Circulation Journal Research Articles

Clinical Application of Remote Ischemic Preconditioning

Ischemic preconditioning1 has been shown to reliably reduce ischemic myocardial cell necrosis in a host of animal models.2 Although preconditioning is one of the most powerful and reproducible phenomena in cardioprotection, it has not readily translated to routine clinical use. One issue is that the timing of the long duration of ischemia must be known in advance and the treatment must be applied before the long duration of ischemia. Thus, although evidence suggests that preinfarction ischemia (angina) before an ST-segment elevation myocardial infarction is associated with smaller infarct size and better clinical outcome,3 there is no reliable way to predict when a myocardial infarction will occur and hence no way to either induce ischemic preconditioning or apply a preconditioning mimetic agent just before the infarction. There are, of course, situations in which myocardial ischemia is planned, eg, during coronary artery balloon angioplasty, during coronary artery bypass surgery, during excision and transportation of a donor heart, and before exercise in a patient with known demand-induced ischemia. Preconditioning has been applied to some of these situations. For example, multiple brief balloon inflations and deflations in the coronary artery reduce the severity of chest pain, ST-segment elevation, and lactate production on subsequent balloon inflations compared with an initial balloon inflation without necessarily recruiting blood flow.4 Intermittent aortic cross clamping before coronary artery bypass surgery has been observed to preserve cardiac high-energy phosphate levels.2 These examples of ischemic preconditioning require an invasive procedure to induce ischemia within the heart and the possibility of showering atherosclerotic emboli either down the coronaries or into the aorta as a coronary angioplasty balloon is repeatedly inflated or deflated or the aortic cross clamp is repeatedly clamped and unclamped. Article p 820 Another approach exists that has the potential to be entirely noninvasive: remote …

Clinical and Diagnostic Features of Delayed Hypoxic Leukoencephalopathy

Clinical and Diagnostic Features of Delayed Hypoxic Leukoencephalopathy

Fibrin Clot Visualized by Optical Coherence Tomography

Optical coherence tomography (OCT) is a recently developed optical imaging technique that provides high-resolution (≈10 to 20 μm) cross-sectional images of vessels.1 It has been reported that OCT images of white and red thrombus were characterized as backscattering protrusions in the coronary lumen.2 However, OCT characteristics of fibrin clot composed of fibrin material and few blood cells have not been described. The coronary arteries of a 75-year-old man …

Diversity of Denizens of the Atherosclerotic Plaque

The atherosclerotic plaque typically harbors cells of several lineages whose conversations, mediated by extracellular or cell surface–associated messengers, influence decisively the biology and clinical consequences of the lesion. Early vascular biology studies defined the resting state of the endothelium, characterized by the elaboration of antithrombotic and vasodilatory mediators. The activated endothelium recruits inflammatory leukocytes, favors clot accumulation, participates in angiogenesis, and can influence the behavior of subjacent smooth muscle cells in ways that favor atherogenesis and vasoconstriction (Figure). More recently, we have come to appreciate that the endothelial cell not only can exhibit a spectrum of functions, but that some may arise postnatally from bone marrow–derived precursors.1 Thus, the heterogeneity of endothelial cells depends not only on the mutability of their function but also on their origin. The diversity of endothelium depends not only on lineage but also location, with increasingly well-understood differences between arterial, microvascular, and venous endothelial cells. Figure. Heterogeneity of major cell types in atherosclerotic plaques. Vascular biologists have long recognized heterogeneity of endothelial cells and smooth muscle cells, now understood to result from local mediator milieu, biomechanical stimuli, and different embryological origins. Indeed, recent data suggest that both of these intrinsic vascular cell types can arise in postnatal life from bone marrow–derived precursors. Immunological dogma recognizes several T-cell populations, exemplified here by the Th1 and Th2 subsets, which on the balance exert opposing influences on atherogenesis. New data now establish the relevance to atherosclerosis and hyperlipidemia of monocyte heterogeneity. Monocytes that bear high levels of the markers Ly6c/Gr-1 and P-selectin glycoprotein ligand exhibit more proinflammatory functions than their …

Cardiovascular Magnetic Resonance of Isolated Left Ventricular Apical Hypoplasia

A 37-year-old white peripartum female was admitted to intensive care with pulmonary edema. She had no past medical history of note. Left bundle-branch block, P mitrale, and left-axis deviation were identified on her ECG, and cardiomegaly on her chest x-ray (Figures 1 and 2⇓). She was referred for cardiovascular magnetic resonance (CMR) after diagnostic coronary angiography revealed normal coronary arteries. Figure 1. ECG showing P mitrale, left-axis deviation, and left bundle-branch block. Figure 2. Chest x-ray showing …

