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PubMed2001

Oral matrix metalloproteinase inhibition and arterial remodeling after balloon dilation: an intravascular ultrasound study in the pig.

BACKGROUND: Inhibition of matrix metalloproteinase (MMP) activity after balloon angioplasty by intraperitoneal injection of batimastat reduces late lumen loss by inhibition of constrictive remodeling. In the present study, we investigated whether the oral MMP inhibitor marimastat inhibits constrictive remodeling in favor of neutral or expansive remodeling. METHODS AND RESULTS: In 26 pigs, balloon dilation was performed in 101 peripheral arteries. Pigs were treated with marimastat or served as controls and were euthanized 42 days after intervention. Intravascular ultrasound was performed at all time points. Vessel area (VA) loss was assessed by calculating the change in VA at termination relative to after intervention. Arteries were divided in 3 categories: expansive remodeling (VA loss < -5%), neutral (-5% +5%). In the marimastat group, a significant reduction (53%) of late lumen loss was observed that was fully explained by impaired constrictive remodeling. In the marimastat group, the prevalence of constrictive remodeling was reduced (38% versus 75% in the control group) in favor of not only neutral but also expansive remodeling (21% and 42% versus 4% and 21% in the control group, respectively, P:<0.01). In contrast to the control group, acute luminal gain in the marimastat group did not correlate with late VA loss. CONCLUSIONS: Irrespective of the acute luminal gain by balloon dilation, the oral MMP inhibitor marimastat inhibited constrictive arterial remodeling in favor of both neutral and expansive remodeling.

Administration, Oral↗

PubMed2004

Small artery remodeling depends on tissue-type transglutaminase.

Remodeling of small arteries is essential in the long-term regulation of blood pressure and blood flow to specific organs or tissues. A large part of the change in vessel diameter may occur through non-growth-related reorganization of vessel wall components. The hypothesis was tested that tissue-type transglutaminase (tTG), a cross-linking enzyme, contributes to the inward remodeling of small arteries. The in vivo inward remodeling of rat mesenteric arteries, induced by low blood flow, was attenuated by inhibition of tTG. Rat skeletal muscle arteries expressed tTG, as identified by Western blot and immunostaining. In vitro, activation of these arteries with endothelin-1 resulted in inward remodeling, which was blocked by tTG inhibitors. Small arteries obtained from rats and pigs both showed inward remodeling after exposure to exogenous transglutaminase, which was inhibited by addition of a nitric oxide donor. Enhanced expression of tTG, induced by retinoic acid, increased inward remodeling of porcine coronary arteries kept in organ culture for 3 days. The activity of tTG was dependent on pressure. Inhibition of tTG reversed remodeling, causing a substantial increase in vessel diameter. In a collagen gel contraction assay, tTG determined the compaction of collagen by smooth muscle cells. Collectively, these data show that small artery remodeling associated with chronic vasoconstriction depends on tissue-type transglutaminase. This mechanism may reveal a novel therapeutic target for pathologies associated with inward remodeling of the resistance arteries.

Amines↗

PubMed2006

Flow-dependent remodeling of small arteries in mice deficient for tissue-type transglutaminase: possible compensation by macrophage-derived factor XIII.

Chronic changes in blood flow induce an adaptation of vascular caliber. Thus, arteries show inward remodeling after a reduction in blood flow. We hypothesized that this remodeling depends on the crosslinking enzyme tissue-type transglutaminase (tTG). Flow-dependent remodeling was studied in wild-type (WT) and tTG-null mice using a surgically imposed change in blood flow in small mesenteric arteries. WT mice showed inward remodeling after 2 days of low blood flow, which was absent in arteries from tTG-null mice. Yet, after continued low blood flow for 7 days, inward remodeling was similar in arteries from WT and tTG-null mice. Studying the alternative pathways of remodeling, we identified a relatively high expression of the plasma transglutaminase factor XIII in arteries of WT and tTG-null mice. In addition, vessels from both WT and tTG-null mice showed the presence of transglutaminase-specific crosslinks. An accumulation of adventitial monocytes/macrophages was found in vessels exposed to low blood flow in tTG-null mice. Because monocytes/macrophages may represent a source of factor XIII, tTG-null mice were treated with liposome-encapsulated clodronate. Elimination of monocytes/macrophages with liposome-encapsulated clodronate reduced both the expression of factor XIII and inward remodeling in tTG-null mice. In conclusion, tTG plays an important role in the inward remodeling of small arteries associated with decreased blood flow. Adventitial monocytes/macrophages are a source of factor XIII in tTG-null mice and contribute to an alternative, delayed mechanism of inward remodeling when tTG is absent.

