Aim — to compare the features of diastolic dysfunction (DD) with preserved left ventricular (LV) ejection fraction (EF) in patients with diabetes mellitus type 2 (DM2) with arterial hypertension (AH) and in patients with essential hypertension (EH) without diabetes.Material and methods. The study involved 87 patients with DD with preserved LV EF: 53 patients with DM2 with AH and 34 patients EH without diabetes. Transthoracic echocardiography was performed by ultrasonic imaging system iE33 xMATRIX («Philips», USA). DD was determined in a complex: type on the basis of the ratio parameters of pulsed-wave (E/A) and tissue (e/a) Doppler; and severity on the Е/e values and pulmonary capillary wedge pressure (PCWP). Myocardial contractile function was assessed by traditional LVEF by Simpson and more exactly, in details on the basis of the longitudinal, radial and circular deformation of the LV myocardium by speckle-tracking echocardiography (using the program Q-lab 3.0 Advanced Ultrasound Quantification software).Results. The groups were comparable in clinical characteristics. The average level of HbA1c in patients with DM2 was 8.2±1.7%. The average LV EF by Simpson in the EH group was 59.9±8.1, in DM2 — 58.3±6.7 (p=0.228). There were more severe disorders of LV Diastolic function in DM2 patients: the values of E/e (p=0.000) and PCWP (p=0.001) were significantly higher in diabetic patients (14,1±5,5 and 15,3±4,7 mm Hg) than in EH (9.7±2.3 and 11.9±1.3 mm Hg). Although that the LV EF (by traditional echocardiographic method of Simpson) was preserved in both groups , the LV global longitudinal strain (12.4±3.0) was significantly lower in DM2 (p=0.005), than patients with EH (16.6±2.0) by speckle-tracking echocardiography.Conclusion. Severity of LV DD are harder in Patients with diabetes and hypertension, than in patients with EH with the similarity of clinical manifestations and data of traditional echocardiographic methods. There were found initial disorders of LV longitudinal myocardial fibers contraction by speckle-tracking echocardiography in patients with DM and preserved LV EF. The combination of impairment of systolic and diastolic function in diabetes is inseparable. Early development of combined systolic and diastolic dysfunction in DM2 is associated with a poor prognosis: a higher risk of early development of atrial fibrillation, ventricular arrhythmias and progressive heart failure.
Aim. To identify profibrogenic mediators, markers of endothelial dysfunction and hemostasis in patients with diabetes mellitus (DM) and chronickidney disease (CKD). Materials and methods. The study included 120 patients with DM and 20 age-matched normotensive subjects without DM showing the glomerularfiltration rate (GFR) > 60 ml/min/1.73 m3. Four groups of patients were distinguished: 1 - DM2 patients without renal pathology (n=33), 2 - DM2 patients with diabetic nephropathy (n=24), 3 - DM2 patients with ischemic nephropathy (IN) (n=33) verified by contrast visualization techniques(multispiral CM of abdominal aorta and renal arteries, abdominal angiography of renal arteries or MR angiography of renal arteries and abdominal aorta), 4 - DM1 patients with DN (n=30). Clinical examination included assessment of complaints, analysis of medical history of the main diseaseand concomitant disorders, determination of the main clinical and biochemical characteristics of blood and urine, measurement of НbА1с and 24-hralbuminuria (AU) by standard methods, estimation of GFR by the MDRD formula, ECG, echocardiography, 24-hr AP monitoring, counseling bycardiologist and ophthalmologist (fundal examination by ophthalmoscopy). Standard kits were used to detect profibrogenic mediators and markersof endothelial dysfunction including transforming growth factor-beta (TGF-b), angiotensin II (AT II), monocyte chemoattractant protein (MCP-1),regulated on activation normal T cell expressed and secreted (RANTES), adhesion factors (intracellular adhesion molecule (ICAM-1), vascular celladhesion molecule (VCAM-1) vascular endothelial growth factor (VEGF), interleukin-6 (IL-6), asymmetric dimethylargnine (ADMA), homocysteine(HCYST), metalloproteinases (MMP), von Willebrand factor (vWF), plasminogen activator inhibitor (PAI-I). Results. DM patients with CKD had elevated blood profibrogenic cytokine (MCP-1, TGF-1b, IL-6) and extracellular matrix degradation factor(MMP-9) levels compared with patients without CKD and healthy subjects. These changes were unrelated to the type of diabetes or the cause ofnephropathy, which suggests their contribution to renal pathology through the universal mechanism of tubulointerstitial fibrosis. Activation of profibrogeniccytokines in DM patients with CKD was closely associated with endothelial dysfunction manifest as enhanced production of blood adhesive angiogenic, thrombogenic factors (FW, PAI, VICAM, sICAM, VEGF), and endothelium-affecting factors (ADMA, homocysteine). Mediators of inflammationand fibrogenesis in these patients negatively correlated with GFR and positively with AU, the main markers of renal dysfunction. Hyperuricemia,TGF-1b, ADMA, and MCP-1 are considered to be the risk factors of impaired renal filtration function. Conclusion. The level of profibrogenic cytokines and ndothelial dysfunction factors in DM patients with different renal lesions reflects severity of tubulointerstitialfibrosis. It may be used for the purpose of prognostication and substantiation of intensification of secondary prophylaxis of renal insufficiency.
It is now well established that clinical use of statins for primary and secondary prevention of cardiovascular complications in patientswith diabetes mellitus (DM) increases life expectancy. At the same time, meta-analysis of major randomized trials shows statins to increaseglycemic levels and incidence of diabetic symptoms, especially in patients at risk for developing glycemic disorders. However,comparison of positive and negative effects of statins suggests prevalence of clinically beneficial factors.
It is known that hypoglycemia is associated with an increased risk of cardiovascular adverse events including death. ACE-inhibitors, when taken withantidiabetic drugs, can cause hypoglycemic episodes by improving insulin sensitivity. This clinical case illustrates the necessity to monitor plasmaglucose in the early phase of the treatment by the ACE-inhibitors in diabetic patients.
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