Kidney and Circadian Blood Pressure Rhythm

Association between nondipper pattern of circadian rhythm of blood pressure (BP) and impaired renal capacity to excrete sodium into urine was confirmed by Bankir et al1 in this issue of Hypertension based on a large number of subjects. Although this association has been observed in small studies,2,3 their study1 is the first to show it in a large-scale setting, and, therefore, is highly welcomed. Because there is a tight link between kidney and hypertension, renal dysfunction causes hypertension, whereas hypertension accelerates renal damage. It is well appreciated that the kidneys play an important role in the long-term regulation of BP. Usually it takes almost 1 week for kidneys to achieve a new steady-state balance of sodium, when sodium intake is altered. Therefore, renal participation in the short-term BP regulation, such as circadian rhythm, has been overlooked. However, the findings of Bankir et al1 strongly suggest that nocturnal hypertension and nondipper pattern of circadian BP rhythm are because of impaired renal capacity to excrete sodium, and circadian BP rhythm is at least in part regulated by kidneys. Sodium sensitivity of BP is also determined by renal capacity to excrete sodium and is regulated by glomerulotubular balance between glomerular ultrafiltration capability and rate of tubular sodium reabsorption.4 Thus, sodium sensitivity is increased in chronic kidney disease (CKD) where glomerular filtration rate (GFR) is reduced and also in disorders with enhanced tubular sodium reabsorption, including primary aldosteronism, diabetes mellitus, and metabolic syndrome, where GFR is augmented. When sodium sensitivity is increased, glomerular capillary pressure is usually elevated, resulting in albuminuria and renal damage. It becomes evident that, in patients with high-sodium sensitivity, the nocturnal dip in …

Central Blood Pressure and Hypertension

During the 20th century, the brachial artery auscultatory method of blood pressure (BP) measurement has been the major basis for our understanding of clinical hypertension. First, the height of systolic (S) and diastolic (D) BP was used to define cardiovascular (CV) risk. Second, BP reduction by drug treatment was shown to be associated with a substantial decrease of CV risk in several varieties of high BP, including systolic hypertension in the elderly.1,2 However, drug treatment often reduced DBP more than SBP, resulting in increased pulse pressures (PP) and the related arterial stiffness. An associated increase in coronary risk was also observed.1,3 Because PP and arterial stiffness did not respond readily to drug treatment and was made even less responsive by aging, it has been suggested and shown that mechanical factors such as PP, arterial stiffness, and wave reflections, preferably measured by central (aortic or carotid) BP, should be fully investigated. Because the majority of the studies used noninvasive peripheral BPs the need arose for invasive methods to verify and validate central BP measurement in the evaluation of CV risk.4 In the present issue of this journal, Jankowski et al5 established, in a 4.5-year follow-up of 1109 patients undergoing coronary angiography, that central BP was a significant and independent predictor of CV risk, as potent as cardiac ejection fraction and more powerful than brachial sphygmomanometric measurements. For these coronary patients, the pulsatile …

Impaired Fetal Growth, Cardiovascular Disease, and the Need to Move on

The final step in the acceptance of a new medical hypothesis is often the approval of significant funding to investigate it. In the case of developmental programming (ie, the notion that the in utero environment determines susceptibility to many diseases later in life), this has recently come in the form of support by the US Congress for the National Children’s Study, a $3 billion project to follow the impact of environmental factors before, during, and after pregnancy on disease manifestation in some 100 000 children up to the age of 25 years.1 This initiative will, no doubt, yield a wealth of correlative data and identify many new factors potentially affecting developmental programming. Article p 405 Much of the concept underlying the National Children’s Study stems from the pioneering work of Barker and colleagues,2 whose epidemiological observation of increased cardiovascular risk in children with low birth weight has spurred a large number of retrospective studies during the past 30 years. Despite some conflicting results, most of these studies support the notion that reduced birth weight is indeed associated with increased hypertension, diabetes mellitus, and cardiovascular disease. However, the strong correlation between birth weight and duration of gestation, plus the fact that a short gestation also may be associated with cardiovascular risk,3 poses the question to what extent low birth weight is truly responsible. In this issue of Circulation , an article by Kaijser and coworkers4 at the Karolinska Institute in Stockholm provides a convincing answer. By scanning 250 000 records of birth at 4 major delivery units in Sweden between 1925 and 1949, they identified a cohort of 6437 subjects, which included 2937 children born preterm (<37 weeks of gestation) and 2181 with a birth weight <2000 g for girls or <2100 g for boys. During the …