Adaptation, Physiological↗

PubMed2000

Temporal events underlying arterial remodeling after chronic flow reduction in mice: correlation of structural changes with a deficit in basal nitric oxide synthesis.

To define the cellular events of vascular remodeling in mice, we measured blood flow and analyzed the morphology of remodeled vessels at defined points after a flow-reducing remodeling stimulus for 3, 7, 14, and 35 days. Acute ligation of the left external carotid artery reduced blood flow in the left common carotid artery (LC) compared with sham and contralateral right common carotid arteries (RCs). In morphometric analyses, the decrease in diameter in LCs was reversible by vasodilator perfusion 3 days after ligation, whereas ligation for 7 days or greater resulted in a permanent diameter reduction. Coincident with structural remodeling at day 7 was an increase in cell death in remodeled LCs. Functionally, rings from remodeled LCs contracted to prostaglandin F(2alpha) and relaxed to acetylcholine in a manner identical to that of control arteries. However, remodeled LCs were hypersensitive to the nitrovasodilator sodium nitroprusside (at day 7) and exhibited a marked reduction in basal NO synthesis at 7 and 14 days after ligation. The impairment of endothelial NO synthase function was likely due to post-translational mechanisms, given that endothelial NO synthase mRNA and protein levels did not change in remodeled LCs. These data define the ontogeny of flow-triggered luminal remodeling in adult mice and suggest that endothelial dysfunction occurs during reorganization of the vessel wall.

Animals↗

PubMed2006

Extracellular matrix remodeling by dynamic strain in a three-dimensional tissue-engineered human airway wall model.

Airway wall remodeling is a hallmark of asthma, characterized by subepithelial thickening and extracellular matrix (ECM) remodeling. Mechanical stress due to hyperresponsive smooth muscle cells may contribute to this remodeling, but its relevance in a three-dimensional environment (where the ECM plays an important role in modulating stresses felt by cells) is unclear. To characterize the effects of dynamic compression in ECM remodeling in a physiologically relevant three-dimensional environment, a tissue-engineered human airway wall model with differentiated bronchial epithelial cells atop a collagen gel containing lung fibroblasts was used. Lateral compressive strain of 10 or 30% at 1 or 60 cycles per hour was applied using a novel straining device. ECM remodeling was assessed by immunohistochemistry and zymography. Dynamic strain, particularly at the lower magnitude, induced airway wall remodeling, as indicated by increased deposition of types III and IV collagen and increased secretion of matrix metalloproteinase-2 and -9. These changes paralleled increased myofibroblast differentiation and were fibroblast-dependent. Furthermore, the spatial pattern of type III collagen deposition correlated with that of myofibroblasts; both were concentrated near the epithelium and decreased diffusely away from the surface, indicating some epithelial control of the remodeling response. Thus, in a physiologically relevant three-dimensional model of the bronchial wall, dynamic compressive strain induced tissue remodeling that mimics many features of remodeling seen in asthma, in the absence of inflammation and dependent on epithelial-fibroblast signaling.

Bronchi↗

PubMed2004

Current perspectives of electrical remodeling and its therapeutic implications.

