Editorial: Defining The Relationship Between Akinesia And Dyskinesia And The Cause Of Left Ventricular Failure After Anterior Infarction And Reversal Of Remodeling To Restoration

AbstractJ Thorac Cardiovasc Surg 1998;116:47-

Left Ventricular Form and Function - Scientific Priorities and Strategic Planning for Development of New Views of Disease

Heart failure continues to be one of the most costly and prevalent medical problems. The increasing age of our population and the increased survival of patients with diseases that lead to heart failure will no doubt further magnify this very serious health problem at a staggering cost, both monetary and human. To address this public health concern, a fuller understanding of what constitutes normal cardiac function is essential to recognize optimal goals for restoration after disease disrupts stability. From micro to macro, our limited understanding of the heart’s function continues to represent an obstacle to our ability to design strategies for effective treatment of heart failure. Thus, there is a critical need to address the existing and emerging issues in this area to develop new safe and effective strategies to address the clinical challenges facing cardiologists and cardiothoracic surgeons. As a result of this need, the National Heart, Lung, and Blood Institute convened a workshop entitled “Form and Function: New Views on Development, Diseases, and Therapies for the Heart” on April 25 to 26, 2002, in Bethesda, Maryland. The objective was an effort to understand the importance of structure/function relationships of the intact ventricles from both the basic science and clinical perspectives, to define where progress is most urgently needed, and to plan research programs that will most effectively integrate understanding of functional geometry into therapy of human heart disease

Right ventricular architecture responsible for mechanical performance: Unifying role of ventricular septum

The right ventricle (RV) is composed of a free wall containing a wrap-around circumferential muscle at its base and a septum composed of helical fibers that are oblique and cross each other at 60° angles. This structure is defined by the helical ventricular myocardial band and defines RV function because the wrap-around transverse fibers constrict or compress to cause the bellows motion responsible for 20% of RV output, whereas the oblique fibers determine shortening and lengthening that produces 80% of RV systolic function. Clinical shortening is quantified by tricuspid annular plane systolic excursion and measured by echocardiography. Destruction of the free wall by electrocautery or patch replacement does not alter RV function if the septum is intact. Conversely, septal damage causes RV dysfunction if pulmonary vascular resistance is increased. The interaction between structure and function to cause RV failure and how these factors become corrected is defined for RV failure, RV relationship to LV failure, resynchronization, pacing, RV dysplasia, left ventricular assist device, intraoperative septal injury during myocardial protection, the septal role in tricuspid insufficiency, pharmacologic decisions on altering pulmonary vascular resistance in RV failure, congenital heart disease, and adult heart disease is considered in this overview. These structure–function relationships emphasize why clinical decisions must be based on knowledge of normality, recognizing how disease offsets normality, and introducing actions that rebuild normality