Justice David J. Brewer and “the Constitution in Exile”

A decade ago, Judge Douglas Ginsburg roiled the waters of constitutional debate with his offhand reference to a “Constitution in Exile” in a book review that appeared in a limited- circulation journal of the libertarian Cato Society.1 The metaphor was irresistible, conjuring up as it does romantic images of Stuart princes wandering about Europe, hoping for the return of the legitimate constitutional order, and either enjoying triumphant Restoration (Charles II) or being doomed to crushing disappointment (Bonnie Prince Charlie after Culloden). Or, on the opposite end of the ideological spectrum, images of Lenin being recalled from Swiss exile to his moment in history at the Finland Station, to inaugurate a new world order.

Scavenger Receptor A and CD36 Are Implicated in Mediating Platelet Activation Induced by Oxidized Low- Density Lipoproteins

See ATVB 2007;2476–2483. CD36, previously known as GPIIIb or GPIV, is an 88-kDa membrane glycoprotein that was isolated from blood platelets soon after being identified on monocytes by monoclonal antibody OKM5. Cloning the CD36 gene showed this cell adhesion molecule to be a member of the scavenger receptor class B family. Moreover, it was observed that CD36 has the capacity to bind oxidized low-density lipoproteins (oxLDL) but not acetylated lipoproteins. Scavenger receptor class A (SRA),1 also expressed on platelets and monocytes/macrophages, is a trimer of 77 kDa, that binds to acetylated and oxidized lipoproteins. SRA is closely associated to macrophage CD36 in initiating atherosclerotic lesions, in some studies but not all.2,3,4 Very little was known, up to now, on the role played by oxLDL in activating platelets via CD36 and SRA and promoting a prothrombotic phenotype. The study, in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology , by Suzanne Korporaal and coworkers,5 shows very elegantly that oxLDL, in tandem with CD36 and SRA, is activating platelets and potentially increasing the risk of thrombosis. This investigation brings some exciting data on a novel platelet-activating pathway triggered by partially oxidized (30% to 60%) LDL and mediated by the combined activity of CD36 and …

Letter by Weidemann et al Regarding Article, “Global Diastolic Strain Rate for the Assessment of Left Ventricular Relaxation and Filling Pressure”