Electrical remodeling involves alterations in the electrophysiologic milieu of myocardium in various disease states, such as ventricular hypertrophy, heart failure, atrial tachyarrhythmias, myocardial ischemia, and infarction that are associated with cardiac arrhythmias. Although research in this area dates back to early part of the 19th century, we still lack the exact knowledge of ionic remodeling, the role of various genes and channel proteins, and their relevance for the newer antiarrhythmic therapies. Structural remodeling may also have an impact on the electrical remodeling process, although differences in both structural and electrical remodeling are associated with different disease states. Various electrophysiologic, cellular, and structural alterations, including anisotropic conduction, increased intracellular calcium levels, and gap junction remodeling predispose to increased dispersion of action potential duration and refractoriness. This constitutes a favorable substrate for early and late afterdepolarizations and reentrant arrhythmias. Studying the role of ionic remodeling in the initiation and propagation of cardiac arrhythmias has significant relevance for developing newer antiarrhythmic therapies, for identifying patients at risk of developing fatal arrhythmias, and for implementing effective preventive measures. Further research is required to understand the specific effects of individual ion channel remodeling, to understand the signal transduction mechanisms, and to address whether detrimental effects of electrical remodeling can be altered.

Action Potentials↗

PubMed2004

[The effect of montelukast on airway remodeling and the expression of interleukins and transforming growth factor-beta2 mRNA].

OBJECTIVE: To study the relation between Interleukin-4 (IL-4), IL-5, IL-13, transforming growth factor-beta(2) (TGF-beta(2)) and airway remodeling and to investigate the effects of Montelukast (MK) on airway inflammation and airway remodeling of asthma. METHODS: Twenty female BALB/c mice were randomly divided into a remodeling group and a treatment group (MK group), with 10 BALB/c mice in each group. The mice were sensitized by ovalbumin (OVA), and only the MK group was treated with MK (15 mg/kg). The number of total cells and eosinophils in bronchoalveolar lavage fluid (BALF) were counted. Light and electronic microscope were used to detect the pathologic histology and morphologic change. In situ hybridization and reverse transcription-polymerase chain reaction (RT-PCR) were used to measure IL-4, L-5, IL-13, and TGF-beta(2) mRNAs in the lung. RESULTS: The numbers of total cells and eosinophils in BALF of the remodeling group were (5.4 +/- 1.1) x 10(5)/ml and 2.32 +/- 0.20, while those of the treatment group were (3.9 +/- 1.6) x 10(5)/ml and 1.64 +/- 0.32, respectively, the difference being significant (P < 0.01). Histological and electronic microscopic examination showed extensive airway inflammation, notably accumulation of significant numbers of eosinophils and lymphocytes in the remodeling group. Other features including prominent proliferation of airway epithelial cells protruded like fingers, increased thickness of smooth muscle, hyperplasia of connective tissue, goblet cell hyperplasia and a marked increase in airway mucus secretion with mucus plugging and extensive collagen deposition around the airways were also noted in the remodeling group. In the treatment group, the inflammation was significantly decreased, with decreased production of mucus, decreased collagen and granule of mucus around airway, less proliferation of airway epithelium, smooth muscle hypertrophy and airway spasm. In situ hybridization showed that the expression of IL-13 mRNA and TGF-beta(2) mRNA in the lung of the remodeling group were 24 +/- 7 and 17 +/- 5 respectively, while those of the treatment group were 17 +/- 4 and 10 +/- 3. RT-PCR results showed that the absorbance of IL-4 mRNA and IL-5 mRNA in the lung of the remodeling group were 0.91 and 0.96, while those of the treatment group were 0.22 and 0.35; the differences between the groups were all significant (all P < 0.01). CONCLUSION: MK could effectively inhibit airway remodeling, which suggests a possible role of cysteinyl leukotrienes in the pathogenesis of chronic allergic inflammation with fibrosis.

Acetates↗

PubMed2005

[Remodelling in atrial fibrillation].

