CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 3, September – October 2024 AFRICA 151 have a trophic effect on the IVS but also a deleterious effect on diastolic function. These findings make the thorny question of ‘the egg and the chicken’ between IR and hyperinsulinaemia appear as a watermark. The cause–effect relationship between IR and hyperinsulinaemia is still debated, since these two conditions are closely associated. It is possible that the two conditions are related by a reciprocal causal relationship, since there are plausible physiopathological explanations justifying the role of the ‘chicken or egg’ for each of the conditions, respectively. The pathophysiological mechanisms by which IR promotes LVH and diastolic dysfunction have been the subject of several experimental studies.22-24 The startingpoint of a complexmetabolic cascade during IR, culminating in structural and functional anomalies of the left ventricle, is the almost exclusive recourse HOMAIR –1 0.75 2.5 4.25 6 LVED (mm) 200 137.5 75 12.5 –50 r = 0.298 p < 0.001 Fig. 1. HOMAIR and left ventricular end-diastole diameter. HOMAIR –1 0.75 2.5 4.25 6 IVS (mm) 50 35 20 5 –10 r = 0.416 p < 0.001 Fig. 2. HOMAIR and interventricular septum. HOMAIR –1 0.75 2.5 4.25 6 PWT (mm) 40 27.5 15 2.5 –10 r = 0.426 p < 0.001 Fig. 3. HOMAIR and posterior wall thickness. HOMAIR –1 0.75 2.5 4.25 6 SWT 100 70 40 10 –20 r = 0.441 p < 0.001 Fig. 4. HOMAIR and sum of wall thickness. HOMAIR –1 0.75 2.5 4.25 6 LVMlh (g/m2.7) 200 137.5 75 12.5 –50 r = 0.239 p < 0.001 Fig. 5. HOMAIR and left ventricular mass indexed to height2.7. HOMAIR –1 0.75 2.5 4.25 6 LVMlbsa (g/m2) 350 237.5 125 12.5 –100 r = 0.249 p < 0.001 Fig. 6. HOMAIR and left ventricular mass indexed to body surface area.
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