Microcirculatory and glycolytic metabolism evaluation in isolated noncompaction cardiomyopathy

• Grant number: 10/18939-3
• Support Opportunities: Regular Research Grants
• Start date: March 01, 2011
• End date: August 31, 2013
• Field of knowledge: Health Sciences - Medicine - Medical Clinics
• Principal Investigator: Vera Maria Cury Salemi
• Grantee: Vera Maria Cury Salemi
• Host Institution: Instituto do Coração Professor Euryclides de Jesus Zerbini (INCOR). Hospital das Clínicas da Faculdade de Medicina da USP (HCFMUSP). Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil

Abstract

The non-compacted cardiomyopathy (MCNC) is a rare disorder characterized by the following aspects: a) change in the myocardial wall due to the prominence of its trabeculae with intertrabecular recesses that may be secondary to intrauterine arrest of myocardial compaction, the result is the myocardium featuring two blades with one another and compressed non-compressed b) continuity between the left ventricular cavity and intertrabecular recesses being filled with blood from the left without communication with the epicardial coronary system, c) reduction of coronary flow reserve, as assessed by PET scanning, being seen in most segments that have abnormalities of ventricular wall movement. The diagnosis of MCNC is usually determined by echocardiography. However, other imaging modalities such as MRI, CT and ventriculography can diagnose or confirm the clinical suspicion. The differential diagnosis of MCNC includes dilated cardiomyopath y, hypertensive heart disease, apical hypertrophic cardiomyopathy, infiltrative cardiomyopathy and endomyocardial disease eosinofílica.Anormalidades in myocardial perfusion may play a crucial role in the pathophysiology of CHF, arrhythmias and sudden death. In a recent study with PET analysis 63 found a significant decrease in microcirculatory flow in response to adenosine infusion. Microcirculatory dysfunction not only remained in segments trabeculation, but also in places without trabeculae, suggesting a diffuse disease. It seems reasonable to assume that microcirculatory dysfunction may be responsible for the worsening of myocardial contractility. (AU)

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

TAVARES DE MELO, MARCELO DANTAS; PINTO GIORGI, MARIA CLEMENTINA; ASSUNCAO, JR., ANTONILDES NASCIMENTO; DANTAS, JR., ROBERTO NERY; ARAUJO FILHO, JOSE DE ARIMATEIA; PARGA FILHO, JOSE RODRIGUES; DE SOUZA BIERRENBACH, ANA LUIZA; DE LIMA, CAMILA ROCON; SOARES, JR., JOSE; MENEGUETTI, JOSE CLAUDIO; et al. Decreased glycolytic metabolism in non-compaction cardiomyopathy by F-18-fluoro-2-deoxyglucose positron emission tomography: new insights into pathophysiological mechanisms and clinical implications. EUROPEAN HEART JOURNAL-CARDIOVASCULAR IMAGING, v. 18, n. 8, p. 915-921, AUG 2017. (10/18939-3)