Key result
In young, asymptomatic patients, type 1 diabetes was associated with a progressive four-stage development of diabetic cardiopathy, which was confirmed in 94% of patients (p<0.001).
Observational (n=211)
p-value: p=<0.001
This study supports a 4-stage progression of diabetic cardiopathy in type 1 diabetes, starting with increased contractility, followed by diastolic dysfunction, and eventually systolic dysfunction.
Supports staged diabetic cardiopathy progression in asymptomatic type 1 diabetes; hypothesis-generating and requires prospective validation before screening adoption.
Based on our recent reports that increased myocardial contractility has been found in newly diagnosed diabetic patients, and that diastolic (D) dysfunction precedes systolic (S) dysfunction, we suggested that the development of diabetic cardiopathy passes through the following stages: (I) increased myocardial contractility, (II) intact S and D function, (III) intact S function and D dysfunction, and (IV) S and D dysfunction. The aim of this pilot study was to test this hypothesis. One hundred fifty‐seven young (26.2 ± 7.4 years) cardiac‐asymptomatic patients with type 1 diabetes and 54 healthy subjects were studied using M‐mode echocardiography. The presence of at least one of the variables for systolic function (ejection fraction, mean velocity of circumference, fiber shortening, and stroke index) or diastolic function [left atrium emptying index (LAEI), EFo slope of anterior mitral leaflet, and isovolu‐metric relaxation time (IRT)] outside the control mean ± 2 SD was interpreted as an increased or depressed myocardial contractility, and diastolic dysfunction, respectively. The severity of diabetic complications (retinopathy, nephropathy, and cardiac autonomic neuropathy) was evaluated by the diabetic complication index (DCI=0 + 6 scores). Our hypothesis was confirmed significantly (p< 0.001) in 148 (94%) patients with diabetes. Duration of diabetes and DCI progressed significantly (ANOVA: F = 36.6, p<0.001; F=70.8, p<0.001) with hypothetical stages. Diastolic dysfunction was more pronounced in stage IV than in stage HI: IRT (80.5 ± 18.6 ms vs. 62.5 ± 16.4, p<0.001), EFo (63 ± 15 mm/s vs. 72 ± 21, p<0.05), LAEI (0.58 ± 0.13 vs. 0.8 ± 0.15, p < 0.001). End‐diastolic volume/LV muscle mass ratio was reduced in stage III (0.73 ±0.16 ml/g) compared with the control value (0.83 ± 0.17, p < 0.01), but was higher than that in stage IV (0.65 ± 0.16, p < 0.05). The left atrium in stage HI (18.2 ± 3.7 mm/m2) was dilated compared with the control value (16.2 ± 3.3, p < 0.01) and more dilated in stage IV (19.6 ± 3.1, p<0.001). The present study demonstrates the following stage development of specific diabetic cardiac changes: (I) increased myocardial contractility; (II) intact S and D function; (III) initial D dysfunction, LV restriction and LA dilation with normal S function; and (IV) progression of the previous changes and appearance of S dysfunction.
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D. Raev (1993) conducted an observational in Type 1 diabetes (n=211). Type 1 diabetes vs. Healthy subjects was evaluated on Confirmation of the four hypothetical stages of diabetic cardiopathy development (p=<0.001). In young, asymptomatic patients, type 1 diabetes was associated with a progressive four-stage development of diabetic cardiopathy, which was confirmed in 94% of patients (p<0.001).
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