Joseph Morales, Sirivan S. Seng, Kainat Faizi, Jaime Simone, Charles M. Geller, Asanthi Ratnasekera
Valvular injury is a rare form of BCI. The most frequently injured valve is the aortic valve, followed by the mitral and tricuspid valves.3 Papillary muscle rupture, chordae tendineae rupture, and valve leaflet lacerations can result in mitral valve injury, resulting in hemodynamic instability.4 Valvular prolapse, rupture, and severe regurgitation is caused by injury secondary to the compressive forces of the thoracic and abdominal cavity. It has been shown that intraventricular pressures exceeding 320 mm Hg cause increased susceptibility to cardiac valve rupture.5 Mitral valve injury occurs when blunt trauma occurs during early systole, when the mitral valve closes and there is isovolumetric contraction.5 It is possible that the presence of preexisting mitral valve prolapse may increase the risk for papillary rupture after blunt thoracic trauma.
Correlation between pathoanatomic findings, imaging modalities, and genetic findings in patients with left ventricular hypertrabeculation/noncompaction
Published in Expert Review of Cardiovascular Therapy, 2021
Claudia Stöllberger, Josef Finsterer
Inter-observer agreement of the Stöllberger definition was assessed between three experienced observers from two centers by reviewing cine-loops of 100 patients, 50 from each center, and 51 with LVHT as the initial diagnosis [71]. In that study, disagreement with the initial diagnosis occurred in 53% about LVHT presence and in 67% about LVHT absence. Agreement was slightly higher among both observers from the same echocardiographic laboratory (kappa 0.793), than among observers from different echocardiographic laboratories (kappa 0.628) and (kappa 0.669), respectively. By reviewing the discordant cases, consensus was achieved about LVHT presence (n = 8) or absence (n = 16). In 11 cases, however, the diagnosis remained questionable, due to poor image quality, lack of views in different apical planes, aberrant bands and chordae tendineae, abnormally sized or inserting papillary muscles, and localized calcifications of the endocardium [71].
Mitral valve prolapse
Published in Expert Review of Cardiovascular Therapy, 2019
Aeshah Althunayyan, Steffen E Petersen, Guy Lloyd, Sanjeev Bhattacharyya
There is a spectrum of disease ranging from fibroelastic deficiency and localized prolapse of an isolated scallop to myxomatous Barlow’s disease where there is excess tissue and elongated chordae leading to thickening of valve leaflets and prolapse of multiple scallops [6]. Recent, histological studies suggest they may be separate disease processes [7]. In Barlow-type valves, expansion of the spongiosa layer due to accumulation of proteoglycans together with intimal thickening on fibrosa and atrialis leads to diffuse leaflet thickening (Figure 1). In fibroelastic deficiency, there is focal thickening on the fibrosa of the leaflet near the chordae with increased perichordal elastin and diminished collagen content of the chordae. There is increased myofibroblastic cell proliferation with increased expression of profibrotic pathways [7]. It is hypothesized that these contribute to chordal rupture. Roberts et al. [8] examined the excised posterior leaflet of 37 patients who had undergone mitral valve repair. Superimposed fibrous tissue was found on both the atrial and ventricular surfaces of the leaflets and chordae and therefore is a major component of leaflet thickening. They found in all 37 patients chordae tendineae were ‘missing’ on gross examination. However, histologically, the leaflet and chordae tendineae could be easily demarcated. The chordae tendineae were often covered by the fibrous tissue on the ventricular aspect of the valve. Therefore, the prevalence of chordal rupture may be higher than previously thought.