Diabetic Cardiomyopathy: Current Approach and Potential Diagnostic and Therapeutic Targets

Gîlcă, Georgiana-Emmanuela; Ştefănescu, Gabriela; Bădulescu, Oana Viola; Tanase, Daniela-Maria; Bararu, Iris; Ciocoiu, Manuela

doi:10.1155/2017/1310265

Cited by 78 publications

(73 citation statements)

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“…With regard to our patient, the onset of the signs and symptoms, the radiologic appearance and clinical evolution support the diagnosis of type I negative pressure pulmonary edema. In the context of general anesthesia, the differential diagnosis includes other life threatening conditions: aspiration pneumonitis, acute respirator y distress syndrome (ARDS), postoperative residual curarization, cardiogenic pulmonary edema, neurogenic pulmonary edema, pulmonary embolism, anaphylaxis, drug induced pulmonary edema [1] and pulmonary edema secondary to diabetic decompensated cardiomiopathy [2].…”

Section: Resultsmentioning

confidence: 99%

Synthetic Phenylpiperidine Derivative Meperidine as a Trigger for Type I Negative Pressure Pulmonary Edema in General Anesthesia

Baracan¹,

Gavris²,

Poroch³

et al. 2017

Rev. Chim.

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We present a case of type I negative pressure pulmonary edema in a healthy 17-year-old boy who underwent an emergent appendectomy under general anesthesia. The particularity of our case revolves around the administration of meperidine for perioperative shivering, along with other anesthetic risk factors, which may have served as the trigger of type I negative pressure pulmonary edema.We present the pathophysiological mechanisms, the formulation of clinical and paraclinical diagnosis and the principles of intensive care therapy. This was the first such case experienced in our practice, with a remarkable learning opportunity.Negative pressure pulmonary edema (NPPE) is an acute, potentially life threatening, uncommon perioperative pathological entity. Two clinical types have been described: type I NPPE, associated with acute airway obstruction, and type II NPPE, associated with chronic partial upper airway obstruction. An early differential diagnosis between various pulmonary edema conditions in critically ill patients and a prompt recognition of high risk of acute morbidity are crucial in certain circumstances. We present a case of type I NPPE in a healthy 17-year-old boy who underwent an emergent appendectomy under general anesthesia. The particularity of our case revolves around the administration of meperidine, along with other anesthetic risk factors, which may have served as the trigger of NPPE. Experimental part Study case presentationA 17-year-old male patient without medical history presented with acute appendicitis. After evaluation in the emergency department, he was admitted for emergency appendectomy. His preoperative physical examination and laboratory tests were within normal limits except for neutrophilic leukocytosis.Physical status: height (H) = 1.60 m; weight (W) = 50 kg; body mass index (BMI) = 19.53 kg/m 2 ; airway assessment by Mallampati classification of oral opening -Mallampati I.Cardiovascular status: blood pressure (BP) = 117/59 mmHg; heart rate (HR) = 75 bpm; heart auscultationnormal.Respiratory status: chest auscultation was clear bilaterally, without murmurs. His baseline pulse oximetry arterial blood oxygen saturation (SpO 2 ) was 99% on room air, with a fraction of inspired oxygen (FiO 2 ) of 0.21. * email: claudiagavris@yahoo.com, Phone: +40723791322; vlader2000@yahoo.com, Phone: +40723271972 Laboratory blood investigations: hemoglobin (Hgb) = 15.2 g/L; hematocrit (Hct) = 42%; leukocytes (L) = 9,450/ µL (neutrophils = 90%); platelets (PLT) = 221,000/µL; activated partial prothrombine time (aPTT) = 24.4 s; international normalized ratio (INR) = 1.09; serum proteins = 71 g/L; fibrinogen = 3.22 g/L; C-reactive protein (CRP) = 11.3 mg/L; glycemia = 110 mg/dL; serum Na + = 135 mmol/L; serum K + = 4.1 mmol/L; serum Cl -= 98,5 mmol/ L; serum total calcium = 9.43 mg/dL; serum Mg + = 1.81 mg/dL; aspartate aminotrasferase (AST) = 20 U/L; alanine aminotransferase (ALT) = 18 U/L; lactate dehidrogenase (LDH) = 374 U/L; blood urea nitrogen (BUN) = 33.3 mg/ dL; creatinine = 1.06 mg/dL.The patient w...

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Section: Resultsmentioning

confidence: 99%

Synthetic Phenylpiperidine Derivative Meperidine as a Trigger for Type I Negative Pressure Pulmonary Edema in General Anesthesia

Baracan¹,

Gavris²,

Poroch³

et al. 2017

Rev. Chim.