It is well known that atrial fibrillation (AF) tends to become permanent with time as illustrated by the fact that it becomes more difficult to maintain sinus rhythm when AF has been present for a long time. Atrial remodelling plays a part in this process and has been studied in experimental models. Atrial remodelling is defined as all the phenomena occurring during AF contributing to its maintenance. The persistence of AF induced by stimulation in the animal depends on the duration and the repetition of the atrial stimulation and it would appear that "AF induces AF". The tendency for AF to persist is associated with a shortening of the effective atrial refractory period with loss of its adaptation to the heart rate. The determining factor of both electrical and structural remodelling is the rapidity of the atrial rhythm of the AF itself. These phenomena lead to a type L calcium cellular overload as shown by its prevention or attenuation by the administration of verapamil, a calcium antagonist. Electrical remodelling is accompanied by a structural remodelling in the experimental model of persistent AF over several weeks. Samples from the two atria examined by electronic microscopy show mitochondrial changes, an accumulation of glycogen, a deficit in myofibrils, a redistribution of the nuclear chromatim and a reduction of sarcoplasmic reticulum with changes in protein structure. This structural remodelling is a reaction of adaptation similar to that observed in hibernating myocardium during ischaemia and aims to prolong cellular viability by decreasing atrial contractility. Another aspect of structural remodelling is the activation of fibroblasts with formation of fibrosis with resulting heterogeneity of the conduction tissue. There is also an increase in converting enzyme and angiotensin II concentrations. Irbesartan, an angiotensin II antagonist, reduced fibroblast growth. This has clinical applications as shown by the reduction in the recurrences of AF after cardioversion when given in association with amiodarone. Persistent AF leads to left atrial dilatation with abnormal atrial contractility. Further studies are necessary to determine the effect of atrial remodelling which might also act on the foci responsible for inducing the AF. Better understanding of atrial remodelling will contribute to the use of new pharmacological agents to prevent AF.

Atrial Fibrillation↗

PubMed2003

Coronary arterial remodeling in differing clinical presentations of unstable angina pectoris--an intravascular ultrasound study.

BACKGROUND: Coronary arterial remodeling influences the clinical presentation of ischemic heart disease; however, there is little information on the relationship between coronary arterial remodeling and the type of angina pectoris that patients manifest. HYPOTHESIS: The study was undertaken to determine the difference of coronary arterial remodeling in patients with different types of angina pectoris. METHODS: We analyzed 100 patients with ischemic heart disease using intravascular ultrasound (IVUS). Intracoronary IVUS images of proximal reference (PR), distal reference (DR), and target lesion were recorded, and intraluminal area (LA) and external elastic membrane (EEM) were measured. We defined a remodeling index as 100 x (lesion EEM - [PR-EEM + DR-EEM]/2) / ([PR-EEM + DR-EEM]/2). Cases were classified into three groups according to the clinical history (Group 1a: de novo unstable angina pectoris, Group 1b: accelerating unstable angina pectoris, and Group 2; stable angina pectoris). RESULTS: The remodeling index in Group 1a was significantly larger than that in Groups 1b and 2 (18.6 +/- 28.5 vs. 5.3 +/- 27.1 and 18.6 +/- 28.5 vs. -2.7 +/- 17.6, p = 0.0347 and p = 0.0005, respectively), but there was no statistical difference in remodeling index between Groups 1b and 2. CONCLUSIONS: Our results indicate that positive coronary arterial remodeling is more prevalent in patients with new onset of angina pectoris. The specific type of coronary arterial remodeling may affect the clinical presentation of patients with coronary artery disease.

Adult↗

PubMed1994

The bone-remodeling transient: implications for the interpretation of clinical studies of bone mass change.

A computer simulation of the bone-remodeling transient is described, in which the focus is explicitly on changes in clinically measurable bone mass (or density). Based upon quantitative remodeling data accumulated by histomorphometry and calcium tracer kinetics, the simulation shows that much of the apparent gain in bone produced by several agents currently employed to treat osteoporosis can be explained as a remodeling transient rather than as a fundamental alteration of remodeling balance. Even gains as large as 30% or more can be produced by nothing more than the remodeling transient under certain plausible combinations of basal remodeling rate, remodeling period, and degree of bone loss. The simulation further highlights the importance, in evaluating bone-active agents, of separating the response across the first remodeling period from bone changes that may ensue thereafter.

Algorithms↗

PubMed1999

Intracapsular hip fracture: increased cortical remodeling in the thinned and porous anterior region of the femoral neck.

