Clinical Trial: Training-induced Increased Left Ventricular Trabeculation

Study Status: Completed
Recruit Status: Completed
Study Type: Observational

Official Title: Increased Left Ventricular Trabeculation in Athletes - a Marker of Left Ventricular Non-compaction or a Physiological Epiphenomenon of Increased Cardiac Preload?

Brief Summary: This project will expand on research conducted by the investigators' group, where the investigators have demonstrated increased LV trabeculation, satisfying currently existing criteria for LV Non-Compaction Cardiomyopathy (LVNC), in groups exposed to high cardiac workloads. To the investigators' knowledge, this will be the first prospective study aiming to demonstrate a direct relationship between high levels of exercise and increased LV trabeculation. This study may add weight to the theory that this entity currently described as LVNC, is a morphological epiphenomenon common to many distinct myocardial remodeling processes associated with increased cardiac preload and afterload and may better define normal adaptive increases in LV trabeculation.

Detailed Summary:

Background of Left Ventricular Non-Compaction Cardiomyopathy Left Ventricular Non-Compaction Cardiomyopathy (LVNC) is a myocardial disorder defined by increased left ventricular (LV) trabeculation and intertrabecular recesses communicating with the LV cavity. The condition is associated with progressive heart failure, systemic thromboembolism and a predilection to fatal ventricular arrhythmia and sudden cardiac death. However, a large proportion of affected individuals may be asymptomatic. One cohort study demonstrated 28% of detected cases of LVNC were asymptomatic, with the majority being identified through family screening. It must be emphasized that currently there is no diagnostic tool, neither genetic nor imaging, that can categorically identify an individual as having LVNC or not. This lack of a 'gold standard' makes the description of increased left ventricular trabeculation difficult, creating a tendency to apply a diagnostic label of LVNC inappropriately.

Traditional thought has been that LVNC results from arrest of the normal trabecular regression and myocardial compaction that occurs during embryological development. However, this concept is challenged by reported cases of 'acquired' LVNC, where serial echocardiograms have demonstrated a transition from a normal endocardial appearance to a hypertrabeculated LVNC phenotype. Whether this is a delayed presentation of a genetically heterogeneous cardiomyopathy or a morphological epiphenomenon shared by many phenotypically distinct cardiomyopathies, remains unknown. This irresolution is exemplified by international discordance, with the American Heart Association classifying LVNC as a genetic cardiomyopathy and the European Society of Cardiology and World Health Organisation taking the view that LVNC remains an 'unclassified cardiomyopathy'.

In the absence of congen
Sponsor: St George's, University of London

Current Primary Outcome:

• Thickness of non-compacted myocardial tissue (mm) [ Time Frame: 7 months ]
  Measured on echocardiography and cardiac MRI
• Thickness of compacted myocardial tissue (mm) [ Time Frame: 7 months ]
  Measured on echocardiography and cardiac MRI
• Myocardial fractal dimension [ Time Frame: 7 months ]
  Measured on cardiac MRI

Original Primary Outcome: Same as current

Current Secondary Outcome: Increase in peak VO2 on CPET during training [ Time Frame: 7 months ]

Original Secondary Outcome: Same as current

Information By: St George's, University of London

Dates:
Date Received: September 28, 2015
Date Started: October 2015
Date Completion:
Last Updated: October 17, 2016
Last Verified: October 2016