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“…Cardiovascular-related complications are responsible for approximately 65% of diabetic death [29]. among which DCM leads to diastolic dysfunction and further systolic dysfunction, and eventually greatly increases the risk of heart failure [10]. Myocardial fibrosis and hypertrophy, as well as cardiomyocyte apoptosis, are vital contributors in the onset and progression of DCM [9].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 attenuates high glucose-induced cardiomyocyte apoptosis via regulation of miR-181a-5p

et al. 2020

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Diabetic cardiomyopathy (DCM) is one of the cardiovascular complications of diabetes mellitus independent of hypertension, coronary disease, and other heart diseases. The development of DCM is multifactorial and hard to detect at an early stage. Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (Malat1) is emerging as a regulator of DCM, the underlying mechanism of its role in DCM has not been elaborated yet. In this study, we established a mouse DCM model via streptozocin injection as evidenced by cell hypertrophy and cell apoptosis of myocardial tissue, and found that Malat1 expression was upregulated in the myocardium in DCM mice. Meanwhile, elevated expression of pro-apoptotic factors p53, p21, cleaved caspase 3, cleaved caspase 9 and BAX, and down-regulation of anti-apoptotic BCL-2 were observed in DCM myocardium. We further investigated the effect of Malat1 on cardiomyocytes under high glucose condition by silencing Malat1 with its specific shorthairpin RNA. Like in vivo, expression of Malat1 in cardiomyocytes was notably raised, remarkable cell apoptosis and changes in apoptosis-related factors were also observed following high glucose treatment. Besides, we validated that Malat1 acted as a sponge of miR-181a-5p. Inhibition of miR-181a-5p could, at least partially, abolish Malat1 knockdown-induced alteration in cardiomyocytes. In addition, p53, a critical regulator of apoptosis, was validated to be a downstream target of miR-181a-5p. In summary, our findings reveal that Malat1 knockdown attenuates high glucose-induced cardiomyocyte apoptosis via releasing miR-181a-5p, and this mechanism may provide us with new diagnosis target of DCM.

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“…DM is characterized by high blood glucose and leads to multiple complications including diabetic retinopathy, diabetic nephropathy, and diabetic neuropathy (Baba and Ishizaki, 1992;Chen et al, 2017;Hung et al, 2017;Ung et al, 2017). Of these, DCM is a major complication, causing high morbidity and mortality (Frati et al, 2017;Gilca et al, 2017;Hu et al, 2017). Evidence indicates that Chinese traditional medicine and phytomedicine have beneficial effects on diabetic complications including DCM.…”

Section: Discussionmentioning

confidence: 99%

Silymarin ameliorates diabetic cardiomyopathy via inhibiting TGF‐β1/Smad signaling

Meng

Yang

Wang

et al. 2018

Cell Biology International

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Diabetic cardiomyopathy (DCM) is the leading cause of morbidity and mortality in diabetes mellitus (DM) patients. Previous studies have shown that the transforming growth factor-beta 1 (TGF-b1)/Smad signaling pathway plays a key role in the development of myocardial fibrosis in DCM. Silymarin (SMN) is used clinically to treat liver disorders and acts by influencing TGF-b1. However, the possible effects of silymarin on DCM remain to be elucidated. In our study, the DM animal model was induced by streptozotocin (STZ) injection. Fasting blood glucose level was measured, and the structure and function of the heart were measured by hematoxylin and eosin (H&E) and Masson staining, echocardiography, and transmission electron microscopy (TEM). Western blot was used to detect the expression of TGF-b1, Smad2/3, phosphorylation Smad2/3(p-Smad2/ 3), and Smad7. Our results showed that silymarin downregulated blood glucose level and significantly improved cardiac fibrosis and collagen deposition in DM rats detected by H&E, Masson staining, and TEM assays. The echocardiography results showed that silymarin administration attenuated cardiac dysfunction in DM rats. Additionally, compared with untreated DM rats, levels of TGF-b1 and p-Smad2/3 were decreased, whereas Smad7 was increased following silymarin administration. These data demonstrate that silymarin ameliorates DCM through the inhibition of TGF-b1/Smad signaling, suggesting that silymarin may be a potential target for DCM treatment.

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Diabetic Cardiomyopathy: Current Approach and Potential Diagnostic and Therapeutic Targets

Cited by 78 publications

References 50 publications

Synthetic Phenylpiperidine Derivative Meperidine as a Trigger for Type I Negative Pressure Pulmonary Edema in General Anesthesia

Synthetic Phenylpiperidine Derivative Meperidine as a Trigger for Type I Negative Pressure Pulmonary Edema in General Anesthesia

Inhibition of long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 attenuates high glucose-induced cardiomyocyte apoptosis via regulation of miR-181a-5p

Silymarin ameliorates diabetic cardiomyopathy via inhibiting TGF‐β1/Smad signaling

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