It has been shown previously that the antero-inferior cortex is subjected to maximal tensile stress during a fall onto the greater trochanter. We have recently shown that in cases of femoral neck fracture, cortical thinning and porosity is greatest in the anterior and antero-inferior region of the femoral neck. To investigate whether this is due to increased remodeling, we have quantified surface-based parameters associated with Haversian remodeling in femoral neck biopsies from women with intracapsular hip fracture and post-mortem controls. Cryostat sections of chilled biopsies were reacted for either tartrate-resistant acid phosphatase (TRAP) or alkaline phosphatase (ALP) activity. Proportions of active canals were determined in each quadrant (inferior, anterior, superior, posterior) of the femoral neck. The biopsies were then embedded in methacrylate to permit histomorphometry using Goldner's and Solochrome sections. In the cases there was no significant increase in the proportion of canals undergoing remodeling in the cortex as a whole (p = 0.846), but the regional distribution of remodeling was markedly different from that in the controls. In the anterior cortex, the proportion of canals undergoing remodeling was increased by 56% (p = 0.0087); in contrast there was a relative decrease of 35% in the superior region (p = 0.0047). In the anterior cortex of cases there were 76% and 42% increases in the proportions of eroded (p = 0.019) and osteoid-bearing (p = 0.041) canals, respectively. In the superior region, the decrease in the proportion of remodeling sites was due to a marked decrease in canals with an osteoid surface (51%; p = 0.0031). Covariance analysis with cortical porosity as the dependent variable showed that porosity was significantly dependent on the regional distribution of eroded (p = 0.033) but not on the distribution of forming (p = 0.153) canals (R(2)adj = 0.51). Cellular levels of TRAP and ALP were significantly elevated in the anterior region of cases compared with the controls (TRAP 55%, p = 0.006; ALP 36%, p = 0.003). For the posterior and inferior regions there were no marked differences in cellular TRAP and ALP levels compared with control values. These data show that the increased cortical thinning and increased porosity we have previously observed in the anterior cortex in cases of hip fracture are associated with increased indices of Haversian remodeling. These findings are consistent with the hypothesis that, in cases of hip fracture, remodeling imbalance in the anterior cortex is a continuing process up to the time of fracture and is due to increased osteoclastic cellular activity associated with an osteoblastic response that is inadequate to prevent bone loss.

Acid Phosphatase↗

PubMed2006

K(ATP) channel current increases in postinfarction remodeled cardiomyocytes.

Adenosintriphosphate-sensitive potassium channels (K(ATP) channels) are an important linkage between the metabolic state of a cell and electrophysiological membrane properties. In this study, K(ATP) channels were studied in myocytes of normal and remodeled myocardium of the rat. Myocardial infarction was induced by ligature of the left anterior descending artery. Remodeled myocytes were obtained from the hypertrophied posterior left ventricular wall and interventricular septum 3 months after infarction. The current through K(ATP) channels was measured in whole-cell and inside-out patches by using the patch-clamp technique. After myocardial infarction, the heart weight/body weight ratio was doubled and the myocytes were hypertrophied yielding a cell capacitance of 266+/-16 pF compared to 122+/-12 pF in control cells. The amount of Kir6.2 protein was indistinguishable in corresponding regions of control and remodeled hearts. The ATP sensitivity of K(ATP) channels in remodeled cells was significantly lower than in control cells (half maximum block at 115 micromol/l ATP in remodeled and at 71 mumol/l ATP in control cells). The maximum I (KATP) density induced by metabolic inhibition was higher in small remodeled (176+/-15 pA/pF) than in control cells (127+/-11 pA/pF), but was unchanged in large remodeled cells. Both, the higher I (KATP) density and the lower sensitivity of the K(ATP) channels to ATP suggest that remodeled cardiomyocytes develop an improved tolerance to ischemia by stabilizing the resting potential and decreasing excitability.

Adaptation, Physiological↗

PubMed1996

Bone remodelling adjacent to intramedullary stems: an optimal structures approach.

