Category Archives: Ventricular Remodeling

"Ventricular Remodeling" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure, which enables searching at various levels of specificity. The geometric and structural changes that the HEART VENTRICLES undergo, usually following MYOCARDIAL INFARCTION. It comprises expansion of the infarct and dilatation of the healthy ventricle segments. While most prevalent in the left ventricle, it can also occur in the right ventricle. C23.300.985 G09.330.190.962.975 Below are MeSH descriptors whose meaning is more general than "Ventricular Remodeling". Below are MeSH descriptors whose meaning is more specific than "Ventricular Remodeling". This graph shows the total number of publications written about "Ventricular Remodeling" by people in this website by year, and whether "Ventricular Remodeling" was a major or minor topic of these publications. Below are the most recent publications written about "Ventricular Remodeling" by people in Profiles. Wenk JF, Klepach D, Lee LC, Zhang Z, Ge L, Tseng EE, Martin A, Kozerke S, Gorman JH, Gorman RC, Guccione JM. First evidence of depressed contractility in the border zone of a human myocardial infarction. Ann Thorac Surg. 2012 Apr; 93(4):1188-93. Xu EZ, Kantores C, Ivanovska J, Engelberts D, Kavanagh BP, McNamara … Continue reading →

Introduction Venous thromboembolic disease (VTE) is estimated to occur in at least 1 to 2 persons per 1000 population annually, manifesting as deep vein thrombosis (DVT), pulmonary embolism (PE) or in combination.1-3 It is the cause of over 100,000 deaths annually and is the most preventable cause of death in hospitalized patients in the United States.4 Despite treatment with anticoagulant therapy, a significant proportion of survivors of acute DVT or PE are at risk of suffering from the disabling sequelae such as the post thrombotic syndrome (PTS), recurrent VTE or chronic thromboembolic pulmonary hypertension (CTEPH).1,5 Given the limitations of medical therapy, promising endovascular treatment modalities have evolved over the past two decades in an effort to mitigate the acute and chronic disability from VTE.6,7 The purpose of this review is to discuss the rationale and evidence for an endovascular treatment approach for high-risk acute DVT and PE patients. The Rationale for an Interventional Approach to Massive and Submassive PE The most dreaded acute complication of PE is death; it is estimated that over 100,000 deaths in hospitalized patients in the United States are attributable to acute PE each year.4 The severity of PE is stratified into massive (PE causing hemodynamic … Continue reading →

Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol. 1993 Oct. 22 (4 suppl A):6A-13A. [Medline]. [Full Text]. American Heart Association. Classes of heart failure. Available at http://www.heart.org/HEARTORG/Conditions/HeartFailure/AboutHeartFailure/Classes-of-Heart-Failure_UCM_306328_Article.jsp#.WUcGf-vyuHs. Updated: May 8, 2017; Accessed: June 18, 2017. [Guideline] Yancy CW, Jessup M, Bozkurt B, et al, American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. 2013 Oct 15. 128(16):e240-327. [Medline]. [Full Text]. [Guideline] Ponikowski P, Voors AA, Anker SD, et al, for the Authors/Task Force Members. 2016 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure: The task force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur Heart J. 2016 Jul 14. 37 (27):2129-200. [Medline]. [Full Text]. [Guideline] Lindenfeld J, Albert NM, Boehmer JP, et al, for the Heart Failure Society of America. HFSA 2010 comprehensive heart failure practice guideline. J Card … Continue reading →

A ventricular septal defect (VSD) is a defect in the ventricular septum, the wall dividing the left and right ventricles of the heart. The extent of the opening may vary from pin size to complete absence of the ventricular septum, creating one common ventricle. The ventricular septum consists of an inferior muscular and superior membranous portion and is extensively innervated with conducting cardiomyocytes. The membranous portion, which is close to the atrioventricular node, is most commonly affected in adults and older children in the United States.[1] It is also the type that will most commonly require surgical intervention, comprising over 80% of cases.[2] Membranous ventricular septal defects are more common than muscular ventricular septal defects, and are the most common congenital cardiac anomaly.[3] Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth. VSD is an acyanotic congenital heart defect, aka a left-to-right shunt, so there are no signs of cyanosis in the early stage. However, uncorrected VSD can increase pulmonary resistance leading to the reversal of the shunt and corresponding cyanosis. The restrictive VSDs (smaller defects) are associated with a louder murmur and more palpable thrill (grade IV murmur). Larger defects may eventually … Continue reading →

The ejection fraction is a measurement doctors very commonly use to assess how well the heart is able to pump blood. Specifically, the ejection fraction is the proportion of blood that is pumped from the left ventricle (the main pumping chamber of the heart) with each heart beat. Typically, the left ventricle ejects 55% or more of its blood volume with each beat, so a "normal" ejection fraction is 55% (0.55) or higher. An ejection fraction of 40 - 50% is considered below normal. Patients with heart failure most often have ejection fractions that are less than 40%. It is important to note that when doctors say the words ejection fraction they are referring to the ejection fraction of the left ventricle. More properly this would be called the left ventricular ejection fraction or LVEF and you may sometimes see or hear this terminology. The right ventricle also has its own ejection fraction (the right ventricular ejection fraction, or RVEF). However, the RVEF is rarely mentioned or talked about by doctors (partly because it is much more difficult to measure than the LVEF, and partly because knowing the precise RVEF is usually not particularly useful.) When your doctor says ejection … Continue reading →

Vol 4, No 4 (Winter 2005) Pulmonary arterial hypertension (PAH) is a disorder characterized by progressive elevation of pulmonary artery pressure (PAP) and vascular resistance in the absence of left-sided cardiac disease, pulmonary vein compression, respiratory disorders, or thromboembolic disease. It is defined by a mean PAP over 25 mmHg at rest or over 30 mmHg with exercise and a pulmonary artery occlusion pressure (PAOP) of less than 15 mmHg. PAH is associated with a poor prognosis. The estimated median survival from diagnosis is 2.8 years and the 1-year and 5-year survival rates are only 68% and 34%, respectively.1 2 More than 70% of PAH patients will die as a result of right ventricular failure and most of the remainder from dysrhythmia. Predictors of a poor prognosis in PAH are related to the development of right ventricular failure.3 4 5 The objectives of this review are to examine the pathophysiologic mechanisms leading to the development of right ventricular failure due to PAH, the diagnostic features of right ventricular failure, and the management of chronic right ventricular failure with emphasis on acute decompensation in this setting. Clinical Manifestations and Hemodynamic DerangementsThe normal right ventricle is a thin-walled (less than 0.6 cm), … Continue reading →