Jeffrey J. Silbiger

Mechanistic Insights into Ischemic Mitral Regurgitation: Echocardiographic and Surgical Implications

Ischemic mitral regurgitation is a common complication of the healing phase of myocardial infarction. A number of mechanisms have been invoked in its pathogenesis, including alterations of papillary muscle position, annular dynamics, and intraventricular synchrony. The echocardiographic hallmark of ischemic mitral regurgitation is systolic tethering of the mitral valve leaflets away from the annular plane. A number of leaflet tethering parameters have been described (tenting height and area, leaflet angles) that provide insight into the mechanism of tethering as well as prognostic information about the durability of mitral valve repair. Restrictive annuloplasty and coronary artery revascularization promote reverse remodeling and remain the most common surgical treatment. Innovative subannular therapies and a number of percutaneous interventions are under investigation.

Anatomy, mechanics, and pathophysiology of the mitral annulus

The mitral annulus plays an important role in leaflet coaptation, in unloading mitral valve closing forces, and in promoting left atrial and left ventricular filling and emptying. Perturbations of annular mechanics figure prominently in a number of disorders including functional and ischemic mitral regurgitation, mitral valve prolapse, atrial fibrillation, mitral annular calcification, and annular submitral aneurysm. This review discusses the role of annular dysfunction in the pathogenesis of these disorders.

Contemporary insights into the functional anatomy of the mitral valve

The mitral valve is a highly complex structure the normal functioning of which requires the coordinated interaction of the leaflets, annulus, chordae tendineae, and papillary muscles. Perturbations of any of these components can interfere with normal valve function. The integrity of the mitral valve is also essential to maintaining normal left ventricular geometry and function through closely coupled ventricular-valvular interactions. This review summarizes recent developments in our understanding of the anatomy and physiology of the mitral valve.

The Cardiac Manifestations of Antiphospholipid Syndrome and Their Echocardiographic Recognition

Antiphospholipid syndrome is an autoimmune disorder characterized by the presence of antiphospholipid antibodies, hypercoagulability, vascular thrombosis, and recurrent fetal loss. Cardiac involvement occurs frequently. Leaflet thickening and vegetations are detected quite often echocardiographically, but hemodynamically significant stenotic and/or regurgitant valvular disease is uncommon. Antiphospholipid syndrome can also cause left and right ventricular systolic and diastolic dysfunction as well as pulmonary hypertension. Other findings include spontaneous echo contrast and in situ mural thrombosis. In this review, the author discusses the major cardiac manifestations of antiphospholipid syndrome and highlights the role of echocardiography in their detection.

Novel pathogenetic mechanisms and structural adaptations in ischemic mitral regurgitation.

Ischemic mitral regurgitation (MR) is a common complication of myocardial infarction thought to result from leaflet tethering caused by displacement of the papillary muscles that occurs as the left ventricle remodels. The author explores the possibility that left atrial remodeling may also play a role in the pathogenesis of ischemic MR, through a novel mechanism: atriogenic leaflet tethering. When ischemic MR is hemodynamically significant, the left ventricle compensates by dilating to preserve forward output using the Starling mechanism. Left ventricular dilatation, however, worsens MR by increasing the mitral valve regurgitant orifice, leading to a vicious cycle in which MR begets more MR. The author proposes that several structural adaptations play a role in reducing ischemic MR. In contrast to the compensatory effects of left ventricular enlargement, these may reduce, rather than increase, its severity. The suggested adaptations involve the mitral valve leaflets, the papillary muscles, the mitral annulus, and the left ventricular false tendons. This review describes the potential role each may play in reducing ischemic MR. Therapies that exploit these adaptations are also discussed.

The Gerbode defect: left ventricular to right atrial communication-anatomic, hemodynamic, and echocardiographic features.

Left ventricular to right atrial (LV–RA) communications were first described in the 19th century by Thurman.1 It was not until 1958, however, that interest in this lesion was renewed following the publication by Gerbode et al.2 of a series of five patients who underwent successful surgical repair. We present herein a case of an acquired Gerbode defect discovered in a young female during pregnancy. A 30-year-old asymptomatic female was referred to our hospital’s cardiology clinic for evaluation of a murmur discovered by her obstetrician in her 18th week of an otherwise uncomplicated pregnancy. At the age of 17, the patient underwent operative repair of a perimembranous ventricular septal defect (VSD). She remained asymptomatic postoperatively and did not seek medical attention until she became pregnant. On examination, there was wide splitting of the second heart sound and a grade 3/6 systolic murmur which was best heard along the left sternal border. A 12-lead electrocardiogram demonstrated normal sinus rhythm at 75 beats per minute with an incomplete right bundle branch block.

