Key result
Higher body weight links strongly to increased LV diameter and cardiomyocyte hypertrophy on autopsy.
Why the study?
Human cardiomyocyte shapes and sizes are generally accessible only at autopsy, limiting study and leaving a major gap in understanding heart failure.
Observational (n=276)
No
Retrospective autopsy data suggests heart failure may result from changes in chamber geometry rather than contractile weakening.
Highlights potential geometric HF drivers in obesity; hypothesis-generating and should not yet change practice.
The shapes and sizes of human cardiomyocytes are accessible to systematic observation under most circumstances only at autopsy. This constraint has seriously curbed the study of these topics, thereby leaving a crippling gap in our understanding of heart failure. In recent years the only published ongoing findings have come from this laboratory. This article is a condensation of these reports, using those sources to develop fresh analyses designed to construct a set of organizing principles. The data are entirely retrospective thereby forbidding hypothesis testing and permitting only hypothesis formation. The hypotheses generated in this way are novel and surprising. In spite of the severe limitations in this methodology is seems possible that some useful new directions of inquiry might evolve from pursuing these original observations.
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Richard E Tracy (2019) conducted an observational in Left ventricular hypertrophy (n=276). Body weight and Type 2 hypertension vs. Normal body weight and normotension was evaluated on Cardiomyocyte longitudinal hypertrophy (LV diameter) and transverse hypertrophy (myocyte breadth) (R2 0.920 (BW vs LVD means); R2 0.203 (LVD vs MyB), p=<0.001).
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