Left ventricle remodelling by double-patch sandwich technique

BACKGROUND: The sandwich double-patch technique was adopted as an alternative method for reconstruction of the left ventricle after excision of postinfarction dysfunctional myocardium to solve technical problems due to the thick edges of the ventricular wall. METHODS: Over a 5-year period, 12 of 21 patients with postinfarction antero-apical left ventricular aneurysm had thick wall edges after wall excision. It was due to akinetic muscular thick tissue in 6 cases, while in the other 6 with classic fibrous aneurysm, thick edges remained after the cut of the border zone. The ventricular opening was sandwiched between two patches and this is a technique which is currently used for the treatment of the interventricular septum rupture. In our patients the patches are much smaller than the removed aneurysm and they were sutured simply by a single row of single stitches. However, in contrast to interventricular septum rupture where the patches loosen the tension of the tissues, in our patients the patches pull strongly and restrain the walls by fastening their edges and supporting tight stitches. In this way they could narrow the cavity and close the ventricle. RESULTS: The resected area varied from 5 × 4 to 8 × 8 cm. Excision was extended into the interventricular septum in 5 patients, thus opening the right ventricle. CABG was performed on all patients but two. Left ventricular volumes and the ejection fraction changed significantly: end-systolic volume 93.5 ± 12.4 to 57.8 ± 8.9 ml, p < 0.001; end-diastolic volume 157.2 ± 16.7 to 115.3 ± 14.9 ml, p < 0.001; ejection fraction 40.3 ± 4.2 to 49.5 ± 5.7%, p < 0.001. All patients did well. One patient suffered from bleeding, which was not from the wall suture, and another had a left arm paresis. The post-operative hospital stay was 5 to 30 days with a mean 10.5 ± 7.5 days/patient. At follow-up, 9 to 60 months mean 34, all patients were symptom-free. NYHA class 2.5 ± 0.8 changed to 1.2 ± 0.4, p < 0.001. CONCLUSION: The double-patch sandwich technique (bi-patch closure) offers some advantages and does not result in increased morbidity and mortality. In the case of excising a left ventricular aneurysm, this technique in no way requires eversion of the edges, felt strips, buttressed and multiple sutures, all of which are needed for longitudinal linear closure. Moreover, it does not require purse string sutures, endocardial scar remnant to secure the patch or folding the excluded non-functional tissue, all of which are needed for endoventricular patch repair

Structure-based finite strain modelling of the human left ventricle in diastole

Finite strain analyses of the left ventricle provide important information on heart function and have the potential to provide insights into the biomechanics of myocardial contractility in health and disease. Systolic dysfunction is the most common cause of heart failure; however, abnormalities of diastolic function also contribute to heart failure, and are associated with conditions including left ventricular hypertrophy and diabetes. The clinical significance of diastolic abnormalities is less well understood than systolic dysfunction, and specific treatments are presently lacking. To obtain qualitative and quantitative information on heart function in diastole, we develop a three-dimensional computational model of the human left ventricle that is derived from noninvasive imaging data. This anatomically realistic model has a rule-based fibre structure and a structure-based constitutive model. We investigate the sensitivity of this comprehensive model to small changes in the constitutive parameters and to changes in the fibre distribution. We make extensive comparisons between this model and similar models that employ different constitutive models, and we demonstrate qualitative and quantitative differences in stress and strain distributions for the different constitutive models. We also provide an initial validation of our model through comparisons to experimental data on stress and strain distributions in the left ventricle

Optimizing Electrode Placement for Hemodynamic Benefit in Cardiac Resynchronization Therapy

Background: Research is needed to explore the relative benefits of alternative electrode placements in biventricular and left ventricular pacing for heart failure with left bundle branch block (LBBB). Methods: A fast computational model of the left ventricle, running on an ordinary laptop computer, was created to simulate the spread of electrical activation over the myocardial surface, together with the resulting electrocardiogram, segmental wall motion, stroke volume, and ejection fraction in the presence of varying degrees of mitral regurgitation. Arbitrary zones of scar and blocked electrical conduction could be modeled. Results: Simulations showed there are both sweet spots and poor spots for left ventricular electrode placement, sometimes separated by only a few centimeters. In heart failure with LBBB pacing at poor spots can produce little benefit or even reduced pumping effectiveness. Pacing at sweet spots can produce up to 35% improvement in ejection fraction. Relatively larger benefit occurs in dilated hearts, in keeping with the greater disparity between early and late activated muscle. Sweet spots are typically located on the basal to mid-level, inferolateral wall. Poor spots are located on or near the interventricular septum. Anteroapical scar with conduction block causes little shift in locations for optimal pacing. Hearts with increased passive ventricular compliance and absence of pre-ejection mitral regurgitation exhibit greater therapeutic gain. The durations and wave shapes of QRS complexes in the electrocardiogram can help predict optimum electrode placement in real time. Conclusions: Differences between poor responders and hyper-responders to cardiac resynchronization therapy can be understood in terms of basic anatomy, physiology, and pathophysiology. Computational modeling suggests general strategies for optimal electrode placement. In a given patient heart size, regional pathology, and regional dynamics allow individual pre-treatment planning to target optimal electrode placement