The internal parameters in bone remodelling theories often are not clearly related to the bony structure which results from the simulations in which they are implemented. For a restricted class of bone remodelling theories, we have previously found a connection between overall structural optimization and the parameters within a continuum-level remodelling rule. In this study, we assess whether a simplified analytical formula based on structural optimization can predict the behaviour of a large-scale finite element bone remodelling simulation. The analytical formula predicts when bone will remain around an intramedullary implant. The predictions of the formula are borne out in the numerical results. This leads to a physical interpretation of one of the two parameters in the remodelling rule used. The results also show some characteristics which are clinically relevant. This study extends earlier results due to Huiskes for internal remodelling around intramedullary implants by using a different, numerically stable remodelling algorithm based on optimization. The study also shows a direct practical application of the optimizing remodelling theory the authors have developed previously.

Biomechanical Phenomena↗

PubMed1991

Bone remodeling in W/Wv mast cell deficient mice.

Strong experimental evidence exists for a relationship between mast cells and bone disease, but the role of mast cells in the regulation of bone remodeling is unknown. In order to address this question, mast cell deficient mice (W/Wv) were paired with their mast cell sufficient (+/+) littermates and evaluated for differences in response to an induced cycle of bone remodeling. This was achieved using a tooth egression protocol, in which a synchronous cycle of bone remodeling was induced in the mandibular buccal alveolar periosteum by extraction of the opposing dentition. Quantitative histomorphometric changes during the activation, resorption, reversal, and formation phases of bone remodeling were documented using standard techniques. Most cell deficient mutants exhibited the following defects in response to an induced cycle of bone remodeling: (a) the onset of the remodeling cycle was delayed by a prolonged activation phase, (b) the duration and extent of the active formation phase was decreased, and (c) the amount of new bone matrix synthesized was diminished while mineralization rates were found to be normal. These results suggest that mast cells and their mediators provide a paracrine mechanism which influences the recruitment of osteoclast and osteoblast progenitors and their participation in bone remodeling. Nonetheless, since bone remodeling occurs in mast cell deficient mice, albeit less efficiently, this mechanism is most likely one of several redundant mechanisms that provide for adequate skeletal homeostasis.

Animals↗

PubMed2004

Ventricular remodeling in heart failure and the effect of beta-blockade.

Left ventricular (LV) remodeling has an important role in the progression of cardiovascular disease. An understanding of the process of LV remodeling has led to greater knowledge of the pathophysiology of heart failure. Drug therapies that slow or reverse the remodeling process seem to have favorable natural history effects in short-term and long-term therapy. Angiotensin-converting enzyme (ACE) inhibitors have been associated with a significant reduction in mortality, and the effect of beta-blockers on the remodeling process has now been studied across much of the spectrum of severity in patients with heart failure. beta-Blockade seems to add favorable and independent effects on the post-myocardial infarction remodeling process over and above those of ACE inhibitors. A combination of both drugs shows the greatest reduction in mortality (ie, the most favorable reverse remodeling). Differences in their effect on remodeling have been recently shown among the beta-blockers. Several studies and a meta-analysis suggest that carvedilol may be more favorable to outcome, having the most effect on LV remodeling.

Adrenergic beta-Antagonists↗

PubMed2006

Ischemic postconditioning protects remodeled myocardium via the PI3K-PKB/Akt reperfusion injury salvage kinase pathway.