HomeCirculationVol. 116, No. 14Letter by Weidemann et al Regarding Article, “Global Diastolic Strain Rate for the Assessment of Left Ventricular Relaxation and Filling Pressure” Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBLetter by Weidemann et al Regarding Article, “Global Diastolic Strain Rate for the Assessment of Left Ventricular Relaxation and Filling Pressure” Frank Weidemann and Joerg M. Strotmann Bart Bijnens Frank WeidemannFrank Weidemann Department of Internal Medicine I, University Hospital Wuerzburg, Germany Search for more papers by this author and Joerg M. StrotmannJoerg M. Strotmann Department of Internal Medicine I, University Hospital Wuerzburg, Germany Search for more papers by this author Bart BijnensBart Bijnens Medical School and Faculty of Electronic Engineering, University of Zagreb, Croatia Search for more papers by this author Originally published2 Oct 2007https://doi.org/10.1161/CIRCULATIONAHA.107.708784Circulation. 2007;116:e368To the Editor:We have read with interest the paper by Wang et al1 on diastolic function assessed by strain rate in the isovolumetric relaxation period (SRIVR) derived from 2-dimensional speckle tracking. In principle, 2-dimensional speckle tracking is a useful progression toward an automated assessment of left ventricular deformation.We would like to comment on the fact that the authors had some difficulties with patients with wall motion abnormalities. It is known from many studies that different conditions such as acute ischemia, regional fibrosis, and increased afterload result in ongoing (postsystolic) deformation during isovolumic relaxation (IVR).2,3 This deformation will change local SRIVR independently from tau, which thus limits the assessment of diastolic function by analysis of SRIVR in a wide range of important clinical conditions.In addition, we agree that E/Ea has some limitations when diastolic function is assessed, especially in the gray zone between 8 and 15. However, although it has merits in the assessment of strain, we think that 2-dimensional speckle tracking is not satisfactory when strain rate is assessed, especially during IVR. It is well known that speckle tracking can only be performed at relatively low frame rates. However, this low frame rate prevents resolution of the fast change in deformation (ie, strain rate) that occurs during IVR. This lack of resolution leads, as correctly mentioned in the paper,1 to an underestimation of peak strain-rate value. Thus, we would suggest use of Doppler-derived strain rate (with its high temporal resolution), and not speckle tracking strain rate, to accurately assess SRIVR.The authors could nicely show the limitations of diastolic function assessment by pulsed-wave tissue Doppler imaging and suggest a greater focus on diastolic deformation. However, we believe that assessment of strain rate during IVR with 2-dimensional speckle tracking and its inherent technical limitations will prove a real challenge in clinical conditions.DisclosuresNone.1 Wang J, Khoury DS, Thohan V, Torre-Amione G, Nagueh SF. Global diastolic strain rate for the assessment of left ventricular relaxation and filling pressures. Circulation. 2007; 115: 1376–1383.LinkGoogle Scholar2 Weidemann F, Dommke C, Bijnens B, Claus P, D’hooge J, Mertens P, Verbeken E, Maes A, Van de Werf F, De Scheerder I, Sutherland GR. Defining the transmurality of a chronic myocardial infarction by ultrasonic strain-rate imaging: implications for identifying intramural viability: an experimental study. Circulation. 2003; 107: 883–888.LinkGoogle Scholar3 Voigt JU, Lindenmeier G, Exner B, Regenfus M, Werner D, Reulbach U, Nixdorff U, Flachskampf FA, Daniel WG. Incidence and characteristics of segmental postsystolic longitudinal shortening in normal, acutely ischemic, and scarred myocardium. J Am Soc Echocardiogr. 2003; 16: 415–423.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Chiang S, Daimon M, Ishii K, Kawata T, Miyazaki S, Hirose K, Ichikawa R, Miyauchi K, Yeh M, Chang N and Daida H (2014) Assessment of Elevation of and Rapid Change in Left Ventricular Filling Pressure Using a Novel Global Strain Imaging Diastolic Index, Circulation Journal, 10.1253/circj.CJ-13-0513, 78:2, (419-427), . October 2, 2007Vol 116, Issue 14 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.107.708784PMID: 17909112 Originally publishedOctober 2, 2007 PDF download Advertisement SubjectsEchocardiography

The Influence of the Regulatory T Lymphocytes on Atherosclerosis

Atherosclerosis is complex inflammatory disease of the arterial wall, in which T lymphocytes play a significant role.1 Since the recognition that T lymphocytes are present in human atherosclerotic plaque nearly 2 decades ago,2 research has focused on the functional importance of these cells in the atherosclerotic process. The majority of T lymphocytes in atherosclerotic lesions are CD4+ T-helper cells with a phenotype characteristic of the proinflammatory T-helper 1 (Th1) subset. These cells recognize specifically antigens that are produced in relative abundance in hypercholesterolemic individuals or in plaques including oxidatively modified LDL (Ox-LDL) and HSP60/65. The T cells are activated when macrophage or dendritic cells present these antigens to the T cells in plaques or lymphoid tissues. The Th1 cells produce inflammatory cytokines IFN-γ, tumor necrosis factor (TNF)-α, and membrane CD40-ligand, which amplify the immune response through activation of macrophages, vascular smooth muscle cells, and endothelial cells.1 See page 2691 Many mechanisms have evolved to maintain immunologic self-tolerance and to limit responses to foreign antigens. One of these mechanisms involves regulatory T cells (Treg) that actively suppress responses of effector T cells. The best- characterized Treg are the natural CD4+CD25+ Treg that mature in the thymus and comprise 5% to 10% of peripheral CD4+ T cells.3 Other surface markers expressed by Treg include CTLA-4 and GITR. FoxP3, a forkhead family transcription factor, is a lineage specification factor for Treg and plays a crucial role in their suppressive function.4 Natural Treg are generated during thymic development, but Treg are also induced in peripheral tissues during immune responses. Treg express antigen receptors typical of effector T cells and are presumably activated by peptide antigens presented by APCs. They also require interleukin (IL)-2 for development and survival. Once activated, Treg may suppress other T …

Solomon Victor: Leading cardiac surgeon in India and long-time supporter of heart, lung and circulation

O 7 July 2006, Professor Solomon Victor, an internationally recognised cardiac surgeon, died in Chennai, India. He was a strong and long time supporter of Heart, Lung and Circulation journal. He was not only an outstanding cardiac surgeon but also a humanitarian, philosopher, botanist and evolutionary biologist. In this issue we publish an obituary for Dr. Solomon Victor, written by one of Britain’s most well known cardiac surgeons –

