Article

Left Ventricular Remodeling in Heart Failure Current Concepts in Clinical Significance and Assessment

Tufts University, Бостон, Georgia, United States
JACC. Cardiovascular imaging (Impact Factor: 7.19). 01/2011; 4(1):98-108. DOI: 10.1016/j.jcmg.2010.10.008
Source: PubMed

ABSTRACT

Ventricular remodeling, first described in animal models of left ventricular (LV) stress and injury, occurs progressively in untreated patients after large myocardial infarction and in those with dilated forms of cardiomyopathy. The gross pathologic changes of increased LV volume and perturbation in the normal elliptical LV chamber configuration is driven, on a histologic level, by myocyte hypertrophy and apoptosis and by increased interstitial collagen. Each of the techniques used for tracking this process-echocardiography, radionuclide ventriculography, and cardiac magnetic resonance-carries advantages and disadvantages. Numerous investigations have demonstrated the value of LV volume measurement at a single time-point and over time in predicting clinical outcomes in patients with heart failure and in those after myocardial infarction. The structural pattern of LV remodeling and evidence of scarring on cardiac magnetic resonance have additional prognostic value. Beyond the impact of abnormal cardiac structure on cardiovascular events, the relationship between LV remodeling and clinical outcomes is likely linked through common local and systemic factors driving vascular as well as myocardial pathology. As demonstrated by a recent meta-analysis of heart failure trials, LV volume stands out among surrogate markers as strongly correlating with the impact of a particular drug or device therapy on patient survival. These findings substantiate the importance of ventricular remodeling as central in the pathophysiology of advancing heart failure and support the role of measures of LV remodeling in the clinical investigation of novel heart failure treatments.

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    • "Limitations of the conventional research paradigm are clearly reflected by the limited number of areas of relative success in heart failure treatment, such as angiotensin converting enzyme inhibitors, β-blockers, aldosterone antagonists, coronary revascularization, heart transplantation, and mechanical devices. While it is true that description of remodelling after myocardial infarction, for example, was first deciphered from experimental work in rodents by Pfeffer and Braunwald [22] (showing that there was a dynamic process post-myocardial infarction that was amenable to being altered in rodents) and was subsequently confirmed in human patients [23] such studies are the exception, not the norm. In reality, the vast majority of basic science experiments have not provided valuable insight into the limited success in heart failure treatment seen to date. "
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    ABSTRACT: Heart failure remains a leading cause of death and it is a major cause of morbidity and mortality affecting tens of millions of people worldwide. Despite decades of extensive research conducted at enormous expense, only a handful of interventions have significantly impacted survival in heart failure. Even the most widely prescribed treatments act primarily to slow disease progression, do not provide sustained survival advantage, and have adverse side effects. Since mortality remains about 50% within five years of diagnosis, the need to increase our understanding of heart failure disease mechanisms and development of preventive and reparative therapies remains critical. Currently, the vast majority of basic science heart failure research is conducted using animal models ranging from fruit flies to primates; however, insights gleaned from decades of animal-based research efforts have not been proportional to research success in terms of deciphering human heart failure and developing effective therapeutics for human patients. Here we discuss the reasons for this translational discrepancy which can be equally attributed to the use of erroneous animal models and the lack of widespread use of human-based research methodologies and address why and how we must position our own species at center stage as the quintessential animal model for 21(st) century heart failure research. If the ultimate goal of the scientific community is to tackle the epidemic status of heart failure, the best way to achieve that goal is through prioritizing human-based, human-relevant research.
    Full-text · Article · Nov 2015 · American Journal of Translational Research
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    • "Subsequent left ventricular dilation by a diffuse myocyte hypertrophy appears associated with a major apoptosis and a major deposition of interstitial collagen. Figure illustration by Craig Skaggs (Adapted from Konstam et al. 2011) "
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    ABSTRACT: Multiple biomarkers have helped us to understand the pathophysiology of cardiovascular medicine, being ischemic heart disease and heart failure the most active fields in which biomarkers have shown to be useful. Furthermore, in several cardiovascular diseases, as heart failure, hypertrophic or dilated cardio-myopathies have demonstrated the presence of remodeling in both ventricles, with mainly changes in the extracellular matrix. The initial post-MI phase of left ventricular remodeling is resulted from a fibrotic repair of the necrotic area with scar formation, elongation, and thinning of the infarcted zone. This book chapter summarizes a review about biomarkers of necrosis and myocardial remodeling and all the knowledge that their study has improved the complex role of this cardiac pathology. The continued research of new molecules that helped us to understand necrosis and remodeling focuses our attention in different groups of biomarkers as troponins, growth factors, matrix metalloproteinases, and collagen peptides. This chapter is also focused on how the renin-angiotensin system influences the cardiac remodeling and the role of microRNAs in extracellular changes.
    Full-text · Chapter · Aug 2015
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    • "Myocardial infarction occurs when blood flow to the heart muscle is lowered and the myocardial cells in the territory start dying. The local contractility is reduced and can lead, if prolonged, to severe remodelling of the heart to maintain physiological constraints [1]. The function of the heart is then impaired [2], and is no longer able to pump as efficiently as it used to, which might cause complications. "

    Full-text · Article · Jan 2015
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