OBJECTIVE: We tested whether ischemic postconditioning (IPostC) is protective in remodeled myocardium. METHODS: Post-myocardial infarct (MI)-remodeled hearts after permanent coronary artery ligation and one kidney one clip (1K1C) hypertensive hearts of male Wistar rats were exposed to 40 min of ischemia followed by 90 min of reperfusion. IPostC was induced by six cycles of 10 s reperfusion interspersed by 10 s of no-flow ischemia. Activation of reperfusion injury salvage kinases was measured using Western blotting and in vitro kinase activity assays. RESULTS: IPostC prevented myocardial damage in both MI-remodeled and 1K1C hearts, as measured by decreased infarct size and lactate dehydrogenase release, and improved function. The reduction in infarct size and the recovery of left ventricular contractility achieved by IPostC was less in 1K1C hearts, but was unchanged in MI-remodeled hearts when compared to healthy hearts. In contrast, the recovery of inotropy was unaffected in 1K1C hearts, but was less in MI-remodeled hearts. Inhibition of the phosphatidylinositol 3-kinase (PI3K) pathway with LY294002 abolished the protective effects of IPostC on both disease models and healthy hearts. Western blot analysis in conjunction with in vitro kinase activity assays identified protein kinase B (PKB)/Akt but not p42/p44 extracellular-signal regulated kinase 1/2 (ERK1/2) as the predominant kinase in IPostC-mediated cardioprotection in remodeled hearts. IPostC increased phosphorylation of the PKB/Akt downstream targets eNOS, GSK3beta, and p70S6K in remodeled hearts. CONCLUSION: Our results offer evidence that IPostC mediates cardioprotection in the remodeled rat myocardium primarily via activation of the PI3K-PKB/Akt reperfusion injury salvage kinase pathway.

Actins↗

PubMed2005

Principles of fracture remodeling in children.

In treating fractures in children, the surgeon must have a good knowledge of the three phases of bone healing, ie, inflammatory, reparative, and remodeling and understand how they contribute to the final recovery of the fracture healing process. By and large, the ability to remodel depends on the bone involved, the patient's age, the proximity to the joint, and its orientation to the joint axis. In the typical long bone, 75% of the remodeling occurs by reorientation of the physis while appositional remodeling of the diaphysis can only be expected to contribute 25% to the remodeling process. The various values of acceptable alignment for each of the major fracture patterns are outlined. These serve only as guidelines. The patient's functional capacity and the surgeon's experience should also be factors in determining whether to depend on the remodeling capacity of the specific fracture or to consider performing a more aggressive, invasive technique to achieve a satisfactory result. There are two advantages in treating children's fractures. First, the healing process is very rapid. Nonunion is a rare event in the pediatric age group. The second perk is that there is a very good remodeling capacity should there be less than anatomical alignment of the affected bone once the fracture has healed. Any individual treating fractures in the pediatric age group should fully understand how pediatric fractures heal and how the remodeling process occurs.

Arm Injuries↗

PubMed2005

Surgical treatment of ischemic mitral regurgitation might not influence ventricular remodeling.

OBJECTIVES: Surgical treatment for ischemic mitral regurgitation has become more aggressive. However, no clinical study has demonstrated that surgical correction of chronic ischemic mitral regurgitation improves survival. We used 4 well-developed ovine models of postinfarction left ventricular remodeling to test the hypothesis that ischemic mitral regurgitation does not significantly contribute to postinfarction left ventricular remodeling. METHODS: Infarction of 21% to 24% of the left ventricular mass was induced by means of coronary ligation in 77 sheep. Infarctions varied only by anatomic location in the left ventricle: anteroapical, n = 26; anterobasal, n = 16; laterobasal, n = 9; and posterobasal, n = 20. Six additional sheep had ring annuloplasty before posterobasal infarction. End-systolic and end-diastolic left ventricular volume, end-systolic muscle-to-cavity area ratio, left ventricular sphericity, ejection fraction, and degree of ischemic mitral regurgitation, as determined by means of quantitative echocardiography, were assessed before infarction and at 2, 5, and 8 weeks after infarction. RESULTS: All infarcts resulted in significant postinfarction remodeling and decreased ejection fraction. Anteroapical infarcts lead to left ventricular aneurysms. Only posterobasal infarcts caused severe and progressive ischemic mitral regurgitation. Remodeling because of posterobasal infarcts was not more severe than that caused by infarcts at other locations. Furthermore, prophylactic annuloplasty prevented the development of mitral regurgitation after posterobasal infarction but had no effect on remodeling. CONCLUSION: The extent of postinfarction remodeling is determined on the basis of infarct size and location. The development of ischemic mitral regurgitation might not contribute significantly to adverse remodeling. Ischemic mitral regurgitation is likely a manifestation rather than an important impetus for postinfarction remodeling.

Animals↗