Contemporary techniques for mitral valve repair-the Mayo Clinic experience.

Mitral valve repair for patients with degenerative or functional mitral valve regurgitation improves symptoms and prognosis, and several techniques have been described. Important principles in operation are simplicity, reproducibility, and durability of repair. At Mayo Clinic, we have operated on more than 6000 patients with degenerative mitral valve disease and valve prolapse, and this review details our approach to mitral valve repair, including robotic and minimally invasive techniques. Most patients with isolated leaflet prolapse can be managed with leaflet plication or triangular resection, and chordal replacement is reserved for repair of anterior leaflet prolapse. Posterior annuloplasty with a standard-sized flexible band is used to reduce annular circumference and improve leaflet coaptation. With these methods, early risk of mortality for mitral valve repair is low in the current era (< 1%), and rate of recurrent valve leakage is 1.5 per 100 patient-years during the first year post-repair and 0.9 per 100 patient-years thereafter. This paper also briefly summarizes important considerations for patients with mitral valve regurgitation and severe calcification, perforations due to endocarditis, and rheumatic heart disease.

Management of the mitral valve in patients with obstructive hypertrophic cardiomyopathy.

Septal myectomy is the gold standard treatment option for patients with obstructive hypertrophic cardiomyopathy whose symptoms do not respond to medical therapy. This operation reliably relieves left ventricular outflow tract gradients, systolic anterior motion of the mitral valve, and associated mitral valve regurgitation. However, there remains controversy regarding the necessity of mitral valve intervention at the time of septal myectomy. While some clinicians advocate for concomitant mitral valve procedures, others strongly believe that the mitral valve should only be operated on if there is intrinsic mitral valve disease. At Mayo Clinic, we have performed septal myectomy on more than 3000 patients with obstructive hypertrophic cardiomyopathy, and in our experience, mitral valve operation is rarely necessary for patients who do not have intrinsic mitral valve disease such as leaflet prolapse or severe calcific stenosis. In this paper, we review anatomical considerations, imaging, and surgical approaches in the management of the mitral valve in hypertrophic cardiomyopathy.

Asymmetric dimethylarginine endogenous inhibition of nitric oxide synthase causes differential vasculature effects.

BACKGROUND: Asymmetric dimethylarginine (ADMA), produced during protein metabolism, is an endogenous inhibitor of nitric oxide synthase, but little is known about its direct vasoactive properties in different arterial beds. MATERIAL/METHODS: Segments of canine coronary, renal, and femoral arteries were pretreated with increasing concentrations of ADMA, and endothelial function was evaluated in organ chambers. RESULTS: In precontracted canine coronary arteries, the highest concentrations of ADMA inhibited endothelium-dependent relaxation mediated by acetylcholine (n=7), but no concentration of ADMA inhibited receptor-independent relaxation mediated by calcium ionophore (n=7) (P<.001). The effect of ADMA on acetylcholine-mediated relaxation was shown to be competitive inhibition of the nitric oxide synthase pathway, because the addition of L-arginine (10(-3) M), but not D-arginine (10(-3) M), reversed the effect produced by 10-5 M ADMA. Further, ADMA did not alter endothelium-independent relaxation mediated by sodium nitroprusside (10(-9) to 10(-6) M; n=7). Femoral arteries (n=7) and renal arteries (n=7) were more sensitive to ADMA than were coronary arteries, and they demonstrated significant ADMA inhibition to receptor dependent relaxation induced by acetylcholine (P=.03 and P=.01, respectively) and to receptor-independent relaxation induced by calcium ionophore (P=.02 and P=.01, respectively). CONCLUSIONS: Endothelium-dependent relaxation mediated by ADMA is more marked in femoral and renal arteries than in coronary arteries. The response in coronary arteries may be overall protective. Considering these different effects in various artery types, the role of ADMA as a confiable and specific cardiovascular risk factor is questioned.

Adaptation of bioassay to detect endothelium-derived relaxing factors from the canine atrial endocardium.

