# Old and Novel Predictors for Cardiovascular Risk in Diabetic Foot Syndrome--A Narrative Review
## 5 Discussions
### Diabetic Foot Syndrome and Diabetic Cardiomyopathy  
The identification among diabetic patients of a multitude of cardiovascular risk factors such as smoking, hypertension and dyslipidemia (\(p\) < 0.05 for each one) with both short- and long-term prognostic value led to the investigation of echocardiographic parameters associated with increased cardiovascular risk [165]. LV systolic dysfunction is initially assessed by reduced longitudinal function, at which stage the ejection fraction is maintained within normal limits by radial and circumferential compensation. Literature data attest to improvement of echocardiographic strain parameters in subclinical systolic dysfunction secondary to treatment of hypertension and obesity in patients with diabetes mellitus [166]. Most patients with DFS also have associated diabetic cardiomyopathy, defined as the presence of systolic dysfunction or at least moderate diastolic dysfunction, independent of the presentation of LV modulation in the absence of chronic ischemic heart disease, hypertension, valvular heart disease or congenital heart disease [167]. Diabetes mellitus induces a number of phenotypic changes assessed by LV mass and LV systolic or diastolic function (Figure 3). Patients with DFS need multimodal imaging evaluation with the aim of early identification of myocardial damage and identification of determinants associated with heart failure [167; 168; 169; 170; 171; 172; 173]. Myocardial fibrosis, microcirculatory damage, metabolic disorders and disorders of cardiac innervation are the pathophysiological mechanisms underlying the development of diabetic cardiomyopathy in patients with DFS. Clinical studies in the literature emphasize the role of renin-angiotensin-aldosterone system dysfunction, oxidative stress, pro-inflammatory status or endothelial dysfunction in the development of systolic and diastolic dysfunction in patients with DFS [174; 175]. Concentric LV hypertrophy in patients with DFS is a common finding secondary to associated lipotoxicity which results in excess lipid accumulation in cardiomyocytes and thus systolic dysfunction [176; 177; 178]. [PERSON] et al. [165] investigated for the first time the change in echocardiographic parameters (ejection fraction, strain parameters) secondary to DF treatment [181]. These investigators analyzed two groups of patients, the first with 54 patients with diabetic foot and the second with 22 patients without diabetic foot, demonstrating that LV dimensions were larger and LV ejection fraction smaller in the group of patients with diabetic foot (\(p<0.05\)). Dynamic assessment of echocardiographic parameters 3 months after the start of diabetic treatment showed a statistically significant improvement in strain parameters of systolic function (\(p<0.001\)), but without an increase in ejection fraction (\(p=0.747\)). A significant proportion of patients with DFS associate heart failure with preserved left ventricle ejection fraction (LVEF), so that the identification in these patients of concentric hypertrophy as well as increased relative wall thickness suggests subclinical involvement [182]. The results of the Irbesartan in Heart Failure With Preserved Ejection Fraction (I-PRESERVE) trial published in 2018 targeted a number of echocardiographic changes in patients with DM such as increased LV size and mass and increased filling pressures (assessed using the E/e\({}^{\prime}\) ratio) in the presence of normal systolic function and mitral annular systolic velocity (similar to patients without DM) [183; 184; 185]. Modern echocardiographic assessment techniques such as speckle tracking reveal alterations in systolic strain that are considered preclinical changes of diabetic cardiomyopathy-opathy [167]. In some patients only changes in longitudinal systolic function compensated by an increase in radial systolic function have been identified, while the majority of cases associate a dysfunction involving both types of alterations [186; 187; 188].