Combating Nitrate Tolerance

Discovered and patented as an explosive by Alfred Nobel in the 1860s, nitroglycerin has been formulated for use in the treatment of symptomatic CAD for over 140 years. In fact, later in life, Nobel himself was prescribed the medication for angina, but refused to take it because of the associated side effect of headache. See page 1729 With glycerol trinitrate (GTN) as the prototype, nitrates represent one of the safest and most rapidly effective pharmacological means to reduce acute symptoms of myocardial ischemia attributable to obstructive coronary disease. This has led, over the years, to the development of long-acting oral and topical preparations. However, efficacy with chronic administration is more difficult to achieve because of the development of therapeutic resistance, generally occurring a few days after initiating treatment. This phenomenon known as nitrate tolerance has been the stimulus for intense investigation of the metabolic fate of nitroglycerin with the idea that modulation of its biotransformation could improve efficacy of chronic treatment. The mechanism of GTN-induced dilation is complex and was not identified until more than 100 years after its discovery. GTN is not a direct vasodilator, rather it must be converted to dinitrate products for vasoactivity. Biotransformation to the active metabolite nitric oxide (NO) occurs in parallel with the formation of glycerol-1,2-dinitrate and involves a dithiol-dependent process.1 It was not until recently that the principal enzyme responsible for biotransformation of GTN was identified. Chen et al1 showed that mitochondrial aldehyde dehydrogenase (ALDH-2) metabolizes GTN to glycerol-1,2-dinitrate and nitrite. This was confirmed by Sydow et al2 using mitochondrial-deficient cultured endothelial cells, although a cytosolic source of ALDH-2 has also been suggested.3 The mitochondrial enzyme converts nanomolar concentrations of GTN to active nitrodilator metabolites in vivo and in vitro, as shown by direct measurements coupled with the use …

Magnetic Resonance Imaging of a Posttraumatic Myocardial Infarction and Ventricular Septal Defect With a Closure Device in Place

A 16-year-old boy sustained blunt trauma as a passenger in a high-speed motor vehicle accident 2 years earlier. Before the accident, he was healthy with no known cardiac disease or murmur. On admission after the accident, he was noted to have a loud IV/VI holosystolic murmur along the left sternal border. One month after admission, an echocardiogram revealed a 1.5-cm muscular ventricular septal defect with a left-to-right shunt, enlargement of the right atrium and ventricle, elevated pulmonary arterial pressure, and moderate tricuspid regurgitation (Figure 1 and Movie I). Figure 1. Delayed contrast enhancement in the short-axis plane demonstrates both sides of the …

Percutaneous Transcatheter Balloon Valvuloplasty for Bioprosthetic Tricuspid Valve Stenosis

A 59-year-old woman was admitted to our hospital because of exertional dyspnea, abdominal distension, and leg edema over the past 2 weeks. She had a history of rheumatic fever at the age of 12 years. In 1983, at the age of 37, she had undergone tricuspid valve replacement with a Carpentier-Edwards bioprosthesis for tricuspid stenosis and mitral valve replacement with a mechanical valve for mitral stenosis. The physical examination on admission revealed marked edema in both legs. There was also presystolic pulsation of the liver, which was palpable 4 cm below the right costal margin. A Levine grade III/VI, rough, diastolic rumble at the lower left sternal border was accentuated during inspiration. Echocardiography revealed severe tricuspid stenosis and a large amount of ascites. The leaflets were thickened, …

Roads to Dysfunction

See related article, pages 951–960 Oxidized low-density lipoprotein (oxLDL) is considered to be the strongest proatherogenic lipoprotein. OxLDL is rapidly taken up by endothelial cells and macrophages and via the steps of foam cell formation and cell death, oxLDL eventually accumulates in the lipid core of atherosclerotic plaques.1 The interaction of oxLDL with cells is mediated by several receptors.2 Members of the scavenger receptor family predominate in macrophages,3 whereas endothelial cells mainly take up oxLDL by the lectin-like ox-LDL receptor-1 (LOX-1).4 On binding to LOX-1, oxLDL activates a multitude of signaling cascades involving MAP kinases,5,6 protein kinase C (PKC),7,8 and protein kinase B9 in endothelial cells. The consequence of this cellular activation, is apoptosis and superoxide anion production, the latter originating from the NADPH oxidase and uncoupling of the endothelial NO synthase (eNOS). OxLDL therefore is a strong inducer of endothelial dysfunction, a state in which the endothelium, instead of generating NO, produces superoxide anions. OxLDL also modulates the specific activity of NOS. It increases caveolin I expression and the interaction of NOS with this protein impairs NO production.10 Furthermore, oxLDL modulates PKC activity and expression and this family of kinases has been shown to acutely attenuate eNOS-dependent NO production and to promote eNOS uncoupling during prolonged exposure times.11 Several observations suggest that the supply of eNOS with the substrate l-arginine is impaired in the presence of oxLDL: In hypercholesterolemia, supplementation of l-arginine improves endothelium-dependent relaxation and NO production;12,13 l-arginine also attenuates the development of atherosclerosis,14 and normalizes leukocyte adhesion …