OBJECTIVE: The aim of this study was to assess the release of endothelium-derived relaxing factors from the endocardium of canine atrial appendage. METHODS: To study the release of endothelium-derived relaxing factor (EDRF) from intact atrial endocardial endothelium, tube-shaped sutures of canine atrial appendages were performed and effluents from these tubes were bioassayed (isolated perfused organ chamber system) for detection of EDRF in canine coronary artery. RESULTS: Effluent from the right atrial appendage caused a relaxation of 58.4 +/- 10.1% and the left atrial appendage 74.9 +/- 8.5% from the initial prostagladin F2alpha contraction in coronary artery. No significant statistical difference was detected in effluent from the right and left atrial appendages. This relaxation was abolished by treating the heart tubes with Triton X-100 and reduced by treatment with LNMMA, a competitive inhibitor of nitric oxide and with indomethacin, an inhibitor of the cyclo-oxygenase pathway, also indicating the release of vasodilatory prostanoids from the endocardial endothelium. CONCLUSION: This study showed for the first time, in vitro luminal release of EDRF and prostacyclin from the canine heart atrium. The ability of the endocardial endothelium to produce these factors could play an important role in preventing thrombus formation in the cardiac chambers.

Adaptação de um sistema de ensaio biológico para detecção de fatores relaxantes endoteliais derivados do endocárdio atrial canino / Adaptation of bioassay to detect endothelium-derived relaxing factors from the canine atrial endocardium

OBJETIVO: Estudar a liberação de fatores relaxantes derivados do endotélio (EDRF) pelo endocárdio de aurículas de corações caninos. MÉTODOS: Aurículas atriais caninas foram suturadas em forma de tubos e o efluente desses tubos foram submetidos a ensaios biológicos (sistema de perfusão isolada em câmaras de órgãos) utilizando artéria coronária canina, para a detecção de EDRFs. RESULTADOS: O efluente da aurícula direita promoveu relaxamento de 58,4 + 10,1 por cento e da aurícula esquerda 74,9 + 8,5 por cento da contração inicial obtida pela ação da prostagladina F2α em artéria coronária. Não houve diferença estatística no relaxamento da artéria coronária induzido pelos efluentes das aurículas direita e esquerda. O relaxamento induzido pelos efluentes das aurículas direita e esquerda foi abolido pelo tratamento das mesmas com Triton X-100. O tratamento das aurículas com L-NMMA, um inibidor competitivo da síntese de óxido nítrico, e com indometacina, um inibidor da via da ciclooxigenase, promoveu redução no relaxamento da artéria coronária induzido pelo efluente auricular, indicando que o endotélio endocárdico libera óxido nítrico e prostanóides. CONCLUSÕES: Esse estudo demonstra, pela primeira vez, a liberação luminal in vitro de EDRF e prostaciclina pelo átrio de coração canino. A habilidade do endotélio endocárdico em produzir esses fatores pode ter um papel importante na prevenção da formação de trombos nas câmaras cardíacas.

OBJECTIVE: The aim of this study was to assess the release of endothelium-derived relaxing factors from the endocardium of canine atrial appendage. METHODS: To study the release of endothelium-derived relaxing factor (EDRF) from intact atrial endocardial endothelium, tube-shaped sutures of canine atrial appendages were performed and effluents from these tubes were bioassayed (isolated perfused organ chamber system) for detection of EDRF in canine coronary artery. RESULTS: Effluent from the right atrial appendage caused a relaxation of 58.4 + 10.1 percent and the left atrial appendage 74.9 + 8.5 percent from the initial prostagladin F2α contraction in coronary artery. No significant statistical difference was detected in effluent from the right and left atrial appendages. This relaxation was abolished by treating the heart tubes with Triton X-100 and reduced by treatment with LNMMA, a competitive inhibitor of nitric oxide and with indomethacin, an inhibitor of the cyclo-oxygenase pathway, also indicating the release of vasodilatory prostanoids from the endocardial endothelium. CONCLUSION: This study showed for the first time, in vitro luminal release of EDRF and prostacyclin from the canine heart atrium. The ability of the endocardial endothelium to produce these factors could play an important role in preventing thrombus formation in the cardiac chambers.