Left ventricular false tendons: anatomic, echocardiographic, and pathophysiologic insights.

Left ventricular (LV) false tendons are chordlike structures that traverse the LV cavity. They attach to the septum, to the papillary muscles, or to the free wall of the ventricle but not to the mitral valve. They are found in approximately half of human hearts examined at autopsy. Although it has been more than 100 years since their initial description, the functional significance of these structures remains largely unexplored. It has been suggested that they retard LV remodeling by tethering the walls to which they are attached, but there are few data to substantiate this. Some studies have suggested that false tendons reduce the severity of functional mitral regurgitation by stabilizing the position of the papillary muscles as the left ventricle enlarges. LV false tendons may also have deleterious effects and have been implicated in promoting membrane formation in discrete subaortic stenosis. This article reviews current understanding of the anatomy, echocardiographic characteristics, and pathophysiology of these structures.

Atheroscerlotic heart disease in Bangladeshi immigrants: risk factors and angiographic findings

BACKGROUND The prevalence of coronary artery disease (CAD) among Bangladeshis greatly exceeds that of Caucasians. Bangladeshis also suffer from premature onset, clinically aggressive and angiographically extensive disease. The role of conventional CAD risk factors (CCRFs) has been questioned. We therefore sought to determine if the CCRFs of Bangladeshis differed from non-Bangladeshis. We also sought to determine whether CAD was more extensive in Bangladeshis and if Bangladeshi ethnicity was independently predictive of extensive i.e., 3-vessel CAD at angiography. METHODS We reviewed the coronary angiograms and medical records of 75 Bangladeshis and 57 non-Bangladeshis presenting with myocardial infarction or angina pectoris. RESULTS Bangladeshis were younger (56.1 vs. 62.4 years, p=.001), had a lower body-mass index (25.2 vs. 27.2 kg/m(2), p=.017) and were less likely to be current or recent smokers (40% vs. 58%, p=.041) than non-Bangladeshis. There were no statistically significant differences in the proportion of subjects in the 2 groups with respect to diabetes mellitus, dyslipidemia, hypertension or family history of CAD. Bangladeshis had twice the rate of 3-vessel CAD of non-Bangladeshis (53% vs. 26%, p=.002). Bangladeshi ethnicity was independently associated with >3X the likelihood of having 3-vessel CAD at angiography (p=.011). CONCLUSIONS This study demonstrated that the CCRF burden of Bangladeshis with CAD is not excessive compared to that of non-Bangladeshis and is therefore unlikely to account for the excessive CAD risk found in this cohort. We also conclude that Bangladeshis have more angiographically extensive CAD than non-Bangladeshis and that Bangladeshi ethnicity is independently predictive of 3-vessel disease.

Abnormalities of the Mitral Apparatus in Hypertrophic Cardiomyopathy: Echocardiographic, Pathophysiologic, and Surgical Insights

Hypertrophic cardiomyopathy is a genetic disorder characterized by increased cardiac muscle mass. This disorder has broad phenotypic expression, including, among others, asymmetric septal hypertrophy, midcavity hypertrophy, and apical hypertrophy. In recent years, it has been recognized that hypertrophic cardiomyopathy is not characterized solely by ventricular hypertrophy but that a number of abnormalities of the mitral apparatus (papillary muscles, leaflets, chords, and annulus) may also occur. These figure prominently in the echocardiographic evaluation and surgical planning of patients with hypertrophic cardiomyopathy and serve as the focus of this review.

Does left atrial enlargement contribute to mitral leaflet tethering in patients with functional mitral regurgitation? Proposed role of atriogenic leaflet tethering.

Papillary muscle repositioning due to left ventricular remodeling is thought to be the primary mechanism responsible for functional mitral regurgitation. This article proposes that remodeling (enlargement) of the left atrium also plays a role in the pathogenesis of functional mitral regurgitation, through a novel mechanism–atriogenic leaflet tethering–described herein.