ESC Textbook of Cardiovascular Medicine

John Camm, Thomas F. Luscher, Patrick W. Serruys, eds 1136 pages. Oxford, UK: Blackwell Publishing; 2006. $295. ISBN 1-4051-2695-7 Editor’s Note: In our effort to provide an insightful, balanced, and constructively critical review of the new first edition of the ESC Textbook of Cardiovascular Medicine edited by Drs A. John Camm, Thomas F. Luscher, and Patrick W. Serruys that was published under the auspices of the European Society of Cardiology by Blackwell Publishing Ltd (2006), we have obtained the opinions of 3 distinguished senior cardiologists, Drs Gottlieb Friesinger, Desmond Julian, and Elliot Rapaport, to serve as a Select Panel for Review. To ensure the book was read in its entirety, the text was divided into thirds and apportioned equally to each reviewer; all 3 reviewers were assigned 4 chapters in common to read as well. This summary review by 3 individuals, each of whom is internationally recognized for expertise in the broad field of general cardiology, is offered in the spirit of helping the ESC achieve its stated objective of providing a textbook that is successful in covering the knowledge that should be required of all general cardiologists. ### General Comments This textbook is primarily targeted at the specific audience of those wishing to be accredited with the European Board for Accreditation in Cardiology (EBAC). It is not intended to be a work of reference, but, as stated in the foreword, of producing “a clinically focused resource for general cardiologists and trainees.” It presents 36 chapters within 1092 pages, each authored by anywhere from 2 to 6 multinational collaborating members of the European Society of Cardiology. One of its remarkable achievements in addition to the high standard of writing is its superb illustrations, figures, and tables that appear on virtually every page. They are well placed within the text and contribute in making …

Spontaneous Left Atrial Dissection and Hematoma Mimicking a Cardiac Tumor

A 59-year-old woman with no history of cardiac surgery or thoracic trauma presented to the emergency department with tachycardia and dyspnea. The ECG showed sinus rhythm (110 bpm). X-rays showed interstitial pulmonary edema. Transthoracic echocardiography revealed a mild enlargement of the left atrium (LA), normal left ventricular function, and a large fixed mass occupying almost entirely the LA and arriving just near the posterior mitral annulus. Moderate mitral regurgitation was present. Transesophageal echocardiography confirmed the presence of an inhomogeneous cyst-like mass with a thin hyperechogenic wall coming from …

Coronary Sinus in the Management of Functional Mitral Regurgitation

The past 5 years have seen the introduction into the preclinical arena of myriad devices for the potential treatment of functional and ischemic mitral regurgitation by a percutaneous approach.1 A number of the device concepts have taken advantage of the relatively easy access to the posterior annulus of the mitral valve provided by the coronary sinus. Although attractive on initial consideration as a delivery route for devices that remodel the posterior mitral annulus, a number of potential shortcomings to this approach may ultimately limit its clinical success. Article p 377 Annular remodeling of the mitral valve for functional mitral regurgitation (FMR) has been demonstrated to have short-term and some intermediate-term efficacy in the clinical surgical setting.2 The pathophysiology of FMR in patients with dilated cardiomyopathy is central regurgitation caused by failure of mitral leaflet coaptation. The causes of this malcoaptation are multifactorial and include annular dilatation and ventricular dilation, which cause apical distraction of the papillary muscles, producing tethering of the mitral leaflets. Although the whole annulus has been demonstrated to dilate in FMR, there is a disproportionate increase in the anterior-posterior or septal-lateral diameter.3,4 The basic premise behind the surgical approach is that through the use of an undersized ring to overcorrect the dilation of the mitral annulus, both the annular dilatation and the tethering of the leaflets from apical papillary muscle displacement can be treated. The tenets for optimal surgical …