Studies of hypoxemic/reoxygenation injury: With aortic clamping XIII. Interaction between oxygen tension and cardioplegiccomposition in limiting nitric oxide production and oxidant damage

AbstractThis study tests the interaction between oxygen tension and cardioplegic composition on nitric oxide production and oxidant damage during reoxygenation of previously cyanotic hearts. Of 35 Duroc-Yorkshire piglets (2 to 3 weeks, 3 to 5 kg), six underwent 30 minutes of blood cardioplegic arrest with hyperoxemic (oxygen tension about 400 mm Hg), hypocalcemic, alkalotic, glutamate/aspartate blood cardioplegic solution during 1 hour of cardiopulmonary bypass without hypoxemia (control). Twenty-nine others were subjected to up to 120 minutes of ventilator hypoxemia (oxygen tension about 25 mm Hg) before reoxygenation on CPB. To simulate routine clinical management, nine piglets underwent uncontrolled cardiac reoxygenation , whereby cardiopulmonary bypass was started at oxygen tension of about 400 mm Hg followed by the aforementioned blood cardioplegic protocol 5 minutes later. All 20 other piglets underwent controlled cardiac reoxygenation , whereby cardiopulmonary bypass was started at the ambient oxygen tension (about 25 mm Hg), and reoxygenation was delayed until blood cardioplegia was given. The blood cardioplegia solution was kept normoxemic (oxygen tension about 100 mm Hg) in 10 piglets and made hyperoxemic (oxygen tension about 400 mm Hg) in 10 others. The cardioplegic composition was also varied so that the cardioplegic solution in each subgroup contained either KCl only (30 mEq/L) or components that theoretically inhibit nitric oxide synthase by including hypocalcemia, alkalosis, and glutamate/aspartate. Function (end-systolic elastance) and myocardial nitric oxide production, conjugated diene production, and antioxidant reserve capacity were measured. Blood cardioplegic arrest without hypoxemia did not cause myocardial nitric oxide or conjugated diene production, reduce antioxidant reserve capacity, or change left ventricular functional recovery. In contrast, uncontrolled cardiac reoxygenation raised nitric oxide and conjugated diene production 19- and 13-fold, respectively ( p < 0.05 vs control), reduced antioxidant reserve capacity 40%, and contractility recovered only 21% of control levels. After controlled cardiac reoxygenation at oxygen tension about 400 mm Hg with cardioplegic solution containing KCl only, nitric oxide and conjugated diene production rose 16- and 12-fold, respectively ( p < 0.05 vs control), and contractility recovered only 43% ± 5%. Normoxemic (oxygen tension of about 100 mm Hg) controlled cardiac reoxygenation with the same solution reduced nitric oxide and conjugated diene production 85% and 71%, and contractile recovery rose to 55% ± 7% ( p < 0.05 vs uncontrolled reoxygenation). In comparison, controlled cardiac reoxygenation with an oxygen tension of about 400 mm Hg hypocalcemic, alkalotic, glutamate/aspartate blood cardioplegic solution reduced nitric oxide and conjugated diene production 85% and 62%, respectively, and contractility recovered 63% ± 4% ( p < 0.05 vs KCl only). Normoxemic delivery of this solution resulted in negligible nitric oxide and conjugated diene production and 83% ± 8% recovery of contractility ( p < 0.05 vs all other groups). These data show correlation between nitric oxide production during initial reoxygenation and the extent of oxidant damage (i.e., conjugated diene production) and link functional recovery to suppression of excessive nitric oxide production and limitation of lipid peroxidation by the interaction of oxygen tension and cardioplegic composition during initial reoxygenation. (J THORAC CARDIOVASC SURG 1995; 110:1274-86